International Diabetes Federation – evidence for 1-hour glucose assessor

International Diabetes Federation has just released a new Position Statement that indicates that an oral glucose tolerance test performed at 1-hour after a glucose load is more effective in screening at-risk individuals for prediabetes and type 2 diabetes than a 2-hour Oral Glucose Tolerance Test (OGTT). 

The International Diabetes Federation is a non-profit umbrella organization of more than 240 national diabetes associations from 161 countries including the United States (represented by the American Diabetes Association), Canada, Australia, as well as many countries in Europe, Asia and Africa. This global reach means that the IDF’s reports and recommendations have significant international implications.

This international Position Statement provides the evidence to support the practice of requisitioning a 1-hour post load glucose test in place of 2 hour Oral Glucose Tolerance Test to diagnose prediabetes and type 2 diabetes in at-risk individuals.

For physicians who prefer to choose to continue to order a 2-hour Oral Glucose Tolerance Test, this new Position Statement provides support for adding an additional extra assessor at 1-hour, something I have asked for over the last several years based on existing evidence

Prediction of Risk of Type 2 Diabetes

The new Position Statement highlights that a 1-hour post-load plasma glucose level of 8.6 mmol/L (155 mg/dL) or higher during in people with normal glucose tolerance strongly predicts the development of type 2 diabetes as well as various complications such as micro- and macrovascular issues, obstructive sleep apnea, metabolic dysfunction-associated fatty liver disease, and death in individuals with risk factors. The recommendations are for  individuals with 1-hour plasma glucose of 8.6 mmol/L (155 mg/dL) or higher to be prescribed lifestyle intervention and referred to a diabetes prevention program.

Diagnosis of Type 2 Diabetes

The Position Statement indicates that a  1-hour post-load plasma glucose level of 11.6 mmol/L (209 mg/dL) or higher confirms a diagnosis of type 2 diabetes and recommends that a repeat test be conducted to confirm the diagnosis of type 2 diabetes and once confirmed, to refer the individual for treatment.

Benefits of the 1-hour Post-Load Glucose Test

The Position Statement indicates that the 1-hour post glucose load test;

    1. shows glucose dysregulation earlier than the 2-hour post glucose load test
    2. provides an opportunity to avoid misclassification of glucose status if fasting blood glucose or HbA1c are used alone.
    3. predicts diabetes and associated complications including death in populations of different ethnicity, sex and age
    4. allows for early detection in high-risk individuals which enables the ability to provide intervention to prevent a progression to type 2 diabetes.

Conclusion

The conclusion of the International Diabetes Federation Position Statement is that there is strong evidence to support redefining current diagnostic criteria for prediabetes and type 2 diabetes to include testing at 1-hour post glucose during an Oral Glucose Tolerance Test.

Final Thoughts

There is strong evidence for the use of a 1-hour post glucose load test to diagnose or rule out prediabetes or type 2 diabetes in at-risk individuals.

Most significantly, use of the 1-hour post glucose load test allows for early detection and provision of dietary and lifestyle intervention support to prevent the progression to type 2 diabetes. 

To your good health,

Joy

 

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/

Reference

 

  1. Bergman M,  Manco M., Satman I., et al, International Diabetes Federation Position Statement on the 1-hour post-load plasma glucose for the diagnosis of intermediate hyperglycaemia and type 2 diabetes, Diabetes Research and Clinical Practice, Vol. 209, 111589, March 6, 2024 https://doi.org/10.1016/j.diabres.2024.111589

 

Copyright ©2024 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

 

Nutrition is BetterByDesign

DEXA Bone Density Scans – accuracy depends on where it is done

If you are considering having a DEXA bone density scan to assess your risk of osteoporosis, where you have it done will significantly impact the accuracy of the results, and whether they will provide you with the information you want.

While dual-energy X-ray absorptiometry (DEXA) bone density scans are considered the gold standard for assessing bone mineral density (BMD), it is important to note that there is a large difference in the accuracy of DEXA scans obtained from non-accredited imaging centers offering bone density scans as a service, and facilities specializing in bone densitometry (the clinical assessment of bone density). An accurate scan enables doctors to rule out or establish a diagnosis and provides opportunity for timely treatment recommendations, including dietary and lifestyle modifications.

To illustrate the difference, the first part of the article will explain the standards for accredited facilities, and then contrast them to non-accredited imaging centers. This comparison will underscore the differences between the two.

Accredited Facilities for DEXA Bone Density Scans

For bone density scan data to be reliable in ruling out or diagnosing osteopenia or osteoporosis, it’s important that the scans are conducted by a trained bone densitometry technologist, in a facility that adheres to accreditation standards established by the International Society for Clinical Densitometry (ISCD), and in Canada, by the local College of Physicians and Surgeons of the province. Finally, the scans must be reviewed by a Radiologist, a doctor who specializes in medical imaging before a report is generated.

In British Columbia, the accreditation of bone densitometry facilities as well ensuring that bone densitometry technologists have the appropriate training is overseen by the College of Physicians and Surgeons of British Columbia (CPSBC). They operate the Diagnostic Accreditation Program (DAP), which ensures the quality and safety of a range of diagnostic services, including DEXA bone density scans. The DAP not only verifies that a facility meets the necessary quality standards but ensures that they consistently maintain those standards.

Accredited facilities must adhere to the Accreditation Standards for Diagnostic Imaging from the College of Physicians and Surgeons(1). This comprehensive 312 page document contains imaging standards for x-rays, mammograms, ultrasounds, MRIs , with the standards for bone densitometry beginning on page 274. These standards ensure the quality and safety of bone density scanning procedures.

These standards also outline that bone densitometry facilities must have a Medical Director overseeing operations, and that bone densitometry technologists performing scans must either be certified with the International Society for Clinical Densitometry (ISCD), or have obtained 12 Continuing Medical Education (CME) credits in bone densitometry. Additionally, technologists in accredited facilities are mandated to regularly update their knowledge by acquiring 24 CME credits in bone densitometry every three years.

Summary of the Accreditation Standards for Diagnostic Imaging for Bone Densitometry

The bone densitometry section of the Accreditation Standards for Diagnostic Imaging (1) consists of ten pages of standards, including;

    • patient preparation for the exam
    • standard imaging procedure protocols to ensure that the examination is appropriate for its intended use in clinical decision making
    • ensuring that current and accurate medical records are kept for each person
    • that diagnostic reports are in a standardized format and provide comprehensive and necessary information for clinical decision making / interpretation 
    • safe operation and maintenance of equipment
    • acceptance testing for equipment to ensure it is tested prior to use, and  quality assurance programs to ensure that the required quality is attained

These standards provide additional mandatory requirements and best practices that supplement the accreditation standards established by the International Society for Clinical Densitometry (ISCD) (2).

Below is the first of the ten pages of standards (this page is on patient preparation).

from page 375 of 312, CPSBC Accreditation Standards for Diagnostic Imaging for Bone Densitometry (1)
from page 375 of 312, CPSBC Accreditation Standards for Diagnostic Imaging for Bone Densitometry (1)

These standards require that the following information be collected before a bone density scan takes place.

(1) taking clinically relevant medical history, including family history, prior fractures, bone trauma, surgery, chronic illness, and any relevant medication that may affect bone density (such as corticosteroids, or thyroid medication),

(2) ensuring that the person has not had any procedures such as a barium x-ray or radionucleotide study that can affect the results,

(3) assessing whether the person has arthritis, deformity or other degenerative changes that can affect measurement,

(4) ensuring the person hasn’t had any implants in the area being assessed, such as a hip replacement,

(5) that a qualified physician is involved in assessing any interference or contraindications,

(6) review of previous bone density scans to determine if a specific site should be excluded from the current scan,

(7) patient height and weight are accurately measured at the time of examination.

None of this, or any of the other 9 pages of standards are required to be followed in an imaging center that provides bone density scans as a service. 

Imaging Center Providing DEXA bone density scans

Imaging centers that provide DEXA bone density scans as a service are business, and are not clinically regulated.  There are no physicians or radiologists involved. These business are not required to meet the international standards of the International Society for Clinical Densitometry (ISCD), or local clinical standards outlined above.

While these centers need to assess height, a construction tape measure attached to the wall with tape may be used, instead of a stadiometer.

Weight may not be asked but rather calculated from the results of a whole body composition scan performed at the same time.

Questions about personal medical history, family medical history, risk factors, medications or procedures that could affect results will be limited.

Image Quality

In accredited facilities, rigorous standards are in place to ensure high image quality, as all scans undergo review by a radiologist prior to report generation.

Images are required to be clear and well defined, such as the top pair of images from HealthLink BC (3). 

Images from imaging centers, such as the pair of images on the bottom often lack the contrast and definition which limits their usefulness.

 

Measurement Accuracy – hips

For hip scans to be useful in diagnosing osteoporosis, it is essential that the neck of the femur (hip bone) is measured at the narrowest part (4), such as the image on the far right (4).

The image on the left from an imaging center does not measure the neck of the femur at the narrowest part, and as illustrated in the middle image, the narrowest part is to the right of where it was measured.

Measurement Accuracy – spine

Spinal images from accredited facilities (left photo from (4)) are clear, and show equal amounts of soft tissue on either side of the spine. In addition, the height of each vertebrae is roughly the same height, with markers in the disk space (4).

   

The image on the right from an imaging center is not clear and has little contrast. It does not show equal amounts of soft tissue on either side of the spine, and the height of each vertebrae varies considerably.

Finding an Accredited Facility

In British Columbia, a full list of accredited diagnostic imaging facilities in the province is available on the College of Physicians and Surgeons web site (5).

The International Society for Clinical Densitometry (ISCD) has a searchable list of accredited facilities by country, as well as US states and Canadian provinces.

The College of Physicians and Surgeons in your province or state may also have a list.

Final Thoughts…

For data from a DEXA bone density scan to be reliable and useful for ruling out or diagnosing osteopenia or osteoporosis, it needs to be performed at an accredited facility.

This can be compared to the difference between home lab test testing and lab tests. While at-home blood testing kits are available to screen for different conditions, diagnoses of a medical condition requires blood tests from an accredited laboratory that are reviewed and assessed by a physician.

If you want to have a DEXA bone density scan to assess your risk of osteoporosis, then speak with your doctor to get a referral to an accredited facility.

How I Can Help

If you have been diagnosed as being at risk for osteoporosis, or have been diagnosed with osteopenia or osteoporosis, implementing appropriate dietary and lifestyle changes can be beneficial.  Please let me know if you would like some support.

To your good health,

Joy

 

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

  1. College of Physicians and Surgeons of British Columbia, Accreditation Standards, Diagnostic Imaging, https://www.cpsbc.ca/accredited-facilities/dap/accreditation-standards-DI
  2. International Society for Clinical Densitometry (ISCD), Official Positions, DEXA Best Practices, https://iscd.org/wp-content/uploads/2021/08/Best-Practices-DXA-Article.pdf
  3. Health Link BC, Bone Density Tests, Treatments, Medications Categories, Media Gallery, https://www.healthlinkbc.ca/tests-treatments-medications/medical-tests/bone-density
  4. Bone Health & Osteoporosis Foundation, DXA Basics- ISO 2021 Interdisciplinary Symposium on Osteoporosis ISO 2024, https://interdisciplinarysymposiumosteoporosis.org/
  5. College of Physicians and Surgeons of British Columbia, Provisional Accreditation Facilities – Diagnostic Imaging, https://www.cpsbc.ca/files/pdf/DAP-Accredited-Facilities-DI.pdf

 

Copyright ©2024 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Nutrition is BetterByDesign

 

DEXA Body Composition Scans as Assessors of Bone Density

DEXA Bone Density Scans are the gold standard for assessing the quality of the inside of bone, and determining whether a person has osteopenia or osteoporosis. More on those scans, soon.

A DEXA Body Composition Scan is designed for assessing the amount of body fat and the distribution of that fat, yet often come with a report that includes “bone mineral density” information. It is essential to understand that “bone mineral density” on a DEXA Body Composition Scan is estimated, not measured. 

This article is about the DEXA Body Composition Scan and what information it reliably provides.

NOTE: (February 14, 2024) If you are thinking of having a DEXA Body Composition Scan, be sure the facility you choose is accredited by the College of Physicians and Surgeons in your area.  More on this in the next article!

DEXA Body Composition Scan

The DEXA Body Composition Scan measures

(a) total amount of fat mass in grams, and

(2) total amount of Lean Body Mass plus bone, in grams.

It does not measure bone mass, but adds both lean body mass and bone mass together. This is important because reports that often accompanying DEXA Body Composition Scans include information about “bone mineral density”, but this information is estimated, rather than assessed. 

The DEXA Body Composition Scan reliably indicates how much total fat someone has, and the distribution of that fat over the body. It does not differentiate between sub-cutaneous fat (the fat under the skin) and visceral fat (the fat around the organs) which is associated with increased health risk.

Since fat mass is what is being directly evaluated in a DEXA Body Composition Scan, the total amount of body fat determined by this method is accurate.

DEXA Body Composition Scan Data of Fat and Lean 

Below are two pages from a DEXA Body Composition Scan report. 

Body Fat Composition and Total Lean Body Mass (muscle) plus bone
Body Fat Composition and Total Lean Body Mass (muscle) plus bone

This above page from a DEXA Body Composition Scan report is mostly related to what it assesses directly, which is Total Fat Mass in grams, and Lean Body Mass plus bone in grams, and evaluates the distribution of that fat.

While a DEXA Body Composition Scan does not differentiate between subcutaneous fat and visceral fat, the report indicates “Estimated Visceral Adipose Tissue (fat)” in the table of adipose (fat) indices. It is important to note that visceral fat is not assessed, but estimated. 

DEXA scanners (both GE and Hologic brands) have the National Health and Nutrition Examination Survey (NHANES) data integrated into their software, this which enables them to generate Z-scores for total amount of fat in grams, as well as localized Z-scores for fat in arms, legs, and trunk (1).

Z-scores compare the an individual subject’s results to those of an aged-matched population, and since a DEXA Body Composition Scan measures total fat directly, the z-score in this report for adiposity (fat) is valid.

T-scores compare an individual’s results to how many standard deviations it is from the results of a 30-year old young adult, and since a DEXA Body Composition Scan measures total fat directly, the t-score for adiposity (fat) is also valid.

DEXA Body Composition Scan Data on Bone Mineral Density and Bone Mineral Composition

This is where reports that may be provided with a DEXA Body Composition Scan can get really crazy.

A DEXA Body Composition Scan does not differentiate between Lean Body Mass as muscle and bone, so any information about “bone mineral density” and “bone mineral composition” is based on estimations!  

Whole Body Composition Scan - estimation of Bone Mineral Content and Bone Mineral Density
Whole Body Composition Scan – estimation of Bone Mineral Content and Bone Mineral Density

Since there is no measurement of bone mass in grams separate from Lean Body Mass (muscle),  z-scores for “Bone Mass Density” from a Whole Body Composition Scan make no sense.  This is a comparison of estimated bone data to actual data from an aged-matched population! 


Have a look at the table below from a 55 year old woman whose DEXA Body Composition Scan report indicates that she had osteoporosis based on estimated bone density numbers. Without having a DEXA Bone Density Scan, of both hips and lower spine she really doesn’t know if she has osteopenia or osteoporosis or not. A DEXA Body Composition Scan is designed to assess fat mass and the distribution of that fat, not bone.

"Bone Mineral Density" based on a DEXA Whole Body Scan
“Bone Mineral Density” based on a DEXA Whole Body Scan

Final Thoughts…

If you have had a DEXA Body Composition Scan and been told that you have osteopenia or osteoporosis remember that this is based on estimates of total amount of bone, and not actual measurement of bone. In such a case, I would recommend discussing with your doctor having a DEXA Bone Density Scan of both hips and lower spine.

If the DEXA Bone Density Scan indicates that you meet the criteria for osteopenia or osteoporosis, then meet with you doctor to discuss the results and their recommendations. In some cases, a doctor may recommend medication to keep bone from breaking down too quickly, and/or a program designed by a Physical Therapist to enable you to safely exercise and retain as much of bone mass you still have, while minimizing the risk of fractures. 

Take Away Message

Remember, that estimated data of “bone mineral density” from a DEXA Body Composition Scan is not the same as data from a DEXA Bone Mineral Density scan which is based on direct assessments.

Getting accurate information using the right diagnostic tool is essential.

How I Can Help

If you are an older adult who wants to optimize your diet and lifestyle to retain as much bone mass as possible as you age, I can help.

To your good health,

Joy

 

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/

Reference

  1. Shepherd JA, Ng BK, Sommer MJ, Heymsfield SB. Body composition by DXA. Bone. 2017 Nov;104:101-105. doi: 10.1016/j.bone.2017.06.010. Epub 2017 Jun 16. PMID: 28625918; PMCID: PMC5659281.

 

 

Copyright ©2024 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Nutrition is BetterByDesign

Is Animal-based and Plant-based Protein Equivalent?

is animal protein and plant protein equivalent and what is the Digestible Indispensable Amino Acid Score [DIAAS]Some people are considering going “plant-based” for perceived health reasons, or for ethical considerations and while these are important, evaluating plant protein quality is a necessary consideration. Evaluating protein quality using the Digestible Indispensable Amino Acid Score [DIAAS] can help.

A recent study found that essential amino acids from animal protein are more bioavailable than from plant protein [1], and these findings are especially important for older adults who need to preserve muscle mass, and for active adults wanting to build muscle. 

Amino Acids and Bioavailability

Amino acids are the building blocks of protein, including muscle. There are twenty amino acids categorized into two groups: essential amino acids (EAA) and non-essential amino acids.

Bioavailability means the degree to which the essential amino acids in a food can be used by the body to make its own proteins [2] such as muscle.

Essential amino acids, including leucine, which is required for muscle growth and repair, must be eating in protein foods in the diet. This is why they are called “essential” amino acids. The leucine content of a protein is vital because leucine is what triggers mTOR signaling in muscle, which stimulates muscle growth[3]. Dietary Recommendations for older adults emphasize obtaining 2.3 g leucine at each of 3 meals to ensure the building of new muscle protein [4], and 3g leucine per meals [5] to rebuild muscle. Protein recommendations for older adults range from between 20g per meal [3] to 25-30g protein per meal [5] for those recovering muscle mass. For physically active adults, the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine recommend a protein intake of 1.2—2.0 g protein / kg per day to optimize recovery from training, and to promote the growth and maintenance of lean body mass [6].

Plant Protein vs Animal Protein for Building Muscle 

chickpeas and hummus as example of plant protein - low Digestible Indispensable Amino Acid Score [DIAAS]Plant protein generally contains lower levels of the essential amino acid leucine than animal proteins[7] but those seeking to eat a more plant-based diet often turn to legumes (“beans”) for protein. Most legumes are incomplete proteins – meaning they are missing essential amino acids. For example, lentils have only 0.7g of leucine per half cup and chickpeas contain only 0.42g of leucine per half cup.  This means that so for an older adult to get the minimum amount of leucine at a meal (2.3 g leucine) they would have to eat more than 3 cups of lentils, or 5 ½ cups of chickpeas at a meal.

But what about the protein content of foods? Are plant-based proteins equivalent to animal-based proteins?

Is Plant Protein Equivalent to Animal Protein?

A newly randomized, investigator-blinded, crossover study was first performed with a group of young adults, and then in a group of older adults [1]. Researchers compared ounce-equivalents (oz-eq) of animal-based protein (lean pork or whole eggs) with plant-based protein (black beans or sliced almonds) in a mixed whole foods meal. The goal was to see how well the body can use essential amino acids from each type of protein to make body protein. To determine essential amino acid bioavailability, as well as blood sugar and insulin levels, blood samples were taken before they ate the meal, and at 30, 60, 120, 180, 240, and 300 minutes after eating.

Researchers chose the measure of ounce-equivalent (oz-eq) because the Dietary Guidelines for Americans (DGA) uses ounce-equivalent to “identify the amount of (protein group) foods with similar nutritional content” [1, 8]. For example, the DGA indicates that one ounce-equivalent equals one ounce of meat, or one whole egg, or 0.25 cups of beans, or 0.5 ounces of nuts but the authors of the study note that the ‘basis for stating these protein foods are “equivalent” and have “similar nutritional content” is unclear’ [1].

plant protein equal to animal protein ? What about the Digestible Indispensable Amino Acid Score [DIAAS]
“ounce-equivalent” from [8] U.S. Department of Agriculture and U.S. Department of Health and Human Services. Dietary Guidelines for Americans, 2020–2025, 9th ed

 

As pointed out by the authors, protein foods differ in energy content and macronutrient contents, including both protein quantity, and protein quality. With regards to protein quantity, one ounce-equivalent of pork loin contains ~7 g of total protein, and one ounce-equivalent of almonds contains only ~3 g of total protein [1]. 

With regards to protein quality, the authors define this ‘as the ability of a dietary protein source to provide adequate amounts and proportions of essential amino acids (EAA) that are digestible and as a result are bioavailable for use in the body for stimulating protein synthesis, and maintaining or growing body tissues’. 

The Bioavailability of Plant Protein – Digestible Indispensable Amino Acid Score

The bioavailability of amino acids in different types of proteins have been determined and is available in the The Digestible Indispensable Amino Acid Score [DIAAS]. In 2013, the DIAAS was recommended by the Food and Drug Administration to replace their previous method called the Protein Digestibility Corrected Amino Acid Score (PDCAAS) [9]. In the DIAAS system, each essential amino acid is recognized as an individual nutrient, rather than lumping all amino acids together and this is very important because the bioavailability of a protein source must to be taken into account when determining if a diet is adequate in protein, and in specific essential amino acids such as leucine.

High quality proteins are those with a DIAAS score ≥100, and are considered excellent quality proteins. DIAAS scores of 75–99 are considered high-quality proteins, and those with scores of <75 are considered to be able to make no quality protein claim [8]. Based on this recent research, plant protein from most grains and legumes (“beans”) are <75 on the DIAAS score, with pea and soy falling between 75 and 100.  Animal protein such as pork consistently score over 100 on the DIAAS [10].

If regulatory guidelines such as the Dietary Guidelines for Americans and Canada’s Food Guide for Health Eating used the protein values generated by the Digestible Indispensable Amino Acid Score, rather than the PDCAAS, consumers would easily be able to see that a 4oz plant-based patty is not equivalent in protein quantity of quality as a 4oz beef patty, and 20g of vegan protein powder is not equivalent to 20g of whey protein powder. Use of the DIAAS in both countries would more accurately reflect protein quality [11] and enable consumers to make better choices.  

Plant Protein versus Animal Proteins – conclusions of the study

plant protein vs animal protein for building muscle - steak as example of animal proteinThe study found that consuming meals with equivalent amounts of animal-based proteins versus plant-based proteins resulted in more essential amino acids in the blood compared with meals containing animal-based proteins in both young and older adults, separately and combined.

Also found was that there was greater essential amino acid bioavailability in lean pork, than in eggs in both young adults and older adults, separately or combined, and there as no difference in essential amino acid bioavailability between black beans and almonds.

The researchers concluded that it is inappropriate to say that different protein sources on an ounce-equivalent basis are “equivalent” .

Final Thoughts…

If you are an active adult seeking to build and repair muscle, then knowing which is better (plant protein vs animal protein for building muscle) is important. If you are an older adult wanting to retain muscle mass, eating high quality protein that contains all the essential amino acids including leucine is essential. While the US Dietary Guidelines states that one ounce of meat or one whole egg or 0.25 cups of beans or 0.5 ounce of nuts are equivalent, this recent study finds that the protein in beans and nuts is not equivalent to that in meat and eggs. 

If you are toying with the idea of becoming more plant-based, be sure that you understand the science of protein bioavailability so you can make a sound decision. 

For those who already eat a vegetarian diet for religious or ethical reasons, ensuring that your meals contain the most bioavailable plant-based proteins at each meal requires knowledge and effort.

More Info

If you would like support ensuring that you or someone you love eats sufficient high-quality protein at each meal needed to trigger muscle synthesis, please reach out to me through the Contact Me form, above.

To your good health, 

Joy

You can follow me on:

 

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

  1. Connolly G, Hudson JL, Bergia RE, Davis EM, Hartman AS, Zhu W, Carroll CC, Campbell WW. Effects of Consuming Ounce-Equivalent Portions of Animal- vs. Plant-Based Protein Foods, as Defined by the Dietary Guidelines for Americans on Essential Amino Acids Bioavailability in Young and Older Adults: Two Cross-Over Randomized Controlled Trials. Nutrients. 2023; 15(13):2870. https://doi.org/10.3390/nu15132870
  2. Gaudichon C, Calvez J. Determinants of amino acid bioavailability from ingested protein in relation to gut health. Curr Opin Clin Nutr Metab Care. 2021 Jan;24(1):55-61. doi: 10.1097/MCO.0000000000000708. PMID: 33093304; PMCID: PMC7752214.
  3. Layne E Norton, Donald K Layman, Leucine Regulates Translation Initiation of Protein Synthesis in Skeletal Muscle after Exercise12, The Journal of Nutrition,
    Volume 136, Issue 2, 2006, Pg 533S-537S, doi.org/10.1093
    (https://www.sciencedirect.com/science/article/pii/S0022316622080956)
  4. Bauer JI, Biolo G, Cederholm T, Cesari M, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. J Am Med Dir Assoc. 2013 Aug;14(8):542-59
  5. Nutrition Heart Beat, Leucine: perform better and maximize your muscle through diet, https://nutritionheartbeat.com/sports-nutrition/leucine-diet-muscle
  6. Thomas DT, Erdman KA, Burke LM. American College of Sports Medicine Joint Position Statement. Nutrition and Athletic Performance [published correction appears in Med Sci Sports Exerc. 2017 Jan;49(1):222]. Med Sci Sports Exerc. 2016;48(3):543-568. doi:10.1249/MSS.0000000000000852
  7. Berrazaga I, Micard V, Gueugneau M, Walrand S. The Role of the Anabolic Properties of Plant- versus Animal-Based Protein Sources in Supporting Muscle Mass Maintenance: A Critical Review. Nutrients. 2019 Aug 7;11(8):1825. doi: 10.3390/nu11081825. PMID: 31394788; PMCID: PMC6723444.
  8. U.S. Department of Agriculture and U.S. Department of Health and Human Services. Dietary Guidelines for Americans, 2020–2025, 9th ed.; U.S. Department of Agriculture and U.S. Department of Health and Human Services: Washington, DC, USA, 2020. Available online: DietaryGuidelines.gov
  9. Herreman, LNommensen, PPennings, BLaus, MCComprehensive overview of the quality of plant- And animal-sourced proteins based on the digestible indispensable amino acid scoreFood Sci Nutr2020853795391https://doi.org/10.1002/fsn3.1809
  10. Food and Agriculture Organization of the United Nations. Dietary Protein Quality Evaluation in Human Nutrition: Paper 92. Rome, Italy: Food and Agriculture Organization of the United Nations; 2013.
  11. Marinangeli CPF, House JD. Potential impact of the digestible indispensable amino acid score as a measure of protein quality on dietary regulations and health. Nutr Rev. 2017 Aug 1;75(8):658-667. doi: 10.1093/nutrit/nux025. Erratum in: Nutr Rev. 2017 Aug 1;75(8):671. PMID: 28969364; PMCID: PMC5914309.

 

Copyright ©2023 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

 

Nutrition is BetterByDesign

Why A Smoothie is “Pre-Chewed” Food

In the interest of time, many people will throw a cup or more of fruit, some green veggies and maybe some protein powder into a blender to make a smoothie for breakfast without realizing the effect that blending has on their blood sugar, gut microbiome, and even the overall amount of food they eat.

Making a Smoothie 

Making a smoothie
For people with pre-diabetes or diabetes, a smoothie that has pureed fruit has a very different effect on blood sugar than eating the same ingredients as whole, intact foods. This is because the carbohydrate from the ingredients is now acellular, meaning “out of the cell”.

Cellular versus Acellular Carbohydrate

Cellular carbohydrates come from whole, intact food that remains in the cell wall. These take longer to be digested and absorbed into our bloodstream than carbohydrates that have been ground or pureed. As well, cellular carbohydrates have a lower “carbohydrate density” than processed carbohydrate, where the carbohydrate density are the grams of carbohydrate in a food, minus  the grams of fiber, based on the total gram weight of the food [1].

Acellular carbohydrates are no longer are contained within their cell wall, because they have been pureed (like fruit in a smoothie), or ground, such as flour, from grain. As a result, these foods have a much higher “carbohydrate density” because the fiber is no longer contained in the cell wall, along with the carbohydrate.

A Smoothie as “Pre-Chewed” Food

Most people think digestion begins in the stomach, but it doesn’t. It starts in the mouth when we chew food. As unpalatable as it sounds, smoothies are really “pre-chewed” food, and consuming carbs this way can disrupt our blood sugar, gut microbiota, and even affect the amount of food we consume.

