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December 20, 2019

New ADA Standards of Medical Care Includes Low Carbohydrate Diet

The American Diabetes Association (ADA) has just released its new Standards of Medical Care in Diabetes (2020) [1] which begins the section on Medical Nutrition Therapy by referring to the ADA’s April 2019 Consensus Report[2] which emphasized that there is no ”one-size-fits-all” eating pattern for the prevention or management of diabetes (more in this article).

In the section on Medical Nutrition Therapy (MNT), the new Standards of Medical Care 2020 underscores that for many people with diabetes, the most challenging part about treatment is determining what to eat — and for this reason the ADA emphasizes that meal planning needs to be individualized.

The ADA also states that all people diagnosed with diabetes should be referred to an a Registered Dietitian (RD/RDN) who is “knowledgeable and skilled in providing diabetes-specific MNT at diagnosis and as needed throughout the life span”[1] and that research indicates that edical Nutrition
Therapy delivered by an RD/RDN is associated with decrease in HbA1C of between 0.3 and 2.0% for people with type 2 diabetes [3].

In the section on Eating Patterns, Macronutrient Distribution and Meal Planning, the new Standards of Medical Care in Diabetes re-iterated what the Consensus Report stated, that evidence suggests that;

“there is not an ideal percentage of calories from carbohydrate, protein, and fat for people with diabetes. Therefore, macronutrient distribution should be based on an individualized assessment of current eating patterns, preferences, and metabolic goals.”

As well, the new Standards of Medical Care re-iterates that a low carbohydrate eating pattern is an example of one that is both healthful and helpful in controlling blood glucose;

“The Mediterranean-style ([4-5], low-carbohydrate* [6-8] and vegetarian or plant-based [9-10] eating patterns are all examples of healthful eating patterns that have shown positive results in research, but individualized meal planning should focus on personal preferences, needs, and goals. “

*In the Consensus Report referred to in this section, a low carbohydrate eating pattern was defined as 26-45% of total calories from carbohydrate and a very low carbohydrate eating pattern (ketogenic) was defined as 20-50 g of non-fiber carbohydrate per day.

The new Standards of Medical Care encourages healthcare practitioners to not only consider a person’s metabolic goals, but also their personal preferences, including tradition, culture, religion, health beliefs, goals, and economic situation in helping them choose a suitable eating patterns.

It encourages each member of the healthcare team;

“to be knowledgeable about nutrition therapy principles for people with all types of diabetes and be supportive of their implementation.”

Given that a low carbohydrate diet is one of the eating patterns that the ADA considers both healthful and helpful in the management of diabetes, healthcare professionals ought to be prepared to be supportive of a person seeking to implement this approach.

The Standards of Medical Care states that until there is stronger evidence surrounding comparative benefits of different eating patterns in specific individuals, “healthcare providers should focus on the key factors that are common among the patterns:

1) emphasize non-starchy vegetables
2) minimize added sugars and refined grains
and
3) choose whole foods over highly processed foods to the extent possible”[2].

Similar to what was stated in the Consensus Report, the Standards of Medical Care reiterates that “research studies on some low-carbohydrate eating plans generally indicate challenges with long-term sustainability, it is important to reassess and individualize meal plan guidance regularly for those interested in this approach”. Given the wide range of “low carbohydrate” diets people may be following, it makes good sense to ensure a person is following one that is evidence-based and appropriate for them.

The Standards of Medical Care restates that at this time a low carbohydrate eating pattern is not recommended for women who are pregnant or lactating, people with or at risk for disordered eating, or people who have renal disease, and should be used with caution in patients taking sodium—glucose cotransporter 2 inhibitors due to the potential risk of ketoacidosis [11-12]. (Note: This caution regarding those taking certain medication is covered in this previous article).

Carbohydrates

The section of the Standards of Medical Care in Diabetes on Carbohydrates re-emphasizes the benefits to blood sugar (glycemic) control of a low carbohydrate eating patterns that was previously outlined in the Consensus Report, namely;

“For people with type 2 diabetes or prediabetes, low-carbohydrate eating plans show potential to improve glycemia and lipid outcomes for up to 1 year [6, 8, 13, 14-17]

The new Standards re-iterates that “part of the challenge in interpreting low-carbohydrate research has been due to the wide range of definitions for a low-carbohydrate eating plan [8, 18]”.

Final Thoughts…

There is nothing really “new” in the section on Medical Nutrition Therapy in the new Standards of Medical Care as it pertains to the safety and efficacy of low carbohydrate eating patterns, or in their ability to help improve blood sugar control. This, in and by itself is very encouraging because it means that the ADA has considers a well-designed low carbohydrate diet to be both healthful and helpful in the management of diabetes for the second year in a row.

When will Diabetes Canada complete their review of the current literature, including that cited by the ADA in the Consensus Report and their new Standards of Medical Care in Diabetes 2020 and update their position on the use of low carbohydrate diets in those with diabetes in Canada?

More Info

If you would like more information about the services I provide and how I can design a Meal Plan for you based on your needs, please have a look under the Services tab, or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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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.

References

American Diabetes Association, Facilitating Behavior Change and Well-being to Improve Health Outcomes: Standards of Medical Care in Diabetes—2020
American, Diabetes Care Jan 2020, 43 (Supplement 1) S48-S65; DOI: 10.2337/dc20-S005
Evert AB, Dennison M, Gardner CD, et al. Nutrition therapy for adults with diabetes or prediabetes: a consensus report. Diabetes Care 2019;42:731—754
Franz MJ, MacLeod J, Evert A, et al. Academy of Nutrition and Dietetics nutrition practice guideline for type 1 and type 2 diabetes in adults: systematic review of evidence for medical nutrition therapy effectiveness and recommendations for integration into the nutrition care process. J Acad Nutr Diet 2017;117:1659—167
Esposito K, Maiorino MI, Ciotola M, et al. Effects of a Mediterranean-style diet on the need for antihyperglycemic drug therapy in patients with newly diagnosed type 2 diabetes: a randomized trial. Ann Intern Med 2009;151:306—314
Boucher JL. Mediterranean eating pattern. Diabetes Spectr 2017;30:72—76
Sainsbury E, Kizirian NV, Partridge SR, Gill T, Colagiuri S, Gibson AA. Effect of dietary carbohydrate restriction on glycemic control in adults with diabetes: a systematic review and meta-analysis. Diabetes Res Clin Pract 2018;139:239—252
van Zuuren EJ, Fedorowicz Z, Kuijpers T, Pijl H. Effects of low-carbohydrate- compared with low-fat-diet interventions on metabolic control in people with type 2 diabetes: a systematic review including GRADE assessments. Am J Clin Nutr 2018;108:300—331
Snorgaard O, Poulsen GM, Andersen HK, Astrup A. Systematic review and meta-analysis of dietary carbohydrate restriction in patients with type 2 diabetes. BMJ Open Diabetes Res Care 2017;5:e000354
Rinaldi S, Campbell EE, Fournier J, O’Connor C, Madill J. A comprehensive review of the literature supporting recommendations from the Canadian Diabetes Association for the use of a plant-based diet for management of
Pawlak R. Vegetarian diets in the prevention and management of diabetes and its complications. Diabetes Spectr 2017;30:82—88
U.S. Food and Drug Administration. FDA Drug Safety Communication: FDA revises labels of SGLT2 inhibitors for diabetes to include warnings about too much acid in the blood and serious urinary tract infections. Accessed 1 November 2019. Available from http://www.fda.gov/Drugs/DrugSafety/ucm475463.htm
Blau JE, Tella SH, Taylor SI, Rother KI. Ketoacidosis associated with SGLT2 inhibitor treatment: analysis of FAERS data. Diabetes Metab Res Rev 2017;33:e2924
Saslow LR, Daubenmier JJ, Moskowitz JT, et al. Twelve-month outcomes of a randomized trial of a moderate-carbohydrate versus very low-carbohydrate diet in overweight adults with type 2 diabetes mellitus or prediabetes. Nutr Diabetes 2017;7:304
Hallberg SJ, McKenzie AL, Williams PT, et al. Effectiveness and safety of a novel care model for the management of type 2 diabetes at 1 year: an open-label, non-randomized, controlled study. Diabetes Ther 2018;9:583—612
van Wyk HJ, Davis RE, Davies JS. A critical review of low-carbohydrate diets in people with type 2 diabetes. Diabet Med 2016;33:148—157
Meng Y, Bai H, Wang S, Li Z, Wang Q, Chen L. Efficacy of low carbohydrate diet for type 2 diabetes mellitus management: a systematic review and meta-analysis of randomized controlled trials. Diabetes Res Clin Pract 2017;131:124—131
Tay J, Luscombe-Marsh ND, Thompson CH, et al. Comparison of low- and high-carbohydrate diets for type 2 diabetes management: a randomized trial. Am J Clin Nutr 2015;102:780—790
Thomas D, Elliott EJ. Low glycaemic index, or low glycaemic load, diets for diabetes mellitus. Cochrane Database Syst Rev 2009;1:CD006296

December 18, 2019December 18, 2019

Is Your New Year’s Resolution to Lose Weight or Improve Your Health?

Many people say they plan to lose weight, lower their blood sugar, pressure or cholesterol in the New Year, but the difference between a “wish” and a “resolution” is having a plan in place to actually do it.

Wish or Resolution?

A “wish” is really just a hope that something will occur — an “it would be nice” type of thought, whereas a “resolution” is a firm decision to do something and is associated with specific qualities that will make it a reality. A resolution is a SMART goal; one which is specific, measurable, achievable, realistic and timely.

A goal to lose weight or eat healthier isn’t specific — it’s just a wish. A resolution to stop eating foods with added sugar is specific, so is a goal to eat whole, real foods that are low in refined carbohydrate. These are specific.

A resolution isl measurable. It decides what success looks like. For someone to say they want to lose 25 pounds is very different than to say they plan to lose a pound a week so that in 6 months they’ve lost 25 pounds.

But is that goal achievable? If someone is significantly overweight, it is achievable to set a goal of losing 25 pounds in 6 months.

What if someone wants to incorporate long periods of intermittent fasting into their lifestyle, but also eat all of their meals with their family? This isn’t realistic — but they can choose to have shorter ‘eating windows’ (such as 18:6), intermittently fast each day and still eat dinner each night with their family. That’s entirely realistic.

For a goal to be timely (or time-bound) means that it will also be achieved in a specific amount of time. So, for example, the resolution to lose 25 pounds in 6 months, is time-bound.

So, while there are lots of people saying they’d like to lose weight, eat healthier, exercise more or have better blood sugar, blood pressure or cholesterol in the New Year, to be successful one needs a go about putting a SMART plan in place now in order to achieve it.