  1. A 1977 study published in the journal Lancet demonstrated that when fruit is pureed fruit or juiced and then eaten, the glucose response 90 minutes later is significantly higher than if the fruit were eaten whole [2]. This is because the blender or juicer has made the carbohydrate acellular, by doing some of the work that chewing does. In this way, carbohydrate-containing smoothies are essentially “pre-chewed”. For those with pre-diabetes or diabetes, having a morning smoothie instead of eating the same foods intact has a very different effect on blood glucose. Keep in mind, that while 60g of a whole fruit, 60g of pureed fruit, and 60g of fruit that has been juiced have the same amount of carbohydrate and similar Glycemic Index (GI), the GI only indicates how quickly a food or drink will increase blood sugar, not how much higher blood sugar will go.  The two-part article, titled The Perils of Food Processing explains in scientific terms the effect of food processing on blood sugar.
  2. Carbohydrates that remain with their cell structure such as whole berries or fruit (i.e. cellular carbohydrates) have their carbohydrate density preserved until the digestive juices in the stomach begin to break down the cell wall of the fruit. Once free from the cell wall, the carbohydrate is absorbed in the large intestine, or colon. Acellular carbohydrates, on the other hand such as fruit-containing smoothies begin to be digested in the small intestine, instead of the colon (where cellular carbohydrates are digested). It is thought that this early fermentation may raise the risk of gut dysbiosis and leaky gut syndrome [1].
  3. Finally, the processing of acellular carbohydrates in a blender so we can drink our food, as opposed to eating it makes it too easy to have more than one would if eating the same amount of the intact food. Since acellular carbohydrates are higher in carbohydrate density than the diets made of intact, whole food, it is thought that this may raise the risk for obesity, and leptin resistance [1]. Leptin is the hormone that tells us when we are hungry, and it is thought that this negative feedback loop becomes dysregulated when we consume large amounts of acellular carbohydrates, including pureed fruit, flour-based baked goods, and refined grains.
  4.  

Final Thoughts…

It is important to keep in mind that digestion begins in the mouth when we chew food and how we absorb the carbohydrate contained in those foods is very different when we eat whole, intact food, as opposed to pureeing them into a smoothie. Smoothies are really “pre-chewed” food that can disrupt our blood sugar, gut microbiota, and affect the overall amount of food we consume.

Instead of throwing some fruit, veggies and protein powder into a blender, why not eat a half cup of berries, with a cup of cottage cheese or plain Greek yogourt, and grab a handful of snap peas for the low carb veggies, instead? This is a quick, light meal that has all the protein and leucine required for adults to preserve their muscle mass — and there is no blender to clean, afterwards!

How I Can Help

I understand that not everyone who wants to eat healthy loves to cook. I often design Meal Plans for people based on easy-to-obtain foods that require minimum preparation and little to no cooking. Whether you love to cook or can’t be bothered, I can help.

For more information, please look under the Service tab or contact me through the Contact Me form above.

To your good health, 

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

  1. Spreadbury, I., Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota and may be the primary dietary cause of leptin resistance and obesity. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy. 2012:5 175-189.
  2. Haber GB, Heaton KW, Murphy D, Burroughs LF. Depletion and disruption of dietary fibre. Effects on satiety, plasma-glucose, and serum-insulin. Lancet. 1977 Oct 1;2(8040):679-82. doi: 10.1016/s0140-6736(77)90494-9. PMID: 71495

Copyright ©2023 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Nutrition is BetterByDesign

 

Types of Protein to Help Older Adults Retain Muscle

The inability to retain muscle and strength associated with aging is called sarcopenia, and it is not only a concern for older adults. Loss of muscle mass begins to occur after the age of thirty at the rate of 1% per year [1], and the gradual inability to retain muscle mass and strength generally begins occurring by age fifty [2]. Muscle loss affects 5-13% of adults between the ages of sixty to seventy, and up to half of adults older than eighty years of age have sarcopenia [3].

Inability to retain muscle affects mobility Not being able to retain muscle mass results in older adults no longer being able to remain active, a reduced quality of life, osteoporosis, increased risk of falls, and a worsening of metabolic health [4].

Most people have never paid attention to the amount and quality of the protein they eat – choosing instead to select protein foods based on taste preference, economics, or ethical or religious reasons. These are all important considerations; however, they are not the only ones. As outlined in a previous article about the role of protein in the diet of older adults, high biological value protein that contain sufficient amounts of the amino acid leucine are necessary for the health of muscle [5], but in this regard not all protein foods are equal.

Amino acids are the building blocks of protein, including muscle, and there are twenty amino acids categorized into two groups: essential and non-essential amino acids. Essential amino acids, including leucine which is required for muscle growth and repair are not produced by the body in sufficient amounts. Leucine must be obtained through diet, which is what makes it an “essential” amino acid.

The leucine content of proteins is critical because leucine is what triggers mTOR signaling in muscle that stimulates muscle growth. For this reason, the proteins people need to contain sufficient leucine – especially older adults who want to retain muscle mass, and mobility.

Plant proteins generally contain lower levels of leucine compared to animal proteins [6]. Grains such as wheat contain less than 7% leucine [7] and even quinoa which is considered a “complete protein” because it has all essential amino acids only contain only 4.5% leucine [8]. People who want to eat a more plant-based diet to retain muscle may turn to legumes (“beans”) for protein, but they are usually incomplete proteins – meaning they are missing essential amino acids, and are generally poor sources of leucine. Even soybeans, which are complete proteins, contain only 8% leucine [9].

Older adult walkingDietary Recommendations for older adults emphasize a minimum of 20g of protein per meal, with more than 2.3 g leucine at each of 3 meals to ensure the building of new muscle protein [10].

Furthermore, to retain muscle and to recover the loss of muscle mass in older adults, the recommended intake of leucine is 3g per at each of 3 meals, along with 25-30g of protein [11].

Protein Sources to Help Retain Muscle 

Animal proteins are highly bioavailable complete proteins and the richest sources of leucine.  Only 1 cup of 1% fat cottage cheese contains 2.9g of leucine per cup – the amount needed for an entire meal! A cup of plain yogurt contains 1.3g of leucine, and a cup of Greek yogurt contains 1.2 g of leucine. Only 3 oz. of ground beef or pork contains 1.8g of leucine and the same amount of chicken breast contains 2.25g – all the leucine that is needed in a meal [11]. These are excellent protein and leucine containing food to help retain muscle. 

Soybeans which are a complete plant-based protein contain only 0.28g leucine per half cup, and firm tofu which is a concentrated form of soy protein has between 0.73g of leucine for three ounces, so to get sufficient leucine from firm tofu would require an older adult to eat ¾ of a pound – well beyond the appetite of many older adults. Incomplete proteins such as lentils have only 0.7g of leucine per half cup, and black beans only 0.61g leucine per half cup – so for an older adult to get the minimum amount of leucine at a meal (2.3 g leucine) from either of these, they would have to eat more than 3 cups at a meal, or 5 ½ cups of chickpeas (0.42g of leucine per half cup). 

For older adults who want to eat a more plant-based diet, ensuring adequate highly bioavailable protein that are also rich sources of leucine is essential to retain muscle – so I recommend “prioritizing protein” along with eating plenty of non-starchy vegetables, like broccoli, green beans, and leafy greens.

Prioritize Protein to Retain Muscle 

“Prioritizing protein” means to first decide what protein you are going to eat at a meal, and then build the rest of the meal around that.  For older adults, the protein should have between 25-30g of highly bioavailable protein, and 2.3-3g of leucine.

For breakfast, choosing high leucine proteins such as a cup of cottage cheese, or a cup of plain Greek yogurt will provide the needed minimum amount of highly bioavailable protein, as well as sufficient leucine. On the other hand, 2 eggs only contain 12 g of highly bioavailable protein, and 1.2g leucine less than half the recommended amount for older adults.

Choosing 4 oz (113g) of canned tuna for lunch will provide 4g of leucine and 21g of protein, and 3 oz of chicken breast (113g) will provide 2.4g of leucine and 26.5g of protein. To top up the leucine contents, you can serve that with some salad greens sprinkled with an ounce (28g) of pumpkin seeds that contains 0.7g of leucine or an ounce (28g) of sunflower seeds that contains 0.46g of leucine.

In terms of dinner options, while steak is one of the richest sources of leucine – having 3.4 g leucine per 4 oz (113g), cost is a factor. More cost-effective options for those that eat it are 4 oz. (113g) of pork chops which contains 27g of protein, and 2.5 g of leucine. Four ounces of ground beef contains only 16 g of protein but has 2.5 g of leucine, so boosting the protein content of the meal can be as simple as adding some Greek yogurt for dessert.

UPDATE (August 20, 2023) – Be sure to read the new article “Is Plant Protein and Animal Protein Equivalent” based on a recently published study.

Final Thoughts…

The quality of life of older adults and their health depends on remaining active, which requires adequate muscle mass, and preventing sarcopenia requires sufficient protein with all the essential amino acids, as well as enough of the amino acid leucine.

Given that we lose muscle mass at the rate of 1% per year after the age of thirty, which proteins we choose to eat at each of our meals is essential.

If you would like support ensuring you or a loved one eats sufficient high quality protein and leucine as well as other nutrients of concern, please reach out to me through the Contact Me form, above.

To your good health, 

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

  1. Keller K, Engelhardt M. Strength and muscle mass loss with aging process. Age and strength loss. Muscles, Ligaments and Tendons Journal. 2013;3(4):346-350.
  2. Lexell J. Human aging, muscle mass, and fiber type composition. Journals of Gerontology Series A: Biological and Medical Sciences. 1995;50:11–16
  3. Cruz-Jentoft AJ, Bahat G, Bauer J, Boirie Y, Bruyère O, Cederholm T, et al. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing. (2019) 48:16–31. 10.1093/ageing/afy169
  4. Hunter GR, Singh H, Carter SJ, Bryan DR, Fisher G. Sarcopenia and Its Implications for Metabolic Health. J Obes. 2019 Mar 6;2019:8031705. doi: 10.1155/2019/8031705. PMID: 30956817; PMCID: PMC6431367.
  5. Tessier AJ, Chevalier S. An update on protein, leucine, omega-3 fatty acids, and vitamin d in the prevention and treatment of sarcopenia and functional decline. Nutrients. (2018) 10:1099. 10.3390/nu10081099
  6. Berrazaga I, Micard V, Gueugneau M, Walrand S. The Role of the Anabolic Properties of Plant- versus Animal-Based Protein Sources in Supporting Muscle Mass Maintenance: A Critical Review. Nutrients. 2019 Aug 7;11(8):1825. doi: 10.3390/nu11081825. PMID: 31394788; PMCID: PMC6723444.
  7. Norton, L.E., Wilson, G.J., Layman, D.K. et al. Leucine content of dietary proteins is a determinant of postprandial skeletal muscle protein synthesis in adult rats. Nutr Metab (Lond) 9, 67 (2012). https://doi.org/10.1186/1743-7075-9-67
  8. El-Sohaimy, Sobhy & Mehany, Taha. (2015). Physicochemical and functional properties of quinoa protein isolate. Annals of Agricultural Sciences. 60. 10.1016/j.aoas.2015.10.007.
  9. Amino Acid Analysis of Soybean, https://www.drugfuture.com/chemdata/Soybean.html
  10. Bauer JI, Biolo G, Cederholm T, Cesari M, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. J Am Med Dir Assoc. 2013 Aug;14(8):542-59
  11. Nutrition Heart Beat, Leucine: perform better and maximize your muscle through diet, https://nutritionheartbeat.com/sports-nutrition/leucine-diet-muscle
  12. Rondanelli M, Nichetti M, Peroni G, Faliva MA, Naso M, Gasparri C, Perna S, Oberto L, Di Paolo E, Riva A, Petrangolini G, Guerreschi G, Tartara A. Where to Find Leucine in Food and How to Feed Elderly With Sarcopenia in Order to Counteract Loss of Muscle Mass: Practical Advice. Front Nutr. 2021 Jan 26;7:622391. doi: 10.3389/fnut.2020.622391. PMID: 33585538; PMCID: PMC7874106.

 

 

Copyright ©2023 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Nutrition is BetterByDesign

 

 

 

A Ketogenic Diet for Mental Health

People’s interest in following a ketogenic diet to see if it offers improvements in mental health is continuing to increase, but not everyone is prepared for what is involved in adopting a Modified Ketogenic Diet that contains 75% fat, and little protein.  Based on emerging evidence and under the oversight of people’s doctors, I now offer clients the option of an alternative approach.

Different Types of Ketogenic Diets

As outlined in a previous article titled “Use of a Therapeutic Ketogenic Diet in Mental Health,” I outlined what a therapeutic ketogenic diet is, and the three basic types of therapeutic ketogenic diets; a Classic Ketogenic Diet that uses a 4:1 ratio of fat to protein plus carbs, a Modified Ketogenic Diet that uses a 3:1 ratio, and a Modified Atkins Diet that uses a 3:1 ratio.

Therapeutic Ketogenic Diets for Mental Health

Since the release of Psychiatrist Dr. Chris Palmer’s book, Brain Energy in November last year, I have had quite a number of people either referred to me by their doctors, or approach me themselves to design a therapeutic ketogenic diet for them. These people knew what the different types of ketogenic diets were, and were quite set on beginning with a Modified Ketogenic Diet (3:1).  As a result, they were fully prepared for how much their diet would change and were willing to trial the diet for three months, as is recommended.  I have clients that started a therapeutic ketogenic diet at the beginning of the year and who are continuing to eat this way, as their doctors oversee their health and medication adjustments. 

Like those who have come to me to design therapeutic ketogenic diets for seizure disorder or as adjunct treatment in glioblastoma (a form of brain cancer), these individuals wanted to do whatever it took to see if they could feel better.  Since all of these people were doing this under the oversight of their physicians, my role was simply to design a diet for them to trial, with some food substitutions to keep it interesting.

Another Type of Ketogenic Diet for Mental Health

Recently, I have had people approach me about wanting to adopt a ketogenic diet for mental health, yet feeling apprehensive about the significant change that would be involved with adopting a Modified Ketogenic Diet (3:1). They wanted something that was easier to adopt and something that they would be more likely to be able to sustain, long term.

I had read some anecdotal reports of individuals doing very well following a Modified Atkins Diet (2:1) under the supervision of their doctors, and very recently (June 3, 2023) a pre-print pilot study came out where this approach was successfully trialed in people with bipolar disorder [2].

As a result, I now offer a 2:1 ketogenic diet approach to those working with their doctors who don’t feel they could maintain a 3:1 ketogenic diet (75% fat, with carbohydrate and protein equaling 25% altogether), but who want to try a ketogenic diet to see if they feel better.

This alternative approach is much less time consuming in terms of the amount of calculations and work I need to do, so the benefit to the individual is that it is less costly. It enables people to get into ketosis and see if they feel any better. Then, in consultation with their doctors they can decide if the improvements are sufficient to maintain their diet as it is, or whether it may be worth seeing if a gradual increase in fat, and decrease in protein may work better.

Working with Your Doctor to Support Mental Health

As mentioned in the previous article, Dr. Palmer recommends that Psychiatrists first determine if trialing a ketogenic diet is appropriate for a specific patient. For people considering using a ketogenic diet as an adjunct treatment for mental health, the first place to start is by having this discussion with your doctor — especially if taking any medications for depression, anxiety disorder, or bipolar disorder or for metabolic conditions such as high blood pressure or to control blood sugar.

Dr. Palmer also recommends that doctors have their patients remain on their medication while trialing the diet for a period of three months, during which they are evaluated to see if there has been any significant change in symptoms [1]. If the doctor finds that the diet is helping, they may begin to gradually deprescribe some medications. As I’ve said in many other articles, changing dosages of medication is not something people should do on their own. 

There is an important point that Dr. Palmer makes that should not be overlooked. With the gradual decrease in medications, people must realize that they are more reliant on the ketogenic diet to keep symptoms under control. Since the diet is therapeutic, taking “cheat days” may result in it taking several days to get back into ketosis — during which symptoms can dramatically reappear [1]. I do not recommend “cheat days” when following a ketogenic diet for therapeutic purposes.  While a 2:1 diet is much easier to maintain long term than a 3:1, consistently maintaining the correct ratio of fat to protein and carbohydrate is essential.

Dr. Palmer recommends the following two steps to doctors that want to use ketogenic diets with their patients [1]; 

  1. Find a licensed Dietitian knowledgeable in therapeutic ketogenic diets and partner with them. 

  2. Read the book “Ketogenic Therapies” by Dr. Eric Kossoff [3]

Dr. Eric Kossoff’s book, Ketogenic Diet Therapies for Epilepsy and Other Conditions is one that have referred to often over the last 5 years of designing therapeutic ketogenic diets for other conditions.

Steps to Getting Started

If you are thinking of adopting a ketogenic for improved mental health, then the first step is to reach out to your doctor.  To assist you in having this type of discussion, please feel free to download this letter

If your have already discussed this and your doctor is willing to oversee your health and medications while you adopt the diet, I can provide you with a Request for Medical Supervision Form. 

More Info

If you would like more information about having a therapeutic ketogenic diet designed for you, please send me a note using the Contact Me form at the top of this page.

To your good health!

Joy

 

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

  1. Dr. David Puder, MD, Psychiatry Podcast, Episode 163, Dr. Chris Palmer: Ketogenic Diet for Mental Health, M=November 15, 2022, https://www.psychiatrypodcast.com/psychiatry-psychotherapy-podcast/163-treating-mental-health-disorders-with-a-ketogenic-diet
  2. Needham Nicole, Campbell Ian, Grossi Helen et al, Pilot Study of a Ketogenic Diet in Bipolar Disorder, June 3, 2023, doi.org/10.1101/2023.05.28.23290595, https://www.medrxiv.org/content/10.1101/2023.05.28.23290595v1
  3. Kossoff, Eric & Turner, Zahava & Cervenka, Mackenzie & Barron, Bobbie. (2020). Ketogenic Diet Therapies For Epilepsy and Other Conditions. 10.1891/9780826149596.

 

 

Copyright ©2023 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Is High Fructose Corn Syrup (HFCS) Linked to Fatty Liver Disease?

A recent social media post about a Canadian woman living in the United States who discovered that the ingredients in a major brand of ketchup manufactured in Canada and the United States were different caused quite a stir.  Online discussion centered around whether the inclusion of high fructose corn syrup (HFCS) in the US product posed an increased risk of fatty liver disease.

twitter post that was almost viral about high fructose ketchup

The ingredients listed in the US and Canadian products were as follows;

Heinz Tomato Ketchup (America): Tomato concentrate from red ripe tomatoes, distilled vinegar, high fructose corn syrup, corn syrup, salt, spice, onion powder, natural flavoring.

Heinz Tomato Ketchup (Canada): Tomato paste (from fresh, ripe tomatoes), sugar, vinegar, salt, spices

One Difference Between the US and Canadian Ketchup 

The significant difference between the two ingredient lists was that the US-manufactured ketchup used high fructose corn syrup (HFCS) and corn syrup to sweeten the product, whereas the Canadian ketchup was sweetened using sugar (sucrose). 

High Intakes of Fructose and Non-Alcoholic Fatty Liver Disease

There have been a few research articles over the last several years which seemed to indicate that large intakes of fructose may be linked to non-alcoholic fatty liver disease (NAFLD) but I had not yet written anything about it, largely due to a lack of time. This recent social media post going viral made me want to write a brief post pointing to some recent evidence that large intakes of fructose, including high fructose corn syrup (HFCS) may pose a risk of NAFLD.

What is fructose?

Fructose is a natural occurring sugar that is present in fruit, some vegetables and honey and which is used as a component in the manufacture of high-fructose corn syrup (HFCS) which is used as a sweetener in soda (soft drinks, pop), in candies, and in condiments such as ketchup.

Approximately a quarter (24%) of US adults have non-alcoholic fatty liver disease (NAFLD) which results in the excess build-up of fat in the liver that is unrelated to heavy alcohol use [1]. NAFLD is a serious condition that can progress to chronic liver damage, and lead to death [1].

academic presentation about fructose and NAFLDAn expert talk given this time last year at Endo 2022, the annual meeting of the Endocrine Society which took place from June 11-14, 2022, in Atlanta, Georgia, titled Fructose Consumption and NAFLD in US Adult Population presented evidence that non-alcoholic fatty liver disease (NAFLD) is associated with high intakes of fructose.

The researchers analyzed data from the 3,292 US adults enrolled in the National Health and Nutrition Examination Survey (NHANES) from 2017-2018 and found that those who consumed the greatest amount of fructose were Mexican Americans (48%), non-Hispanic Blacks (44%), with a lower percentage of fructose consumption amongst non-Hispanic whites (33%).

The researchers found the highest prevalence of non-alcoholic fatty liver disease (NAFLD) amongst Mexican Americans who consumed the highest amount of fructose (70%) which was significantly different than the prevalence of NAFLD in Mexican Americans that consumed the lowest amount of fructose (52%) [2]. When researchers adjusted for body composition and laboratory variables, they found that high fructose consumption was related to a higher risk of NAFLD in the total population, not only in Mexican Americans [2].

The researchers concluded that “there is an association between fructose consumption and the odds of developing non-alcoholic fatty liver disease (NAFLD)” and that “interventions should aim to decrease consumption of fructose overall” [1,2].

The researchers recommended that health care providers encourage people to consume less food and beverages with high-fructose corn syrup to prevent the development of NAFLD [1].

Final Thoughts…

Consuming small amounts of ketchup sweetened with high-fructose corn syrup in and by itself does not pose a risk of developing non-alcoholic fatty liver disease.

Where the risk lies is for people who are consuming fruit juice, soda pop, candy and condiments including ketchup that contain high-fructose corn syrup.

The recommendation of the Endocrinologists above is to encourage people to consume less of these foods and beverages to prevent the development of non-alcoholic fatty liver disease.

To your good health!

Joy

 

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

 

  1. Williams, Colleen, Reports and Proceedings of the Endocrine Society, News Release June 12, 2022, People who consume too much high fructose corn syrup could be at risk for NAFLD, https://www.eurekalert.org/news-releases/955131
  2. Kermah D, Najjar S, Puri V, Schrode K, Shaheen M, Zarrinpar A, Friedman T. OR10-5 Fructose Consumption and NAFLD in US Adult Population of NHANES 17-18. J Endocr Soc. 2022 Nov 1;6(Suppl 1):A17. doi: 10.1210/jendso/bvac150.035. PMCID: PMC9625025.

 

Copyright ©2023 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Nutrition is BetterByDesign

Use of a Therapeutic Ketogenic Diet in Mental Health

Most people have heard of the high fat, low carb “keto” diet that is often followed for weight loss and for improving blood sugar, but a  therapeutic ketogenic diet is very different. Therapeutic ketogenic diets have been used for more than 100 years in the treatment of epilepsy and diabetes and more recently, in the treatment of various mental health disorders, including depression, bipolar disorder, and schizophrenia.

Therapeutic Ketogenic Diet for Mental Health 

A research article published on July 6, 2022 in Frontiers of Psychiatry was my first exposure to the use of a therapeutic ketogenic diet in the treatment of mental health disorders. This was of great interest to me because my graduate research was in the area of mental health nutrition, and for the last 5 years I have supported people following therapeutic ketogenic diets for seizure disorder, and as adjunct treatment in specific forms of cancer. The use of a therapeutic ketogenic diet in mental health brings these two formerly separate areas of my experience together. 

In this pilot study, thirty one adults in a psychiatric hospital in Toulouse, France who had treatment-resistant depression, bipolar disorder, and schizoaffective disorder were placed on a therapeutic ketogenic diet that restricted their carbohydrate intake to 20g per day. Of the 28 patients that followed the diet for longer than two weeks, symptoms of depression and psychosis improved in all 28 patients, with improvements becoming noticeable within three weeks or less. Most impressive was that 43% of patients achieved clinical remission of symptoms, and 64% were discharged from the hospital on less psychiatric medication [1]. 

“Brain Energy” Book – role for therapeutic ketogenic diet 

The release of the best-selling book Brain Energy in mid-November 2022, written by Harvard psychiatrist Dr. Chris Palmer, one of the pioneers in the use of a therapeutic ketogenic diet in treating psychiatric disorders [2,3,4], brought the use of this type of diet in mental health to public awareness. As a result of the book, I have had many more individuals contact me about designing such a diet to see if it would improve their mental health.  

But what is a therapeutic ketogenic diet?

Types of Therapeutic Ketogenic Diets

There are several types of therapeutic ketogenic diets, each designed according to a specific “ketogenic ratio” which specifies the amount of fat in the diet compared to the total amount of protein plus carbohydrate.

Classic Ketogenic Diet (KD)

The Classic Ketogenic Diet uses a 4:1 ratio which means it is made up of 4 grams of fat for every 1 gram of protein plus carbohydrate. That is, for every 5 grams of food eaten, there are 4 grams of fat and 1 gram of protein and/or carbohydrate. A 4:1 ketogenic diet contains 80% fat (4÷5=80%) and 20% protein plus carbohydrate (1÷5=20%), and protein may be set at 15% of calories with a maximum of 5% of calories coming from carbohydrate, or protein may be set lower at 10%, and carbohydrate as high as 10%. This type of diet may be used when the need to achieve and maintain high levels of ketones is necessary.

It is important to note that the ketogenic ratio compares the amount of fat, protein, and carbohydrates in grams, which is a measure of weight. The diet is calculated in grams, since food is measured by weight, in grams.

As you will see below, the amount of fat, protein and carbohydrate in the diet can also be calculated as a percentage of calories.

Modified Ketogenic Diet (MKD)

The Modified Ketogenic Diet uses a 3:1 ratio which means it is made up of 3 grams of fat for every 1 gram of protein plus carbohydrate. For every 4 grams of food eaten, there are 3 grams of fat and 1 gram of protein and carbohydrate. A 3:1 ketogenic diet contains 75% fat (3÷4=75%) and 25% protein plus carbohydrate (1÷4=25%). Some psychiatrists will start their patients on a 3:1 therapeutic ketogenic diet and once their patient is producing significant levels of ketones and is stable with respect to symptoms, may gradually have them transition over to a Modified Atkins Diet (see below) while monitoring their symptoms.

Modified Atkins Diet (MAD)

The Modified Atkins Diet uses a 2:1 ratio and is often used when people are taking a break from a 4:1 or 3:1 therapeutic ketogenic diet, and is also used as a therapeutic diet in mental health as it is the easiest for people to sustain long term. As mentioned above, some psychiatrists will start their patients on a 3:1 ketogenic diet to generate higher levels of ketones and then gradually have their clients transition over to a Modified Atkins Diet as it is more sustainable long term. This diet is also very helpful for those who do not tolerate the very high fat content of a 4:1 or 3:1 diet. In a Modified Atkins Diet, for every 3 grams of food eaten, there are 2 grams of fat and 1 gram of protein and carbohydrate. A 2:1 ketogenic diet contains 67% fat (2÷3=67%) and 33% protein plus carbohydrate (1÷3=25%).

Calculating Ratios Based on a Percentage of Calories

The first step for me, as a Dietitian in designing a therapeutic ketogenic diet is to determine the amount of calories (kcals) a person requires. This is routine work in designing any Meal Plan.

The next step is unique to the design of therapeutic ketogenic diets and that is calculating the specific percent of calories that needs to come from fat, protein and carbohydrate.

It is important to note that calculating the ratio provided from fat, protein and carbohydrate based on calories arrives at a different percentage than when calculating the ratio based on grams of food. This is because fat provides more calories per gram (9 kcal/g) than protein and carbohydrates (4 kcal/g).

To get 500 calories as protein, one would need to eat 125g of protein (500÷4=125), but to get the same 500 calories as fat, one would only need to eat 55.5 g of fat (500÷=55.5), because fat is much more calorically dense. Therapeutic ketogenic diets have much smaller meals because fat provides the same number of calories, for much less mass (weight, in grams).

Classic Ketogenic Diet – 90% fat as a percentage of calories

On a 4:1 ketogenic diet, 90% of the calories in the diet comes from fat when measuring by calories (80% fat if you are measuring by weight, in grams). This can be confusing, but remember that a 4:1 ketogenic ratio represents 4 grams of fat for every 1 gram of carbohydrate plus protein.

    • Four grams of fat (which provides 9 calories per gram) provides a total of 36 calories (4 x 9 = 36).
    • One gram of protein or carbohydrate (which provides 4 calories per gram) provides a total of 4 calories (1 x 4 = 4). 

That is, the ratio of calories from fat to calories from protein plus carbohydrate is 36:4. This means that for every 40 calories consumed, 36 calories come from fat and 4 calories come from protein and/or carbohydrate. Thus, 90% of the calories comes from fat (36÷40=90%), and 10% comes from protein and carbohydrate (4÷40=10%) [5]. 

Modified Ketogenic Diet (MKD) – 87% fat as a percentage of calories

On a 3:1 ketogenic diet, about 87% of the calories comes from fat, and 13% comes from protein plus carbohydrate. 

  • Three grams of fat (which provides 9 calories per gram) provides a total of 36 calories (3 x 9 = 27).
    • One gram of protein or carbohydrate (which provides 4 calories per gram) provides a total of 4 calories (1 x 4 = 4) [5]. 

On a Modified Ketogenic diet, the ratio of calories from fat to calories from protein plus carbohydrate is 27:4. This means that for every 31 calories consumed, 27 calories come from fat and 4 calories come from protein and/or carbohydrate. Thus, 90% of the calories comes from fat (27÷31=87%), and 13% comes from protein and carbohydrate (4÷31=13%) [5]. 

A Dietitian’s Role in Therapeutic Ketogenic Diets

In a recent Psychiatry and Psychotherapy podcast where Dr. Chris Palmer was interviewed, he talks about how Psychiatrists can incorporate use of a therapeutic ketogenic diet in their practice [6].  The first thing he said was that there was a need for the physician to determine if this approach is appropriate for a specific patient.

 

As outlined in a 2018 article titled “Don’t Try This at Home – when medical supervision is needed“, beginning a ketogenic diet is something that needs to be done with the knowledge and oversight of one’s doctor — especially when taking specific types of medication such as;

    1. insulin (or insulin analogues)
    2. medication to lower blood glucose such as sodium glucose co-transporter 2 (SGLT2) medication including Invokana, Forxiga, Xigduo, Jardiance, etc.,
    3. medication to control blood pressure such as Ramipril, Lasix (furosemide), Lisinopril / ACE inhibitors, Atenolol / βeta receptor antagonists, etc.,
    4. mental health medications such as antidepressants, medication for anxiety disorder, bipolar disorder (such as Lithium), and schizophrenia

Dr. Palmer recommends that doctors have their patients remain on their medication while starting a therapeutic ketogenic diet, and be evaluated during the stages of ketosis to see if there has been any significant change in symptoms [6]. 

[People who follow a therapeutic ketogenic diet for medical reasons are often asked to track their Glucose-Ketone Index (GKI) so their doctors can monitor the benefit of the diet. I teach people how to do that.]

Dr. Palmer suggests that individuals should trial a therapeutic ketogenic diet for a period of three months [6], and if the doctor finds that the diet is helping, they may begin to gradually deprescribe some medications. As mentioned in the “Don’t Try This at Home” article, changing dosages of medication is not something people should do on their own. 

In the podcast, Dr. Palmer makes an important point. With the gradual decrease in medications, people must realize that they are more reliant on the ketogenic diet to keep symptoms under control. Since the ketogenic diet is therapeutic, taking “cheat days” is not an option. Dr. Palmer notes that it takes several days to get back into ketosis after breaking the diet and during this time, symptoms can dramatically reappear [6].

Dr. Palmer says that if a Psychiatrist is interested in beginning to use a therapeutic ketogenic diet in their clinical practice, they must be “well-informed on the science behind a therapeutic ketogenic diet, as well as metabolic functioning as a whole”.

Dr. Palmer recommends that doctors begin with the following first two steps [6]:

    1. Find a licensed dietician knowledgeable in therapeutic ketogenic diets and partner with them. 

    2. Read the book “Ketogenic Therapies” by Dr. Eric Kossoff

Dr. Eric Kossoff’s book, Ketogenic Diet Therapies for Epilepsy and Other Conditions is one that have referred to often over the last 5 years of designing therapeutic ketogenic diets in different applications. 

Steps to Getting Started 

If you are thinking of adopting a ketogenic for improved mental health, then the first step is to reach out to your doctor.  To assist you in having this type of discussion, please feel free to download this letter. 

If your have already discussed this and your doctor is willing to oversee your health and medications while you adopt the diet, I can provide you with a Request for Medical Supervision Form. 

[UPDATE (June 21, 2023): There is emerging evidence from a June 3, 2023 pre-publication paper that the easier-to-follow 2:1 ketogenic diet may work well as an adjunct treatment in mental health disorders, such as bipolar disorder. You can read more about that in this more recent article.

More Info

If you would like more information about having a therapeutic ketogenic diet designed for you, please send me a note using the Contact Me form at the top of this page.

To your good health!

Joy

 

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

  1. Danan A, Westman EC, Saslow LR, Ede G. The Ketogenic Diet for Refractory Mental Illness: A Retrospective Analysis of 31 Inpatients. Frontiers in Psychiatry, 06 July 2022. https://doi.org/10.3389/fpsyt.2022.951376 

  2. Palmer, C.M., J. Gilbert-Jaramillo, E.C. Westman. “The Ketogenic Diet and Remission of Psychotic Symptoms in Schizophrenia: Two Case Studies.” Schizophrenia Research. 2019 June; 208: 439-440, ISSN 0920-9964. https://doi.org/10.1016/j.schres.2019.03.019
  3. Sarnyai, Z, Palmer, C.M.,Ketogenic Therapy in Serious Mental Illness: Emerging Evidence, International Journal of Neuropsychopharmacology, Volume 23, Issue 7, July 2020, Pages 434–439, https://doi.org/10.1093/ijnp/pyaa036

  4. Norwitz, N., G.A. Dalai, S. Sethi; C. Palmer. “Ketogenic diet as a metabolic treatment for mental illness.” Current Opinion in Endocrinology & Diabetes and Obesity: 2020 Oct: 27(5): 269-274. 

  5. Eastman, M., KetoConnect, The Ketogenic Ratio Explained, September 16, 2014, https://www.myketocal.com/blog/the-ketogenic-ratio-explained/

  6. Dr. David Puder, MD, Psychiatry Podcast, Episode 163, Dr. Chris Palmer: Ketogenic Diet for Mental Health, M=November 15, 2022, https://www.psychiatrypodcast.com/psychiatry-psychotherapy-podcast/163-treating-mental-health-disorders-with-a-ketogenic-diet

 

Copyright ©2023 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Nutrition is BetterByDesign - therapeutic ketogenic diets

Thyroid Medication can Worsen Blood Sugar Control in People with Diabetes

Did you know that thyroid medication can worsen blood sugar? The ‘highlights of prescribing information” sheets available to pharmacists and doctors for medications such as Synthroid® (generic: levothyroxine) and Cytomel® (generic liothyronine) warn that both these types of thyroid medication can worsen blood sugar control in diabetics, and increase the need for diabetes medications, including insulin. 

I didn’t know this.

Even though I had been diagnosed with type 2 diabetes more than twelve years ago and with hypothyroidism this past August, when I was prescribed thyroid medication, the pharmacist didn’t mention it when I first filled my prescription, nor was I provided with any printed information when my thyroid medication was delivered. My doctor didn’t mention it either but understandably, he knew I had been in remission of diabetes for three years prior to be diagnosed with hypothyroidism and probably didn’t think of me as being diabetic.  He was well-aware that for three years prior to be diagnosed with hypothyroidism, I did not meet the diagnostic criteria for type 2 diabetes either on the basis of fasting blood glucose or HbA1C because I controlled my blood sugar through diet.

When I began taking thyroid medication after my diagnosis of hypothyroidism, I began to periodically feel unwell as I did when I had high blood sugar.  I began to test my blood glucose more often and discovered that it was routinely spiking as high as the mid- to high 10 mmol/L (~190 mg/dl) for seemingly no reason. 

Effect of thyroid medication on blood sugar

I was totally puzzled as to why.  I didn’t eat simple carbs or starch-based food. I wasn’t sick, or under any new stress. I was sleeping well, was  properly hydrated, and there was no reason that I could think of that my blood sugar would keep spiking. In my search for answers, I stumbled across information that indicated that it should be well known that thyroid medication can worsen blood sugar control in people diagnosed with diabetes. For some reason, this information was not communicated to me, and when I asked others with both disorders, they were also unaware.

While I have already been eating low carb for the past three years, I began eating very low carb in order to get a better handle on the blood glucose spikes, and it is helping. I am also, in conjunction with my doctor, adjusting the timing of my thyroid medication around the timing of my meals to minimize the impact of the thyroid medication on my blood sugar and will continue to monitor my blood sugar several times per day. If need be, I will have my doctor either prescribe a medication such as Metformin to support normal blood sugar and/or trial different doses of thyroid medications. The important factor is I now know and can monitor this and make changes, as necessary. 

How many people have no idea?

Diabetes and Thyroid Medication 

It is essential that people diagnosed with any form of diabetes (type 1, type 2, gestational diabetes) as well as hypothyroidism know that their thyroid medication can impact their blood sugar control, as well as their need for diabetes medications, if they take any. Since those with type 1 diabetes and gestational diabetes have to monitor their blood glucose very closely, they would notice any changes, but many people with type 2 diabetes rarely regularly check. 

Thyroid Medication — highlights of prescribing information (product monographs) 

The “Highlights of Prescribing Information” sheets for both Synthroid® and Cytomel® that are available to doctors and pharmacists warn that therapeutic used of “these medications in patients with diabetes mellitus may worsen glycemic control and result in increased antidiabetic agent [i.e., diabetes medications] or an “increase in insulin requirements.” In addition, there is a warning on prescribing both medications to “carefully monitor glycemic control (i.e., blood sugar) after starting, changing, or discontinuing thyroid hormone therapy.” This means that people with diabetes need to be continuing to monitor their own blood sugar and contact their doctors if there is a need to address worsening blood sugar control related to taking thyroid replacement medication.

The “Highlights of Prescribing Information” for Synthroid® [1] is a 19-page product monograph about this medication which states that it does “not include all the information needed to use this medication safely and effectively.” For that, there is the need to read the full prescribing information. In other words, these 19 pages are only a summary of all that is needed to use the medication safely and effectively! 

Below is page 1 of the 19 of the “Highlights of Prescribing Information” for Synthroid®.

Highlights of Prescribing Information for Synthroid – page 1 of 19 highlighted

If the relevant section wasn’t highlighted in yellow by me, how likely would it be that a pharmacist or physician would have noticed this warning amongst the 19 pages of fine type?

The “Highlights of Prescribing Information” for Cytomel® [2] is an 11-page product monograph about that medication. It also states that it does “not include all the information needed to use this medication safely and effectively.” Those sheets are just a summary, and there is the need to read the full prescribing information.

Below is page 1 of the “Highlights of Prescribing Information” for Cytomel®.

Highlights of Prescribing Information for Cytomel – page 1 of 11 highlighted

Again, if the relevant section wasn’t highlighted in yellow by me, how likely would it be that a pharmacist or physician would have noticed this warning amongst the 11 pages of fine type?

 


[Post publication note (May 1, 2023)] 

Since natural desiccated thyroid (NDT) also called natural desiccated extract (NDE) are not approved by the FDA or Health Canada as medications, there are no Prescribing Information sheets for products such as the US product Armour Thyroid®, or equivalent ERFA desiccated thyroid®,  in Canada, but both products contain the same warning.

Page 3 of 24 of the Product Monograph from Armour®  contains a warning under Contraindications;

“Thyroid hormone therapy in patients with concomitant diabetes mellitus or diabetes insipidus or adrenal cortical insufficiency aggravates the intensity of their symptoms. Appropriate adjustments of the various therapeutic measures directed at these concomitant endocrine diseases are required.”

Page 3 of 24 of the Product Monograph from Armour thyroid®

Page 1 of 9 of the Product Monograph from ERFA desiccated thyroid®  contains the same warning under Precautions;

page 4 of 9 Product Monograph Erfa Thyroid®

Recently published studies report that 11%–23% of people with type 2 diabetes also have hypothyroidism [6] making it essential that people with both diagnoses know about the possible effect of thyroid replacement on blood sugar control.

For those interested in the mechanism, a paper published last month explains how thyroid hormones contribute to a rise in blood glucose.  In the liver, thyroid hormones increases expression of glucose transporter 2 (GLUT2), which increases in both gluconeogenesis and glycogenolysis.  In liver, the thyroid hormone T3 increases gluconeogenesis by increasing activity of phosphoenolpyruvate carboxykinase (PEPCK), and in adipose tissue, thyroid hormones increase lipolysis, resulting in an increase in free fatty acid that stimulates hepatic gluconeogenesis [7].

Additional References

4.  Product monograph for Armour Thyroid: https://dailymed.nlm.nih.gov/dailymed/getFile.cfm?setid=56b41079-60db-4256-9695-202b3a65d13d&type=pdf

5. Product monograph for Erfa: https://pdf.hres.ca/dpd_pm/00034857.PDF

6. Talwalkar P, Deshmukh V, Bhole M. Prevalence of hypothyroidism in patients with type 2 diabetes mellitus and hypertension in India: a cross-sectional observational study. Diabetes Metab Syndr Obes. 2019 Mar 20;12:369-376. doi: 10.2147/DMSO.S181470. PMID: 30936734; PMCID: PMC6431000.

7. Eom YS, Wilson JR, Bernet VJ. Links between Thyroid Disorders and Glucose Homeostasis. Diabetes Metab J. 2022 Mar;46(2):239-256. doi: 10.4093/dmj.2022.0013. Epub 2022 Mar 24. PMID: 35385635; PMCID: PMC8987680.


Final Thoughts…

If you have any type of diabetes and have also been diagnosed with hypothyroidism (including Hashimoto’s disease, the autoimmune form), it is very important that you monitor your blood glucose regularly. 

Contact your doctor if you notice a worsening in your blood sugar control, and to have your doctor evaluate your need for an increased dosage of existing diabetes medications, or the introduction of these medications if you don’t currently take any.

Consider adopting a style of eating that is lower in carbohydrate than you currently eat. According to a 2019 consensus report from the American Diabetes Association, reducing overall carb intake has “the most evidence for improving glycemia [blood sugar]” [3] . But please keep in mind that while a low carb diet is safe and effective for those with diabetes, if you take certain types of medications it is necessary to have medical oversight before adopting a very low carbohydrate (“keto”) diet.

More Info

If you have diabetes or pre-diabetes* and would like information on how I can support you in better managing your blood sugar, please send me a note through the Contact Me form at the top of this page.

To your good health!

Joy

*Please note that I do not design Meal Plans for people currently taking insulin or insulin-analogue medication for diabetes as I do not have CDE certification.

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

  1. Food and Drug Administration, Highlights of Prescribing Information for Synthroid, https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/021402s034lbl.pdf
  2. Food and Drug Administration, Highlights of Prescribing Information for Cytomel, https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/010379s054lbl.pdf
  3. Evert, AB, Dennison M, Gardner CD, et al, Nutrition Therapy for Adults With
    Diabetes or Prediabetes: A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014

 

Copyright ©2023 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Hypothyroidism Update – six months of treatment since diagnosis

This update marks just over six months since I was diagnosed with profound hypothyroidism and began medication and nutritional treatment. It is written from a subjective perspective and thus is categorized as part of my personal story.


At the beginning of June 2022, our family was in Tofino (Vancouver Island) for the marriage of my youngest son. The groom’s eldest brother assumed that my inability to walk on the sand for family photos, up the path to the hotel, or to get up out of a chair was a result of me having “aged.” He had no idea that I was hiking in North Vancouver and Golden Ears Provincial Park for several hours at a time just the summer prior.

I knew something was wrong, and for several months, I assumed my feeling exhausted and having joint and muscle pain was a carry-over effect from having had Covid. But a cell phone picture of myself taken just before the wedding told me it had to be something else. Gradually, over several months, I went from looking as I had been the previous two years after losing 55 pounds to looking like I had regained everything. I later found out, it wasn’t fat but an accumulation of mucin in the skin that is one of the hallmark signs of myxedema. You can read more about myxedema and the skin changes associated with hypothyroidism here

Since it was a special occasion, I didn’t say anything to my family about how sick I felt, but I was beginning to think that I had become significantly hypothyroid since I last saw my doctor in person (due to Covid protocols). My plan was to contact him when I returned to the mainland, which I did.

Two weeks later, my doctor confirmed that my symptoms were consistent with a diagnosis of hypothyroidism. In fact, I was surprised when he mentioned that it was not unexpected in light of my lab work over the previous nine years, my past thyroid surgery several decades ago, and my having experienced periodic hypothyroid symptoms since that time. Nevertheless, it took almost a decade for me to get diagnosed because of the limitations placed on doctors regarding which tests they can requisition under what circumstances (more about the challenges of getting diagnosed with hypothyroidism here).

In addition to the clinical challenges of getting diagnosed, there is also the reality that the most common symptoms of hypothyroidism are often assumed to be “just aging.” For example, many people believe it is normal for ‘older adults’ to have body aches, joint pain, fatigue, feel chilled when others do not, experience constipation, have dry skin or hair loss, be forgetful, or to even experience depression. Unfortunately, many don’t realize that these are not typical signs of aging but ARE common symptoms of hypothyroidism. What compounds the challenge of getting diagnosed is that the symptoms of hypothyroidism are so non-specific that many would not give them a second thought. An older person limited to a “one-issue-ten-minute remote doctor’s appointment” would be unlikely even to bring them up.

For those who have been following this story, my diagnosis was not the end but the beginning of my journey. Three months later, I lost half my hair due to telogen effluvium, the most common form of diffuse hair loss that can occur after a profound stress, shock or traumatic event including childbirth, a thyroid disorder, or rapid weight loss. You can read more about that here.

When my hair loss continued due to androgenic alopecia (also common in hypothyroidism), I began to research which nutrients of importance had evidence for helping restore hair loss, and wrote this article. Knowing I had a second son’s wedding mid-February, I incorporated both nutritional supplements (oral and topical) to support me in my recovery from what my doctor called “profound hypothyroidism.”

This weekend was my second son’s wedding, and the difference between how I felt in June and now is incredible! Instead of wearing medical compression stockings and orthopedic shoes so I could walk, I wore regular nylons and dress pumps.

While my doctor said it would still take another six months or longer for the mucin to resolve in my legs and trunk of my body, I was SO pleased that my legs didn’t look like water-logged tree stumps, as they did in June! In addition, my face was no longer swollen beyond recognition. I looked like “me” rather than like I had been “inflated” with an air pump.  I felt human and presentable and unlike I did in June, I wasn’t self-conscious being in the family photos.

Looking at the two wedding pictures side-by-side (see below), it is evident that being on the correct dose and mix of thyroid hormones (thanks to the excellent support of my doctor) has made a significant difference! In addition to thyroid medication, I have also been supplementing with nutrients of importance in hypothyroidism, as well as nutritional supplements with evidence to restore hair loss in androgenic alopecia which I developed secondary to my diagnosis. My hair is gradually growing back in, and where once there was a bald shiny scalp, I have hair an inch or two long. I also have eyelashes again, and the outer thirds of my eyebrows are also coming back in. 

 

It is my hope that when the most recent newlyweds celebrate their first anniversary, that the residual symptoms of hypothyroidism will be behind me.

Final thoughts…

If you have wondered if you have symptoms that may be consistent with hypothyroidism, you can download a checklist of common hypothyroid symptoms here to help you have an informed discussion with your doctor to determine whether thyroid hormone testing is warranted.

More Info?

If you would like more information about how I could support you from a nutritional perspective, please send me a note through the Contact Me form at the top of this page.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

Copyright ©2023 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

 

Alopecia Universalis – a clinician’s personal story of complete hair loss

Three years ago, Tim Rees, a clinician from Germany, lost all his hair a second time to alopecia universalis (AU).  As a registered clinical nutritionist he felt he had lost his credibility to help others with autoimmune conditions, and when he expressed those feelings in a recent blog (link below), it struck a chord with me. 

Tim Rees with his son in 2022

“All my hair fell out, but it was my response to it that destroyed me. You could be forgiven for thinking this is all centered around vanity, but the thing that crushed me was that it made me feel like a fraud.” ~Tim Rees, registered clinical nutritionist

As a clinician, I felt similarly when I lost half my hair in September of 2022. I wondered if others would consider me a “failure” for not having been able to prevent it.

Neither Tim nor I are physicians and thus are not qualified to diagnose conditions (in ourselves or in others). Our role is to provide nutrition education or medical nutrition therapy for conditions diagnosed by physicians. 

I was so struck by Tim’s recent post sharing about his complete hair loss and how he felt about it as a clinician, that I asked his permission to share his story. Below is an excerpt of his recent post. My goal in sharing this is so that people can understand what alopecia universalis is, and how it feels as a clinician to be diagnosed with an auto-immune disorder. It is my hope that sharing Tim’s post will enable people to better understand that clinicians with health conditions (whether autoimmune or not) are no less able to support their clients. What makes a clinician knowledgeable is their training and ongoing study in their area of clinical practice and I do not believe that a clinician diagnosed with an autoimmune disorder or metabolic disease is disqualified from being able to help others. On the contrary, provided they remain objective, I think a clinicians’ ability to understand their clients’ clinical struggles from “both sides of the clinical desk” while offering evidence-based support may be an asset.

I will begin with a very brief explanation of the disorder itself, so Tim’s words make sense.

Alopecia Universalis

Alopecia universalis (AU) is an advanced form of alopecia areata (AA) which is a condition that causes round patches of hair loss. This recent article describes alopecia areata and shows pictures of what it looks like.

In alopecia universalis, there is a complete loss of hair on the scalp and all over the body and it is thought to be an autoimmune condition in which the person’s immune system mistakenly attacks the hair follicles [1].


This Year I Stopped Hiding – a clinician story

(written by registered clinical nutritionist, Tim Rees)

“Three years ago my hair started falling out for the second time. In fact, I’d only had it all back for about 6 months before I got gut-punched standing before the mirror. “It’s not as bad as last time,” I said to myself.

But like an unstoppable rebel force (name the movie) my immune system killed my hair follicles and the hair dropped away like oak leaves in autumn, minus the orange. Alopecia Universalis, not a single hair remained on or in (I’m told) my body.

At the same time, the entire world went into lockdown and the corporate presenting side of my business died along with my self-esteem, my confidence and my monthly hairdressing appointment. There had never been a better time to hide.

You could be forgiven for thinking this is all centered around vanity, but the thing that crushed me was that it made me feel like a fraud. I was so embarrassed the thought of people discovering my secret presented as physical pain. Alopecia, one of the most visible autoimmune diseases one can have, undermined my work and, I thought, my credibility as a nutritionist helping people with autoimmune conditions.

But that’s not true. I’ve done amazing things with nutrition for myself and my clients. Until fairly recently I had lost my hearing to the point that I could no longer use the phone and was conducting sessions using Skype subtitles and talking non-stop in the hope I’d cover their questions before they thought them up. I have a whole list of reasons-why-I’m-not-a-fraud but I won’t bore you with them, after all, most of these insecurities are in my head.

But, here’s the thing. I think I can reverse this condition. Two years ago I stuck to my exclusion diet for four months by which time I had quite a lot of regrowth. Fluffy like a baby owl but still, living follicles. In fact, I remarked to my helpless doctor that I wasn’t worried about the hair, that it was coming back and all was fine. Ever the optimist. But after some bad luck, I began compromising a little here, and a little there, it was Christmas after all, and before I knew it I was doing a passable impression of a bowling ball again.

This year will be different. I’m plastering this all over social media for a number of reasons. Firstly, it’s a part of my acceptance. I fought hard against acceptance mistaking it for defeat. The truth is, you must accept how things are today in order to make a difference tomorrow.

Secondly, after posting a couple of photos on Twitter, I already feel better. And, thirdly it’ll help to keep me motivated and compliant for however long it takes to allow my body to heal.

I’ve been drifting and failing as a husband, as a new father and as a man. Not because I have alopecia but because I’ve let it destroy me. There’s a stoic lesson in there.”

[Shared with permission from Tim Rees’ blog.]


As Tim outlines in the full article, it is his goal this year to reverse his alopecia universalis, and like I did when I set out to recover my own hair loss from telogen effluvium and androgenic alopecia, he will be sharing his progress on social media for all the world to see. 

Tim plans to use an exclusion diet as well as nutritional supplements and to document why he is using them.  He also intends to integrate other approaches which he hopes will support his goal, including the use of sauna, cold thermogenesis, exercise, circadian rhythm / light exposure, etc. and document what he found helpful. While this will be Tim’s personal account of what he is doing to improve his hair loss, I am confident that as a clinician, he will document his choice of approaches and provide references.

I applaud Tim’s boldness and bravery to stop “hiding” and to live his hair loss story and goal of hair loss restoration in a public way. I wish him all the very best in achieving his goal.  

Final Thoughts…

It is important to keep in mind that what may work for Tim may not work for others diagnosed with the alopecia universalis, anymore than the nutrients I took would work for others diagnosed with telogen effluvium and androgenic alopecia. I chose to not write about which nutrients I took and in what dosages because it was not relevant to anyone other than me. I did write two referenced articles related to nutrient supplementation and hair loss and the first one was Hair Loss in Hypothyroidism (Part 2) – Nutrients of Importance  and the second was Nutritional Supplements With Evidence to Restore Hair Loss.

Since taking some nutritional supplements is not without risk, I would encourage anyone considering doing this to first consult with a qualified healthcare professional. Let them assess you to help determine which nutrients may be low or deficient based on dietary intake, and lab work.

A registered clinical nutritionist such as Tim Rees, BSc mBANT rCNHC from Ebersberg, Germany is licensed to support people in that country and I can support people in several provinces in Canada. If you would like more information on how I can help, please send me a note through the Contact Me form at the top of this page and you can reach out to Tim on his blog.

[Please note that I do not know Tim personally and as such this article is not an endorsement.]

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

  1. National Institute of Health, Genetic and Rare Diseases Information Centre, Alopecia universalis, https://rarediseases.info.nih.gov/diseases/614/alopecia-universalis

 

Copyright ©2023 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

The Androgen Paradox of Hair Growth and Hair Loss

Androgens are male hormones and as explained below, contribute to hair growth in both men and women. But, androgens also contribute to hair loss, such as in androgenetic alopecia. This is known as the “androgen paradox”.

As explained in the previous article, one of the main contributors to both male pattern baldness and female pattern baldness, also known as androgenetic alopecia, is the hormone dihydrotestosterone (DHT). DHT is a male hormone (androgen) that is a metabolite of testosterone made by the enzyme  5 alpha-reductase (5-AR) acting on testosterone. 

But androgens also play an important role in hair growth.

The Androgen Paradox

Before people go through puberty, most parts of the body (except for the scalp) are covered in thin, fine hair known as vellus hair (“peach fuzz”). Vellus hair is generally lighter and shorter than terminal hair that grows on the scalp, which is longer and thicker [1]. As androgens increase during puberty, vellus hair follicles are change into terminal hair follicles which then produce larger, curlier, and darker hair which appears in the public area, and “arm pits” (axillary area) [1].

During puberty, androgens stimulate beard growth in men [1], but even though androgens such as testosterone, androstenedione, dehydroepiandrosterone (DHEA), and DHEA sulfate (DHEAS) are produced by the ovaries and adrenal glands of healthy women, these are not in large enough quantities to stimulate hair growth on the face. In women with Polycystic Ovarian Syndrome (PCOS) however, hair on the upper lip and chin area (hirsutism) is common and is believed to be due to high levels of male androgens and abnormal levels of luteinizing hormone (LH) from the pituitary interfering with the normal function of the ovaries [2,3].

Paradoxically, androgens also contribute to hair loss in androgenetic alopecia (AGA) [4].  A double blind control study from 1994 of people with androgenetic alopecia found that DHT levels were significantly higher in areas of bald scalp, than in areas of the scalp that contained hair [5]. In 1996, it was determined that the parts of the scalp that show balding in androgenetic alopecia have higher levels of the enzyme 5 alpha-reductase (5-AR) in the hair follicles, than the hair follicles in the parts of the scalp that do not bald [6]. These higher levels of 5-AR in the hair follicles converts testosterone to DHT, and when DHT binds to the receptors in the oil glands of hair follicles, it causes the follicles to shrink, or “miniaturize” until they eventually stop producing hair, resulting in baldness. 

As mentioned in the previous article, 5 alpha-reductase (5-AR) can be inhibited by the drug Finasteride® which lowers levels of DHT in the hair follicle, reducing the attack and slowing, or stopping hair loss.  Finasteride® also reduces the amount of DHT in the blood and scalp [7,8] and slowing androgenic alopecia progression.

As outlined in the first article in the three-part series titled, “Lotions, Potions, and Pills”, there are nutritional supplements available that are documented to restore hair growth and that are supported with the highest-quality evidence. A few of them are 5 alpha-reductase (5-AR) Inhibitors, and function similarly to Finasteride®.

The upcoming second article in the series will outline several oral hair growth supplement mixtures with the best quality scientific evidence to support hair growth — some of which also act as 5 alpha-reductase (5-AR) Inhibitors.

In addition, the third upcoming article in the series will outline evidence-based topical hair supplements that either serve as 5-AR reductase inhibitors to reduce the effect dihydrotestosterone (DHT) on hair follicles, support scalp health through their antibacterial or antimicrobial properties, or stimulate hair growth by increasing blood flow to hair follicles.

Final thoughts…

Androgens can paradoxically stimulate hair growth and cycling and this results in men having more hair on their face, and both men and women having hair in their pubic region and arm pits. Androgens can also contribute to balding on the scalp in the same individual, regardless of gender [9].

The balding effect of dihydrotestosterone (DHT) acting on hair follicles of the scalp can be reduced with use of medication treatment such as Finasteride®, as well as by evidence-based oral nutritional supplements and topical applications of essential oils, botanicals, and herbals.

While  Finasteride® is very effective at treating the hair loss associated with androgenic alopecia (as well as benign prostate hyperplasia (BPH)), its use is not without potential side effects. These can include decreased libido, the inability of men to have or maintain an erection, or problems with ejaculation [10]. 