Without such a plan, January will arrive and a week into the New Year, 50% of people will have already given up on their goal [1] and by the end of the month, 83% will have quit [1]. Those are pretty discouraging statistics!

Why is that?

Because it takes ~66 days (more than 2 months) for a habit to become ingrained [2], so having professional support during that critical time is important!

I can help you get off to a good start in achieving your New Year’s resolution, but the best time to put a plan in place is now — before all the festivities begin.

Why not make this the year you actually achieve your health and weight-loss goals?

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

References

Norcross, JC et al, Auld lang syne: success predictors, change processes, and self-reported outcomes of New Year’s resolvers and nonresolvers. J Clin Psychol. 2002 Apr;58(4):397-405
Lally, P., van Jaarsveld, C. H. M., Potts, H. W. W. and Wardle, J. (2010), How are habits formed: Modelling habit formation in the real world. Eur. J. Soc. Psychol., 40: 998—1009.

November 22, 2019November 22, 2019

When to Eat and Not Eat, How Many Meals and Snacks

The whole matter of ‘when we eat’ meals and ‘when we don’t eat’ was historically a non-issue; we ate when it was daylight and we had food available, and we didn’t eat when it was dark or had no food. With the creation of indoor lighting and electricity, “day” lasted as long as we keep the lights on and for most of us, food is available in our fridges around the clock. Before elaborating on the current science surrounding when to eat meals and to not eat, let’s look at a short history of the origins of eating 3 meals per day, and when the idea of ‘snacks’ became prominent.

Timing of Meals

According to food historian Ivan Day[1], during the Middle Ages, availability of daylight shaped meal times, as there was no electricity. People got up and began to work in the fields at first daylight and by mid-day they were hungry after working for 6 hours or so and lunch was the first and main meal of the day. As there was no artificial lighting, cooking large meals in the evening simply wasn’t possible, so dinner was really a smaller meal, such as bread and cheese.

Breakfast became popular during the mid-19th century when labourers needed an early meal to sustain them at work. It became widely popularized in the early 20th century when John Harvey Kellogg invented the first breakfast cereal. Dinner became the main meal of the day with the creation of artificial (gas) lighting, and by the early 1900s, people were eating 3 meals per day, with the last meal occurring after work. Gas lighting was expensive to run, so after dinner was eaten and cleaned up from, bedtime was shortly after.

Snacks

“Snacks” were frowned upon by the middle class during Victorian era because they did not require use of “proper” utensils (cutlery, plates), were seen as unhygienic and were associated with the lower class [2].

Snacks as we know them took root in the 1950s due to the manufacturing industry’s drive to sell new products in a growing economy after the end of WWII, along with an ability to create inexpensive disposable packaging and unique labelling to market these products. Sale of snack foods escalated in the late 1970s [2], and between 1977 and 2006, Americans were eating approximately 570 calories more per day, much of it as snacks rather than during meals [3].

Historic Dietary Treatment of Diabetes

Before the discovery of insulin, successful management of diabetes involved restricting carbohydrates eaten at meals.

In his text book titled “The Principles and Practice of Medicine” (1892), Dr. William Osler recommended a diet of 65% fat, 32% protein, and 3% carbohydrate, as well as abstaining from ”all fruits and garden stuff.” [4] — not dissimilar to some of the high-fat “keto” diets available today.

In the early 1900s, Bernard Naunyn encouraged a strict carbohydrate-free diet [5], with energy being provided as fat and protein.

In 1914, Dr. Frederick M. Allen treated people for several days with a period of fasting to clear the excess blood sugar via the urine, and then followed that with a diet that was mostly fat and protein, with a small amount of carbohydrates, mostly as vegetables â [6].

Dr. Elliot P. Joslin was the first doctor in the United States to specialize in treating diabetes, and in 1916 adopted the same low-carbohydrate approach as Fredrick Allen [7].

Medications as Treatment in Diabetes

Type 1 Diabetes

The discovery of insulin by Dr. Fredrick Banting and Dr. Charles Best in 1921 provided life-saving therapy for those with type 1 diabetes (which results from failure of the insulin-producing β-cells of the pancreas). The insulin was initially isolated from the pancreases of beef and pigs, but “human insulin” became possible in the 1980s due to recombinant DNA technology which enabled the development of both basal insulin, as well as rapid acting insulin. This was life-changing and life-saving to those with type 1 diabetes.

Type 2 Diabetes

Metformin initially became available as a first-line treatment for type 2 diabetes in the late 1990s, and enabled those with type 2 to better control their blood sugar levels along with dietary changes — but when people were unable, or unwilling to adequately limit carbohydrate intake, insulin was prescribed.

Insulin went from being a life-saving therapy for those with type 1 diabetes to also being a ‘treatment’ for people with type 2 diabetes who ate what they wanted at meals and snacks and “covered it with insulin“. The problem is that this type of “liberalization” of the diet creates a “vicious cycle” for those with type 2 diabetes, described as follows in a new study published ahead of print in September 2019, and to appear in the December 2019 journal, Diabetes Care[8];

“Dietary intervention is usually accompanied by sequential addition of several anti-hyperglycemic agents, including glucagon-like peptide 1 (GLP-1) analogs and sodium—glucose cotransporter 2 (SGLT2) inhibitors. Despite this medical treatment, many patients require insulin therapy, which is gradually augmented according to the glucose target-driven strategy. However, this progressive increase in insulin dose often leads to weight gain, which may increase insulin resistance, leading to a vicious cycle further increasing insulin doses, continued weight gain, decreased likelihood of achieving glycemic targets, a high risk for diabetes complications and increased insulin dose-dependent cardiovascular risk and mortality. It is, therefore, important to prevent the weight gain when insulin treatment is required.”

Of course, medications such as biguanides, sulfonylureas, SLP-1 analogues and SGLT2 inhibitors are very important tools for doctors to add in helpong manage blood sugar levels, but too often they are used instead of / in the absence of carbohydrate reducing dietary changes and this results diabetes becomes “a chronic, progressive disease“. It need not be so if people are willing to reduce their carbohydrate intake and time when they do eat some carbohydrate-containing food, in accordance with when their body handles them best.

Dietary Recommendations – meals and snacks

Since 2009, people with type 2 diabetes have been advised to eat 3 meals per day plus several snacks per day â — with carbohydrates evenly distributed across the meals and snacks, in order to achieve the best weight management and blood sugar control [9-11]. They’ve been told to aim for between 45-60 grams of carbohydrate at each meal, and 15-20 grams of carbohydrate for each of 3 daily snacks (between breakfast and lunch, between lunch and dinner, and before bed). Surprisingly, the new study referred to above that will appear in the December 2019 issue of Diabetes Care states that there were no research studies to support these practices [8].

The 45-60 g of carbs for each of 3 meals per day and 15-20 g per snack distribution is still being recommended as goals to those with type 2 diabetes — resulting in between 190 -240 g of carbohydrate being eaten each day. That is a lot of carbohydrate for people who’s bodies can no longer handle that much. Presumably the snacks are to lower the risk of hypoglycemia (low blood sugar) that can result from the anti-hyperglycemic medications that have become necessary to prescribe because these people do not restrict carbohydrate and as a result have blood sugar levels that are too high.

Most concerning is that recent studies have found that snacks consumed later in the day have been associated with an increased risk of obesity and type 2 diabetes, with higher overall blood sugar and higher glycated hemoglobin (HbA1C) [12-13]. These are some of the “costs” of people being told to eat an afternoon and evening snack in order to avoid low blood sugar that can result from taking medication to lower blood glucose, and in an absence of being willing to reduce carbohydrate intake.

Would it not make far more sense to encourage people with type 2 diabetes to eat less carbs and eat less often — along with doctors de-prescribing anti-hyperglycemic medication, including insulin? That way, no snacks are needed to keep them from having low blood sugar and their average blood sugar levels can fall.

In fact, a soon-to-be-published pilot study [8] found that those with type 2 diabetes who ate the same calories each day as 3-meals per day, rather than as 6 meals per day [i.e. 3 meals and 3 snacks] reduced body weight, blood glucose, and insulin doses! Without even changing how many carbs they ate or how many calories they ate, in just 12 weeks, the subjects in the 3 meal per day group, lost on average 12 pounds (5.4 kg) more than those in the 6 meal per day group, had 1.2% lower HbA1C than the 6 meal per day group and their total daily insulin dose was reduced by 26 units ± 7 (with no reduction in the 6 meal per day group). On top of this, this study found that “there was a significant decrease in hunger and cravings only in the 3 meal per day group“. This makes sense of course, because they were able to lower their injected insulin, which drives hunger and fat storage, leading to weight gain. The mechanism was thought to be an up-regulation in the clock genes of those that ate 3 meals per day, which contributed to the improved glucose metabolism.

Note: it’s important to keep in mind that it is the eating of carbohydrate-containing food that triggers the release of insulin from our pancreas, so even in healthy people i.e. those who are not diabetic, eating the same amount of food as 3 meals per day with no snacks (versus 3 meals plus 3 snacks) will result in less insulin being released. Less insulin means less hunger and less fat storage — whether it is the natural insulin from our own pancreas or it is injected insulin. If our goal is weight management, eating the same amount of food as 3 meals, rather than as meals and snacks makes sense.

This study verified that when we eat and when we don’t eat matters a great deal because our body has evolved over hundreds of thousands of years to function in response to light and day cycles, called circadian rhythms.

When We Eat – especially which meals to eat carbs

Chronobiology is the study of the effect of time of day on living systems and is emerging as an important player in human health.

We now know that the body’s processes involved in the maintaining of blood sugar control such as β-cell function, glucose uptake by the muscles, and glucose production by the liver, are all under the control of circadian rhythms. The body’s “master clock” which controls these circadian rhythms is found in a part of the hypothalamus of our brain, called the suprachiasmatic nucleus (SCN) and is “set” by exposure to light.

Note: Historically, the only light that set the SCN was sunlight, but our increasing exposure to bright lights emanating from office- and store- lights, TVs, computers and smart phones has disrupted this once tightly regulated system.

Similar “peripheral clocks” are found in our body’s tissues, including muscle cells, liver cells, β-cells of our pancreas which produce and release insulin, and fat cells (adipose), and these are controlled by the “master clock” in our SCN, and by when we eat [14,15].

As it turns out, our circadian rhythms are optimized for us to eat during periods of light (daytime), and to fast and sleep in periods of dark (night time) [16,17] — so fasting after supper and overnight is consistent with our body’s built-in circadian rhythms.