Use oral nutritional supplements supported by robust scientific studies to promote hair growth and/or the use of topical applications of essential oils, botanicals, or herbals that have been demonstrated to be both safe and effective at reducing or stopping hair loss is also an available option.  Click here to read the first of three articles in a series on this topic.

More Info?

If you would like more information about how I could support you from a nutritional perspective, please send me a note through the Contact Me form at the top of this page.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

    1. Inui, S., Itami, S. (2013). Androgen actions on the human hair follicle: perspectives. Exp. Dermatol. 22, 168–171. doi: 10.1111/exd.12024
    2. Barbieri RL, Ehrmann, DA. UpToDate Patient education: Polycystic ovary syndrome (PCOS) (Beyond the Basics), December 20, 2021, https://www.uptodate.com/contents/polycystic-ovary-syndrome-pcos-beyond-the-basics/
    3. Abdelazim IA, Alanwar A, AbuFaza M, et al. Elevated and diagnostic androgens of polycystic ovary syndrome. Prz Menopauzalny. 2020;19(1):1-5. doi:10.5114/pm.2020.95293
    4. Randall, V. A. (2007). Hormonal regulation of hair follicles exhibits a biological paradox. Semin. Cell Dev. Biol. 18, 274. doi: 10.1016/j.semcdb.2007.02.004
    5. Dallob, A. L., Sadick, N. S., Unger, W., Lipert, S., Geissler, L. A., Gregoire, S. L., et al. (1994). The effect of finasteride, a 5 alpha-reductase inhibitor, on scalp skin testosterone and dihydrotestosterone concentrations in patients with male pattern baldness. J. Clin. Endocr. Metab. 79, 703–706. doi: 10.1210/jcem.79.3.8077349
    6. Itami, S., Nakanishi, J., Yoshikawa, K., Takayasu, S. (1996). 21 Expression of androgen receptor, type I and type II 5 α-reductase in human hair follicle cells. J. Dermatol. Sci. 12, 86–86. doi: 10.1016/0923-1811(94)90434-0
    7. Drake, L., Hordinsky, M., Fiedler, V., Swinehart, J., Unger, W. P., Cotterill, P. C., et al. (1999). The effects of finasteride on scalp skin and serum androgen levels in men with androgenetic alopecia. J. Am. Acad. Dermatol. 41, 550–554. doi: 10.1016/s0190-9622(99)80051-6
    8. Price, V. H. (1999). Treatment of hair loss. New Engl. J. Med. 341, 964–973. doi: 10.1056/NEJM199909233411307
    9. Miranda, B. H., Charlesworth, M. R., Tobin, D. J., Sharpe, D. T., Randall, V. A. (2018). Androgens trigger different growth responses in genetically identical human hair follicles in organ culture that reflect their epigenetic diversity in life. FASEB J. 32, 795–806. doi: 10.1096/fj.201700260RR
    10. MedlinePlus [Internet]. Bethesda (MD): National Library of Medicine (US); [updated 2022 Jun 15]. Finasteride, Available from: https://medlineplus.gov/druginfo/meds/a698016.html 

Copyright ©2022 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Nutritional Supplements With Evidence to Restore Hair Loss

People’s identity is tied to their appearance, which makes significant hair loss at any age or gender devastating, but can nutritional supplements help?

Those experiencing different types of hair loss are often desperate to find a solution, and there is no shortage of lotions, potions, and pills promising new hair growth. Are these safe and effective, or are they simply “snake oil”? This article is about evidence-based nutritional supplements that may help restore hair loss, depending on its cause. It’s important to keep in mind that nutrient needs between people differ, so supplementation is not one-size-fits-all.

Androgenic Alopecia

Androgenic alopecia is commonly known as “male pattern baldness” or “female pattern baldness,” and the leading cause of it is an androgenic hormone known as dihydrotestosterone (DHT). DHT binds to the hair follicle, causing it to shrink, and eventually, the hair stops growing entirely. Some nutritional supplements positively affect DHT and help support hair growth, but many “hair growth nutritional supplements” contain ingredients for which evidence of benefit is lacking.

A study at an alopecia clinic [1] found that 81% of the patients were female, and 63% of them used nutritional supplements, compared to the US average of 40% [2]. The most common hair loss supplements used include biotin, vitamin B12, and B-complex multivitamin and while taking these nutritional supplements may seem benign, biotin, for example, is well-known to interfere with diagnostic tests for Thyroid Stimulating Hormone (TSH). The implication of this is that people taking biotin-containing supplements to self-treat hair loss without first being evaluated for a thyroid disorder may result in missing the diagnosis and underlying cause of their hair loss. In addition to interfering with diagnostic tests, some ‘hair loss nutritional supplements’ may be toxic in high doses, while still others may interact with medications, or supplements that people are taking to restore a diagnosed nutrient deficiency [3]. 

A systematic review that was recently published in the Journal of the American Medical Association (JAMA) Dermatology (November 30, 2022) evaluated the effectiveness of nutritional supplements for treating hair loss in people without nutritional deficiency [4]. This first article is based on this current systematic review.

Three Main Types of Hair Loss

There are three main types of hair loss, telogen effluvium, androgenic alopecia (AGA), and alopecia areata (AA).

Telogen effluvium (TE) is the most common form of diffuse hair loss [5] and usually occurs after a profound stress, shock or traumatic event including childbirth,  a thyroid disorder, or rapid weight loss. This type of hair loss was covered in this earlier article. But TE is not the only type of hair loss in hypothyroidism. In a study of more than 1200 people with thyroid disorder, half (50%) of people aged 40 years old and older had either alopecia areata, or androgenetic alopecia [6].

Androgenic alopeciaAndrogenic alopecia (AGA) affects up to 50% of men and women. In men is called ‘male pattern baldness’ and is mainly seen on the crown of the head and the temples. In women, it is called ‘female pattern baldness’ and is primarily seen at the crown of the head, with a broader center part. Androgenic alopecia is a genetic disorder that involves both maternal (mother’s) and paternal (father’s) genes, with sons being 5-6 times more likely to have it if their fathers were balding [7]. 

Alopecia areataAlopecia areata (AA) is an autoimmune disorder where the body’s immune system attacks the follicles. As a result, hair often comes out in clumps, usually the size and shape of a quarter, but it can affect more expansive areas of the scalp [8]. It can occur in those with other autoimmune conditions, including thyroid disease. 

There are medication treatments available for the different types of hair loss, and there is increasing evidence that taking specific nutritional supplements can be helpful in helping restore hair loss.

A systematic review published in JAMA Dermatology [4] published November 30, 2022 — just a month ago, evaluated the effectiveness of nutritional supplements for treating hair loss in people without nutritional deficiency. The dietary supplements with the highest-quality evidence of potential benefit were categorized according to their mechanism of action and are outlined in this article.

Dihydrotestosterone (DHT) as a Main Cause of Hair Loss

One of the main contributors to androgenetic alopecia (AA) is the male hormone (androgen) called dihydrotestosterone (DHT). DHT is made by an enzyme called 5 alpha-reductase (5-AR) acting on testosterone. When DHT binds to the receptors in the oil glands of hair follicles, it causes the follicles to shrink, shortening their life span. Eventually, these follicles shrink so much that they stop producing hair. The end result is baldness. DHT can be suppressed by medications such as Finasteride®, which lowers levels of DHT. This reduces the attack on hair follicles, slowing or stopping hair loss.

(Minoxidil® is a hair loss medication that works by an entirely different mechanism. It acts as a vasodilator, increasing blood flow in the scalp by making blood vessels wider. It is thought that this increased blood flow slows hair loss and encourages hair to regrow.)

[Update, December 29, 2022: While androgens such as DHT contribute to baldness by their detrimental effect on hair follicles in the scalp, androgens like DHT are also a key player in hair growth. This contradictory role of androgens is known as the “androgen paradox”. This short supplemental article explains more. ]

Nutritional Supplements – the role of 5-α reductase (5-AR) inhibitors in restoring hair loss

Pumpkin Seed Oil as a nutritional supplement in hair loss

nutritional supplements - Pumpkin seedsPumpkin seed oil is known to be effective in treating benign prostate hyperplasia (BPH) because it acts as a 5AR inhibitor [9,10], so it was an excellent candidate to study for its effect on hair growth. In a 2014 study, 76 male androgenic alopecia (AGA) patients were divided into two groups. For 24 weeks, one group of subjects took a 400 mg capsule of pumpkin seed oil each day, while the other group took a placebo. The group taking the pumpkin seed oil nutritional supplement showed significantly superior hair growth, with a mean hair count increase of 40% in the pumpkin seed oil-treated men compared to 10% in the placebo-treated men. There were no differences in adverse effects between the two groups.

Nutritional Supplements in Hair Loss – Saw Palmetto

nutritional supplements -Saw PalmettoIn a 2004 pilot study, six of ten subjects (60%) that took an extract made from 200 mg Saw Palmetto extract (Serenoa repens), 50 mg betasitosterol, along with 50 mg lecithin, 100 mg inositol, 25 mg phosphatidyl choline, 15 mg niacin, and 100 μg biotin for 5 months were reported to have improved hair growth compared to the placebo controlled group (11%), however the difference was not statistically significant [11]. Studies with larger groups of both treatment and control groups is needed before conclusions can be made. Most importantly, it is hard to know if the benefits were due to the Saw Palmetto, or some of the other ingredients in the supplement.  For this reason, I think this next study is more helpful.

A two year randomized control study of 100 male patients with mild to moderate androgenic alopecia took either 320 mg of dry Saw Palmetto nutritional supplement extract (Serenoa repens) daily for 24 months, or 1 mg Finasteride daily for the same time period.  While Finasteride was significantly more effective at slowing hair loss, at 24-months the Saw Palmetto extract did stabilize hair loss. [12].

The results of this study suggest that Saw Palmetto can stabilize hair loss over two years, but is less effective than the medication Finasteride.

The Role of Specific Micronutrients in Restoring Hair Loss

Nutritional Supplements for Hair Loss – Vitamin D

Three studies from the last 5-10 years have demonstrated that that lower levels of vitamin D, or vitamin D deficiency have been associated with all three forms of hair loss, including androgenic alopecia [13], alopecia areata [14], and telogen effluvium [15].

A small 2021 study supplemented 40 women with telogen effluvium with very high oral vitamin D3 (200,000 IU every two weeks for six weeks). The study reported that more than 80% had improved results on a hair pull test after six months, with no adverse side effects [16]. However, the limitation of this study was that it was unknown if any of these subjects were deficient in vitamin D before taking the supplements, there was no control group, and telogen effluvium tends to resolve by itself over the same six-month period without treatment.

nutritional supplements - vitamin D capsulesBefore beginning supplementation, it would be prudent to assess vitamin D status and to determine how low or deficient it is, then increase dietary intake of vitamin D, and supplement as necessary to attain and maintain sufficient blood levels of vitamin D.

nutritional supplements - salmon as a source of vitamin DFoods that are naturally good sources of vitamin D include fatty fish such as salmon, mackerel and tuna.

Nutritional Supplements for Hair Loss – Zinc

A deficiency of zinc is associated with telogen effluvium, and lower zinc levels have been observed in people with alopecia areata (AA) [17-19]. Two small studies of zinc supplementation in patients with alopecia areata both reported benefits. The first study with 38 subjects was from 1981 [20] and supplemented using 220 mg of zinc sulfate per day. The second study from 2012 [21] had 67 subjects supplemented with 5 mg/kg body weight per day of zinc sulfate. Both studies reported benefits at three months; however, larger studies are needed.

It would be best to assess zinc status for those with hair loss (especially alopecia areata) prior to supplementing with zinc.

sea urchin roe as a source of zincIf zinc status is low, increasing dietary intake of zinc would be a great place to start. Good sources of zinc include red meat, poultry, seafood such as oysters, crab, lobster, and sea urchin (uni, in Japanese), as well as nuts.

If needed to achieve adequate blood levels of zinc, a supplement can be added to attain, and maintain zinc adequacy, but it’s important to ensure there is adequate copper intake as well, as zinc depletes copper. Beef liver is a very good source of dietary copper, but eating 3 or 4 ounces once a week may be enough, as it has 6 times the recommended dietary intake of copper, and high amounts of preformed vitamin A. It is also important not to take zinc supplements within several hours of taking iron supplements, as they complete for binding sites.

Nutritional Supplements for Hair Loss – Vitamin B12

Vitamin B12 is necessary for DNA synthesis and it was proposed in a 2017 report on the role of micronutrients in alopecia areata that vitamin B12 could be helpful in increasing the number of hair follicles [17].

A 2018 study of people with telogen effluvium that included symptoms of itching, pain, soreness, and/or burning were evaluated for symptoms of B12 deficiency. While lab normal values were 200-400 pg/mL, deficiency was evaluated to be <550 pg/ml, a cutoff limit reported to be used in other countries. After four months, 90% of subjects that received either a daily B12 tablet or monthly B12 injection had significant decrease or even an absence of hair shedding [23]. The main shortcoming of this study was the self-resolving nature of telogen effluvium — which means that over the same period of time, doing nothing could have resulted in improvement is hair loss.

nutritional supplements - liver as a source of vitamin B12The best dietary sources of vitamin B12 are organ meats, including liver and kidney, clams, sardines, and beef, however, some disorders and advanced age can result in reduced dietary absorption of vitamin B12. Testing vitamin B12 status is important especially in older adults who have decreased absorption of B12 due to decreased intrinsic factor, as well as testing B12 status in those taking medication to lower stomach acid. 

Nutritional Supplements – the role of antioxidants in restoring hair loss

Oxidative stress has been thought to play a role in all three types of hair loss [24-26] and antioxidants such as selenium, vitamins A, E and C, and carotenoids (yellow, orange or red coloured fat-soluble pigments found in vegetables, fruit, and some fish. 

A 2015 randomized control study compared the effects of giving a supplement containing omega 3 fat from fish, omega 6 fat from blackcurrant seed oil, as well as the antioxidants lycopene (from tomato), vitamin C, and vitamin E versus giving no supplement to 188 women diagnosed with stage 1 androgenic alopecia [27]. The intervention group had significantly increased hair density and hair thickness at six months.

A 2010 randomized control study compared giving a supplement containing mixed tocotrienol from the vitamin E family versus a placebo to patients with unspecified hair loss. The 50 mg mixed capsules given to the intervention group had 30.8% alpha-tocotrienol, 56.4% gamma-tocotrienol, and 12.8% delta-tocotrienol, as well as 23 IUs alpha-tocopherol). Twenty one subjects were randomly assigned receive 2 x 50 mg (100 mg) of mixed tocotrienols daily, while 17 subjects were assigned to receive an oral placebo capsule. At 8-months, the number of hairs of the subjects in the intervention group increased by 34.5% compared to the placebo group which had a 0.1% decrease [28]. The shortcomings of this study were the small sample size and that the study did not define hair loss in the inclusion criteria of subjects. 

Nutritional Supplements – more is not always better

Caution needs to be taken when choosing types and amounts of antioxidant supplements as excessive use of supplements such as selenium, for example has been tied both to toxic effects and hair loss [29]. Even when getting selenium in the diet by eating Brazil nuts, only 2 is already at the maximum daily amount. Eating 4 or 5 Brazil nuts can exceed the safe upper tolerance of selenium for adults, so more is not better. 

Excess vitamin A intake can result in vitamin A intoxication which can result in seizures or blurred vision, and long term (chronic) over supplementation with vitamin A can result in several symptoms, including muscle and bone pain, high blood lipids and ironically alopecia, or hair loss [30].

nutritional supplements - cod livers as a source of vitamin AThe best sources of preformed vitamin A (retinol) are beef liver, fish, and eggs and a delicious and very rich source is Icelandic cod livers.

Cod livers are very high in retinol, and just half a 115g can contains 450% the recommended daily intake for vitamin A. To avoid getting too much preformed vitamin A, it is best not to eat cod livers more than once every week or two, and even further apart if also regularly consuming beef liver which is also high in preformed vitamin A.

Before beginning to take supplements it is important to assess intake form food sources, so as not to take too much as a supplement.

Other Nutritional Supplements – probiotics and growth hormone modulators

kim chee as a probioticProbiotics have been hypothesized to improve blood flow to the scalp and one study from 2020 used a kimchi and fermented soybean paste (cheonggukjang) probiotic product.

Twenty-three men and twenty-three women with androgenic alopecia (AGA) were given the supplement and at four months, 93% showed significant improvement in either hair thickness and/or hair count, with no serious side effects [31]. The limitations of this study were the small sample size and lack of a control group.

capsaicin Capsaicin, is the chemical that give hot chilis their spiciness and is used as a topical pain reliever. When  applied to the scalp has been found to increase Insulin-like Growth Factor I (IGF-1) which is involved in hair growth [32].

A randomized control study of a capsaicin and isoflavone supplement (6 mg capsaicin, 75 mg isoflavone (from soy) in 48 adults with either androgenic alopecia (AGA) or alopecia areata (AA) compared to controls found significantly more hair growth in the capsaicin and isoflavone group at 5 months, and no adverse effects were reported. The limitations of this study were its small sample size as well as the inclusion of various types of alopecia.

Final Thoughts…

In the United States, dietary supplements are normally considered a food and as such, their safety or effectiveness are not evaluated by the Food and Drug Administration (FDA). It is only if a product is labelled to treat a disease that the product meets the definition of a drug and needs to establish its efficacy [33].

In Canada, however, dietary supplements are considered Natural Health Products (NHP) by Health Canada and are treated as non-prescription drugs which are regulated under the Natural Health Product Regulations. According to Health Canada, in the ten years from 2004 (when the Natural Health Product Regulations came into existence) and 2014, nearly 55,000 licenses for NHPs were issued [34].

The ease by which Canadians can order supplements online from the US essentially bypasses any governmental safeguards put into place by Health Canada so it is important that people in both countries are aware that there is no FDA oversight for safety or efficacy for supplements purchased from the US. For this reason, it is best that before people begin using dietary supplements to self-treat hair loss, that they discuss this with a knowledgeable healthcare professional, such as their doctor or Registered Dietitian. In addition, for those already taking dietary supplements, it is important before going for lab tests to mention to your doctor and Dietitian which supplements you are taking so that they can ensure that you discontinue use of specific supplements for an sufficiently long period of time before the test (such biotin before a Thyroid Stimulating Hormone (TSH) test).

More Info?

Hair loss can be devastating, but before parting with substantial sums for money for lotions, potions, or pills that promise new hair growth, first take the time to find out what you need. 

Consider finding out if your diet or lifestyle may put you at risk for nutrient deficiencies, and if so to have those evaluated. Ask yourself if it is possible you may have a thyroid disorder (this article may help) so that you can have diagnostic tests before taking supplements that can interfere with getting accurate results.

Finally, if blood tests come back indicating that you may have low nutrient status or a deficiency, find out which nutrients can be adequately obtained from food, and which may need to be supplemented.

Nutritional supplements can be very helpful if used correctly, but taken in the wrong dosage, or at the wrong timing, supplements can interfere with the absorption of medications you may take, and/or with other nutrients you are already low on.

If you would like more information on how I can help assess your dietary intake or nutrient status of specific nutrients, please send me a note through the Contact Me form at the top of this page.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

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    2. E.D. Kantor, C.D. Rehm, M. Du, E. White, E.L. Giovannucci, Trends in dietary supplement use among U.S. adults from 1999–2012, JAMA, 316 (14) (2016), pp. 1464-1474
    3. Ronis MJJ, Pedersen KB, Watt J. Adverse effects of nutraceuticals and dietary supplements. Annu Rev Pharmacol Toxicol. 2018;58:583-601. doi:10.1146/annurev-pharmtox-010617-052844
    4. Drake L, Reyes-Hadsall S, Martinez J, Heinrich C, Huang K, Mostaghimi A. Evaluation of the Safety and Effectiveness of Nutritional Supplements for Treating Hair LossA Systematic ReviewJAMA Dermatol. Published online November 30, 2022. doi:10.1001/jamadermatol.2022.4867
    5. Malkud S. Telogen Effluvium: A Review. J Clin Diagn Res. 2015;9(9):WE01-WE3. doi:10.7860/JCDR/2015/15219.6492
    6. Vincent M, Yogiraj K. A descriptive study of alopecia patterns and their relation to thyroid dysfunction. Int J Trichol 2013;5:57-60
    7. Ho CH, Sood T, Zito PM. Androgenetic Alopecia. Updated Nov 15, 2021. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing, https://www.ncbi.nlm.nih.gov/books/NBK430924/#_NBK430924_pubdet_
    8. Medical News Today, Alopecia areata: Causes, diagnosis and treatments, April 7, 2022, https://www.medicalnewstoday.com/articles/70956
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    14. Rasheed H, Mahgoub D, Hegazy R, et al. Serum ferritin and vitamin D in female hair loss: do they play a role? Skin Pharmacol Physiol. 2013;26(2):101-107. doi:10.1159/000346698
    15. Lee S, Kim BJ, Lee CH, Lee WS. Increased prevalence of vitamin D deficiency in patients with alopecia areata: a systematic review and
      meta-analysis. J Eur Acad Dermatol Venereol. 2018;
      32(7):1214-1221. doi:10.1111/jdv.14987
    16. Sattar F, Almas U, Ibrahim NA, et al. Efficacy of oral vitamin D3 therapy in patients suffering from diffuse hair loss (telogen effluvium). J Nutr Sci
      Vitaminol (Tokyo). 2021;67(1):68-71. doi:10.3177/jnsv.67.68
    17. Thompson JM, Mirza MA, Park MK, Qureshi AA, Cho E. The Role of micronutrients in alopecia areata: a review. Am J Clin Dermatol. 2017;18(5):
      663-679. doi:10.1007/s40257-017-0285-x
    18. Abdel Fattah NS, Atef MM, Al-Qaradaghi SM. Evaluation of serum zinc level in patients with newly diagnosed and resistant alopecia areata. Int J
      Dermatol. 2016;55(1):24-29. doi:10.1111/ijd.12769
    19. Mussalo-Rauhamaa H, Lakomaa EL, Kianto U, Lehto J. Element concentrations in serum, erythrocytes, hair and urine of alopecia patients.
    20. Ead RD. Oral zinc sulphate in alopacia areata-a double blind trial. Br J Dermatol. 1981;104(4): 483-484. doi:10.1111/j.1365-2133.1981.tb15323.x
    21. Sharquie KE, Noaimi AA, Shwail ER. Oral zinc sulphate in treatment of alopecia areata (double blind; cross-over study). J Clin Exp Dermatol Res.
      2012;3(150).
    22. Siavash M, Tavakoli F, Mokhtari F. Comparing the effects of zinc sulfate, calcium pantothenate, their combination and minoxidil solution regimens
      on controlling hair loss in women: a randomized controlled trial. J Res Pharm Pract. 2017;6(2):89-93. doi:10.4103/jrpp.JRPP_17_17
    23. Daly T, Daly K. telogen effluvium with dysesthesia (ted) has lower B12 levels and may respond to B12 supplementation. J Drugs Dermatol.
      2018;17(11):1236-1240.
    24. Prie BE, Iosif L, Tivig I, Stoian I, Giurcaneanu C. Oxidative stress in androgenetic alopecia. J Med Life. 2016;9(1):79-83.
    25. Savci U, Senel E, Oztekin A, Sungur M, Erel O, Neselioglu S. Ischemia-modified albumin as a possible marker of oxidative stress in patients with
      telogen effluvium. An Bras Dermatol. 2020;95(4): 447-451. doi:10.1016/j.abd.2020.01.005
    26. Öztürk P, Arıcan Ö, Kurutaş EB, Mülayim K. Oxidative stress biomarkers and Adenosine deaminase over the alopecic area of the patients with alopecia areata. Balkan Med J. 2016;33(2):188-192. doi:10.5152/balkanmedj.2016.16190
    27. Le Floc’h C, Cheniti A, Connétable S, Piccardi N, Vincenzi C, Tosti A. Effect of a nutritional supplement on hair loss in women. J Cosmet
      Dermatol. 2015;14(1):76-82. doi:10.1111/jocd.12127
    28. Beoy LA,WoeiWJ, Hay YK. Effects of tocotrienol supplementation on hair growth in human volunteers. Trop Life Sci Res. 2010;21(2):
      91-99.
    29. Sutter ME, Thomas JD, Brown J, Morgan B. Selenium toxicity: a case of selenosis caused by a nutritional supplement. Ann Intern Med. 2008;148
      (12):970-971. doi:10.7326/0003-4819-148-12-200806170-00015
    30. Olson JM, Ameer MA, Goyal A. Vitamin A Toxicity. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-.
    31. Park DW, Lee HS, Shim MS, Yum KJ, Seo JT. Do kimchi and cheonggukjang probiotics as a functional food improve androgenetic alopecia? a clinical pilot study. World J Mens Health. 2020;38 (1):95-102. doi:10.5534/wjmh.180119
    32. Harada N, Okajima K. Effect of topical application of capsaicin and its related compounds on dermal insulin-like growth factor-I levels in mice
      and on facial skin elasticity in humans. Growth Horm IGF Res. 2007;17(2):171-176. doi:10.1016/j.ghir. 2006.12.005
    33. US Food and Drug Administration. Questions
      and Answers on Dietary Supplements. Accessed December 27, 2022. https://www.fda.gov/food/information-consumers-using-dietary-supplements/questions-and-answers-dietary-supplements
    34. Health Canada, Natural Health Products Program Quarterly Snapshot – Quarter 1 (Fiscal year 2014-2015), https://www.canada.ca/en/health-canada/services/drugs-health-products/natural-non-prescription/activities/quarterly-snapshot-quarter-1-2014-2015.html

 

Copyright ©2022 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Hair Loss in Hypothyroidism – nutrients of importance

In the previous article titled Hair Loss – root causes was about the three most common types of hair loss, including androgenic alopecia, alopecia areata, and the most common form of diffuse hair loss, telogen effluvium which is the type often associated with hypothyroidism.  This article explains the role of specific vitamin and mineral deficiencies in hair loss and how treating them can help restore hair growth.

As explained in the previous article, telogen effluvium (TE) is the most common form of hair loss in hypothyroidism and is where the hair often comes out in clumps in the shower or a brush. Hair loss is usually from all over the scalp but may occur more on the temples, the part, and the crown of the head [1]. But TE is not the only type of hair loss in hypothyroidism. In a study of more than 1200 people with thyroid disorder, half (50%) of people aged 40 years old and older had either alopecia areata, or androgenetic alopecia [2].

What makes the hair loss associated with thyroid dysfunction particularly challenging is that it occurs 2-3 months after the overt symptoms of thyroid disorder began, which is usually once they’ve already begun thyroid hormone treatment for hypothyroidism.

The pictures below are of me. The one on the left was taken at one of my son’s wedding in June 2022, just prior to being diagnosed with hypothyroidism.  I clearly had the symptom of edema (facial swelling, leg and hand swelling) associated with undiagnosed / untreated hypothyroidism, the hair on my head was minimally affected. The photo on the right was taken three months later, after beginning hormone replacement treatment for hypothyroidism, and the hair loss and shiny scalp is very apparent. 

No hair loss at height of untreated hypothyroidism, telogen effluvium hair loss 3 months later

Hair loss in hypothyroidism

Normally,  90-95% of hair follicles are in the growth (anagen) phase, with only 5–10% being in the resting (telogen) phase. Only a few follicles are in the transitional (catagen) phase [1] at any one time.  At the end of the telogen phase, the hair falls out and under normal circumstances that would amount to ~ 100-150 hairs per day.

Hair growth stages

 

In telogen effluvium, the growth (anagen) phase slows down and up to 50% of the follicles move into the telogen phase, where shedding occurs. i.e., hair loss becomes 5-10 greater than normal, with people losing up to 50% of their hair.  As can be seen in the photo above, at 3 months I had lost 50% of my hair. 

It wasn’t only half the hair on my head that I lost, also lost 1/2 my eyelashes and part of the outer third of my eyebrows.

Since the period of the most dramatic loss occurs approximately 2-3 months after the triggering event, many people don’t relate the shedding to the event that caused it. 

Hypothyroidism can result in hair loss, but nutrient deficiencies can sometimes underlie hypothyroidism (such as in iodine or iron deficiency) and can often make the symptoms of hypothyroidism worse.  Each person is different and the degree to which underlying nutrient deficiencies may make hair loss worse, varies.  As a result, the sufficiency of the key nutrients related to hypothyroidism should be evaluated. 

If any of these nutrients are found to be deficient or suboptimal, correct supplementation can support the regrowth of hair, but it should be noted that the timing of supplements with respect to each other and in relation to the timing of thyroid medication is essential. The reason for this is that some nutrients complete for binding sites (e.g., iron, zinc and copper) and need to be taken separated from each other. In addition, thyroid medication needs to be taken at least a half hour before and food or vitamin / mineral supplementation, or two hours afterwards. When there are several nutrient deficiencies and multiple doses per day of thyroid medication, this can take quite a bit of planning to get the timing right.

Iron deficiency is very common and one of the deficiencies that contributes to telogen effluvium [3,4], and iron is often low in hypothyroidism [5]. In some cases, treating iron deficiency may in itself be sufficient to restore thyroid function [5]. The reason is that the body requires sufficient iron to convert the inactive thyroid hormone thyroxine (T4) into the active thyroid hormone triiodothyronine (T3) and insufficient iron stores could interfere with this conversion. 

It has been recommend that to reverse significant hair loss due to telogen effluvium to maintain serum ferritin at levels of >157 pmol/L (70 ng/dL) [4].

Some of the best food sources of heme iron (the most bioavailable form) are oysters, clams and liver.

Adequate vitamin C intake is required for intestinal absorption of iron, so ensuring adequate vitamin C intake is important those with hair loss associated with iron deficiency.

Selenium was identified in the 1990s as a component of the enzyme that activates thyroid hormone through the conversion of (inactive) T4 to (active)T3 [6]. Selenium is also used to by the body for the formation of glutathione, a powerful antioxidant that protects the thyroid from inflammation and oxidative stress.

Food sources of selenium include Brazil nuts, with 2 Brazil nuts meeting the daily requirement of 200 mcg of selenium. Other good sources of selenium are mushrooms, eggs, fish such as cod and halibut, chicken and eggs. 

Selenium deficiency is a significant problem in the developing world, but thought to be rare in the West. Research from 2012 indicates that the selenium content of the soil in the US was already lowest in the major agricultural areas of the Northwest, Northeast, Southeast, and areas of the Midwest near the Great Lakes[7] and at the time, only the Great Plains and the Southwest were reported to have adequate selenium content in the soil [6].

Zinc plays a key role in the metabolism of thyroid hormones, specifically by regulating the enzymes that are involved in the activation of T4 to T3, as well as regulating thyrotropin releasing hormone (TRH), and thyroid stimulating hormone (TSH) synthesis [8]. Zinc also modulates structures of essential transcription factors that are involved in the synthesis of thyroid hormones, as well as influence the levels of TSH, T4,  and T3 in the blood [8]. It is important to be tested first to know if there is a zinc deficiency before taking a supplement, because supplemental zinc can result in a reduction in copper, and if taking zinc, it is important not to take it with iron or calcium supplements as they complete for binding sites.

Eating foods rich is zinc is the safest way to ensure adequate intake and good sources of zinc include red meat, poultry, seafood such as oysters, crab and lobster, as well a nuts. 

Vitamin D – in Canada which is above the 49th parallel, it is  known that between 70% and 97% of the population demonstrates vitamin D insufficiency, with 32% in Canada being Vitamin D deficient [9].  Deficiency of Vitamin D in the US is even higher, at 42% [10]. It has been known that there was a relationship between Hashimoto’s (autoimmune) hypothyroidism and Vitamin D deficiency [11], it is now known that non-autoimmune hypothyroidism is associated with vitamin D deficiency [12]. A randomized, double-blind, placebo-controlled trial from 2018 in over 200 hypothyroid patients aged 20-60 years old found that supplementing with vitamin D improved TSH levels and calcium levels in hypothyroid patients [13]. 

In addition to dairy foods that are fortified with Vitamin D, foods that are naturally good sources of Vitamin D include fatty fish such as salmon, mackerel and tuna.

 

Vitamin B12  – It is known that people with Hashimoto’s disease (autoimmune hypothyroidism) have a higher prevalence of pernicious anemia [14], which is caused by a deficiency of vitamin B12, either due to a lack of B12 the diet or an inability to absorb it. In addition, vitamin B12 deficiency can mimic many of the symptoms of hypothyroidism such as fatigue, weakness, yellowish skin, some of the mental health symptoms. The best sources of vitamin B12 are organ meats, including liver and kidney, clams, sardines, and beef.


[UPDATE: December 11, 2022] The photo on the top, below was taken three months after being diagnosed with hypothyroidism and beginning hormone replacement treatment. The hair loss is obvious, as is my shiny scalp. The photo on the bottom was taken today — three months later. It clearly shows the regrowth of hair which is the result of both hormone replacement treatment, and three months of nutrient supplementation to support regrowth. [Note: Each person’s results will be different of course, depending which nutrient deficiencies they may have, and whether these deficiencies were due to the hypothyroidism itself, the result of inadequate dietary intake, or both].

 

Hair regrowth after 3 months thyroid treatment and nutrient supplementation

…and the hair regrowth wasn’t only on my scalp.  When I first lost so much hair, I also lost most about half of my eyelashes, too.  A month ago (Nov. 18, 2022), I took a picture of them growing back in, and below is that photo and what they look like almost a month later (December 13, 2022), without any mascara or eyeliner.

Eyelashes growing back in

POSTSCRIPT (November 18, 2022):  In writing this post yesterday, I came across several research papers that referred to the role of several of the nutrients of importance to hair loss in hypothyroidism, to premature hair greying. While my grey hair certainly was not “premature,”  look what I found today! 

A recent study mapped hundreds of proteins inside of hair and found that white hairs contained more proteins linked to mitochondria and energy use which suggests that metabolism and mitochondria may play a role in hair greying. Since thyroid hormones are known to be the major controllers of metabolic rate, it makes sense that hair that was previously dark might turn grey as the result of hypothyroidism, and revert back to dark with thyroid hormone correction. 

[Rosenberg AM, Rausser S, Ren J, et al. Quantitative mapping of human hair greying and reversal in relation to life stress. Elife. 2021;10:e67437. Published 2021 Jun 22. doi:10.7554/eLife.67437]


Final Thoughts…

While treating hypothyroidism is a medical prescription of thyroid replacement medication in an optimal dosage, determining if any nutritional deficiencies may be contributing to the condition, or mimicking its symptoms, is essential.

Having dietary intake assessed and, if indicated, having blood tests to determine if nutrient deficiencies exist and correcting them can go a long way to helping people feel better and supporting regrowth from hair loss.

It is important to remember that taking supplements needs to be done wisely. “More is not better” when it comes to taking nutrient supplements.

For example, nutrients such as selenium can be toxic in excess amounts, even when eaten as Brazil nuts.

Some nutrients, such as biotin which is often taken by people for hair growth can interfere with thyroid hormone tests.

Iodine is another nutrient that should not be supplemented when people are taking thyroid hormone replacement medication.

If you aren’t sure if your nutrient intake or nutrient status of specific nutrients sufficient, then having a nutritional assessment and blood tests when needed is a great place to start. 

More Info?

If you have been diagnosed with hypothyroidism and would like to better understand the condition and make sure that you have adequate intake of nutrients known to be important in thyroid health, please send me a note through the Contact Me form.

To your good health!

Joy

 

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
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References

    1. Malkud S. Telogen Effluvium: A Review. J Clin Diagn Res. 2015;9(9):WE01-WE3. doi:10.7860/JCDR/2015/15219.6492
    2. Vincent M, Yogiraj K. A descriptive study of alopecia patterns and their relation to thyroid dysfunction. Int J Trichol 2013;5:57-60
    3. Almohanna HM, Ahmed AA, Tsatalis JP, Tosti A. The Role of Vitamins and Minerals in Hair Loss: A Review. Dermatol Ther (Heidelb). 2019;9(1):51-70. doi:10.1007/s13555-018-0278-6
    4. Trost LB, Bergfeld WF, Calogeras E. The diagnosis and treatment of iron deficiency and its potential relationship to hair loss. J Am Acad Dermatol. 2006;54(5):824–844.
    5. Ghiya R, Ahmad S. SUN-591 Severe Iron-Deficiency Anemia Leading to Hypothyroidism. J Endocr Soc. 2019 Apr 30;3(Suppl 1):SUN-591. doi: 10.1210/js.2019-SUN-591. PMCID: PMC6552785.
    6. Winther, K.H., Rayman, M.P., Bonnema, S.J. et al. Selenium in thyroid disorders — essential knowledge for clinicians. Nat Rev Endocrinol 16, 165–176 (2020). https://doi.org/10.1038/s41574-019-0311-
    7. Mistry HD, Broughton Pipkin F, Redman CW, Poston L. Selenium in reproductive health. Am J Obstet Gynecol. 2012 Jan;206(1):21-3
    8. Severo JS, Morais JBS, de Freitas TEC, et al. The Role of Zinc in Thyroid Hormones Metabolism. Int J Vitam Nutr Res. 2019;89(1-2):80-88. doi:10.1024/0300-9831/a00026
    9. Schwalfenberg GK, Genuis SJ, Hiltz MN. Addressing vitamin D deficiency in Canada: a public health innovation whose time has come. Public Health. 2010;124(6):350-359. doi:10.1016/j.puhe.2010.03.00
    10. Forrest KY, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US adults. Nutr Res. 2011;31(1):48-54. doi:10.1016/j.nutres.2010.12.001
    11. Botelho IMB, Moura Neto A, Silva CA, Tambascia MA, Alegre SM, Zantut-Wittmann DE. Vitamin D in Hashimoto’s thyroiditis and its relationship with thyroid function and inflammatory status. Endocr J. 2018;65(10):1029-1037. doi:10.1507/endocrj.EJ18-0166
    12. Ahi S, Dehdar MR, Hatami N. Vitamin D deficiency in non-autoimmune hypothyroidism: a case-control study. BMC Endocr Disord. 2020;20(1):41. Published 2020 Mar 20. doi:10.1186/s12902-020-0522-9
    13. Talaei A, Ghorbani F, Asemi Z. The Effects of Vitamin D Supplementation on Thyroid Function in Hypothyroid Patients: A Randomized, Double-blind, Placebo-controlled Trial. Indian J Endocrinol Metab. 2018;22(5):584-588. doi:10.4103/ijem.IJEM_603_17
    14. Ness-Abramof R, Nabriski DA, Braverman LE, et al. Prevalence and evaluation of B12 deficiency in patients with autoimmune thyroid disease. Am J Med Sci. 2006;332(3):119-122. doi:10.1097/00000441-200609000-00004

 

Copyright ©2022 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

 

 

Hypothyroid 101

Hypothyroid 101 provides an overview of what the thyroid does, the main thyroid hormones, the main causes of hypothyroidism, how hypothyroidism is diagnosed, as well as options for having thyroid blood tests done.

The Thyroid Gland

hypothyroid - the thyroidThe thyroid is butterfly-shaped gland situated in the middle of the lower front part of the neck. While it isn’t very big, it plays a very important role in the regulation of metabolism which is the process by which the food we eat is converted to energy.

When the thyroid doesn’t function properly, it affects metabolism. In the case that the thyroid is underactive (hypothyroid) this results in a slowing of everything from heart rate, our ability to generate heat to stay warm, for muscles to do work, and for us to think properly and process information.

The Two Main Thyroid Hormones – T4 and T3

The thyroid produces two main hormones, T4 (thyroxine) and T3 (triiodothyronine). When it’s working properly, 93% of the thyroid hormone produced by the body each day is T4, and only 7% is T3 [1]. The thyroid manufactures ~85mcg of T4 and 6.5mcg of T3 per day [1], which is a T4 to T3 ratio of 13:1.  

T4 is the inactive form of thyroid hormone and has four molecules of iodide bound to it. When it becomes activated, it loses one of the iodides and becomes T3, which is the active form.

In its free, unbound form, thyroxine is known as free T4 (abbreviated fT4) and in its free, unbound form triiodothyronine is known as free T3 (abbreviated fT3). 

The production of T4 and T3 in the thyroid is regulated by the pituitary gland, but the signal for the pituitary gland to tell the thyroid gland to make thyroid hormones comes from the hypothalamus region of the brain.  The hypothalamus releases a hormone called TRH (Thyrotropin-Releasing Factor) that acts on the pituitary gland, causing it to release a hormone called TSH (Thyroid Stimulating Hormone). It is TSH released from the pituitary gland that acts on the thyroid gland, causing it to release thyroxine.

 

hypothyroid - the Hypothalamus Pituitary Thyroid Axis
from [2] The Merck Manual of Medical Information (1997)

Hypothyroid – how it is diagnosed

In Canada and many places in the US, the standard screening test for abnormal thyroid function, including hypothyroid, is a blood test measuring thyroid stimulating hormone (TSH), which is a pituitary hormone. 

If TSH results falls within normal range, no testing of thyroid hormones occurs. The thyroid response to TSH is presumed to be normal. 

Central Hypothyroidism occurs when there is a problem with either the hypothalamus or the pituitary gland.

On lab tests, a low TSH and low free T4 indicates central hypothyroidism and this is often treated by prescribing medication, including T3 containing medications. 

Primary hypothyroidism is where there is no abnormality in the hypothalamus or the pituitary gland. It is diagnosed when there is high TSH, and normal or low free T4.

Hypothyroid – main causes 

In the developed world, the most common form of primary hypothyroid in is Hashimoto’s disease. In developing countries, it is mostly caused from a lack of iodine in the diet. Other causes of hypothyroid includes the trauma from surgery to remove a benign or cancerous tumour, or the result of radioactive iodine treatment for overactive thyroid.

Hashimoto’s disease is the most common cause of hypothyroid in the West. It is an autoimmune disorder where the body’s immune system, specifically the lymphocytes attack the thyroid. In response to this attack,  the thyroid produces antibodies, specifically thyroperoxidase antibodies (TPO-ab) and thyroglobulin antibodies (TG-ab) [3]. A diagnosis of Hashimoto’s is made based on both the presence of symptoms of hypothyroidism, as well as the presence of TPO-ab or TG-ab.


One of the main challenges with getting diagnosed as hypothyroid is that many of the early symptoms of hypothyroidism are non-specific  — meaning they can have several different causes.

In a post-pandemic world of telephone doctor appointments, such vague symptoms may seem too inconsequential to bring up.

Below is a downloadable checklist that can help you have a conversation with your doctor.


Symptoms such as body aches, joint pain, fatigue, feel chilled, weight gain, frequently being constipation, having dry skin don’t seem ‘serious’ enough to make an appointment with one’s doctor and could be due to a number of different causes from  not eating well, to having a virus, and are very often discounted as being due to “age”. Even forgetfulness and depression which are known symptoms in more advanced hypothyroidism are often attributed to aging. 

Hypothyroid – getting evaluated and diagnosed 

As outlined in an earlier article, in British Columbia unless a person is of advanced age, has a family history or personal medical history of thyroid disease or another autoimmune disorder, takes medications such as lithium or amiodarone, or is from a developing country with iodine deficiency, they do not even qualify for TSH testing unless they display the specific symptoms listed in Table 1, below [4].

hypothyroid signs and symptoms
Table 1: Signs and Symptoms of Hypothyroidism (from [4])

One drawback to the above approved checklist is that it does not include some of the well-documented symptoms of hypothyroidism, such as non-pitting edema of the lower legs and ankles, a puffy swollen face, an enlarged tongue (with or without scalloped edges), loss of the outer third of eyebrows, or having pale or bluish lips.

Even if one has a blood test for TSH, if it comes back at the high end of the normal range, no further testing is done [4]. 

hypothyroid diagnosis decision tree (in British Columbia)

Without a person having known risk factors, or having symptoms that appear in the official  list in the Guidelines and Protocols [4] (Table 1, above), diagnostic tests may not be requisitioned unless or until a person becomes sicker and the reason for this is explained below, in the section about ordering lab tests.

To help people have an informed discussion with their doctor, below is a 2-page downloadable, fillable checklist that contains a list of common hypothyroid symptoms, along with a simple explanation of what that symptom is. For example, in this checklist “periorbital edema” is explained as ‘swelling under eyes.’

Please note that this checklist list is not exhaustive and is NOT intended to be used for self-diagnosis purposes. It is only provided so that people who think they may have symptoms of hypothyroidism can consult with their doctor, and discuss the matter with them. Remember, only a medical doctor can diagnose and treat. 

Signs and Symptoms of Hypothyroidism – 2-page downloadable and fillable checklist

 

Thyroid Panel Lab Tests –  3 options to diagnose hypothyroid

[updated: November 3, 2022]

In Canada, there is no such thing as a standard “thyroid panel,” although naturopaths offer thyroid assessment panels on a client-pay basis. Medical doctors can order thyroid function tests based on the guidelines of their specific province, and naturopaths can order different thyroid assessment panels, depending on the province they are located in.

1. Medical Doctor (MD)

Thyroid function blood tests can be ordered by medical doctors (MDs) including family practice physicians, general practitioners (GPs), and specialists such as Endocrinologists and the cost of testing will be covered by the provincial health plan if it meets their guidelines. 

In most provinces in Canada, a requisition needs to be written by a licensed medical doctor for the cost of the test to be covered by the provincial health plan. In New Brunswick and Nova Scotia Health authorities and lab regulators have placed restrictions on how lab tests can be ordered, and patents are charged fees to order them privately.

In Ontario, Saskatchewan and British Columbia, the following guidelines apply;

Furthermore, in British Columbia, physician-ordered lab tests must be requisitioned in accordance with the Laboratory Services Act to be covered by MSP (Medical Service Plan). Doctors are in a very challenging position in BC as MSP can seek recovery for lab-test cost from a doctor if they feel that the test(s) ordered were not clinical  justified. 

Most physician-initiated lab test investigation for hypothyroid begins with a TSH test. One reason for this is to rule out Central Hypothyroidism which is where there is a problem with either the hypothalamus, or the pituitary gland. As explained above, a low TSH will likely result in a free T4 test being requisitioned. If free T4 is also low, then T3 medication or some other type of medication might be prescribed, or the person referred to an endocrinologist.

If the TSH test comes back high (above the upper limit of normal) this will likely result in a free T4 test being requisitioned. Depending on whether the free T4 is normal or low, and how far above the upper limit the TSH is, the doctor may recommend one of a variety of treatment options, and/or refer their patient to an endocrinologist.
 
The provincial health plan in British Columbia (MSP) pays the laboratory that performs the analysis the following amount for thyroid function tests, and thyroid antibody tests:
 
      • TSH: $9.90
      • free T4: $12.12
      • free T3: $9.35
      • thyroperoxidase antibody (TPO-ab): $20.22 (payable only for possible autoimmune thyroid disease)
      • thyroglobin antibody (TG-ab): $27.90 (only performed as an adjunct to thyroglobulin measurement for the conditions such as thyroid tumors, cancer, etc.)
      • reverse T3: uninsured test 
 
from http://www.bccss.org/bcaplm-site/Documents/Programs/laboratory_services_schedule_of_fees.pdf
Where it becomes challenging is when TSH is in the high-normal range and/or the person has symptoms consistent with being hypothyroid but no symptoms listed on Table 1 of the Guidelines & Protocols for Thyroid Function Testing [4]. In BC, it used to be up to a physician’s discretion to requisition blood tests based on their best clinical judgement, but since the Laboratory Services Act (LSA) came into effect on October 1, 2015 [5], the Medical Service Plan (MSP) can seek recovery for lab-test cost from the doctor if they feel that the test(s) ordered were not clinical  justified. Needless to say, this puts doctors in a very challenging position.
 
As a clinician, when I provide one of my clients with a Lab Test Request Form to bring to their doctor, with their permission I will mark the clinical reason that I am requesting specific tests to rule out hypothyroid on the form, so that their doctor can consider whether they feel the test(s) are warranted.
 

2. Naturopathic doctor (ND)

[updated: November 3, 2022] 
 
In British Columbia, Ontario and Saskatchewan, thyroid assessment panels require a visit to a naturopath, and would take at least two sequential visits; one to get the lab test requisition to go to the lab, and the second to have the naturopath provide their interpretations of the results, and their recommendations. The costs of naturopath’s services are not covered by provincial health care, so clients need to pay out of pocket.  Fees for naturopathic visits and blood test vary between provinces and within the same province between practitioners.
 
In Ontario, fees for visits to a naturopath are regulated by the College of Naturopaths of Ontario and are set per block of time . Typically the cost of first visit, second visit and subsequent visits vary, with the first visit of 75 minutes costing ~$200, and the second visit of 45 minutes) costing ~$115. 
 
In the first visit the naturopath would ask questions as part of their assessment and complete and sign a Naturopathic Requisition Form which enables their client to go to the lab and have the tests done. The client pays the naturopath for the visit as well as the cost of the lab tests. In Ontario, the College of Naturopaths of Ontario allows naturopaths to add a markup to goods and services they offer, such as supplements, and blood test panels. With respect to blood tests, the naturopath pays a special negotiated lab fee for the thyroid panel to the lab, then bills their clients, often with a mark-up.   In the second visit, the naturopath will interpret the results.
 
In BC, fees are set by the BC Naturopathic Association Fee Guidelines. Naturopaths are also able to add a mark-up to the cost of supplements and blood tests. From experience, some naturopaths in BC keep their mark-up for lab tests minimal (e.g. $7 per test).  
 
The Enhanced Thyroid Assessment available in Ontario has the following 6 tests ;
    • TSH
    • Free Thyroxine (FT4)
    • Free Triiodothyronine (FT3)
    • Reverse T3
    • Thyroperoxidase Antibody (TPO-ab)
    • Anti-Thyroglobulin (TG-ab)
Prices for thyroid panels charged to naturopaths are available online for Ontario (see above) but in BC the prices aren’t marked.
 
Compared to the (MSP) government pricing, the above tests (minus the Reverse T3 which isn’t paid for by MSP) costs $80, so presumably naturopaths are charged prices similar to what MSP pays and then can add a mark-up to them. From the client’s perspective, they need to pay for the two naturopath visits, as well as the cost of the lab tests. 
    • TSH: $9.90
    • free T4: $12.12
    • free T3: $9.35
    • thyroperoxidase antibody (TPO-ab): $20.22 (payable only for possible autoimmune thyroid disease)
    • thyroglobin antibody (TG-ab): $27.90 (only performed as an adjunct to thyroglobulin measurement for the conditions such as thyroid tumors, cancer, etc.)
Total: $79.49
 
In British Columbia, naturopaths can only order the Basic Thyroid Assessment which includes the following 4 tests;
    • TSH
    • Free Thyroxine (FT4)
    • Free Triiodothyronine (FT3)
    • Thyroperoxidase Antibody (TPO-ab)

Reverse T3 and Anti-Thyroglobulin (TG-ab) are not available.

3. Patient-Pay 

If a doctor does not want to take the risk of requisitioning specific lab tests that the provincial plan may seek to recover costs from them, there is the option of the doctor writing on the requisition that specific test(s) to rule out hypothyroid will be “patient-pay” and the individual can pay for that specific lab test themselves. 
It should be made clear that a person does need a requisition from a doctor that indicates “patient pay” for the specific test(s) and cannot go to the lab directly and request the test themselves.
 
***It should also be noted that the cost of thyroid lab tests paid for by the individual are NOT the same as the cost paid for by MSP, and naturopaths, but are significantly higher. 
 
Last week, as a private individual with a physician lab requisition, I was charged 3 times the MSP cost for a free T3 test. As I found out at that lab visit, there is no patient-pay price list available at the lab, online, or by writing the lab office. The staff at the lab will disclose the cost of the test once the person is at the lab with the requisition, but this first requires the individual making an appointment, and going there at their appointment time.  
 
A fellow clinician told me several days later that there is a patient-pay price list available to Physicians, Registered Dietitians, Nurse-Practitioners, and other healthcare professionals, and I now have a copy of this list. It is titled the British Columbia Private Price List for Commonly Ordered Lab Tests, and is dated April 2021. It is labelled as “a confidential document,” and it is indicated at the top that clinicians are not to disclose their prices publicly, however we are able to share that information in conversations with our patients / clients. 
 
 
 
While I am unable to disclose the patient-pay lab test prices publicly (such as in this article), I am able to share the patient-pay prices of lab tests with any of my clients who are considering asking their doctor to requisition patient-pay test(s).  
 
 

Final Thoughts

Determining whether the symptoms one has may be related to their thyroid, and going about getting tested can be challenging. It is my hope that by providing the information in this article, you can have an informed discussion with your doctor.

If you would like more information about how I can support you in your goal of improved health, please send me a note through the Contact Me form above.

To your good health!

Joy

 

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

  1. Jonklaas J, Bianco AC, Bauer AJ, et al, Guidelines for the treatment of hypothyroidism: prepared by the American thyroid association task force on thyroid hormone replacement. thyroid. 2014 Dec 1;24(12):1670-751.
  2. Berkow, R., Beers, M. H., & Fletcher, A. J. (1997). The Merck Manual of Medical Information. Whitehouse Station, N.J.: Merck Research Laboratories.
  3. Puszkarz, Irena, Guty, Edyta, Stefaniak, Iwona, & Bonarek, Aleksandra. (2018). Role of food and nutrition in pathogenesis and prevention of Hashimoto’s thyroiditis. https://doi.org/10.5281/zenodo.1320419
  4. BC Guidelines & Protocols Advisory Committee, Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder, October 24, 2018
  5. Laboratory Services Act, Laboratory Service Regulation, October 1, 2015 (last amended September 20, 2020 by B.C. Reg. 263/2020)

 

Copyright ©2022 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

To Hell and Back – recovering from hypothyroidism (a Dietitian’s Journey)

Last Monday, I went to the lab for updated blood work, including a thyroid hormone panel, additional thyroid antibody tests, and an iron panel. I have moved past the frustration of there being no pricelist available for consumers who are self-paying for lab tests, and am now focusing on the lab test results, and the dietary changes that I need to make in light of those, as I am recovering from hypothyroidism.


DISCLAIMER: This article is a personal account posted under A Dietitian’s Journey. The information in this post should in no way be taken as a recommendation to self-diagnose, self-interpret diagnostic tests, or self-treat any suspected disorder. It is essential that people who suspect they may have symptoms of any condition consult with their doctor, as only a medical doctor can diagnose and treat.


The results came back late Monday afternoon and I met with my doctor to discuss them on Thursday, The good news is that based on calculation estimates converting the bovine Natural Desiccated Thyroid (NDT) medication that I had been taking, to a mixture of Synthroid® (a synthetic T4 medication) and Cytomel® (a synthetic T3 medication), my free T4 and free T3 are almost perfect. As my doctor said when we met, “between your research and my experience, we got this”.

This is a beautiful picture.

 
TSH, fT4 and fT3 levels on T4/T3 thyroid hormone replacement medication

It shows, as my doctor and I had hoped, that my free T3 (the active thyroid hormone) is in the higher part of the reference range (65.5%); a level considered optimal by endocrinologists and thyroidologists who are well-versed in the use of the combination T4/T3 medications that I have been prescribed.

While my free T4 could be in the higher part of the range on the type of medication that I am taking, it may slightly lower because of the feedback from having sufficient free T3. That’s okay! I am feeling so much better, although it will take another year or more until I am really well again.

As expected, my TSH (Thyroid Stimulating Hormone, the pituitary hormone that tells the body how much thyroid hormone to make) is low because the amount of free T3 is optimal. This is a classic feedback loop where free T3 provides feedback on the pituitary gland, indicating that there isn’t a need to make more thyroid hormone. Think of it like a thermostat.  When the room gets warm enough, there is feedback on the thermostat that no additional heat is required, and it turns it off until the room gets cold again.

Of importance, my TSH is not considered “suppressed” (TSH ≤0.03 mU/L) but “low” (TSH = 0.04-0.4 mU/liter) [1], so there is no increased risk of cardiovascular disease or bone fractures. Those with a “high” TSH (>4.0 mU/liter) — which was the level that I was at before being treated, and those with a “suppressed” TSH (≤0.03 mU/L) both have an increased risk of cardiovascular disease, abnormal heart rhythms and bone fractures. Those with “low” TSH (0.04-0.4 mU/liter) like I have, do not [1,2]. So more good news.

I have been diagnosed with Hashimoto’s disease (also known as Hashimoto’s thyroiditis) which is an autoimmune disease and diagnosis is based both on symptoms of hypothyroidism, along with the presence of thyroperoxidase antibodies (TPO-ab) and thyroglobulin antibodies (TG-ab) in the blood [3].

In many cases of hypothyroidism, it is these antibodies that contribute to the gradual disappearance of thyroid cells and the development of hypothyroidism.  In my case, it was the trauma to the thyroid that resulted from surgery that I had 30 years ago to remove a benign tumour that was the major contributor to the eventual decrease in thyroid function.

Prior to being diagnosed, as you can read about here, I had all the classic symptoms of hypothyroidism, including body aches, joint pain, fatigue, feeling chilled, constipation, dry skin, hair loss, being forgetful, and even feeling depressed.

By the point I realized that these symptoms were not consistent with long-Covid (which is what I initially suspected) or aging (which my sons assumed), I had developed some of the symptoms of severe hypothyroidism [3], including difficulty with speech, significant water retention, and peripheral edema (swelling) of the ankles and face [3]. There are more photos of what I looked like when I was very sick here as well as photos from the beginning part of my recovery.

 

To hell and back – 5 months of recovery from hypothyroidism

 

 

The blood tests confirm that I have both thyroperoxidase antibodies (TPO-Ab) and thyroglobulin antibodies (TG-Ab), which along with my symptoms, confirms my diagnosis of Hashimoto’s disease, but thankfully my blood test results indicate that neither are elevated.

Thyroperoxidase-Ab = 9 (<35 IU/mL)

Thyroglobulin Ab = 14 (<40 IU/mL)

While they are not elevated, they are present. 

Gliadin and Transglutaminase

For many years I avoided gluten containing products because I thought I was gluten intolerant, although not celiac.