In addition, blood sugar control is not the same at all times of the day, but fluctuates according to our body’s circadian rhythms. It has been shown in both healthy individuals and those with type 2 diabetes that identical foods eaten in the afternoon and evening cause much higher elevations in blood sugar, compared with the same foods eaten in the morning [18-20] . Based on this, it makes the most sense for any major carbohydrate sources (milk, fruit, root vegetables etc.) that are going to be eaten during the day to be consumed at breakfast, rather than evenly distributed across the whole day and evening.

When We Don’t Eat – intermittent fasting

It has been shown for those with type 2 diabetes that fasting until noon time actually results in much higher after-meal blood sugar levels (postprandial hyperglycemia), as well as an impaired insulin response after lunch and dinner [21], so while it is currently popular for people to chose their “eating windows” based on a wide range of popular protocols, it seems to me that choosing them in a way that is consistent with our circadian rhythms makes the most sense — especially if the goal is weight loss, appetite control and blood sugar regulation.

More Info

If you would like more information about having me design a Meal Plan for you that arranges your eating times and non-eating times around your schedule and in accordance with your natural circadian rhythms, please have a look under the Services tab or in the Shop. If you have service-related questions, please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

References

BBD News Magazine, Winterman, Denise, Breakfast, lunch and dinner; Have we always eaten them? Nov 15 2012, https://www.bbc.com/news/magazine-20243692
Carroll, Abigail (30 August 2013). “How Snacking Became Respectable”. Wall Street Journal. August 30, 2013, https://www.wsj.com/articles/how-snacking-became-respectable-1377906874
Duffey KJ, Popkin BM, Energy Density, Portion Size, and Eating Occasions: Contributions to Increased Energy Intake in the United States, 1977—2006, June 28, 2011, https://doi.org/10.1371/journal.pmed.100105
Osler W. The Principles and Practice of Medicine. New York, D. Appleton and Company, 1892
Woodyatt RT, Bernhard Naunyn. Diabetes 1952;1:240—241, pmid:1493683
Allen FM, Studies concerning diabetes. JAMA 1914;63:939—94
Joslin EP, Treatment of Diabetes Mellitus. 2nd ed. Philadelphia, Lea & Febiger, 1917, p. 409
Jakubowicz D, Landau Z, Tsameret S et al, Reduction in Glycated Hemoglobin and Daily Insulin Dose Alongside Circadian Clock Upregulation in Patients With Type 2 Diabetes Consuming a Three-Meal Diet: A Randomized Clinical Trial, Diabetes Care 2019 Dec; 42(12): 2171-180.https://doi.org/10.2337/dc19-1142
Seagle HM, Strain GW, Makris A, Reeves RS; American Dietetic Association. Position of the American Dietetic Association: weight management. J Am Diet Assoc 2009;109:330—346
Beyond the Basics: Meal Planning for Healthy Eating, Diabetes Prevention and Management. Canadian Diabetes Association, 2014.
Arnold L,MannJI, Ball MJ. Metabolic effects of alterations in meal frequency in type 2 diabetes. Diabetes Care 1997;20:1651—1654
Mekary RA, Giovannucci E, Willett WC, van Dam RM, Hu FB. Eating patterns and type 2 diabetes risk in men: breakfast omission, eating frequency, and snacking. Am J Clin Nutr 2012;95:1182—1189
Gouda M, Matsukawa M, Iijima H. Associations between eating habits and glycemic control and obesity in Japanese workers with type 2 diabetes mellitus. Diabetes Metab Syndr Obes 2018;11:647—658
Dyar KA, Ciciliot S, Wright LE, et al. Muscle insulin sensitivity and glucose metabolism are controlled by the intrinsic muscle clock. Mol Metab 2013;3:29—41
Sadacca LA, Lamia KA, deLemos AS, Blum B, Weitz CJ. An intrinsic circadian clock of the pancreas is required for normal insulin release and glucose homeostasis in mice. Diabetologia 2011;54:120—124
Poggiogalle E, Jamshed H, Peterson CM. Circadian regulation of glucose, lipid, and energy metabolisminhumans. Metabolism2018;84:11—27
Saad A, Dalla Man C, Nandy DK, et al. Diurnal pattern to insulin secretion and insulin action in healthy individuals. Diabetes 2012;61:2691—2700
Bo S, Fadda M, Castiglione A, et al. Is the timing of caloric intake associated with variation in diet-induced thermogenesis and in the metabolic
pattern? A randomized cross-over study. Int J Obes 2015;39:1689—1695
Jakubowicz D, BarneaM, Wainstein J, Froy O. High caloric intake at breakfast vs. dinner differentially influences weight loss of overweight and obese women. Obesity (Silver Spring) 2013; 21:2504—2512
Morgan LM, Shi JW, Hampton SM, Frost G. Effect of meal timing and glycaemic index on glucose control and insulin secretion in healthy volunteers. Br J Nutr 2012;108:1286—1291
Jakubowicz D, Wainstein J, Ahren B, Landau Z, Bar-Dayan Y, Froy O. Fasting until noon triggers increased postprandial hyperglycemia and impaired
insulin response after lunch and dinner in individuals with type 2 diabetes: a randomized clinical trial. Diabetes Care 2015;38:1820—1826

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October 27, 2019September 14, 2020

Vitamin D Supplementation Can Help Protect Against the Flu

DISCLAIMER: This article does NOT recommend not getting a flu shot, nor does it recommend taking Vitamin D instead of getting a flu shot.

This article is about the use of Vitamin D supplementation to help protect against the flu.

Studies Showing that Vitamin D Attenuates the Flu

There are two large-scale meta-analyses — one from 2013 and the other from 2017 that indicate that Vitamin D supplementation can reduce the risk of getting an upper respiratory infection (URI) including influenza (“the flu”).

The first study by Bergman et al [4] analyzed data from 11 placebo controlled trials that involved more than 5,600 subjects and found that those taking a daily dose of Vitamin D had half the risk of developing an upper respiratory infection (URI), including influenza (‘the flu”). This held true even though many of the studies used very low dose of supplementation.

The second of the two large-scale meta-analysis by Martineau et al [5] analyzed the data from 25 randomized controlled trials and involved more than 11,300 subjects. This study found that Vitamin D supplementation reduced the risk of developing an upper respiratory infection (URI), including the flu and those who were the most deficient experienced the most benefit. Even those subjects with very low Vitamin D status had 1/3 the risk when supplementing with Vitamin D, compared to those who did not take any.

Both meta-analysis found that daily dosing with Vitamin D was more effective than taking larger (bolus) doses once a week, or once a month.

There are numerous studies which indicate that people with lower levels of Vitamin D are more likely to get the flu and a 2010 study with healthy adults found that people with lower levels of were twice as likely to get the flu than people with high levels of Vitamin D [6].

Supplementing with Vitamin D

Health Canada’s recommended daily intake (RDAs) for Vitamin D (updated in 2011) are 600 International Units (IUs) for everyone aged one year old to 70 years old and 800 IU for adults over 70 years of age. Health Canada’s safe upper limit (UL) is listed as 4,000 IU per day, however recent scientific publications indicate that there was an error in the calculations used to determine them.

Two researchers from the School of Public Health at the University of Alberta published a paper in October 2014 which indicates that the Institute of Medicine (IOM) that develops the Recommended Dietary Allowances (RDAs) used by both Canadians and Americans made a serious error in their calculations in determining the RDAs for Vitamin D [7] and that rather than 600 IUs being needed to prevent deficiency in 97.5% of individuals, the actual amount is estimated to be 8895 IU of Vitamin D per day — which is above the Health Canada’s tolerable upper intake of 4000 IU per day.

On top of that, researchers from the University of California at San Diego and Creighton University in Omaha, Nebraska published a letter in the same online journal in March 2015 which said that they have confirmed the Institute of Medicine’s miscalculation that was noted by the Canadian investigators [8].

A press release published in Science News on March 17, 2015 indicated that;

“The recommended intake of vitamin D specified by the IOM is 600 IU/day through age 70 years, and 800 IU/day for older ages. Calculations by us and other researchers have shown that these doses are only about one-tenth those needed to cut incidence of diseases related to vitamin D deficiency.“

How much Vitamin D should we supplement?

The Vitamin D Council (a US-based group) recommends adults take 5,000 to 10,000 IU/day, depending on body weight and recommend people have their levels checked to make sure it is > 40 ng/ml (100 nmol/l) and to maintain serum levels at 50 ng/ml (125 nmol/L). Since Vitamin D toxicity manifests as high levels of calcium in the blood and urine, the Vitamin D Council recommends monitoring via blood tests that serum levels don’t exceed 150 ng/ml (374 mmol/L).

Since Health Canada’s current upper limit is 4,000 IUs per day (which may be based on an error in calculation, as noted above), a prudence dosage for supplementation for a healthy adult would not exceed 4,000 IUs per day.

Note: I also recommend people take 100 mcg of Vitamin K2 (menaquinone-4, or menaquinone-7) as Vitamin K2 plays a synergistic role with Vitamin D which regulates blood levels of calcium. Vitamin K prevents calcium from accumulating in soft tissues, such as the blood vessels (contributing to Coronary Artery Calcification)[10]. Put simply, Vitamin K helps ensure that calcium ends up in bone, not arteries.

NOTE: People taking Warfarin (Coumadin) or other anticoagulant medication should not supplement with Vitamin K2 except under the advice of the physician prescribing Warfarin.

Keep in mind that food also provides Vitamin D with natural sources being salmon (447 IU per 3 ounces), tuna (154 IU per 3 ounces), eggs (41 IU per yolk) and cheese (14 IU per 2 ounces of cheddar) and milk and non-dairy beverages made as ‘milk replacements’ are fortified, with 100 IU per cup (250 ml).

If you are a healthy adult under 50 years old with no family risk of cancer* or osteoporosis, 1000 IU Vitamin D3 per day (plus 100 mcg of Vitamin K2) is probably sufficient. Be sure to choose the D3 form (not D2) as it is more efficient at raising serum levels. For adults under 50 with a family history of cancer or who are at risk for osteoporosis, a dosage of 2000 IU Vitamin D3 per day (plus 100 mcg of Vitamin K2) may be more appropriate.

Healthy adults over the age of 50 can safely double the amounts above â — so 2,000 IUs Vitamin D3 per day (plus 100 mcg of Vitamin K2) and for those with a family history of cancer to take 3,000 IUs Vitamin D3 per day (plus 100 mcg of Vitamin K2).

Remember though that Vitamin D is a fat soluble vitamin, so be sure to have your serum levels checked periodically as your body is able to stores for long periods of time. The best indicator of Vitamin D status is a routine blood test called 25-hydroxy vitamin D.