A year ago that I stumbled across some novel ingredients and had an idea to create low carb breads to provide dietary options for those with diabetes. My goal was to enable people who would not otherwise consider a low carbohydrate diet to be able to adopt one, for health reasons.   I was mainly thinking of those from bread-centric cultures such as South East Asians (Indian) and Hispanics but in time, I developed many more types of low carb bread. 

I was aware of the connection between high gluten consumption and leaky gut syndrome, but against that I weighed the serious morbidity and mortality linked to uncontrolled diabetes. I had come across many people who would rather stay diabetic, and potentially lose their toes or vision than give up bread and developing these breads seemed like the lesser of two evils. 

Since being diagnosed with hypothyroidism that I had been developing over the previous 9 years (more about that here), I learned that the gliadin fraction of gluten structurally resembles transglutaminase. Transglutaminase is an enzyme that makes chemical bonds in the body, and while present in many organs, there are higher concentrations of transglutaminase in the thyroid.

In leaky gut syndrome, gliadin (and other  substances) result in the gaps in between the cells of the intestinal wall to widen. This results in the immune system of the body reacting to food particles that are inside the intestine, that it normally would not see. It is thought that the immune system reacts to gliadin and creates antibodies to it, seeing it as a foreign invader.  Since gliadin and transglutaminase have very similar structural properties, it is thought that in those with leaky gut syndrome, the immune system begins to attack the transglutaminase in the thyroid, and other tissues, contributing to the development of auto-immune conditions, including hypothyroidism. 

A-1 Beta Casein and Gluten

A few years ago, I had leaky gut syndrome but it resolved with dietary changes, including avoiding gluten and A-1 beta casein dairy (you can read about what A-1 beta casein dairy is here).  Naturally, as I had been working on recipe development for the low carb bread book, I had been eating gluten as I tested them. I also became more liberal in including dairy products from A1-beta casein cows, when I hadn’t used it in years. That started when there was severe flooding last year in Chilliwack last year due to heavy rains after the summer, and that was where my goat milk came from.  Even once the roads were open again and the highways rebuilt, I never really went back to using goat milk, which is naturally A-2 beta casein. In the interest of an abundance of caution, I will go back to using dairy products from A-2 beta casein cows, or from goat or sheep milk (that are naturally A-2). Humans produce A-2 beta casein protein, and using milk from A-2 beta casein animals does not result in an immune response. It is not seen as “foreign.”

From what I’ve read and in discussing it with my doctor, it is likely that my hypothyroidism has been developing over the last 30 years, related to the surgery I had to remove a benign tumour. Further supporting that me becoming hypothyroid has been a long time in the making, I have had high-normal levels of TSH over the last 9 years — which happens to be a time period over which I was avoiding both gluten and A-1 dairy. Given that, I think it’s logical to conclude that my hypothyroidism is primarily related to the destruction of thyroid tissue in the invasive surgery connected to removal of the tumour. Further supporting this hypothesis, I currently have fairly low levels of TPO and TG antibodies, so I suspect they have begun developing fairly recently. Since a 2018 study reported that  both TPO-antibodies and TG antibodies are decreased in hypothyroid patients following a gluten-free diet [4], it seems wise for me to go back to avoiding gluten, with the goal of lowering my TPO-antibodies and TG-antibodies down to as close to zero, as possible.

Cruciferous Vegetables

Cruciferous vegetables such as Brussels sprouts, broccoli, bok choy, cauliflower, cabbage, kale are known goitrogens. Goitrogens are naturally occurring substances that are thought to inhibit thyroid hormone production. The hydrolysis of a substance known as pro-goitrin that is found in cruciferous vegetables produces a substance known as goitrin, that is thought to interfere with thyroid hormone synthesis [5]. Since cooking cruciferous vegetables limits the effect on the thyroid function, and eating cruciferous vegetables have many health benefits, I will usually eat them cooked, but not in huge quantities. There are studies that found a worsening of hypothyroidism when people ate very large quantities of these (e.g. 1 – 1 ½ kg / day) so it is recommended that intake of these vegetables be kept relatively constant day to day, and limited to no more than 1-2 cup / day. I’ve decided that when I do eat them, to keep intake to the lower end of that range, and eat more non-cruciferous vegetables instead.

Iron Deficiency and Low Stomach Acid (hypochlorhydria)

I now know why I am still so tired. I asked my doctor to run an iron panel and the results show I have low iron. Previous results indicate my vitamin B12 are fine and I continue to supplement methylated folate and B12, so I know those are not a problem.

While my iron stores (ferritin) are okay, they are not optimal i.e., ferritin = 93 (15-247 ug/L) instead of >100ug/L.

My hematology panel is low-normal i.e. hemoglobin = 122 (115-155 g/L), hematocrit = 0.37* (0.35-0.45 L/L), MCV = 88 (82-98 fl), MCH = 29.5 (27.5-33.5 pg), MCHC = 334 (300-370 g/L)

My serum iron and iron saturation are very low i.e., serum iron = 11.9 (10.6-33.8 umol/L), iron saturation = 0.15 (0.13-0.50)

Low iron status is common with hypothyroidism, but it was surprising to me because I eat beef liver, or chicken livers every week, and also take a heme polysaccharide supplement (like Feramax®), so it may be due to an absorption problem.

Low stomach acid (hypochlorhydria) is common in hypothyroidism, and since low pH is needed for iron absorption, I have made dietary changes to improve that.

Final Thoughts…

I am very grateful that my doctor recognizes my knowledge as a clinician and is receptive to me advocating for my health. I am incredibly fortunate that he involves me in decisions regarding blood tests, as well as discussing medication types and dosages.  As for the dietary changes and supplementation, he is content to let me handle that!

I hope that out of my experience that I have called “to hell and back” that I am able to help others better understand hypothyroid symptoms, diagnosis and treatment options so that they can discuss them with their doctor.

To your good health,

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

Copyright ©2022 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

 

Blood Tests and Lab Frustrations – a Dietitian’s Journey

NOTICE: This my personal experience as a private consumer of lab services, and is not related to my profession as a Dietitian. This article is posted in a separate section of the web page titled “A Dietitian’s Journey” which is about my personal health journeys.

“A Dietitian’s Journey – Part I” was about my two year journey recovering from obesity, and poor metabolic health and “A Dietitian’s Journey-Part II” is my current  personal journey recovering from hypothyroidism.

This article is written as a private consumer, which is why it is categorized as a personal account, and an editorial.


This past Monday, I went to the lab to have blood tests to measure my thyroid hormones, anti-thyroid antibodies, and an iron panel. When I had met with my doctor last week, I learned that I would need to pay for the free T3 test because the British Columbia guidelines and protocols for ordering thyroid tests state that a free T3 test is only covered to rule out suspected cases of hyperthyroidism [1]. As I wrote last Thursday, I was “more than willing to pay for a $9.35 test to have all the data.” 

I think most people are aware that the healthcare system is economically stretched, and I certainly understand and accept the need to reduce costs. One way to do that is to restrict the ordering of laboratory tests to only medically justifiable circumstances, which makes good sense. 

While I recognize that I am not objective in this situation, it would seem to me that when someone is on thyroid hormone replacement medication that includes both synthetic T4 and T3 hormones, that the expense of both a free T4 test and free T3 test should be covered by the provincial healthcare system as the cost is justifiable because the prescribing doctor needs to determine if the dosage of both synthetic hormones is adequate, but not too high. 

As I said above, I knew last week that I would be paying for the free T3 test and was fine with that, but what I wasn’t prepared for was that I would be expected to pay three times the cost the government pays for the same test, and that there would no patient-price list available.

When I arrived at the lab on Monday, I was told that the free T3 test would cost $32.00.  I replied that there must be a mistake, because the cost of the test is $9.35. I was informed that the government pays $9.35 for the free T3 test, but the patient-pay cost for the same test is $32.00. I explained to the person at the desk that I could understand the test costing more if there was a set-up fee for a stand-alone test, or for a separate blood draw, but this test was going to be run with others using the same blood draw.  I was informed that $32.00 is the patient-pay cost of the free T3 test regardless of whether it is done with other tests, or by itself.

I asked if I could please see the price list with the patient-pay costs, and was told that there isn’t one. I was asked if I wanted to have the free T3 test period formed, and if I did that I would need to pay $32.00. What choice did I have?  It was not as though I could go to one of the lab’s competitors, as this private lab company is the only one providing laboratory services in this city. 

[NOTE (October 28, 2022: I have spoken to people in other provinces, and it appears from what people have said that the practice of diagnostic laboratories not disclosing patient-pay prices occurs in Manitoba, Ontario, and British Columbia. This practice may also occur in others provinces as well, but I don’t know. This article written as private consumer is about the practice of diagnostic labs not disclosing patient-pay prices to consumers, irrespective of which province the practice occurs in, or by what company.]

I paid the $32.00 for the test because I needed this information to know the effect of the medication on my thyroid hormones, and for my doctor to know whether a medication adjustment was needed. I had the disposable income to pay for it, but what about consumers who need a laboratory test to make health decisions or for their doctor to be able to, and who cannot afford that? 

… and why are patient-pay clients charged 3 times as much as the government pays for the same test?  Even if a private consumer was only requesting a stand-alone test and had to pay the ~$15 blood draw fee, this test would only cost $25, not $32.

After my appointment, I wrote the regional office of the lab company and asked “to have the patient-pay lab prices for British Columbia.” I heard back from a Client Service Advisor who told me that “We do not provide a list of what we charge to patients”.

I was flabbergasted. 

I’ve always made the assumption that private businesses are required to post their prices, or at least make them available when asked.

As an individual consumer, what happened at the lab would be like going to the grocery store to buy food, but none of the items for sale have marked prices. You are required to pick out the things you need, but only find out at the cash register what the price is. 

When you get to the cash, you ask the cashier about the prices, and she tells you there’s no price list,  but she can give you the total cost at the end, and you can either pay, or put the items back. Needing the items, you pay what you are told, and take your receipt.

When you get home, you decide to write the head office and ask if they can send you a price list, and are told there IS one, but that they can’t give it to you.

[UPDATE October 29, 2022: The way things are currently set up, one has to make an appointment with the lab, go there, line up and give the person at the desk their requisition, and only then can find out how much the patient-pay part will cost.

After investing so much time, consumers are put in a position of having to make a decision on the spot — pay whatever is being asked, or leave without the test.

Consumers should be able to access the prices online and make a decision at their leisure, before investing so much time.] 

I don’t know whether private businesses in Canada required to post their prices, or make them available when asked. I’ve always assumed they were, but I could be wrong. If there is a requirement to do so, do diagnostic labs have an exemption that enables them not to make their prices available to members of the public?


UPDATE October 28, 2022: I have since found out the same company provides a price list to allied health professionals so that they can provide laboratory assessment services to their clients, and if they choose they can mark up the cost in their own billing.

There are 2 versions of this test list available. They are identical except the one for British Columbia does not have the prices indicated, whereas the Ontario one does (see below).

I have also since found out that the company DOES have patient-pay price list that is titled “British Columbia Private Price List for Commonly Ordered Lab Tests” and is dated April 2021. It is marked “confidential” and as a result cannot be publicly shared.  See #3, below.

    1. The allied healthcare price list available in Ontario, dated November 2018 has the prices marked. See below.
    2. The allied healthcare price list available in British Columbia, dated June 2020 does not have the prices marked.

Above is the allied health professional cost (November 2018) for an entire thyroid panel of 6 thyroid-related lab tests, including;

          • TSH
          • free T4
          • free T3
          • reverse T3
          • thyroperoxidase antibody (TPO)
          • anti-thyroglobin antibody (TG-ab)

Compared to what the BC government pays for the same tests (minus the reverhttp://from http://www.bccss.org/bcaplm-site/Documents/Programs/laboratory_services_schedule_of_fees.pdfse T3 which isn’t paid for by MSP) the above panel costs $80. Presumably naturopaths are charged prices similar to what MSP pays.

3.    I have since found out that there IS a patient-pay price list and it is titled “British Columbia Private Price List for Commonly Ordered Lab Tests” and is dated April 2021.

 

The prices cannot be posted because the notice at the top of the price list reads;

“This is a confidential document. Please do not disclose our prices publicly except in conversations with your patients.”

Why is the private-pay price of lab tests a confidential document, and why can’t the prices of lab tests be disclosed to the public?

Are business in British Columbia required to disclosed their prices and if so, are diagnostic labs exempt from making their private-pay prices available to consumers?

I don’t know.

How many people would be willing to order dinner at a restaurant that did not post the price of its menu items until after they ordered?

 

My Thoughts on Patient-Pay Prices

I believe that as consumers, private-pay individuals have a right to have access to the prices for laboratory tests in advance, so that they can consider their decision to purchase, or not purchase these services. Consumers expect grocery stores and department stores to post their prices, and it is my personal opinion that privately owned laboratories from whom private consumers purchase services should be no different.

I also think private-pay individuals have a right to know why they are required to pay a premium price for the same services that the government gets for a third the cost, and allied healthcare professionals obtain for approximately half the cost.

This differential pricing for allied health professionals is a little like retailers selling supplements to practitioners at wholesale prices, while expecting the consumer to pay full price. Even car dealerships have “employee pricing” events so that the average consumer can take advantage of the same discounts provided to their employees, but at these diagnostic labs, consumers are unable to know in advance how much they will be paying for services before they arrive at the cash.

I believe that as private businesses, diagnostic laboratories are free to set their prices as they see fit but it would seem that (1) consumers should be able to know what those prices are in advance, and (2) that consumers should also know that they are paying a premium price for the same services, compared to what the government and allied health professionals are paying.

I am very grateful to live in a country where publicly funded medical care is available. I am thankful to have access to excellent diagnostic lab tests, and don’t even mind paying the same cost the government pays for tests that I want to have done. But as a private consumer, I believe the cost of services need to be available and that there needs to be transparency with regards to pricing discounts provided to others.

To your good health,

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

  1. BC Guidelines & Protocols Advisory Committee, Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder, October 24, 2018

 

Copyright ©2022 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Hypothyroidism Signs and Symptoms Checklist

DISCLAIMER (October 14, 2022): The information in this post and in the checklist contained in it should in no way be taken as a recommendation to self-diagnose, self-interpret diagnostic tests, or self-treat any suspected disorder. It is essential that people who suspect they may have symptoms of any condition consult with their doctor, as only a medical doctor can diagnose and treat.


As outlined in a previous article, the standard screening test for abnormal thyroid function is thyroid stimulating hormone (TSH), but if those results come back within normal range and a person has not known risk factors or obvious symptoms of thyroid disease, no testing of thyroid hormones occurs,  and thyroid function is presumed to be normal.

In British Columbia, unless a person is of advanced age, has a family history or personal medical history of thyroid disease or an autoimmune disorder, takes medications such as lithium or amiodarone, or is from a a developing country with iodine deficiency, they do not qualify for TSH testing unless they display the specific symptoms listed in Table 1, below.

British Columbia Checklist of Symptoms and Signs of hypothyroidism

This approved checklist does not include some of the well-documented symptoms of hypothyroidism, such as non-pitting edema of the lower legs and ankles, a puffy swollen face, enlarged tongue with or without scalloped edges, loss of the outer third of eyebrows, or having pale or bluish lips. The downloadable checklist below contains a list of these, and other common symptoms.

Signs and Symptoms of Hypothyroidism – downloadable checklist

This downloadable checklist of common hypothyroid symptoms is not intended to self-diagnose. It is provided to help people who feel unwell to have an informed discussion with their doctor as to whether thyroid hormone testing should be considered.

Signs and Symptoms of Hypothyroidism – larger type, 4-page downloadable checklist

 

   NEW – Signs and Symptoms of Hypothyroidism – 2-page downloadable and fillable checklist

 

More Info?

If you would like to know how I can help support your nutritional needs, please send me a note through the Contact Me form.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

  1. BC Guidelines & Protocols Advisory Committee, Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder, October 24, 2018

 

Copyright ©2022 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

What Does Success Looks Like Now – A Dietitian’s Journey

This article is the fourth entry in A Dietitian’s Journey and is about how I will measure success as I recover from hypothyroidism.

A Dietitian’s Journey – Part I

“A Dietitian’s Journey” (Part I) was my personal weight-loss and health-recovery journey that began on March 5, 2017 when I decided to make dietary and lifestyle changes so that I could reclaim my health. At that time, I was obese, had type 2 diabetes for the previous 8 years, and extremely high blood pressure. 

Two years later, on March 5, 2019, I accomplished all but one of my goals, and the last one I achieved three months later. In all, I lost 55 pounds and more than a foot off my waist, and met the criteria for partial remission of type 2 diabetes, and remission of hypertension (high blood pressure).

To get an idea of what I looked like at the beginning and the end of that journey, there are two short videos on my Two Year Anniversary post that tell the story well.  The first video was taken when I started and it is very apparent how obese I was, and how difficult it was for me to walk and talk at the same time. The second clip was taken when I completed my journey, and the difference is unmistakable.  

A Dietitian’s Journey – recovery from hypothyroidism

Without much difficulty I maintained my health and my weight-loss from March 2019 until August 2020 but then I came down with Covid.  This was at the very beginning of the pandemic and no one really knew what to expect in terms of symptoms. As you can read about in the first post in what has effectively become A Dietitian’s Journey Part II, (When a New Diagnosis is a Long Time Coming ) I had symptoms that both my doctor and I assumed were related to the virus, including muscle aches and joint pain, being exhausted, having ‘brain fog,’ headaches, and having the shivers.

Afterwards, I had to work very hard to regain my mobility. No one knew this wasn’t ‘normal.’

At first, I could barely walk up a flight of stairs. At the time, “success” was being able to walk around the block.  Then I began taking several dietary supplements to help strengthen my immune system and in retrospect, the reason I felt better was likely due to the fact that these were all supplements involved in thyroid support. Success at the time was being able to walk around the man-made lake at the local park, but over the weeks and months of supplementing my diet and walking every weekend, success was being able to complete several medium difficulty hikes in the local mountains. 

Unfortunately, in March of 2022,  I came down with what my doctor assumed was Covid again. At first the symptoms were similar to what I experienced in August 2020, including muscle aches, joint pain, being exhausted, feeling cold all the time, with the only difference being that I didn’t have headaches. The symptoms persisted for several months and I was beginning to think that I had “long-Covid.” As most people did over the pandemic, I put on 20 pounds, but from March to May, I began to look as though I was putting on significant weight, but every time I got on the scale it indicated only a few pounds of difference. I had no idea what was going on.

The next symptom that I became aware of was swelling in my ankles. It wasn’t just a little bit of swelling, but significant enough that I needed to wear compression stockings all day.

At my youngest son’s wedding at the beginning of June, I looked like I did when I was 55 pounds heavier, but I wasn’t.

LEFT: March 5, 2017, RIGHT: June 3, 2022

About three weeks after the wedding, I was diagnosed with hypothyroidism, and started taking desiccated thyroid. At first, I felt significantly better, and within several weeks, the edema in my legs began to subside. 

 

There is still a fair amount of mucin accumulation in my legs, but as of this weekend, I can begin to grab a very small amount of flesh between my fingers. From what I have read it will take at least 6 months for this to resolve. You can read a referenced article about the skin symptoms associated with hypothyroidism here.

It is easy to see from the above photo that in less than 3 months on thyroid medication treatment, my face has lost its puffy, “inflated” look yet amidst the positive improvements of decreased edema and looking more like myself in some respects is the reality that I have lost ~1/2 of my hair due to telogen effluvium that often occurs with sustained hypothyroidism. You can read more different causes for hair loss here.

Loss of half my hair in 3 months due to telogen effluvium.

Even though I have already been on thyroid replacement hormones for several months, it usually takes ~3-6 months for hair loss to stop and another 3-6 months for regrowth to be seen and 12-18 months to complete regrowth [3]. For someone like my who has lost half their hair, six months to a year to begin to see hair growth can seem like an eternity.

I recently changed medication forms from desiccated thyroid to a mixture of T4 medication (Synthroid®) and T3 medication (Cytomel®). The overall distribution of T4:T3 is about the same, but it is hoped that this mixture will result in more stable thyroid hormones day-to-day.

In six weeks I will have new blood tests to re-evaluate whether my levels have improved.  At last check, my TSH was still high-normal (3.47 mU/L) when in most patients on thyroid hormone replacement the goal TSH level is between 0.5 to 2.5 mU/L [7]. My Free T4 =  14.0 pmol/L which is still in the lower end of the range (10.6-19.7 pmol/L) when it is considered optimal to be in the higher end of the range. 

Metabolic Changes due to Hypothyroidism

It’s well known that people with hypothyroidism experience several clinical changes including different type of anemia, changes in how their heart functions, changes in blood pressure, blood sugar and cholesterol and weight gain due to a slower metabolism. My recent medical work up indicates that I was no different in this regard.

Different Types of Anemia

People with hypothyroidism have a decrease in red blood cells and experience different types of anemia, including the anemia of chronic disease. In addition, 10% of people with hypothyroidism develop pernicious anemia, which is associated with vitamin B12 and folate (folic acid). Iron deficient anemia is also common due to decreased stomach acid that results in decreased absorption of iron.

I was supplementing with B12 and folate and as a result have no signs of pernicious anemia, however my hematology panel indicates that I may have iron deficient anemia. An iron panel would be able to quantify this, however I am already taking heme iron supplements, along with vitamin C to support absorption.

Heart Changes

The slowing of metabolism associated with hypothyroidism also results in a decrease in cardiac (heart) output, which results in both slower heart rate and less ability for the heart to pump blood.  This is what results in the unbearable fatigue.

High Blood Pressure

The decreased ability of the heart to pump leads to increased resistance in the blood vessels, which results in increased blood pressure (hypertension).

In those who had normal blood pressure previous to developing hypothyroidism, blood pressure can rise as high as 150/100 mmHg. Hypothyroidism may increase it further for those previously diagnosed with high blood pressure. While my blood pressure had been normal for more than a year, it gradually started increasing the last year, which in retrospect is the period of time over which I was exhibiting more and more symptoms of hypothyroidism. I have since been put back on medication for hypertension to protect my kidneys, which I hope to be able to get off of again within the next six month to a year, as my thyroid hormones normalize.

Weight Gain

Thyroid hormones act on every organ system in the body, but the thyroid is well-known for its role in energy metabolism. When someone has overt hypothyroidism, there is a slowing of metabolic processes, which results in symptoms such as fatigue, cold intolerance, constipation, and weight gain. 

Weight gain is not only about diet or how much someone eats versus how much they burn off. It is also about the person’s metabolic rate, which can be impacted by several things, including decreased thyroid hormones. I gained 20 pounds over the pandemic (much of which overlaps with the period of time over which I was exhibiting more and more symptoms of hypothyroidism. I also gained 10 pounds from March to June which is mostly water weight, due to the mucin accumulation.

High Cholesterol

It has long been known that those with hypothyroidism have high total cholesterol, high low-density lipoproteins (LDL) [4], and high triglycerides (TG) [5], which results from a decrease in the rate of cholesterol metabolism. My doctor deliberately did not want to check these last time, because he knew they would be abnormal only as a result of the hypothyroidism. He plans to evaluate them once I have been stable on hormone replacement for several months.

So, What Does Success Look Like Now?

Just as I had a clear idea of what success looked like in my first A Dietitian’s Journey, I have a clear idea of what I would like success to look like this time, as I recover from my hypothyroid diagnosis.
 

Over the next year, this is what I want to accomplish;

    1. weight same as March 5, 2019 (end of A Dietitian’s Journey, part I)
    2. waist circumference same as March 5, 2019 (end of A Dietitian’s Journey, part I)
    3. regrowth of my hair to same thickness as before clinical symptoms of hypothyroidism
    4. restoration of iron deficient anemia:
      (a) normal ferritin 11-307 ug/L
      (b) iron 10.6-33.8 umol/L
      (c) TIBC 45–81 µmol/L
      (d) transferrin  2.00-4.00 g/L
    5. Blood pressure ≤  130/80 mmHg
    6. Blood sugar:
      (a) non-diabetic range fasting blood glucose ≤  5.5 mmol/L
      (b) non-diabetic range HbA1C ≤  5.9 %
    7. Thyroid Hormones:
      (a) optimal TSH= 0.5 to 2.5 mU/L
      (b) optimal Free T4 = 15-18 pmol/L (10.6-19.7 pmol/L)
    8. Cholesterol:
      (a) LDL ≤ 1.5 mmol/L
      (b) TG ≤ 2.21 mmol/L

Final Thoughts…

While I don’t know if it will be possible to achieve all of these within the time frame or within adjustments to medication that my doctor will be willing to make, these are my goals. I believe that most of these are possible, and as far as they are within my control, this is what I would like to accomplish.

I have achieved a lot the last 3 months, but I am not “done.” I want the rest of my life back!

I want to be able to do the things that I enjoy, and to have the freedom to make plans in the evening knowing I will have the energy to follow through.

I think this is reasonable to ask and I will do everything I can to make this a reality.

A Dietitian’s Journey Part II continues…

To your good health,

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

Copyright ©2022 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Hair Loss – root causes (Part 1)

Hair loss can be a very distressing symptom, especially when it is noticeable to ourselves and others. However, before outlining strategies for addressing it, we first need to understand what’s causing it. That is the purpose of this article.  The next article will address strategies for helping to restore hair loss through diet and nutrient supplementation.

There are different types of hair loss with various causes, including genetic, autoimmune, severe stress, as well as nutrient deficiency and nutrient excess. Below are a three of the most common types of loss. 

Male pattern baldness

Androgenic Alopecia is the most common type and affects up to 50% of men and women [1]. In men, it is called ‘male pattern baldness,’ and is mainly seen on the crown of the head and on the temples.  In women, it  is called ‘female pattern baldness,’ and is mainly seen at the crown of the head, with a wider center part [2].  Androgenic alopecia is a genetic disorder that involves both maternal (mother’s) and paternal (father’s) genes, with sons being 5-6 times more likely to have it if their fathers were balding [1]. Since it is genetic, there is no ‘cure,’ but growth may be improved by using products such as minoxidil (Rogaine®) or rosemary extract which has been found to be as effective as minoxidil in studies [2]. One drawback is that treatment needs to continue indefinitely or loss will reoccur when treatment is discontinued [6].

Alopecia areata is an autoimmune disorder where the body’s immune system attacks the follicles. Hair often comes out in clumps, usually the size and shape of a quarter but it can affect wider areas of the scalp [3]. It can occur in those who already have some form of autoimmune conditions, including thyroid disease. Treatment may involve use of oral or topical corticosteroid medication [3] which are very powerful anti-inflammatory medications, or other medications used in autoimmune conditions. Individual bald spots may be treated using Minoxidil (Rogaine®) [3]. 

Telogen effluvium – is the most common form of diffuse hair loss [7]. It usually occurs after a profound stress, shock or traumatic event including after childbirth, as the result of a thyroid disorder, as well as rapid weight loss. It has been reported after a sudden and significant calorie restriction diet (“crash dieting”) [8],  and has also been reported associated with the popularized ‘keto’ diet [9,10], but I am in agreement with Dr. Stephen Phinney of Virta Health that it should not occur in a well-designed keto diet [11].  

In telogen effluvium, hair often comes out in clumps in the shower, or in a brush [6]. Loss is usually from all over the scalp, but may occur more on the temples, the part and the crown of the head [7].  Once the cause telogen effluvium is removed, regrowth will usually begin within two to six months [6].

There are three phases of growth; the growth (anagen) phase, the transition (catagen) phase, and the resting (telogen) phase [5]. During the growth phase, follicles produce a shaft beginning from tip to root [5]. During the catagen and telogen phase, the follicles reset and prepare to start making a new hair. 

hair growth phases – based on Reference [7]

Normal Hair Loss vs Hair Loss in Telogen Effluvium

Normally,  90-95% of follicles are in the growth (anagen) phase, with only 5–10% being in the resting (telogen) phase. Only a few follicles are in the transitional (catagen) phase [7] at any one time.  At the end of the telogen phase, the hair falls out and under normal circumstances that would amount to ~ 100-150 hairs per day [7].

In telogen effluvium, the growth (anagen) phase slows down and up to 50% of the follicles move into the telogen phase, where shedding occurs. i.e., loss becomes 5-10 greater than normal, with people losing up to 50% of their hair.  Since the period of the most dramatic loss occurs approximately 2-3 months after the triggering event, many people don’t relate the shedding to the event that caused it.

Identifying the cause of hair loss is essential, as once identified, and corrected, regrowth will occur [7], but it can take 3-6 months for hair shedding to stop. While many people are anxious that they will go bald, hair loss does not usually exceed 50% of their hair [7].  Once the cause is identified and corrected, regrowth can begin to be seen 3-6 months later [7], but significant regrowth can take 12-18 months [7].

Medications that can interfere with hair regrowth include beta-blockers such as metoprolol and propranolol used in the treatment of abnormal heart rhythms, after a heart attack, or high blood pressure, anti-thyroid medication used in the treatment of hyperthyroidism and anticoagulants [7].

As outlined in this previous article, hair loss is one of the identifying markers of hypothyroidism that results from a lack of thyroid hormones. Hair growth will begin to occur once optimal thyroid hormone replacement is reached, however as mentioned above, it may take 3-6 months for hair shedding to stop, and another 3-6 months for regrowth to be able to be seen [7].  For someone dealing with hair loss, six months to a year to begin to see hair growth can seem like an eternity.  