Final thoughts…

There is good evidence that adding Vitamin D3 supplementation to your daily routine may boost your ability to fight of upper respiratory infections, including the flu.

…and if you supplement with Vitamin D, don’t forget to add the Vitamin K2 to help keep the calcium where it ought to be.

More Info

If you would like more information about my services, please have a look under the Services tab or in the Shop and if you have any questions, please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

CTV News, Canadian warns against vaccine apathy after flu sends him to hospital for two months, https://www.ctvnews.ca/health/canadian-warns-against-vaccine-apathy-after-flu-sends-him-to-hospital-for-two-months
Dairy Nutrition, Vitamin D status of Canadians — Results from the Canadian Health Measures Survey, https://www.dairynutrition.ca/nutrients-in-milk-products/vitamin-d/vitamin-d-status-of-canadians-results-from-the-canadian-health-measures-survey
Vitamin D Council, Dr. John Cannell, MD, Influenza, https://www.vitamindcouncil.org/health-conditions/influenza/
Bergman P, Lindh AU, Bjí¶rkhem-Bergman L et al, Vitamin D and Respiratory Tract Infections: A Systematic Review and Meta-Analysis of Randomized Controlled Trials, PLoS One. 2013 Jun 19;8(6):e65835.
Martineau AR, Jolliffe DA, Hooper RL, Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data, BMJ. 2017 Feb 15;356:i6583
Sabetta, J.R., DePetrillo, P., Cipriani, R.J., et al., Serum 25-hydroxyvitamin d and the incidence of acute viral respiratory tract infections in healthy adults. PLoS One, 2010. 5(6): p. e11088.
Veugelers PJ, Ekwaru JP. A statistical error in the estimation of the recommended dietary allowance for vitamin D. Nutrients. 2014;6(10):4472—4475. Published 2014 Oct 20. doi:10.3390/nu6104472
Heaney R, Garland C, Baggerly C, French C, Gorham E. Letter to Veugelers, P.J. and Ekwaru, J.P., A statistical error in the estimation of the recommended dietary allowance for vitamin D. Nutrients 2014, 6, 4472-4475; doi:10.3390/nu6104472. Nutrients. 2015;7(3):1688—1690. Published 2015 Mar 10. doi:10.3390/nu7031688
Science News, Recommendation for vitamin D intake was miscalculated, is far too low, experts say, https://www.sciencedaily.com/releases/2015/03/150317122458.htm
Theuwissen E, Smit E, Vermeer C, The role of vitamin K in soft-tissue calcification, Adv Nutr. 2012 Mar 1;3(2):166-73.

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September 10, 2019September 10, 2019

Why Eating Less and Exercising More DOES Matter As We Age

There is much “push back” when it comes to the standard advice to “eat less and exercise more” as a means of losing weight, and for good reason. For one, metabolism will slow as a result of caloric restriction — making it that much more difficult to lose weight when deliberately cutting calories. Another reason is that it is exceedingly difficult for an obese person to exercise. For many, just getting around is a chore. It is for this reason that I focus on helping people be less hungry by eating a different mix of protein, fat and carbohydrate — because a natural byproduct of being less hungry, is eating less. Being active is possible once a person is losing weight and not feeling hungry all the time. Yes, they are still “eating less and moving more” — but as a result, not as the focus.

Addendum (Sept 10 2019) — Weight loss is not only about what we eat. It’s also about when we don’t eat; whether it’s having times between meals where we don’t eat, or not eating from the end of supper until the first meal of the following day (whenever that is). Thanks Dr. Andy Phung for the reminder!

A new study published yesterday (September 9, 2019) in the journal Nature Medicine[1] has found that “eating less and exercising more” may actually be good advice as we age — because it turns out that we have decreased fat turnover as we age. If we eat the same amount as we always have and don’t increase the amount we exercise, we will end up gaining approximately 20% over a 10-15 year period [3].

Until recently little was known about fat turnover [2] — which is the storage and removal of fat from adipocytes (fat cells). A 2011 study showed that during the average ten-year lifespan of human fat cells, the fat in them (triglycerides) turns over six times, in both men and women [2], and that when people are obese, the fat removal rate decreases and the amount of fat as triglyceride stored each year increases [2]. What we didn’t know until now is what happened to fat turnover as we age. This follow-up study headed by the same lead researcher as the 2011 study explored this issue, as well as differences in fat turnover after people have bariatric surgery which helps explain why some people regain their weight after weight loss, where as others don’t.

Eating Less Matters as We Age

Fat turnover is a difference between the rate of fat uptake into fat cells and the fat removal rate. High fat storage but low fat removal is what results in the accumulation of fat and in obesity. The “bad news” of this new study is that fat accumulation due to decreased fat turnover is what happens as we age, leading to accumulation of fat. That is, even if we don’t eat more or exercise less than previously, we will store more fat — which can result in as much as a 20% increase in body weight over 13 years [3].

“Those who didn’t compensate for that (i.e. decrease fat turnover) by eating less calories gained weight by an average of 20 percent”[3].

Researchers from the University of Uppsala in Sweden and the University of Lyon in France studied the fat cells of 54 men and women over an average 13 year period [3] and regardless of whether the subjects gained weight or lost weight, they had a decreased fat turnover.

Since fat turnover is decreased as we age, to prevent weight gain we need to take in less calories than we used to, even if we are just as active.

Why We Regain Weight After Weight Loss

The study also looked at fat turnover in 41 women who underwent bariatric surgery. Results showed that only those who had a low lipid turnover rate before the surgery were able to increase their lipid turnover after surgery and maintain their weight loss 4-7 years after surgery [1]. Researchers think that if people had a high lipid turnover rate before surgery, there is less ‘room’ for them to increase their lipid turnover rate after surgery, which is why they regain the weight. This could explain why so many people who lose incredible amounts of weight following any one of a number of “diets” regain it (and then some) afterwards.

Exercise and Lipid Turnover

Previous studies have reported that fat turnover increases as we exercise [2], so based on this new study, the idea of ‘eating less and exercising more’ actually matters as we age. We can either decrease our intake as we age and/or be a little more active and avoid gaining weight — which is easy enough to do for those who are slim, if they know.

But what about those who are already overweight or obese and now find out they are more prone to storing fat now that they’re older, even though they eat the exact same way and haven’t changed their activity level?

I believe the solution is the same regardless of a person’s age — focusing on the person eating in such a way as to be less hungry, so that in the end they end up eating less. As they lose weight because they’re not hungry all the time, being more active is easier to implement. The difference between it being “doable” depends on what we focus on. As covered in a previous article, we understand why a person who eats foods that are a combination of fat and carbs together eat more, but my approach is to gradually adjust the amount of carbohydrate in the diet, so that people can eat more protein and healthy fat, and end up feeling less hungry. When they aren’t being driven by the reward system of their brain (see linked article) to want more and more foods with carbs and fat together, it is much easier for them to eat when they are actually hungry. As they do, their weight drops as a result.

In light of this new study, what is important is that as people age there is a natural tendency to put on weight, even if they eat the same and don’t change their activity level. This means older people need to modify the amount of calories they take in and/or expend more energy, the question is how.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

References

Arner P, Bernard S, Appelsved K-Y et al. (2019). “Adipose lipid turnover and long-term changes in body weight.” Nature Medicine 25(9): 1385-1389.
Arner, P. et al. Dynamics of human adipose lipid turnover in health and metabolic disease. Nature 478, 110—113 (2011).
Karolinska Institutet, New study shows why people gain weight as they get older, Published: 2019-09-09 18:35, https://news.ki.se/new-study-shows-why-people-gain-weight-as-they-get-older

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September 8, 2019September 10, 2019

Treating Small Intestinal Bacterial Overgrowth (SIBO)

In the first article in this series about Small Intestinal Bacterial Overgrowth (SIBO) I covered what SIBO is, how common it is, as well as its symptoms. In the second article, I outlined different tests used to diagnose SIBO, some of the challenges with those, the difference between hydrogen-dominant and methane-dominant SIBO, and why Irritable Bowel Syndrome (IBS) that does not improve despite adopting appropriate dietary changes may be SIBO. In this article (which is part 3 in the series), I outline the main dietary approaches used in treating SIBO along with antibiotic and evidence-based herbal antimicrobial therapy, and elaborate as to whether dietary changes should come before- or after antimicrobial treatment.

In discussing the treatment of Small Intestinal Bacterial Overgrowth, it’s important to keep in mind that SIBO is the presence of types of bacteria in the small intestine that are not supposed to be there. While dietary changes can help by improving the symptoms, in and by themselves they will not result in the elimination of the bacteria that are contributing to the symptoms. The bacteria that are foreign to the small intestine need to be eradicated and the underlying cause of the SIBO needs to be addressed. As outlined in the first article, Small Intestinal Bacterial Overgrowth may be caused by a number of conditions, including low stomach acid (achlorhydria), pancreatic insufficiency, anatomical abnormalities such as small intestinal obstruction, diverticula, or fistula (which are abnormal connections between an organ and the intestine), as well as slowing of intestinal movements (motility disorders) that are common in those with diabetes mellitus, as well as due to alcohol consumption and a number of other factors. Addressing those underlying causes is needed, along with correcting intestinal flora imbalance.

NOTE: As a Dietitian, my role is to support treatment of a diagnosed condition from a dietary perspective, but not to diagnose. Diagnosis is the realm of medicine, and diagnosis of SIBO is for a gastroenterologist or Functional Medicine MD to make, using established medical testing protocols. It is also the role of MDs to prescribe antimicrobials. I provide dietary support during the three phases of treatment with the goal of reducing the person’s symptoms, increasing the likelihood of eradication during antimicrobial treatment, and reducing the likelihood of recurrence of SIBO after eradication.

There are two important factors to keep in mind when it comes to Small Bacterial Overgrowth treatment; (1) despite antibiotic treatment, an older (2008) study found that recurrence of SIBO as diagnosed by glucose breath tests occurs in almost half of all people within a year of treatment [1], however individuals in this study that relapsed were older aged (which is associated with decreased stomach acid), and had a history chronic use of proton-pump inhibitor medication (which also results in lower stomach acid), (2) addressing the underlying cause of SIBO is necessary, otherwise recurrence is likely.