[I understand this firsthand, as the two photos below are of me.  The one on the left was taken June 3, 2022 at my youngest son’s wedding — a few weeks before being diagnosed of hypothyroidism, and the one on the right was taken yesterday, September 3, 2022, exactly three months later. I share these photos so that people can better understand what the hair loss associated with hypothyroidism may look like.]

Hair loss 3 months after diagnosis

Dr. Izabella Wentz, a clinical pharmacist who focuses on thyroid disorders believes that hair loss is best improved on a medication that contains both T4 and T3, such as desiccated thyroid extract like WP Thyroid®, Nature-Thyroid® or Armour Thyroid®, or a mixture of T4 medication (such as Synthroid®) and a T3 medication such as Cytomel®.  Dr. Wentz also provides a general “rule of thumb” that TSH after treatment should be between 0.5 and 2 μIU/mL [12].

Hair Loss in Nutrient Deficiencies and Nutrient Excess

There are specific nutrient deficiencies that are also linked to different types of hair loss, with the most well-known being iron deficiency. Vitamin C deficiency is also a factor as it is needed  for intestinal absorption of iron.  Zinc deficiency, as well as some B-vitamin deficiency (e.g. niacin, biotin, riboflavin) as well as vitamin D deficiency can also be associated with hair loss [13].  As importantly, excess in vitamins such as vitamin E, vitamin A and folic acid are also associated with hair loss [13]. Ensuring  adequate but not excess nutrient intake is essential and this will be covered in the next part of this article.

Final Thoughts…

Hair loss can be a very distressing symptom, especially when it is noticeable to ourselves and others. Once the cause has been identified and treated, can all we do is be patient and wait for the hair to grow?

Hair regrowth can be supported by ensuring a nutrient-adequate diet, as well as with nutrient supplementation, when there is nutrient deficiency. This will be the topic in Hair Loss – Part 2.

More Info

If you would like more information about how I might be able to support your nutritional needs, please send me a note through the Contact Me form, above.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

  1. Ho CH, Sood T, Zito PM. Androgenetic Alopecia. Updated Nov 15, 2021. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing, https://www.ncbi.nlm.nih.gov/books/NBK430924/#_NBK430924_pubdet_
  2. Panahi Y, Taghizadeh M, Marzony ET, Sahebkar A. Rosemary oil vs minoxidil 2% for the treatment of androgenetic alopecia: a randomized comparative trial. Skinmed. 2015;13(1):15-21.
  3. Medical News Today, Alopecia areata: Causes, diagnosis and treatments, April 7, 2022, https://www.medicalnewstoday.com/articles/70956
  4. Medical News Today, Is Telogen Effluvium reversible? April 23, 2018, https://www.medicalnewstoday.com/articles/321590
  5. Alonso L, Fuchs E; The Hair Cycle. J Cell Sci 1 February 2006; 119 (3): 391–393. doi: https://doi.org/10.1242/jcs.02793
  6. Phillips TG, Slomiany WP, Allison R. Hair Loss: Common Causes and Treatment. Am Fam Physician. 2017;96(6):371-378.
  7. Malkud S. Telogen Effluvium: A Review. J Clin Diagn Res. 2015;9(9):WE01-WE3. doi:10.7860/JCDR/2015/15219.6492
  8. Goette DK, Odom RB. Alopecia in crash dieters. JAMA. 1976;235(24):2622-2623.
  9. Hallberg, S., Do Ketogenic diets cause hair loss? https://www.youtube.com/watch?v=PxkfM84lxMU
  10. Westman E., Hair Loss and Keto, https://www.youtube.com/watch?v=Cgv92mfTj4k
  11. Phinney S., Virta Health, Does Keto Cause Hair Loss, https://www.virtahealth.com/faq/keto-hair-loss
  12. Wentz I., Hair Loss and Your Thyroid, https://thyroidpharmacist.com/articles/hair-loss-and-thyroid/
  13. Guo EL, Katta R. Diet and hair loss: effects of nutrient deficiency and supplement use. Dermatol Pract Concept. 2017;7(1):1-10. Published 2017 Jan 31. doi:10.5826/dpc.0701a01

 

Copyright ©2022 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

More Than Skin Deep – skin symptoms associated with hypothyroidism

According to the American Thyroid Association, 6% of the population have some type of thyroid disease and 60% of them (~12 million people) are unaware of it. Assuming the same rate applies in Canada, 2.3 million people in Canada have thyroid disease and almost 1.4 million people are unaware of it. Since changes in the skin may be one of the first clinical signs of hypothyroidism [2] and are often important indications of its progression [4], this article outlines how some of those skin changes may appear.

DISCLAIMER (August 26, 2022): The information in this post should in no way be taken as a recommendation to self-diagnose, self-interpret skin symptoms or diagnostic tests, or self-treat any suspected disorder. It is essential that people who suspect they may have symptoms of any condition consult with their doctor, as only a medical doctor can diagnose and treat.

NOTE: This article also contains aspects of my personal story which are clearly marked. My personal experience is not objective data. The pictures are provided only so that people can better understand what some skin symptoms of hypothyroidism may look like. Many more pictures are available in clinical online. 


INTRODUCTION: My interest in hypothyroidism is more than academic, as I was recently diagnosed with it. I realize in retrospect that I missed almost all the early signs because I didn’t know what the range of possible symptoms could be. Just as my interest in hyperinsulinemia and type 2 diabetes was birthed in my own diagnosis and eventual partial remission, my interest in this hypothyroidism is no different. Since hypothyroidism can be dangerous if left untreated, my goal in writing this series of articles is to help people know the wide range of symptoms that may be associated with it, and to seek medical attention for themselves or their loved one, when necessary.

As outlined in the article Symptoms of Hypothyroidism Mistakenly Blamed on Aging, people think it is normal for ‘older adults’ to have body aches, joint pain, fatigue, to feel chilled when others do not, experience constipation, hair loss, be forgetful, or to experience depression. However, these are NOT typical signs of aging but ARE common symptoms of hypothyroidism. 

In retrospect, in my case, these types of symptoms came long after the skin symptoms, but cutaneous symptoms were so non-specific that I had no idea they might indicate that something clinical was going on.  

Of course, as a Dietitian, I knew that people often gained weight before they were diagnosed with hypothyroidism, and that they needed to take one of several medications prescribed as treatment. I knew they had to take their medication a half an hour before eating but until recently, my support was limited to teaching them what hypothyroidism is, the nutrients of importance in thyroid function, and foods and beverages that may impact thyroid function.

Until recently, I didn’t know that undiagnosed hypothyroidism can be dangerous and can progress to a myxedema crisis that can be fatal, with a death rate between 20-60%, even with treatment [3]. 

Until today, I had no idea that the majority of people with thyroid disease (60%) are undiagnosed [1].

Putting these two sets of statistics together was concerning to me.  Since many of the symptoms of hypothyroidism such as joint and muscle pain, difficulty getting up from a seated position, or feeling cold are often discounted as normal signs of aging, I wanted people to also know what some of the skin symptoms of hypothyroidism are in the hope that is might help them put the clues together, and seek medical attention.

Skin Symptoms Associated with Hypothyroidism

As mentioned in a previous article about the role of hormones in metabolic disease, thyroid hormones act on every organ system of the body, and their affect on the skin is no exception. Some skin symptoms such as myxedema don’t appear until much later in the progression of hypothyroidism, while other appear early on.

In this article, I will describe the later symptoms first because they are hallmarks of the progression of disease and indicate that getting medical attention is important. In my own case, it was the symptoms associated with myxedema that made me begin to realize that the tiredness and achy muscles and sore joints that I had been experiencing for over a year was more than post-Covid symptoms.

As explained in Symptoms of Hypothyroidism Mistakenly Blamed on Aging, myxedema describes advanced hypothyroidism that occurs when the condition is left untreated or inadequately treated and is also applied to hypothyroidism’s effects on the skin, where it looks puffy and swollen and takes on a waxy consistency [4]. 

[Personal note: It was me looking for clinical answers this morning that resulted in me stumbling across the some of the other skin symptoms associated with hypothyroidism. I wanted to know how long it would take since beginning treatment with thyroid hormone medication for the myxedema to resolve in my legs.]


NOTE: these photos are for illustrative purposes only. Photos of myxedema in the clinical literature are available but are copyrighted. It is for this reason that I am posting my photos only as example, or illustrations.

Below is a photo showing the change in appearance in my left leg from November 3, 2021 (left), to July 16, 2022 (middle), to August 26, 2022 (right).

The photo on the left was taken by me last November while I was doing some stretches. It was still on my phone in mid-July when I took a picture of the swelling in my lower legs and ankles caused by mucin accumulating in the skin. The photo on the right was taken this morning, and while much of the swelling has been reduced, I am still unable to pinch any skin on my legs due to the remaining mucin. I have read that it can take 6 – 8 months for this to resolve.

It has been only 2 months since I began treatment for hypothyroidism, beginning with a very low dose. The above photo shows what I looked like 2 ¾ months ago at my son’s wedding, and how quickly the myxedema in my face resolved with treatment. 


What Causes the Skin Change Known as Myxedema

Myxedema is one several skin significant changes associated with the progression of hypothyroidism. A recently updated dermatology textbook describes myxedema as ‘skin that is cold and pale with abnormally widespread dryness (xerosis) and where a diffuse loss of hair (alopecia) may be present [5].’

When I first saw my doctor after my son’s wedding at the beginning of June, he pointed this out on my legs and said that the cold, waxy skin, along with the swelling is “benchmark symptom” of hypothyroidism.  He showed me how it was impossible to pinch and lift any skin on my legs and that pressing on it left no ‘dent’ mark.  This lack of a dent means the type of edema (swelling) is “non-pitting edema.” Pitting edema occurs in many other conditions, but this non-pitting edema, along with the cold, waxy skin is characteristic of progressing hypothyroidism. The coldness of the skin is the result in the drop in body temperature due to decreased metabolism [2] and is another hallmark symptom of hypothyroidism, discussed in a previous article. The swelling is caused by the accumulation of mucin in the skin.

Mucin is a type of glycoprotein (a protein with a side chain of hyaluronic acid, a sugar molecule) [5] which is naturally produced in the skin. Hyaluronic acid normally binds water to collagen, trapping it in the skin and is injected into the skin by dermatologists to cause aging skin to appear plump, moist and younger looking. The problem is, in hypothyroidism mucin accumulates under the skin, giving it that “tight, waxy” texture. (I would describe it as feeling like an over-inflated balloon). The accumulation of mucin around hair follicles contributes to the resulting hair loss on the arms and legs (and other areas where it occurs). 

[Personal Note: if you look at the composite picture of my left foot (above), you can see in the right hand photo taken this morning (more than 2 months after beginning thyroid hormone medication) that I still cannot pinch any skin on my legs.  While my face has improved, there is still significant improvement yet to occur in my legs, and other parts of my body. ]

Other Skin Symptoms of Hypothyroidism

In addition to myxedema, other skin changes that are associated with hypothyroidism include;

    • dry skin (xerosis)
    • thin scaly skin
    • carotinemia
    • purpura
    • telogen effluvium (hair loss)
    • decrease sweating
    • poor wound healing

As explained in an earlier article, since the presentation of symptoms in hypothyroidism varies so much between individuals, symptoms that were “early” for me, may not be for others, and may not appear at all. 

Purpura is caused when small blood vessels burst, resulting in blood pooling just under the skin. It looks a bit like a bruise, but without pain or swelling and it does not change colour in time.  Purpura is a non-serious skin hemorrhage that is almost always a symptom of something else and looks like small, reddish-purple spots just beneath the skin’s surface.

[Personal account: This morning, when I saw the term “purpura” it jumped out at me. Since May of 2021, I have had a large purple area on my left ankle that I had first attributed to a particularly grueling hike I did in Maple Ridge, BC with one of my young adult sons.  I noticed it when I got home, as did my son, and I assumed it would clear up on its own, but it never did. When I saw my doctor right after my son’s wedding, I showed it to him and he nodded as if to take note, but didn’t say anything. I now know that in my case, it was one of the very early skin signs of hypothyroidism.  I thought I had taken photos of what my purple ankle looked like at its worse, but I may have deleted them because I thought it was simply leftover damage to blood vessels from a hike. The good news is, that two months after beginning thyroid hormone treatment, the purpura is ~75% resolved.] 

August 20, 2022: purpura 75% resolved, thin dry skin, telogen effluvium (hair loss) yet to be resolved

Another early symptom of hypothyroidism for me, was telogen effluvium, a loss of hair on my arms and legs and to a lesser extent, on my scalp. 

[Personal account: Last summer I was joking with a family member that one of the advantages of getting older was no longer needing to shave my legs.  I didn’t realize until recently that the loss of hair on my legs and arms as long as two years ago was NOT a perk of aging (like no longer having a “period”), but was an early symptom of hypothyroidism! I also didn’t realize that decreased sweating wasn’t a benefit of aging, either. I feel stupid in retrospect, but I wasn’t taught it and when I looked it up it said that hair on the body “thins” as one ages, so I thought it was normal.  I hadn’t realized that I had NO hair on my arms and legs. Two months after beginning thyroid medication, that is beginning to change. I feel like a pubescent boy excited by his first facial hair.

I mentioned the dry skin in previous posts, so won’t do so again here, but that was a very early sign for me.  Again, I thought it was a normal part of aging.]

Another term that jumped out at me this morning, was the term carotinemia. This is where beta-carotene accumulates in the blood and gives skin a yellowish pigmentation. In my case, it was not due to eating too much beta-carotene rich foods like carrots, squash or sweet potato, but was a skin symptom of hypothyroidism.  

Two days ago, I posted the photo below on social media. I now understand the significance of what I wrote;

“Update from A Dietitian’s Journey – Part II: It’s been exactly 2 ½ months since my son’s wedding and 2 months since I began thyroid treatment. I think what is most noticeable is that the yellowish skin colour is gone.”

I now know this was carotinemia which has recently resolved —  between the photo of last week (August 17, 2022) and this week (August 24, 2022).
 

 

How my Clinical Practice is Impacted

Just as my clinical practice changed 5 years ago when I came to understand what hyperinsulinemia was, and how early clinical signs of developing type 2 diabetes are evident as long as 20 years before diagnosis, it is changing again as a result of what I am learning about hypothyroidism.

Understanding the wide range of clinical and subclinical symptoms that people may have leads me to ask additional questions, to look at lab test results differently, and to ask for additional ones if it seems clinical warranted. While it is beyond the scope of practice of a Dietitian to diagnose any disease or to treat hypothyroidism, I am more aware of what to look and this helps me to refer people back to their doctor if I feel there may be a clinical concern.

Final Thoughts…

The list of skin symptoms in hypothyroidism in this article is by no means exhaustive.  There are others discussed in the literature that present, particularly as the disease progresses.  Since the goal of this article was to present symptoms that may present early or with advancing hypothyroidism, additional symptoms are beyond the scope of this article.

If you think that you, or someone you know may have symptoms of hypothyroidism, please consult with a medical doctor. 

More Info

If you would like more information about the services I provide people who are newly diagnosed with hypothyroidism, please send me a note through the Contact Me form, above.

To your good health!

Joy

 

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

    1. American Thyroid Association, Prevalence and Impact of Thyroid Disease, https://www.thyroid.org/media-main/press-room/, accessed August 26, 2022
    2. Kasumagic-Halilovic E. Thyroid Disease and the Skin. Annals Thyroid Res. 2014;1(2): 27-31.
    3. Elshimy G, Chippa V, Correa R. Myxedema. [Updated 2022 May 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK545193/#_NBK545193_pubdet_
    4. Medical News Today, What is Myxedema and How is it Treated, April, 22, 2022, https://www.medicalnewstoday.com/articles/321886
    5. Patterson, JW, Weedon’s Skin Pathology, Cutaneous Mucinoses, Elsevier Canada; 5th edition (April 20, 2020)

 

Copyright ©2022 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Beyond Diet – the role of hormones in metabolic health

DISCLAIMER: (August 14, 2022): The information in this post should in no way be taken as a recommendation to self-diagnose, change one’s diet, self-interpret diagnostic tests, or self-treat any suspected disorder. It is essential that people who suspect they may have symptoms of any condition consult with their doctor, as only a medical doctor can diagnose and treat.

The role of diet in metabolic health is well-known, but many people do not realize that hormones, including those from the thyroid impact that.

The Role of Thyroid Hormones

from The Merck Manual of Medical Information (1997)

The thyroid and the hormones it produces play an important role in metabolic health but it is a hormone from the pituitary gland called Thyroid Stimulating Hormone (TSH) that causes the thyroid gland to release the hormone thyroxine, also called free T4. Free T4 is the inactive form of thyroid hormone. Free T4 is activated (reduced) to free T3 (triiodothyronine), the active form of thyroid hormone.

Overt hypothyroidism is where TSH >10 mU/L, with normal or low free T4). 

Subclinical hypothyroidism (SCH), which is where TSH is higher than the normal cutoffs (TSH >4 mU/L) but less than the criteria for overt hypothyroidism (TSH >10 mU/L), but with normal free T4. 

Metabolic Changes due to Hypothyroidism

It has been well established for decades that people with overt (established) hypothyroidism experience several clinical changes that one might assume to be diet-related at first glance. For example, people with hypothyroidism have a decrease in red blood cells and experience different types of anemia, including the anemia of chronic disease. In addition, ten percent of people with hypothyroidism develop pernicious anemia, which is associated with vitamin B12 and folate (folic acid).  

The slowing of metabolism associated with hypothyroidism also results in a decrease in cardiac (heart) output, which results in both slower heart rate and less ability for the heart to pump blood. 

High Blood Pressure

The decreased ability of the heart to pump leads to increased resistance in the blood vessels, which results in increased blood pressure (hypertension).

In those who had normal blood pressure previous to developing hypothyroidism, blood pressure can rise as high as 150/100 mmHg. Hypothyroidism may increase it further for those previously diagnosed with high blood pressure.

It is not only diet that can contribute to high blood pressure but thyroid hormones (as well as other factors).

Weight Gain

Thyroid hormones act on every organ system in the body, but the thyroid is well-known for its role in energy metabolism. When someone has overt hypothyroidism, there is a slowing of metabolic processes, which results in symptoms such as fatigue, cold intolerance, constipation, and weight gain. 

Weight gain is not only about diet or how much someone eats versus how much they burn off. It is also about the person’s metabolic rate, which can be impacted by several things, including decreased thyroid hormones.

High Cholesterol

It has long been known that those with overt hypothyroidism have high total cholesterol, high low-density lipoproteins (LDL) [14], and high triglycerides (TG) [15], which results from a decrease in the rate of cholesterol metabolism. While many assume that “high cholesterol” results from diet, such as the assumption it is related to eating too many eggs, thyroid hormones may also play a role.

Subclinical Hypothyroidism

It has been found that some people with subclinical hypothyroidism have high low-density lipoproteins (LDL) and triglycerides (TG) and low high-density lipoproteins (HDL) [16]. 

But it is not only high cholesterol that is also found in subclinical hypothyroidism. For example, a 2016 paper referred to above reported that previous studies found no significant difference in symptoms between people with subclinical hypothyroidism and those with overt hypothyroidism [9]. That is, all the symptoms associated with overt hypothyroidism are also seen in subclinical hypothyroidism. Therefore, to assume that high blood pressure, serum cholesterol, or blood sugar is solely the result of diet is to possibly overlook the role of the pancreas and/or the thyroid.

As I wrote about in the previous post, all too often common symptoms of hypothyroidism are assumed to be normal signs of aging. Given the potentially serious consequences leaving hypothyroidism undiagnosed and untreated, it is important that people are able to recognize these symptoms in themselves, and loved ones.

Thyroid Hormones Affect Insulin Secretion of the Pancreas

Just as we cannot look at diet without considering the role of hormones such as insulin, we cannot look at pancreas function in isolation from thyroid function. 

As mentioned above, thyroid hormones influence every organ in the body, including the pancreas. It is now known that there are functional thyroid receptors in the pancreas that affect insulin secretion, and it is thought that thyroid hormones may play a role in the development of diabetes. 

Diagnosis and Treatment

The most recent population-based study data from the US with almost 26,000 adults aged 18 – 74 years found 9.5% had TSH levels >5.1 mIU/L, with a higher prevalence in women and older adults. Among the 9.5% with elevated TSH, 74% had subclinical hypothyroidism (TSH 5.1 and 10 mIU/L), and 26% had overt hypothyroidism (TSG >10 mIU/L) [17].

Note (August 14, 2022): From a practical point of view, this study shows that almost 10% of adults have some form of hypothyroidism, with 7/10% being subclinical and 2½ % having clear hypothyroidism. Given its prevalence and significant risk of being undiagnosed, identifying symptoms and lab markers before it progresses is essential. 

In British Columbia, a diagnosis of subclinical hypothyroidism is made at a TSH > 4 mIU/L, but treatment is only recommended when TSH is above 10 mIU/L [18]. This leaves those with a TSH >4 mIU/L but <10 mIU/L in the situation where they need to get much sicker before treatment is recommended.

The goal of treatment with thyroid hormone replacement is to reduce the patient’s serum TSH concentration into the normal reference range. Since the mean serum TSH for the general population is around 1.4 mIU/L, with 90% having serum TSH levels <3.0 mIU/L, many experts recommend a therapeutic TSH target ranging from 0.5 to 2.5 mIU/L in young and middle-aged patients [19] to 7.7 mIU/L in elderly people over the age of 80 years [20].

Studies with 10 to 20-year follow-up have reported that 33 to 55% of people with subclinical hypothyroidism progress to overt hypothyroidism [21,22,23]. This means that 1/3 to >1/2 of people with subclinical hypothyroidism will develop overt hypothyroidism within that period.

Most experts do not recommend treating people with a TSH > 10 mIU/L but with no symptoms (asymptomatic). However, since a meta-analysis of data from 1950-2010 found no increased risk of coronary heart disease in asymptomatic people with a TSH of 4.5 to 6.9 mIU/L, treating them is generally not recommended [24]. 

There is, however, an increased risk of coronary heart disease in those with a TSH of 7.0 to 9.9 mIU/L, so some experts recommend treating those with a TSH > 7.0 mIU/L whether or not they have symptoms [24]. Unfortunately, despite this elevated risk, individuals in British Columbia do not currently have access to treatment with a TSH < 10 mIU/L under the guidelines [18].

Final Thoughts…

Making recommendations on how someone should change their diet can’t be made in a vacuum and it is for this reason, I evaluate a person’s lab test results in light of their medical history and enquire about family history of type 2 diabetes, heart disease, high cholesterol, blood pressure, thyroid disorders and other conditions as part of my assessment. Then I look at how people eat in light of their risk factors for those conditions.

If I feel that it would be beneficial to have additional lab work such as fasting insulin, or thyroid stimulating hormone (TSH), then I will request that their doctor requisition these tests. Often, when I provide the doctor with my clinical reasons for asking for them, they write the requisition; however, sometimes, they decline. If I don’t think it would not be a financial burden and that having the results will provide the client with a much better understanding of how their diet relates to their weight or health, I will discuss the option of obtaining the tests on a patient-pay basis.  If self-paying for the tests is not feasible, and the risk factors are significant, then I will tailor my dietary recommendation to lower the risk.

NOTE (August 15, 2022): It is important to keep in mind that too little, or too much thyroid hormone can have serious consequences.

Untreated or under-treated hypothyroidism can be serious and is when the body gets too little thyroid hormone. This can lead to a myxedema crisis (covered in this article).

Thyrotoxicosis can also be serious and is when the body gets too much thyroid hormone. This can occur in untreated hyperthyroidism, or by self-treating hypothyroidism (covered in this article).

If you suspect you may have hypothyroidism (or any other clinical condition), consult with your doctor, and “don’t try this at home.”

More Info

If you would like more information about how I can support you in your goal of improved health, please send me a note through the Contact Me form above.

To your good health!

Joy

 

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

    1. Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.
    2. Pareek, M., Bhatt, D.L., Nielsen, M.L., et al,  Enhanced Predictive Capability of a 1-Hour Oral Glucose Tolerance Test: A Prospective Population-Based Cohort Study. Diabetes Care 1 January 2018; 41 (1): 171–177. https://doi.org/10.2337/dc17-1351
    3. Sagesaka H, S.Y., Someya Y, et al, Type 2 Diabetes: When Does It Start? Journal of the Endocrine Society, 2018. 2(5): p. 476-484.
    4. Government of British Columbia, Ministry of Health, Schedule of Fees for Laboratory Services – Outpatient, Payment Schedule, revised April 1, 2022, http://www.bccss.org/bcaplm-site/Documents/Programs/laboratory_services_schedule_of_fees.pdf
    5. BC Guidelines, Hormone Testing – indications and appropriate use, Insulin, https://www2.gov.bc.ca/gov/content/health/practitioner-professional-resources/bc-guidelines/special-endocrine-testing#Insulin
    6. BC Guidelines, Hormone Testing – indications and appropriate use, C-peptide, https://www2.gov.bc.ca/gov/content/health/practitioner-professional-resources/bc-guidelines/special-endocrine-testing#C-peptide
    7. Canadian Diabetes Association, The Burden of Out of Pocket Costs for Canadians with Diabetes, 2011,  http://www.diabetes.ca/CDA/media/documents/publications-and-newsletters/advocacy-reports/burden-of-out-of-pocket-costs-for-canadians-with-diabetes.pdf
    8. Statistics Canada. Table 11-10-0239-01 Income of individuals by age group, sex and income source, Canada, provinces and selected census metropolitan areas, DOI: https://doi.org/10.25318/1110023901-eng
    9. Javed Z, Sathyapalan T. Levothyroxine treatment of mild subclinical hypothyroidism: a review of potential risks and benefits. Ther Adv Endocrinol Metab. 2016;7(1):12-23. doi:10.1177/2042018815616543
    10. Danese MD, Ladenson PW, Meinert CL, Powe NR. Clinical review 115: effect of thyroxine therapy on serum lipoproteins in patients with mild thyroid failure: a quantitative review of the literature. J Clin Endocrinol Metab 2000; 85:2993.
    11. Caraccio N, Ferrannini E, Monzani F. Lipoprotein profile in subclinical hypothyroidism: response to levothyroxine replacement, a randomized placebo-controlled study. J Clin Endocrinol Metab 2002; 87:1533.
    12. Nakajima Y, Yamada M, Akuzawa M, et al. Subclinical hypothyroidism and indices for metabolic syndrome in Japanese women: one-year follow-up study. J Clin Endocrinol Metab 2013; 98:3280.
    13. Janovsky CCPS, Bittencourt MS, Goulart AC, et al. Unfavorable Triglyceride-rich Particle Profile in Subclinical Thyroid Disease: A Cross-sectional Analysis of ELSA-Brasil. Endocrinology 2021; 162.
    14. Lithell, H., Boberg, J., Hellsing, K., Ljunghall, S., Lundqvist, G., Vessby, B., & Wide, L. (1981). Serum lipoprotein and apolipoprotein concentrations and tissue lipoprotein-lipase activity in overt and subclinical hypothyroidism: the effect of substitution therapy. European journal of clinical investigation11(1), 3–10. https://doi.org/10.1111/j.1365-2362.1981.tb01758.x
    15. Nikkila E, Kekki M, Plasma triglyceride metabolism in thyroid disease, J Clin Invest. 1973;51:203. 
    16. Kung, A. W., Pang, R. W., & Janus, E. D. (1995). Elevated serum lipoprotein(a) in subclinical hypothyroidism. Clinical endocrinology43(4), 445–449. https://doi.org/10.1111/j.1365-2265.1995.tb02616.x
    17. Canaris, G. J., Manowitz, N. R., Mayor, G., & Ridgway, E. C. (2000). The Colorado thyroid disease prevalence study.  Archives of internal medicine160(4), 526–534. https://doi.org/10.1001/archinte.160.4.526
    18. BC Guidelines & Protocols Advisory Committee, Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder, October 24, 2018, pg. 6
    19. Biondi B., The Normal TSH Reference Range: What Has Changed in the Last Decade?, The Journal of Clinical Endocrinology & Metabolism, Volume 98, Issue 9, 1 September 2013, Pages 3584–3587, https://doi.org/10.1210/jc.2013-2760
    20. Surks MI, Hollowell JG.2007Age-specific distribution of serum thyrotropin and antithyroid antibodies in the US population: implications for the prevalence of subclinical hypothyroidismJ Clin Endocrinol Metab 92:4575–4582
    21. Kabadi U. M. (1993). ‘Subclinical hypothyroidism’. Natural course of the syndrome during a prolonged follow-up study. Archives of internal medicine153(8), 957–961. https://doi.org/10.1001/archinte.153.8.957Huber, G., Staub, J. J., Meier, C.,
    22. Vanderpump, M. P., Tunbridge, W. M., French, J. M., Appleton, D., Bates, D., Clark, F., Grimley Evans, J., Hasan, D. M., Rodgers, H., & Tunbridge, F. (1995). The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey. Clinical endocrinology43(1), 55–68. https://doi.org/10.1111/j.1365-2265.1995.tb01894.x
    23. Mitrache, C., Guglielmetti, M., Huber, P., & Braverman, L. E. (2002). Prospective study of the spontaneous course of subclinical hypothyroidism: prognostic value of thyrotropin, thyroid reserve, and thyroid antibodies. The Journal of clinical endocrinology and metabolism87(7), 3221–3226. https://doi.org/10.1210/jcem.87.7.8678
    24. Rodondi, N., den Elzen, W. P., Bauer, D. C., Cappola, A. R., Razvi, S., Walsh, J. P., Asvold, B. O., Iervasi, G., Imaizumi, M., Collet, T. H., Bremner, A., Maisonneuve, P., Sgarbi, J. A., Khaw, K. T., Vanderpump, M. P., Newman, A. B., Cornuz, J., Franklyn, J. A., Westendorp, R. G., Vittinghoff, E., … Thyroid Studies Collaboration (2010). Subclinical hypothyroidism and the risk of coronary heart disease and mortality. JAMA304(12), 1365–1374. https://doi.org/10.1001/jama.2010.1361
  1.  