Three Phases of Dietary Treatment for SIBO

Some clinicians take a single dietary approach with SIBO and prescribe one of several low fermentable carbohydrate diets; either a low-FODMAP diet or the Specific Carbohydrate Diet (SCD), or some combination or variation of these. These diets limit the food sources for bacterial that live in the gut (both small and large intestine), thereby reducing symptoms and at first glance, this may seem like an effective approach, except it has two drawbacks;

following a diet low in fermentable carbohydrate for periods of longer than a month has been shown to also reduce beneficial bacteria in the gut, such as bifidobacteria [2].
Some researchers such as Dr. Mark Pimentel’s group at the Gastrointestinal Motility Program at Cedars-Sinai Medical Center suggest that some fermentable carbohydrates remain in the diet while treating with antimicrobials based on the concept that bacterial are easier to eradicate when they’re active. Antimicrobials act on the replicating cell wall of bacteria, so when bacteria are being starved, they aren’t replicating.

A 2010 study found that treatment of SIBO with the first-line antibiotic Rifaximin alone was only 62% effective, however when Rifaximin was combined with a specific fermentable carbohydrate called partially hydrolyzed guar gum (PHGG), eradication rate was 85% [3]. In addition, the addition of PHGG during the antibiotic treatment phase also prevented the eradication of both of the beneficial bacteria lactobacilli and bifidobacteria from the large intestine.

I take a 3-phase approach to dietary support treatment of SIBO.

Phase I

A first phase of dietary treatment includes the use of a low fermentable carbohydrate diet for 4-6 weeks which enables people to begin to feel better. This is of huge importance to quality of life, after so long of feeling quite unwell! By also including the addition of partially hydrolyzed guar gum (PHGG) in the diet, it allows for the small amount of bacterial growth needed so that once the person is treated with antimicrobials, it is likely to be more successful.

Use of PHGG is also well-known to reduce the symptoms of IBS in both the constipation and diarrhea subtypes [4,5] and since most people with SIBO experience one of these symptoms, or both alternating, addition of PHGG is also beneficial for helping people feel much better, while preparing for the antimicrobial treatment phase.

Phase II

The second phase of dietary treatment coincides with the 4-week period of antimicrobial treatment prescribed by the gastroenterologist or Functional Medicine MD. During this phase, the low fermentable carbohydrate diet is maintained along with the PHGG intake, but begins to include some additional fermentable carbohydrate food, as tolerated. This helps feed the bacteria just enough so that the antimicrobials are more likely to be effective, but without making the person feel unwell.

As mentioned above, studies have shown that the antimicrobials along with PHGG may result in up to 85% eradication[3], a study from 2009 found that eradication rates with Rifaximin alone is only about 50% [6]. It is thought that this may be due to a failure to distinguish between hydrogen-positive and methane-positive types of SIBO. In methane-positive SIBO, eradication has been found to be as high as 85% when Rifamixin is combined with another antibiotic, Neomycin [7]. In methane-positive SIBO, Dr. Pimentel and his group recommend 550 mg Rifaximin three times per day in combination with neomycin 500 mg twice a day for 14 days, or Rifaximin 550 milligrams three times per day with Metronidazole 250 milligrams three times per day for 14 days [8].

Antimicrobials prescribed by some MDs may include herbal antimicrobials. Herbal antimicrobials (FC Cidal® with Dysbiocide® or Candibactin-AR® with Candibactin-BR®) were shown in a 2014 study to be even more effective in eradication of SIBO bacteria as Rifaximin [8]. Of those treated with one of the herbal therapy combinations, 46% of subjects had a negative result upon re-testing, whereas only 34% of those using Rifaximin had a negative result upon re-testing. Furthermore, approximately 57% of those who failed to achieve eradication on Rifaximin as measured by repeat breath testing, achieved eradication on one of the two herbal antimicrobial regimens [8]. Also of significance, in 2014 when the study was conducted, standard treatment with a 4-week supply of Rifaximin (two 200 mg Rifaximin tablets 3x daily) cost $1247.39, whereas the cost for the herbal therapy (2 capsules twice daily of either treatment) was no more than $120 for a one-month supply [9]. The high treatment response rate of the herbal formulations, reduced cost of treatment and long term Generally Recognized As Safe (GRAS) safety record of specific herbs used in the formulations [8], and the fact that these supplements can be purchased by the general public without a prescription provides individuals and their practitioners with several treatment options.

Phase III

The last phase of dietary treatment is the gradual liberalization of the low-fermentable carbohydrate diet. After antimicrobial treatment, once the gut microbiome has been restored, a person should be able to tolerate a healthy, whole food diet. That said, it may be advantageous for a person who has had SIBO previously to continue to avoid unnecessary additions to the diet such as sugar alcohols (xylitol, erythritol, etc.) or gums such as carrageenan, xanthan gum and guar gum (not to be confused with hydrolyzed guar gum!), as well as to limit high fructose and lactose intake.

However, if a person begins to have symptoms again, then having a new hydrogen breath run to ensure there is no recurrence of SIBO makes sense. If the breath test is negative, then further medical investigation for other underlying causes of causes, including low stomach acid, pancreatic insufficiency or intestinal motility disorders may be next. Given that no other underlying cause is identified, food intolerances , including histamine intolerance, A1 beta-casein intolerance might be worth evaluating.

Final Thoughts

SIBO, like IBS is not easy-to-diagnose. More clear-cut diagnoses such as IBD, celiac disease, food allergies etc. need to be ruled out first and while IBS has now gained acceptance as a “real” diagnosis, SIBO is still one of those in which there is much debate.

I have more confidence in the jejeunal aspirate method of diagnosis and wonder if the breath tests really measure what they purport to measure. That said, when people previously diagnosed and unsuccessfully treated for IBS are treated with diet plus antimicrobials, many get better. Are IBS and SIBO really two diagnoses or one?

A low fermentable carbohydrate diet has long been used in the treatment of IBS and the use of partially hydrolyzed guar gum has a successfully and safe long-term history in the treatment of IBS), so continuing to use these in the treatment of SIBO, along with evidence-based antimicrobial treatment prescribed by an MD is a sensible and safe approach.

The Gut Microbiome – so much to learn

There is so much we are discovering about the gut microbiome (the bacteria in our intestines that we live in symbiosis with) and the relationship between alterations in the gut microbiome and chronic disease.

For example, a study published on June 19, 2019 in the journal Pain [10] found a correlation between fibromyalgia (another one of those diseases that medical professionals debate the legitimacy of) and abnormalities in the gut microbiome. In this study conducted in Montreal, approximately 20 different species of bacteria were found to be abnormally high, or abnormally low in the microbiomes of subjects suffering from the disease, compared with healthy controls. It was found that “fibromyalgia and the symptoms of fibromyalgia — pain, fatigue and cognitive difficulties – contribute more than any of the other factors to the variations we see in the microbiomes of those with the disease” [11].

There is much we don’t know in terms of IBS and SIBO but at the end of the day, there are people suffering with these conditions whose quality of life is greatly affected. If the best we have to offer people diagnosed with SIBO at this time is the use of a low fermentable carbohydrate diet along with the addition of well-studied PHGG used in conjunction with antimicrobial agents prescribed by a physician — and this helps people feel significantly better, then this is the most evidence-based approach we have at this time.

More Info?

If you would like to know more about the hourly consultations and packages I provide, including SIBO support, then please click on the Services tab or have a look in the Shop. If you would like additional information, please send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

References

Lauritano EC, Gabrielli M, Scarpellini E, Small intestinal bacterial overgrowth recurrence after antibiotic therapy. Am J Gastroenterol. 2008 Aug;103(8):2031-5.
Staudacher HM, Lomer MCE, Anderson JL, Fermentable Carbohydrate Restriction Reduces Luminal Bifidobacteria and Gastrointestinal Symptoms in Patients with Irritable Bowel Syndrome, The Journal of Nutrition, Volume 142, Issue 8, August 2012, Pages 1510—18, https://doi.org/10.3945/jn.112.159285
Furnari M, Parodi A, Gemignani L, Clinical trial: the combination of rifaximin with partially hydrolysed guar gum is more effective than rifaximin alone in eradicating small intestinal bacterial overgrowth, Alimentary Pharacology and Therapeutics, Volume 32(8) August 2010, page 1000—1006 https://doi.org/10.1111/j.1365-2036.2010.04436.x
Quartarone G, Role of PHGG as a dietary fiber: a review article, Minerva Gastroenterol Dietol. 2013 Dec;59(4):329-40, https://www.ncbi.nlm.nih.gov/pubmed/24212352
Russo L, Andreozzi P, Zito FP, Vozzella L, Partially hydrolyzed guar gum in the treatment of irritable bowel syndrome with constipation: effects of gender, age, and body mass index, Saudi J Gastroenterol. 2015 Mar-Apr;21(2):104-10. doi: 10.4103/1319-3767.153835.
Peralta S, Cottone C, Doveri T, Almasio PL, Craxi A. Small intestine bacterial overgrowth and irritable bowel syndrome-related symptoms: experience with Rifaximin. World J Gastroenterol. 2009;15(21):2628—2631. doi:10.3748/wjg.15.2628
Low K, Hwang L, Hua, J.,A Combination of Rifaximin and Neomycin Is Most Effective in Treating Irritable Bowel Syndrome Patients With Methane on Lactulose Breath Test, Journal of Clinical Gastroenterology: September 2010 – Volume 44 – Issue 8 – p 547-550, doi: 10.1097/MCG.0b013e3181c64c90
Scarlata K, Small Intestinal Bacterial Overgrowth (SIBO), For a Digestive Peace of Mind blog, https://blog.katescarlata.com/2014/01/22/small-intestinal-bacterial-overgrowth/
Chedid V, Dhalla S, Clarke JO, et al. Herbal therapy is equivalent to rifaximin for the treatment of small intestinal bacterial overgrowth. Glob Adv Health Med. 2014;3(3):16—24. doi:10.7453/gahmj.2014.019
Minerbi A, Gonzalez E, Brereton NJB, et al (2019). Altered microbiome composition in individuals with fibromyalgia. PAIN, Articles in Press. https://doi.org/10.1097/j.pain.0000000000001640
McGill University Health Centre Press Room, Gut bacteria associated with chronic widespread pain for first time, June 19th, 2019, https://muhc.ca/news-and-patient-stories/press-releases/gut-bacteria-associated-chronic-widespread-pain-first-time

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September 4, 2019September 9, 2019

Diagnosing Small Intestinal Bacterial Overgrowth (SIBO)

In the first article of this series about Small Intestinal Bacterial Overgrowth (posted here), I covered what SIBO is and how common it is, as well as its symptoms. If you haven’t yet, I’d encourage you to read that article first as it will serve as a good introduction. In this second article, I cover the different tests used in diagnosing SIBO, as well as some of the advantages and drawbacks of each. In the next article will cover various treatment options for SIBO, including dietary protocols combined with antibiotic or herbal therapies (which interestingly have been found in research studies to be equally effective as the first-line antibiotic).

Diagnosing SIBO

One of the first challenges in diagnosing SIBO is finding a physician that is knowledgeable about the condition and current in its treatment. In the past only gastroenterologists diagnosed and treated SIBO and only after very invasive and expensive surgical tests were performed.

Before the invention of endoscopy, diagnosing SIBO required an invasive surgical procedure where a gastroenterologist would take a small amount of liquid from the jejeunum of the small intestine, and that fluid would be cultured to see what types of bacteria grew, and in what quantities. A positive diagnosis of SIBO would occur when > 10⁴colony-forming units of bacteria grew per milliliter of jejunal liquid [1]. The problem with this type of testing was that it was very invasive and expensive.

The medical invention of the endoscope in the mid-1980s enabled gastroenterologists to obtain fluid from the duodenum of the small intestine using a much less invasive procedure. In endoscopy, a long, flexible tube (endoscope) is passed into the throat of a sedated patient, then into the esophagus, past the stomach and into the duodenum, where a fluid sample is collected for culturing. One drawback to this test was that the sample was easily contaminated as it was withdrawn and the procedure was still quite invasive and expensive [1]. A second drawback is that only 30% of gut bacteria taken from the small intestine in this procedure and the one above are able to be cultured [3]. This surgical test is still invasive and expensive and as such is not widely used, although it is still considered the “gold standard” for diagnosing SIBO [2].

A brilliantly simple solution to testing for SIBO came as the result of the discovery that certain gases such as hydrogen or methane are only produced in the small intestine as the by-product of unabsorbed or incompletely absorbed carbohydrate in the diet. Simple breath tests to detect the presence of either gas provides not only the evidence of carbohydrate malabsorption (such as lactose and fructose malabsorption [3]), but the specific gas produced indicates the types of bacteria that are fermenting them (more on that below). The two breath tests for diagnosing SIBO that have become the most widely used are the glucose breath test and the lactulose breath test.

Glucose Breath Test or Lactulose Breath Test?

Either lactulose or glucose are used as substrates in hydrogen and methane breath testing for diagnosing SIBO, with some believing that glucose provides greater test accuracy [2] because glucose is absorbed completely in the upper small intestine [3], but may not be able to detect SIBO in the ileum, the far part of the small intestine, that connects to the large intestine [3]. Lactulose may be able to detect small-bowel bacterial overgrowth in the ileum [2,3].

Depending on which clinician one goes to, they likely will have a preference for using either glucose or lactulose breath test for diagnosing SIBO, whereas some gastroenterologists prefer to use jejeunal sampling via endoscopy.

How Does a Breath Test Work?

Hydrogen or methane exhaled in the breath following consumption of either glucose or lactulose is estimated using a gas chromatograph.

Normally, a small amount of hydrogen is produced from the limited amounts of unabsorbed carbohydrate that reaches the large intestine, however large amounts may be produced if there is malaborption of carbohydrate (such as fructose or lactose) in the small intestine, or if there are the wrong types of bacteria in the small intestine.

The hydrogen (or methane) is produced by the bacteria in the intestine, absorbed through the wall of the small-intestine, large-intestine or both, and the the hydrogen (or methane) containing blood travels up to the lungs. During a breath test, the hydrogen (or methane) is exhaled in the breath, and measured by the gas chromograph.

It is estimated that about 15%-30% of people have gut bacteria that contain Methanobrevibacter smithii, a methane-producing bacteria that recycles hydrogen by combining it with carbon dioxide, to produce methane. This bacteria converts 4 atoms of hydrogen into 1 molecule of methane [4], so people with this intestinal bacteria won’t exhale much hydrogen during the breath test (even if they have carbohydrate malabsorption or SIBO) because the hydrogen that they produce is converted into methane [3].

How the Breath Test is Performed

The person having the breath test first needs to fast overnight and have to brush their teeth and rinse their mouth with mouthwash to make sure oral bacteria don’t affect the test. At baseline, fasting breath hydrogen is estimated 3 – 4 times and averaged as basal breath hydrogen. If the person is found to have high breath hydrogen before they eat the sugar, then it may be attributed to SIBO. Then the person eats a specific amount of the test sugar; either 10 g lactulose or 100 g glucose, and the person’s breath is analyzed for hydrogen and methane every 15 minutes for 2 to 4 hours [3]. Diagnosing SIBO on the basis of a glucose breath test requires a rise in breath hydrogen by 12 ppm above baseline [3].

Based on a study published in 2000, Dr. Mark Pimentel, a key researcher in the area of SIBO from Cedar-Sinai Medical Center believes that a rise in breath hydrogen 20 ppm above basal levels within 90 minutes in a lactulose breath test should be considered a positive diagnosis of SIBO [5]. Some researchers maintain [3] that lactulose should not be used at all for diagnosing SIBO because it assumes that the time from when the lactulose is eaten until it reaches the junction of the small and large intestine (the cecum) is always greater than 90 minutes, whereas other studies indicate that it can range from 40 to 110 minutes [6]. As well, use of lactulose may only be able to diagnose 1/3 of people with SIBO [3].

A recent consensus paper from 2017 [7] published by 10 medical doctors involved in The North American Consensus group on hydrogen and methane-based breath testing concluded that both glucose breath testing and lactulose breath testing were reliable and were considered the least invasive tests for diagnosing SIBO [7]. The consensus group considered a rise in hydrogen of â‰¥20 ppm by 90 minutes* during glucose or lactulose breath test for SIBO to be positive for SIBO, and methane levels â‰¥10 ppm was considered methane positive.

*It should be noted that some clinicians such as Dr. Mark Pimentel consider a positive hydrogen test to be anything >20 ppm, and not necessarily a 20 ppm rise above baseline. In addition, Dr. Pimentel considers a positive methane test to be a reading of >3 PPM within 90 minutes (which is significantly lower than the levels set by the consensus group, of which he was a part [8]). Since different clinicians use different cutoff points to indicate a positive test for SIBO, this leads to what some consider to be a tendency to “overdiagnose” the condition [3].

As mentioned above, since a hydrogen breath test using glucose may miss SIBO in the far part of the small intestine (ileum), and a hydrogen breath test using lactulose may only be able to diagnose 1/3 of people with SIBO, some practitioners take the approach to treat patients “as if” positive for SIBO, in the absence of a positive breath test. If the person gets better on antimicrobial therapy along with appropriate dietary support, then it is deemed that the end goal for the person to feel better has been reached. There are two challenges that come to mind with respect to this approach; first of all, often more than one round of antibiotics or herbal antimicrobials are needed to completely eradicate the bacteria population in the small intestine that are responsible for the symptoms of SIBO. Does one do one round of treatment and hope for the best, or two rounds as that is the most likely to be effective? While Generally Recognized As Safe, even herbal treatments are not without risks, so treating “as if” is not a preferred option. The second drawback (that I will cover just below) is that the treatment for methane-dominant bacteria is different than the treatment for hydrogen-dominant bacteria. One could treat with herbal antimicrobials based on symptoms (i.e. the presence of constipation), but having a positive methane breath test (perhaps at the level of positive indicated by the consensus report, above) would enable an evidence-based treatment decision. While not without drawbacks, it is my opinion that breath testing should at least be tried unless doing so could cause a person severe gastro-intestinal discomfort.

UPDATE (Sept 5 2019): It should be noted that a recent (2018) study found that a glucose-based hydrogen and methane breath test does not detect bacterial overgrowth in the jejunum, but that a positive breath test may indicate altered jejunal function and microbial dysbiosis. This calls into question the validity of using breath tests in diagnosing SIBO. (Sundin OH, Medoza-Ladd A, Morales E et al, Does a glucose”based hydrogen and methane breath test detect bacterial overgrowth in the jejunum, Neurogastroenterology & Motility 30 (11), https://doi.org/10.1111/nmo.13350).

Positive Breath Test for Methane

As mentioned above, whether a breath test is positive for hydrogen or methane indicates something about the types of bacteria involved in SIBO. In several studies, positive methane results on breath tests have been associated with symptoms of constipation [9-12] and are 5 times more likely to have constipation than those with hydrogen dominant overgrowth [12] and the severity of constipation was found to be directly related to the level of methane [9]. Identifying whether SIBO is methane-predominant is important because the methane-producing bacteria Methanobrevibacter smithii is resistant to many antibiotics [7].

Distinguishing SIBO from IBS

As mentioned in the first article in this series on SIBO (available here) many of the symptoms of Irritable Bowel Syndrome (IBS) and SIBO are similar, including abdominal pain, bloating, gas, bouts of diarrhea or constipation or alternating diarrhea and constipation.

To make matters more confusing, Pimentel et al found that almost 80% (78%) of subjects in their study that had an abnormal lactulose breath test which suggested they had SIBO also met the Rome I criteria for IBS [5]. This begs the question how many of those who have been diagnosed with IBS based on the current Rome IV criteria [13] might actually meet the criteria for SIBO?

It is my opinion that someone who has been unsuccessful at resolving their symptoms of IBS using appropriate dietary treatment with the help of a knowledgeable Dietitian would benefit by undergoing glucose or lactulose breath testing to determine if their symptoms may be caused by SIBO.

In the next article, I will cover the main dietary approaches that are used in SIBO treatment, along with antibiotic or studied herbal antimicrobials. I will also cover why some clinicians do NOT change the person’s diet until after antimicrobial treatment has been completed.

More Info?