Copyright ©2022 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Symptoms of Hypothyroidism Mistakenly Blamed on Aging

DISCLAIMER (August 14, 2022): The information in this post should in no way be taken as a recommendation to self-diagnose, self-interpret diagnostic tests, or self-treat any suspected disorder. It is essential that people who suspect they may have symptoms of any condition consult with their doctor, as only a medical doctor can diagnose and treat.

NOTE: This article contains aspects of my personal story which are clearly marked. My personal experience is not objective data. The pictures are provided only so that people can better understand what the “weight gain” of hypothyroidism can look like, and how different it is from ordinary weight gain. 


In-person visits to the doctor have been minimal over the past two years, and it has been easy for people to discount symptoms such as body aches,  headaches, fatigue, and ‘brain fog’ to having had Covid, or to having ‘long Covid’ [1]. It was only when I began having symptoms that were not consistent with Covid that I began to think that it might be hypothyroidism. You can read my personal account here.

I am not that old, but at the beginning of June (two months ago), our family was in Tofino (Vancouver Island) for the marriage of my youngest son. The groom’s eldest brother assumed that my inability to walk on the sand, up the path to the hotel, or get up from a chair was a result of me having “aged.”

He had no idea that I was hiking in North Vancouver and Golden Ears Provincial Park for several hours at a time last summer. I knew that it was abnormal for me to feel so exhausted and for my muscles to feel so weak, and one look in the mirror told me something was very wrong.

In a matter of just a few weeks, I went from looking as I have the last two years to looking as I did when I was 55 pounds overweight. For the sake of this special occasion, I said nothing to my family, but was very concerned for my health.  It was also exceedingly hard for me to be in family photographs that I knew would be viewed for years to come.

I planned to contact my doctor when I returned home and have him assess me to determine whether I had what I suspected was hypothyroidism. 

Last Friday, my doctor confirmed that my symptoms were consistent with that diagnosis. I was surprised when he said that it was not unexpected in light of my lab work over the previous nine years, my past thyroid surgery many years ago, and my having experienced periodic hypothyroid symptoms since that time. Unfortunately, it took almost a decade for me to get diagnosed because of the limitations placed on doctors regarding which tests they can requisition under what circumstances. 

Common Hypothyroid Symptoms May Often be Assumed to be Aging

from https://www.thyroid.org/thyroid-disease-older-patient/

People assume that it is normal for ‘older adults’ to have body aches, joint pain, fatigue, feel chilled when others do not, experience constipation, have dry skin or hair loss, be forgetful, or to even experience depression. However, these are NOT typical signs of aging but ARE common symptoms of hypothyroidism. 

The above-mentioned symptoms are so non-specific that many would not give them a second thought. An older person who is already limited to a one-issue-ten-minute remote doctor’s appointment would likely be hesitant to book a phone call to discuss these symptoms with their doctor. After all, they would conclude, these could be the result of so many different things, or “just the normal effect of aging”. 

Consider constipation as an example. Chronic constipation affects 15% of adults and is the sixth most commonly reported GI symptom [3]. Within the context of a lack of mobility that we have all faced due to lockdown restrictions, how many people would give increased constipation a second thought?

Consider mood changes as another example. It is well-documented that the social isolation associated with the pandemic lockdowns has taken a toll on the mental health of people of all ages. It is easy to attribute symptoms of  decreased cognitive function, forgetfulness, or even depression in older adults to increased social isolation rather than considering a diagnosis of hypothyroidism.

Symptoms such as loss of hair on the legs or arms may be attributed to the natural process of aging, and while it is normal to have less hair on the arms or legs as people age, it is not normal to lose all the hair. Although no longer needing to shave or wax one’s legs may be perceived as a benefit of aging (like no longer having a ‘period’ after menopause), a complete loss of hair on the legs or arms is something that is not a normal part of aging. Symptoms like these should be brought to the attention of one’s doctor. Likewise, while it may be nice for someone not to feel as sweaty in the heat of the summer as one did when they were younger, sweating is how humans stay cool, and decreased sweating can be dangerous! 

Symptoms of constipation, hair loss on legs and arms, decreased sweating, forgetfulness, and mood changes such as depression are not part of “aging” but are symptoms that one’s doctor should assess.  

Untreated Hypothyroidism can be Dangerous

Myxedema describes advanced hypothyroidism that occurs when the condition is left untreated or inadequately treated [4]. This term is also applied to hypothyroidism’s effects on the skin, where it looks puffy and swollen and takes on a waxy consistency [4]. 

Below is a photo of what I looked like hiking 3 months before my son’s wedding, what I looked like with myxedema at his wedding, and what I look like today. I don’t share these photos easily because my son’s wedding was a special occasion, and not only did I look and feel terrible, in retrospect, I was very unwell. I am sharing them so that people can understand what the edema / myxedema of hypothyroidism looks like and how quickly it can progress, and how serious hypothyroidism can be if left untreated or undertreated.

Myxedema of hypothyroidism is very different from ordinary weight gain. I hope that by sharing these photos people will be better equipped to recognize this symptom in themselves or in others, and ensure that medical attention is sought. 

Getting Diagnosed

Each province in Canada sets its policy for provincial medical plans covering laboratory tests. In the US, which testing is covered is determined by whether they are performed by in-network or out-of-network labs. 

In British Columbia, thyroid testing covered by the provincial health plan is determined by a 2018 document titled Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder [2]. These guidelines outline testing for thyroid stimulating hormone (TSH), free thyroxine (fT4), free triiodothyronine (fT3), and anti-thyroid peroxidase (TPO).  

Unless someone has specific risk factors for thyroid disease (older age, strong personal or family history of thyroid disease, taking drugs such as lithium (used in bipolar disorder) or amiodarone (used in cardiac dysrhythmia), or grew up in a developing country known to have either iodine excess or deficiency),  individuals are required to exhibit several of the specific symptoms listed below to even qualify for thyroid hormone testing. 

The problem is that typical symptoms such as cold intolerance,  edema,  decreased sweating, and skin changes often don’t appear until much later in the progression of the disease.  Moreover, in some individuals, these symptoms do not appear at all.

Furthermore, as outlined in the previous article, even if a person meets the criteria for a TSH test, the results would need to come back significantly higher than the cutoffs to qualify for a free T4 (fT4) or free T3 (fT3) test. 

People here and in other places with similar policies have no choice but to live with many symptoms documented to be associated with hypothyroidism but outside narrowly defined diagnostic criteria until they become sick enough to warrant testing. 


NOTE: these photos are for illustrative purposes only. 

[LEFT: me hiking March 5, 2022.  MIDDLE: me at my youngest’s son’s wedding on June 3, 2022, only 2 months ago. RIGHT: Me today (August 8, 2022), only two months after my son’s wedding with 75% of the edema resolved.

UPDATE [August 25, 2022] The photo on the left was taken 2 ¾ months ago. The photo on the right was taken today, 2 months after beginning treatment for hypothyroidism. They are provided only as an illustration of what symptoms can look like and how quickly they can resolve with medical treatment. (I deliberately left the lines marking the hairline and chin to make comparison easier.) 

LEFT: before diagnosis and treatment RIGHT: 2 months after diagnosis and starting treatment [for illustrative purposes only]

The photos below are of my left leg without edema and with it. While my legs are still ‘waxy’ looking from the myxedema, the extreme swelling resolved within a few days of beginning thyroid hormone replacement. This photo is for illustrative purposes only and does NOT provide any clinical information.

While each person may exhibit different symptoms, this is fairly typical of the length of time over which the “weight gain” of hypothyroidism can occur, and also the time-frame over which it can resolve with treatment.


It is important to understand that untreated hypothyroidism can progress and the results of a myxedema crisis which can be fatal. The death rate for a myxedema crisis is between 20-60%, even with treatment [5]. 

A myxedema crisis is often incorrectly called a ‘myxedema coma,’ but this term is misleading since the person rarely experiences a coma.

The most noticeable feature of a myxedema crisis is the person’s significant deterioration in mental function [5]. The slowness of thought, decrease in attention, and apathy can easily be confused with symptoms of depression[6], but in severe untreated hypothyroidism, people can exhibit significant agitation and even psychosis and paranoia, referred to as “myxedema madness” [6]. In addition, there have been cases reported in the literature of people hospitalized with suspected affective (mood) disorders such as bipolar disorder– even psychosis that turned out to be a myxedema crisis and that resolved with thyroid hormone treatment [7].

A myxedema crisis may occur because someone had untreated hypothyroidism. It can also happen because someone stopped taking their medication or was taking an incorrect dosage. Therefore, being correctly diagnosed, treated and followed by a physician is essential.

I found the following explanation from a recent article on hypothyroidism [8] very helpful as it explains how different people with the condition may have various symptoms.

“It is important to maintain a high index of suspicion for hypothyroidism since the signs and symptoms can be mild and nonspecific and  different symptoms may be present in different patients. Typical features such as cold intolerance,  puffiness,  decreased sweating and skin changes may not be present always. Inquire about dry skin, voice changes, hair loss, constipation,  fatigue, muscle cramps, cold intolerance, sleep disturbances,  menstrual cycle abnormalities,  weight gain, and galactorrhea  (nipple discharge not associated with lactation / breastfeeding). Also obtain a complete medical, surgical, medication, and family history” [8].

Note (August 15, 2022): Over-treatment with thyroid hormones also poses a risk of thyrotoxicosis, or “thyroid storm,” outlined in this newer article.

Final Thoughts…

By virtual of their age, older adults in British Columbia qualify for thyroid testing. If older people exhibit even a few of the common symptoms of hypothyroidism, such as long standing body aches or joint pain, unexplained fatigue, feeling usually chilled, constipation, dry skin or hair loss, forgetfulness or depression, this should be brought to their doctor’s attention. These are not typical signs of aging but are common symptoms associated with hypothyroidism. 

For younger individuals without preexisting risk factors and that do not have the specific symptoms listed on the diagnostic criteria, the reality is that they do not qualify for testing. Unfortunately, they will need to get quite unwell before they are able to be diagnosed and treated, and their doctor’s hands are tied by a system that will not enable them to test T3 or T4 — even in the presence of high-normal TSH, or symptoms known to be associated with hypothyroidism, but not on the diagnostic criteria list.

Surely, there has to be a way that people can be tested, but that does not put additional financial strain on an already overtaxed public healthcare system?

Currently people have two alternative options;

(1) pay significant out of pocket costs to see a Functional Medicine MD or Integrative Health MD where they can be properly diagnosed and treated.

(2) pay a naturopath added costs for them to requisition thyroid tests, but one concern is since they are not medical doctors, they do not have the training to rule out liver, kidney or heart disease that can mimic many of the same symptoms as hypothyroidism, and that requires medical attention.

In the previous post, I mentioned the option of enabling patients to self-pay at the same cost as the government pays for TSH, T3 and T4 tests. This way if the lab tests results come back abnormal, their doctor can oversee both diagnosis and treatment (or refer them to an endocrinologist).

In British Columbia, someone can pay (at government rates) $9.90 for a TSH test, $12.12 for a free T4 test, or T4 or total thyroxine test, and pay $9.35 for a free T3 test [9]. Under the current system, the government only applies a lab volume discount (based on 2011-2012 volumes) for some fee-for-service (FFS) tests [10] so under this model, only 38% of tests are reimbursed at 100% of the published fee, whereas 62% are only reimbursed at 50% of the published fee [3].  It is not clear from the government publication which rate applies to thyroid testing, but even if people are required to pay 100% of the costs, the total cost of a TSH test, and a free T4 test, and a free T3 test is just over $30.  

I was disheartened to learn recently that even if patients are willing to pay the full cost of thyroid testing, their doctor is under no obligation to write the lab requisition. This is because licensing requirements require doctors who write a lab test requisition to also take responsibility to oversee care based on those results. Unfortunately, not all doctors are willing to treat those with subclinical hypothyroidism. 

How I May be Able to Assist

I currently assist my clients in requesting that their doctor refer them to an allergist if I believe there is clinical reason to suspect IgE mediated food allergies. I also will request that a doctor requisition a fasting insulin (or c-peptide test) along with a fasting glucose if based on assessment I have reason to suspect a person’s pancreas may be working too hard to keep fasting blood glucose and HbA1C in the normal range. In the same way, if I have clinical reason to be concerned about a person’s thyroid function, I will request that a doctor requisition thyroid testing. These requests are by no means a guarantee that a person’s doctor will agree to requisition blood tests, but it has been my experience that when clinical concerns are documented, most doctors are willing investigate further. 

More Info

If you would like more information about the services I provide people who are newly diagnosed with hypothyroidism, please send me a note through the Contact Me form, above.

To your good health!

Joy

 

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

    1. John Hopkins Medicine, Long COVID: Long-Term Effects of COVID-19, June 14, 2022, https://www.hopkinsmedicine.org/health/conditions-and-diseases/coronavirus/covid-long-haulers-long-term-effects-of-covid19
    2. BC Guidelines & Protocols Advisory Committee, Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder, October 24, 2018
    3. Bharucha AE, Lacy BE. Mechanisms, Evaluation, and Management of Chronic Constipation. Gastroenterology. 2020;158(5):1232-1249.e3. doi:10.1053/j.gastro.2019.12.034
    4. Medical News Today, What is Myxedema and How is it Treated, April, 22, 2022, https://www.medicalnewstoday.com/articles/321886
    5. Elshimy G, Chippa V, Correa R. Myxedema. [Updated 2022 May 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK545193/#_NBK545193_pubdet_
    6. Samuels MH. Psychiatric and cognitive manifestations of hypothyroidism. Curr Opin Endocrinol Diabetes Obes. 2014;21(5):377-383. doi:10.1097/MED.0000000000000089
    7. Heinrich TW, Grahm G. Hypothyroidism Presenting as Psychosis: Myxedema Madness Revisited. Prim Care Companion J Clin Psychiatry. 2003;5(6):260-266. doi:10.4088/pcc.v05n0603
    8. Patil N, Rehman A, Jialal I. Hypothyroidism. [Updated 2022 Jun 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;
    9. Government of British Columbia, Ministry of Health, Schedule of Fees for Laboratory Services – Outpatient, Payment Schedule, revised April 1, 2022, http://www.bccss.org/bcaplm-site/Documents/Programs/laboratory_services_schedule_of_fees.pdf
    10. BC Agency for Pathology and Laboratory Medicine (BCAPLM), Outpatient Payment Schedule, Laboratory Volume Discounting (LVD), http://www.bccss.org/clinical-services/bcaplm/health-professionals/outpatient-payment-schedule

 

Copyright ©2022 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Thyroid Function Assumed to be Normal When Only TSH is Tested

DISCLAIMER (August 14, 2022): The information in this post should in no way be taken as a recommendation to self-diagnose, self-interpret diagnostic tests, or self-treat any suspected disorder, including thyroid function. It is essential that people who suspect they may have symptoms of any condition consult with their doctor, as only a medical doctor can diagnose and treat.


In Canada and many places in the US, the standard screening test for abnormal thyroid function is thyroid stimulating hormone (TSH). As outlined below, TSH is a hormone that is released from the pituitary gland, not the thyroid. If TSH results falls within normal range, no testing of thyroid hormones occurs. Thyroid response to TSH is presumed to be normal.

Thyroid Hormones and Lab Tests Used to Assess Thyroid Function

different organs involved in thyroid function
from [5] The Merck Manual of Medical Information (1997)

Thyroid Stimulating Hormone (TSH) is a hormone that is produced by the pituitary gland in response to a hormone called Thyrotropin-Releasing Factor (TRF) that is released by the hypothalamus of the brain.

Thyroid Stimulating Hormone (TSH) released from the pituitary gland acts on the thyroid gland, a butterfly shaped gland in the front of the neck. The action of pituitary TSH on the thyroid results in the release of thyroxine, also called Free T4 (fT4).  Thyroxine (fT4) is reduced to Triiodothyronine also called Free T3 (fT3), which is the active form of thyroid hormone.

Central Hypothyroidism is where a problem exists in either the hypothalamus or the pituitary gland that results in a decreased in TSH release from the pituitary gland. On lab tests, a low TSH and low T4 indicates central hypothyroidism. This is often treated by administration of growth hormone, or using T3 containing medications. 

Primary hypothyroidism is where there is no abnormality in the hypothalamus or the pituitary gland. Primary hypothyroidism is diagnosed when there is high TSH and normal or low free thyroxine (free T4 / fT4). In many places in Canada and the USA, if TSH is normal, no further testing is done. It is assumed that the action of pituitary TSH on the thyroid gland results in sufficient release of T4.

Thyroid Function – different causes of primary hypothyroidism

Hashimoto’s Disease

The most common form of primary hypothyroidism in the western world is Hashimoto’s disease which is an autoimmune disorder where the body attacks the thyroid. Thyroid Peroxidase Antibody (TPO antibody) is the marker for Hashimoto’s hypothyroidism [6]. 

Prior Thyroid Surgery or Radiation of the Neck

According to Endocrinologist, Dr. Theodore C. Friedman MD, PhD,  Professor of Medicine at UCLA, primary hypothyroidism can also result from prior thyroid surgery to remove a tumor or nodule, or due to radiation of the neck [6].

Dietary Deficiency

Iodine is essential for thyroid function and in the developing world, the most common type of primary hypothyroidism is related to iodine deficiency. Iodine deficiency is assumed to be rare in the West since iodine is added to salt (iodized salt), in the same way that vitamin D is routinely added to milk.  I have noticed a significant increase in the use of Himalayan pink salt and sea salt for home use in the last decade or so, and wondered how much of the salt being used currently is iodized. Data from 2015 indicates that only 53% of salt sales in the US were iodized [7], so I have to wonder what effect this decreased intake of iodized salt may be having on the prevalence of hypothyroidism. 

Selenium is another mineral that is essential for thyroid function as it functions in the conversion of (inactive) T4 to (active)T3. Like iodine deficiency, selenium deficiency is a significant problem in the developing world, but thought to be rare in the West. Research from 2012 indicates that the selenium content of the soil in the US was already lowest in the major agricultural areas of the Northwest, Northeast, Southeast, and areas of the Midwest near the Great Lakes[8] and at the time, only the Great Plains and the Southwest were reported to have adequate selenium content in the soil [8].

Given the decreased use of iodized salt and decreased presence of selenium in the soil where much of domestic food is grown, I wonder what effect this may be having on formerly rare incidence of nutrient-related hypothyroidism in the US and Canada.

Assessing Thyroid Function – testing for hypothyroidism

Each province in Canada sets its own policy for which laboratory tests are covered by provincial medical plans, and in the US which testing is covered is determined by whether they are performed by in-network or out-of-network labs. 

In British Columbia, thyroid testing covered by the provincial plan is determined by a 2018 document titled Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder [9]. These guidelines outline testing for thyroid stimulating hormone (TSH), free thyroxine (fT4), free triiodothyronine (fT3) and anti-thyroid peroxidase (TPO).

According to the guidelines, risk factors for thyroid disease include [9]:

• men: age ≥ 60 years
• women: age ≥ 50 years
• personal history or strong family history of thyroid disease
• diagnosis of other autoimmune diseases
• past history of neck irradiation
• previous thyroidectomy or radioactive iodine ablation
• drug therapies such as lithium and amiodarone
• dietary factors (iodine excess and iodine deficiency in patients from developing countries)
• certain chromosomal or genetic disorders

Note: Iodine nutrient deficiency for those who are not from developing countries is not included. 

Indications for Testing

    1. Routine thyroid function testing is not recommended in asymptomatic patients Testing may be indicated when non-specific symptoms or signs are present in patients who have specific risk factors for thyroid disease.
    2. Testing is indicated for patients with a clinical presentation consistent with thyroid disease as delineated in Table 1: Symptoms and Signs of Thyroid Disease, below.
    3. Where thyroid testing in an asymptomatic patient has occurred and the patient has been diagnosed with subclinical thyroid disease (subclinical hypothyroidism: TSH is elevated in the presence of normal levels of fT4)
    4. If initial testing (i.e. TSH) is normal, repeat testing is unnecessary unless there is a change in clinical condition*.  

The Guidelines (page 3) states, “A TSH value within the laboratory reference interval excludes the majority of cases of primary thyroid dysfunction.

[The reference provided for this is: Jameson, JL., Weetman, A.P.,  Disorders of the Thyroid Gland, Harrison’s Principles of Internal Medicine. 17th ed. New York: McGraw-Hill; 2008. p. 2224–47]

The guide also indicates that “the TSH reference interval will vary depending on the testing laboratory. ” What that means is the cutoff points for an abnormal level of TSH vary between labs in BC.

*What this means is, if TSH lab test results come back in the normal range, no further testing is performed unless the person begins to show some of the accepted hypothyroid signs and symptoms in Table 1, below.

Note: As outlined above, if TSH is found to be normal we know that TSH release from the pituitary gland is normal. There is no testing for the thyroid gland’s response to TSH released from the pituitary gland, it is assumed to be functioning.

Below are the accepted hypothyroid signs and symptoms that warrant testing (from Table 1 [9]).

Signs and Symptoms used in British Columbia to assess thyroid function
Table 1: Signs and Symptoms of Hypothyroidism [9]

Only the above list of clinical presentation symptoms is recognized as consistent with hypothyroidism, warranting lab testing.

Looking at the list in Table 1, how many other conditions, including having Covid-19 result in people feeling depressed, having decreased mental function (“brain fog”), feeling physically tired, feeling cold, having reduced degree of movement and muscle weakness, dry flaking skin, and a hoarse voice?  Unless a person has burning or prickling sensation in their hands or feet, or swelling under their eyes, or are sweating less than usual, it is unlikely they would notice anything unusual outside of common flu or Covid symptoms that would have them mention the above to their doctor.

Below is a fuller list of clinical presentation symptoms associated with hypothyroidism, with the ones NOT recognized for testing in italics.

fuller list of symptoms to evaluate signs and symptoms of thyroid function - page 1
Hypothyroid signs and symptoms 1 of 3 (the ones in italics do NOT warrant TSH testing in British Columbia)
fuller list of symptoms to evaluate signs and symptoms of thyroid function - page 2
Hypothyroid signs and symptoms 2 of 3 (the ones in italics do NOT warrant TSH testing in British Columbia)
fuller list of symptoms to evaluate signs and symptoms of thyroid function - page 3
Hypothyroid signs and symptoms 3 of 3 (the ones in italics do NOT warrant TSH testing in British Columbia)

The Guidelines Summarized

Unless you are either a man ≥ 60 years, or a woman ≥ 50 years with a personal history or strong family history of thyroid disease, a diagnosis of other autoimmune diseases, a past history of neck irradiation or previous removal of your thyroid or destruction of your thyroid for medical reason using radioactive iodine, are not on medications such as lithium or amiodarone, and aren’t from a developing country with either iodine excess or iodine deficiency, or have a specific chromosomal or genetic disorder listed, you do not qualify for TSH testing unless you display the specific symptoms listed in Table 1, above).

What if the other common presentations that are NOT also common in colds, flu or Covid-19 were included in the checklist such as;

    • non-pitting edema (swelling) in the lower legs and ankles
    • a puffy swollen face
    • an enlarged tongue (with or without scalloped edges)
    • enlarged saliva glands including under the tongue
    • hair thinning
    • loss of the outer third of eyebrows
    • pale or bluish lips

…would it be more likely that people experiencing these symptoms would go to their doctors, and be tested?

Summary of Assessing Thyroid Function

  1. To be diagnosed with hypothyroidism, requires a high TSH and normal or low free free T4 but in many places in Canada and the USA, if TSH is normal, no further testing is done.

2. How one defines “high TSH” is important. In British Columbia, the cutoff points vary between labs, but lab normal values at the labs near me are the normal range is 0.27-0.42 mU/L, but is a result of 3.9 mU/L or 4.0 mU/L really “normal”?

Thyroid Function

TSH                    4.0  (0.27-4.2) mU/L

It is “normal enough” that no further testing is done.

3. Someone can have common clinical manifestations of hypothyroidism (non-pitting edema in the lower legs and ankles, a puffy swollen face, enlarged tongue (with or without scalloped edges), enlarged saliva glands, hair thinning, loss of the outer third of eyebrows or pale or bluish lips but if their symptoms are not on the list in Table 1, they are not eligible for testing of thyroid hormones, fT4 / fT3.

4. Unless a person is from a family with specific risk factors (older age with other autoimmune conditions, or had neck irradiation, a thyroidectomy or radioactive iodine ablation,  or take lithium or amiodarone, or are from a developing country that had iodine excess and iodine deficiency) they are not eligible for testing of thyroid hormones, fT4 / fT3.

Final Thoughts…

If some one has their TSH tested and the results come back in the normal range for that particular lab, no further testing is done — even if they have symptoms documented in the literature to be associated with hypothyroidism. 

My concern is if the definition of who qualifies for fT4 testing may be too narrow,. People with high-normal TSH and symptoms that are associated with hypothyroidism, but not on the “list” in Table 1, will not be tested. Could it be that some people could have greatly improved quality of life if thyroid hormones were evaluated, found to be low, and treatment initiated? [Please see note added July 17, 2022 about a diagnosis of subclinical hypothyroidism where TSH > 4mIU/ with normal T4.]

NOTE, July 16, 2022: It is not the normal TSH test result in the absence of symptoms that I am addressing in this article, but the absence of T4 testing in someone with presenting symptoms of hypothyroidism beyond the official “list”. It is my hope that if someone has those symptoms and a TSH value that is normal, that physicians would remain curious and ask for additional testing.

NOTE: July 17, 2022: I came across an academic paper from 2016 that indicates that diagnosis of subclinical hypothyroidism (SCH) exists in western countries for TSH >4 mIU/L, with normal T4 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740939/], whereas the cutoff here for a diagnosis of SCH is >10 mIU/L. (which is based on 2008 reference, as outlined above). Also of interest, another paper I came across from 2016 reported that several previous studies found no significant difference in symptoms between people with  subclinical hypothyroidism  and those with overt hypothyroidism [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740939/] . The most common symptoms reported of both SCH and overt hypothyroidism were poor memory, slow thinking, muscle cramps, muscle weakness, tiredness, dry skin, feeling colder, hoarse voice, puffy eyes, more constipation.

More Info?

If you have been diagnosed with hypothyroidism and would like to better understand the condition, or would like make sure that you have adequate intake of nutrients known to be important in thyroid health, please send me a note through the Contact Me form and I will reply when I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

  1. Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.
  2. Pareek, M., Bhatt, D.L., Nielsen, M.L., et al,  Enhanced Predictive Capability of a 1-Hour Oral Glucose Tolerance Test: A Prospective Population-Based Cohort Study. Diabetes Care 1 January 2018; 41 (1): 171–177. https://doi.org/10.2337/dc17-1351
  3. Bergman M, Chetrit A, Roth J, Dankner R (2016) One-hour post-load plasma glucose level during the OGTT predicts mortality: observations from the Israel Study of Glucose Intolerance, Obesity and Hypertension. Diabet Med 33:1060–1066
  4. Hulman, A., Vistisen, D., Glümer, C. et al. Glucose patterns during an oral glucose tolerance test and associations with future diabetes, cardiovascular disease and all-cause mortality rate. Diabetologia 61, 101–107 (2018). https://doi.org/10.1007/s00125-017-4468-z
  5. Berkow, R., Beers, M. H., & Fletcher, A. J. (1997). The Merck Manual of Medical Information. Whitehouse Station, N.J.: Merck Research Laboratories.
  6. Freidman, Theodore C., Nuances of Hypothyroidism, The MAGIC Foundation’s Annual Conference for Adults With Endocrine Disorders (Phoenix, AZ),  March 3, 2019
  7. Maalouf J, Barron J, Gunn JP, Yuan K, Perrine CG, Cogswell ME. Iodized salt sales in the United States. Nutrients. 2015 Mar 10;7(3):1691-5. doi: 10.3390/nu7031691. PMID: 25763528; PMCID: PMC4377875.
  8. Mistry HD, Broughton Pipkin F, Redman CW, Poston L. Selenium in reproductive health. Am J Obstet Gynecol. 2012 Jan;206(1):21-30
  9. BC Guidelines & Protocols Advisory Committee, Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder, October 24, 2018

 

Copyright ©2022 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.