You can find out more about the hourly consultations and packages I offer by visiting the Services tab or the Shop, and if you would like additional information please send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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Facebook: https://www.facebook.com/BetterByDesignNutrition/
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References

Quigley EMM. The Spectrum of Small Intestinal Bacterial Overgrowth (SIBO), Current Gastroenterology Reports, (2019) 21:3, https://doi.org/10.1007/s11894-019-0671-z
Dukowicz AC, Lacy BE, Levine GM. Small intestinal bacterial overgrowth: a comprehensive review. Gastroenterol Hepatol (N Y). 2007;3(2):112—122.
Ghoshal UC How to interpret hydrogen breath tests. J Neurogastroenterol Motil. 2011; 17: 312—317
Levitt MD, Furne JK, Kuskowski M, Ruddy J. Stability of human methanogenic flora over 35 years and a review of insights obtained from breath methane measurements. Clin Gastroenterol Hepatol. 2006;4:123—129.
Pimentel M, Chow EJ, Lin HC, Eradication of small intestinal bacterial overgrowth reduces symptoms of irritable bowel syndrome.
Am J Gastroenterol. 2000 Dec; 95(12):3503-6
Ghoshal UC, Ghoshal U, Ayyagari A, et al. Tropical sprue is associated with contamination of small bowel with aerobic bacteria and reversible prolongation of orocecal transit time. J Gastroenterol Hepatol. 2003;18:540—547
Rezaie A, Buresi M, Lembo A et al, Hydrogen and Methane-Based Breath Testing in Gastrointestinal Disorders: The North American Consensus, Am J Gastroenterol 2017; 112:775—784; doi: 10.1038/ajg.2017.46
Scarlata K, Small Intestinal Bacterial Overgrowth (SIBO) blog article, January 22, 2014, https://blog.katescarlata.com/2014/01/22/small-intestinal-bacterial-overgrowth/
Chatterjee S , Park S , Low K et al. Th e degree of breath methane production in IBS correlates with the severity of constipation . Am J Gastroenterol 2007 ; 102 : 837 — 41.
Attaluri A , Jackson M , Valestin J et al. Methanogenic fl ora is associated with
altered colonic transit but not stool characteristics in constipation without
IBS . Am J Gastroenterol 2010 ; 105 : 1407 — 11.
Hwang L , Low K , Khoshini R et al. Evaluating breath methane as a diagnostic
test for constipation-predominant IBS . Dig Dis Sci 2010 ; 55 : 398 — 403.
Kunkel D , Basseri RJ , Makhani MD et al. Methane on breath testing is
associated with constipation: a systematic review and meta-analysis .
Dig Dis Sci 2011 ; 56 : 1612 — 8.
Schmulson MJ, Drossman DA. What Is New in Rome IV. J Neurogastroenterol Motil. 2017;23(2):151—163. doi:10.5056/jnm16214

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September 1, 2019September 4, 2019

What is Small Intestinal Bacterial Overgrowth (SIBO)?

I used to believe that SIBO was a condition that only alternative medicine practitioners such as naturopaths identified & ‘treated’, and it wasn’t a real diagnosis at all and it seems I was not alone in this belief.

This is the first article about SIBO which will outline what it is, it’s symptoms and risk factors and a subsequent article will outline how SIBO is diagnosed and some of the treatment options.

Last week I asked on Twitter “Do you believe that SIBO is a credible diagnosis?” and of the sixty one people that responded, here’s what people thought;

Fifteen percent of people thought SIBO wasn’t a legitimate medical diagnosis, while the remainder thought that either it was a credible diagnosis that not all doctors know about (62%), or that only Functional Medicine MDs diagnose and treat it (18%), or only naturopaths (5%) do.

My interest in searching the scientific literature about SIBO came when a rheumatologist suggested that it may be SIBO that was underlying the increase in joint pain that I was experiencing. While I had been diagnosed with osteoarthritis many years ago — which is a degenerative joint disease and not a normal part of aging (more in this article), the pain in my fingers had become excessive, even though there had not been any additional deterioration or deformation in those joints. If it wasn’t a rheumatologist that was suggesting SIBO as a possible cause, I would have discounted it without a thought but because the possibility was raised by a credible clinician, I decided to search the scientific literature to see what I could find. To be honest, I was quite surprised to find that it was not only well-researched, but that there were academics at well-known universities that have been studying it!

What is SIBO?

Small Intestinal Bacterial Overgrowth (SIBO) is an increase in the type of bacteria present in the small intestine that are normally found in the large intestine (also called the colon) [1].

The small intestine consists of three parts; the duodenum connects to the stomach, the middle part is the jejunum and the last part called the ileum, attaches to the colon. It is called the small intestine because its diameter is smaller than the large intestine, although it is actually longer in length than the large intestine [2].

Normally, the small intestine contains very few bacteria and when it does, the type of bacteria found in the duodenum and jejunum are usually a specific type (i.e. lactobacilli and enterococci, gram-positive aerobes or facultative anaerobes) and are found in small amounts (< 10⁴organisms per mL)[1] and research indicates that samples taken from the jejunum of healthy volunteers found no bacteria present at all. When the bacteria that normally populate the large intestine spills over into the small intestine, it is called Small Intestinal Bacterial Overgrowth or “SIBO”.

The body has several built-in defense mechanisms for normally preventing bacterial overgrowth of the small intestine. The major defense against small intestine bacterial overgrowth is (1) the very high acid environment of the stomach (gastric acid) which kills most bacteria, as well as (2) a normally intact ileocaecal valve which is the sphincter muscle that separates the small intestine from the large intestine. In addition, there are additional defense mechanisms such as immunoglobulins in the secretions of the small intestine, as well as secretions from the pancreas and bile-related secretions that keep bacteria from reproducing [1].

SIBO can occur for different reasons, including low stomach acid (achlorhydria), pancreatic insufficiency, as well as anatomical abnormalities including small intestinal obstruction, diverticula (more about this in this article), fistula (which is abnormal connection between an organ and the intestine which can be created after some infections), as well as slowing of intestinal movements (motility disorders) that are common in those with diabetes mellitus, and other conditions. It has been known for many years that those that consume significant amounts of alcohol are known to be at risk for SIBO [3] but a more recent study found an association between moderate alcohol consumption and SIBO [4], which was defined as up to one drink per day for women and two drinks per day for men. It is thought that alcohol consumption may cause injury to the mucosal cells of the small intestine which contributes to a slowing of intestinal contractions (i.e. motility disorder), which is associated with SIBO. In some people, a combination of the above factors may be involved.

[Note: in my case, an underlying diagnosis of SIBO was certainly possible as I had been on a long-term, high dose of H2 antihistamines due to having Mast Cell Activation Disorder (MCAD) — medications which are known to also significantly reduce stomach acid, and I had also been diagnosed with type 2 diabetes 8 years before going into remission 2 1/2 years ago.

How Common is SIBO?

The prevalence of SIBO in young and middle-aged adults appear to be between 6 and 15% , but higher in the older adults (14.5—15.6%) [5]. Perhaps this is due to decreasing amounts of stomach acid associated with aging, as well as increase prevalence of diverticulosis and type 2 diabetes, all of which are associated with SIBO risk.

What are the Symptoms of SIBO?

Many of the symptoms of SIBO are similar to those of Irritable Bowel Syndrome (you can read more about that here), including abdominal pain, bloating, gas, bouts of diarrhea or constipation or alternating diarrhea and constipation. As mentioned above, there are other lesser known symptoms of SIBO, including joint pain.

Update (September 4, 2019): In the second article (posted here), I outlined different tests used to diagnose SIBO, the difference between hydrogen-dominant SIBO and methane-dominant SIBO and why Irritable Bowel Syndrome (IBS) that does not improve despite adopting appropriate dietary changes may be SIBO.

More Info?

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd
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References

Bures J, Cyrany J, Kohoutova D, et al. Small intestinal bacterial overgrowth syndrome. World J Gastroenterol. 2010;16(24):2978—2990. doi:10.3748/wjg.v16.i24.2978
Medscape, Small Intestine Anatomy, Dec 8 2017, https://emedicine.medscape.com/article/1948951-overview
Hauge T, Persson J, Danielsson D: Mucosal Bacterial Growth in the Upper Gastrointestinal Tract in Alcoholics (Heavy Drinkers). Digestion 1997;58:591-595. doi: 10.1159/000201507
Gabbard SL, Lacy BE, Levine GM et al, The Impact of Alcohol Consumption and Cholecystectomy on Small Intestinal Bacterial Overgrowth, Digestive Diseases and Sciences, 2014, Volume 59, Number 3, P. 638
Dukowicz AC, Lacy BE, Levine GM. Small intestinal bacterial overgrowth: a comprehensive review. Gastroenterol Hepatol (N Y). 2007;3(2):112—122.

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August 19, 2019August 20, 2019

When Real Food is Deemed Offensive and Disturbing, not Processed Food

Note: This article is not one of my usual Science Made Simple posts, but a comment about something that occurred on social media yesterday.

Yesterday, I posted a photo on Instagram, Facebook and Twitter of some fresh chicken that I had bought and that I had cut up into legs and breasts. Real food is perfectly normal for a Dietitian to write about, right?

The photo I posted is above.

The caption under the photo indicated that this shouldn’t look foreign and that real chicken comes with a head, feet and bones (in contrast to chicken we buy in a supermarket that usually comes boneless or pre-cut, in Styrofoam trays, and covered in plastic wrap).

Presumably, someone found this photo of chicken before and after cutting as being offensive and reported it to Instagram. I was not notified that the photo had been censored, and it looks the same from my end, but several people that follow me told me that my photo was deemed to contain “sensitive content”.

To anyone viewing the post now, it now looks like this:

This photo contains sensitive content which some people may find offensive or disturbing.

A physician posted the following comment about the censoring;

“I cannot believe a photo of food is blurred as “sensitive content”. It is absolutely mind boggling. But it’s totally fine to be constantly inundated with ads for crap that make us feel bad about ourselves, making us buy junk we don’t need.“

This physician is right! There’s a huge difference between real food and the processed food-like substances (“crap”) that we are encouraged to buy and eat. You can read more about telling the difference between these in this previous article.

The two photos of chicken that I posted before and after being cut up has been blurred on Instagram because “some might find offensive or disturbing“.

Do you know what I consider offensive and disturbing?

I find people having to have toes amputated because of uncontrolled diabetes offensive.

I find obese people trying desperately to lose weight, yet finding themselves unable to curb an insatiable craving for processed food that was deliberately created by its producers, disturbing.

I find the fact that many young children in Canada and the US (and likely in many other countries) think of chicken as something that comes boneless, deep fried in batter and packaged in small individual packages with various flavours of sweetened sauce to dip it in, disturbing.

I find pea protein isolate, industrial seed oil, methyl cellulose and a host of other processed ingredients masquerading in the meat counter, offensive. But please don’t misunderstand…

I have absolutely no problem with vegetarians and vegans having a wide variety of plant-based food available to eat as alternatives to animal-based foods, but it should not be marketed to consumers as “meat”, but ‘better’.

It may be “better” or “ultra” or “beyond” for those who choose a plant-based lifestyle, but an ultra-processed mixture of pea protein isolate, canola oil, refined coconut oil, cellulose from bamboo, methylcellulose, potato starch, maltodextrin, yeast extract, sunflower oil, vegetable glycerin, dried yeast, gum arabic along with seasoning and flavourings is not ‘better’ or preferable to whole, real food with a single ingredient, “beef”.

These are choices…

…and people have the right to choose what they want to eat, without condemnation and judgement.

There is no one-sized-fits-all-diet and individuals who choose to eat meat, fish or poultry should not be vilified or censored for doing so.

To your good health,

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
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August 7, 2019March 16, 2021

Tyramine Intolerance – underlying cause of migraine headaches?

A migraine is more than just a really bad headache. While migraine is characterized by intense, debilitating headache, it also may include nausea, vomiting, difficulty speaking, sensitivity to light and sound, and may- or may not be preceded by an aura (sensory, motor, visual or speech symptoms that act like a warning signal that a migraine is about to begin). People with a reduced ability to clear the amino acid tyramine (which is called tyramine intolerance) often experience migraine, along with other symptoms including heart palpitations and GI issues, including nausea and vomiting.

In those who have insufficient amounts of an enzyme called monoamine oxidase (MAO), levels of tyramine can build up, and this is called tyramine intolerance. A tyramine intolerance diet can be helpful in helping reduce people’s symptoms.

Tyrosine combines with other amino acids to form proteins, and just like the amino acid histadine breaks down to histamine (see this previous article on histamine intolerance), tyrosine breaks down to form tyramine. Normally, the excess tyramine is broken down by the enzyme monoamine oxidases (MAO) — in the same way that excess histamine is broken down by the enzyme diamine oxidase (DAO). In individuals that take certain types of medications such as MAO inhibitors (used in treating some types of depression) and certain medications used for treating Parkinson’s disease, levels of tyramine will build up in the body because the enzyme that breaks it down is inhibited.

In those who have insufficient amounts of the enzyme monoamine oxidase, levels of tyramine can also build up and this is called tyramine intolerance [1].

Symptoms of Tyramine Intolerance

The body naturally responds to the presence of tyramine by making catecholamines such as epinephrine and norepinephrine which are neurotransmitters involved in the “fight or flight” response. If tyramine accumulates, too much of these chemicals are released, which leads to an increase in blood pressure and heart rate [2]. If these chemicals go high enough (such as is the case with those taking certain medications) this can lead to a very rapid and dangerous increase in blood pressure called a ‘hypertensive emergency’ which can result in bleeding in the brain (hemorrhagic stroke)[3] and rarely, even death. At very least, the very high blood pressure can cause damage the body’s tissues and organs.

Those with a reduced ability to clear tyramine due to tyramine intolerance may experience migraine, heart palpitations or GI issues, including nausea and vomiting [2].

Tyramine Intolerance Diet

In those taking MAO Inhibitor medication or specific medications for treating Parkinson’s disease, a tyramine-free diet is prescribed. Since the adverse effects of eating tyramine-containing foods can be so serious, strict adherence is needed.

For those with diagnosed tyramine intolerance, a low tyramine diet will be recommended, and for those with suspected tyramine intolerance a low tyramine diet may be trialed to see if symptoms improve. This is especially the case in people who experience migraine— as it has long been thought that tyramine may underlie the constriction of blood vessels that increases blood pressure associated with migraine[4].

Low Tyramine Diet — not as easy as following a ‘list’

Tyramine naturally occurs in small amounts in protein-containing foods, but as foods age, mature or ripen, tyramine levels increase.

Avoiding strong or aged cheeses, cured, smoked or processed meats, pickled, cultured or fermented foods (including many Asian condiments), nuts and nut butters and some seeds and seed butters, aged spreads such as Marmite and Vegemite, and alcoholic beverages [3,5] is a good place to ‘start’, however reducing tyramine in the diet isn’t as straight forward as simply following a “list’.

Knowing which cheeses, for instance have high levels of tyramine and which have moderate levels can be looked up, but some tyramine-containing foods may act as a trigger to migraine in one person, but not in another — so it is often unnecessary to restrict all tyramine-containing foods. Sometimes by me helping people systematically eliminate the most common tyramine triggers is sufficient to provide them significant relief — without them having to eliminate all tyramine-containing foods. That’s where experience helps!

More Info?

If you have been diagnosed with tyramine intolerance or suspect you may be sensitive to tyramine, I can help.

You can learn more about the Histamine / Tyramine Intolerance Specialty Hourly Service here and I also offer a migraine add-on option to the Complete Assessment Package which you can learn about here. If you would like information as to which is a better fit for your needs, please send me a note using 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/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

References

Joneja, J. Histamine and tyramine sensitivity — how closely are they linked? Food Matters, October 2017, https://www.histamine-sensitivity.com/histamine-tyramine-similaraties-10-12.html
Van Eaton J. Tyramine-Free Diets. Healthline, Feb 1, 2019, https://www.healthline.com/health/tyramine-free-diets
Hall-Flavin D. Mayo Clinic, MAOIs and diet: Is it necessary to restrict tyramine? https://www.mayoclinic.org/diseases-conditions/depression/expert-answers/maois/faq-20058035
Costa MR, Glória MBA. Migraine and Diet, Encyclopedia of Food Sciences and Nutrition (Second Edition), 2003, https://www.sciencedirect.com/science/article/pii/B012227055X007835
Skypala IJ, Williams M, Reeves L, Meyer R, Venter C. Sensitivity to food additives, vaso-active amines and salicylates: a review of the evidence. Clin Transl Allergy. 2015;5:34. Published 2015 Oct 13. doi:10.1186/s13601-015-0078-3

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August 4, 2019May 23, 2023

Why So Many Post Menopausal Women and Older Men Have Low Iron

Why do so many post menopausal women and older men have low iron stores or iron-deficient anemia — especially given that the women are no longer menstruating, and men never had this regular blood loss?

It should be noted that in this article, I am only discussing low iron stores and iron-deficient anemia and not anemia of other types, such as accompanies low vitamin B12 status or a problem with intrinsic factor that helps absorb it; both of which are common as people age, nor they type that is the result of low folate intake. This is a different type of anemia, called macrocytic anemia, where the blood cells are fewer, but larger than normal (macro means larger).

Microcytic anemia is where there are fewer red blood cells and they are smaller than normal (micro means small) and this is caused by conditions that keep the body from making enough hemoglobin, the oxygen carrying part of the blood. Low levels of hemoglobin in red blood cells results in the red blood cells appearing paler in colour and this is called hypochromic (hypo means low, chromic means colour). Iron deficient anemia is the most common type of hypochromic microcytic anemia.

Low iron stores or iron deficient anemia

May be caused by;

1. inadequate dietary intake such as is common in those who are vegetarian (eat no meat from animals) or vegan (eat no animal products, including no eggs or cheese).
2. decreased absorption which is common in conditions such as Celiac disease or in those that have h. pylori; a type of bacteria that causes stomach ulcers (or may be without symptoms at all
3. chronic blood loss, such as is common in women with heavy menstrual periods or in those with inflammatory gastrointestinal (GI) diseases and experience internal bleeding, such as those Crohn’s Disease or Ulcerative Colitis.
4. pregnancy due to increased blood needs of the fetus.

Post-menopausal women are past the age where they can either be pregnant or have periods, so low iron stores or iron-deficient anemia in older women are for reasons similar to older men; either due to decreased iron absorption or chronic blood loss.

In older adults with low iron stores or iron deficient anemia, the first thing I rule out is Celiac Disease because it is as simple as a routine blood test, and a fair number of people with the disease (immune reaction to gluten) have no symptoms whatsoever. The second thing I rule out is any history of- or symptoms of stomach ulcers, which is caused by the heliobacter pylori (h. pylori) bacteria. This bacteria takes up iron and can contribute to iron status in its host. Ruling this out can be done by a breath test looking for urea given off by the bacteria.

Assuming an older adult tests negative for both Celiac disease and h. pylori and does not have any chronic disease that may be causing the anemia — then what can be contributing to them having lower than normal iron stores or iron deficiency?

Iron deficient anemia (IDA) occurs in ~2%-5% of adult men and postmenopausal women; with blood loss from chronic blood loss from gastrointestinal bleeding being the most common cause [1,2] and malabsorption being the second most common 2,3]. Goddard et al [2] found that 5-10% of of iron deficient anemia is due to malabsorption mainly from Celiac disease, but since there was very little research assessing iron deficient anemia in post menopausal women, a 2015 study from Pakistan sought to do that [4].

Chronic blood loss is not only caused by inflammatory bowel diseases such as Crohn’s and Colitis, but with long term used of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) such as Advil® (ibuprofen) and Naproxen®. For years, doctors often recommend that older adults take a “baby aspirin” (low dose ASA, 81 mg) to lower their risk of heart disease, but long term use of even the small dose has been associated with GI bleeding. A study published in October 2018 in the New England Journal of Medicine found that for every 1,000 people taking low dose ASA, 11 avoided a serious cardiovascular event (heart attack, stroke) but 9 experienced GI bleeding serious enough to result in hospitalization or even death [5]. As a result, physicians are re-thinking the previous recommendation for people without a previous heart attack or stroke to take low dose aspirin [6]. Older adults who have been taking NSAIDs for pain or a low dose ASA to protect against heart attack and stroke may have low iron stores or even iron-deficiency as a result.

A major contributor to iron deficiency caused by malabsorption other than Celiac Disease in older adults is the use of Histamine-2 Receptor Antagonists (H2 antihistamines) such as Ranitidine which is the active ingredient in over-the-counter stomach acid reducer, Zantac®, as well as the commonly prescribed Proton Pump Inhibitors (PPIs). Gastric acid inhibitor use of either H2 antihistamines or PPIs for ~2 years is known to be associated with an increased risk of iron deficiency [7], so those with Gastroesophageal Reflux (GERD), chronic heartburn or indigestion or Histamine Intolerance taking these medications are at risk.

Reduced iron status in older adults taking NSAIDs, including low dose aspirin or gastric acid reducers such as Zantac® or PPIs is quite common, so finding ways to decrease dependence on NSAIDS for pain reduction strategies by exploring dietary strategies including an Anti-Inflammatory Diet can be very helpful.

In addition, weight loss especially reduction of weight carried around the abdomen can result in a reduction of- and often a discontinuation of the need for gastric acid inhibitors.

Finally, a major challenge in determining the cause of lower iron stores or iron deficient anemia in older adults is that chronic diseases such as diabetes and chronic kidney disease can cause the anemia of chronic disease (ACD) also called anemia of inflammation, which is very similar to iron deficient anemia (IDA). It is important to distinguish the two. The 2015 study from Pakistan had a rather simple, but ingenious way of doing so. Subjects who were deficient were given iron supplementation and most improved indicating that there was no malabsorption, but low intake. However, if there was no change in serum iron when serum iron was re-tested, these individuals were concluded to be iron deficient due to malabsorption In those with malabsorption due to Celiac disease for example or the use of gastric acid inhibitors that can’t be reduced, recommendation is for intravenous iron administration, as oral iron administration is not effective.

More Info?

If you are an older adult and have lower than optimal iron stores or have been diagnosed with iron deficiency, working with your doctor I can help rule out whether it may be a result of asymptomatic Celiac Disease, over the counter or prescribed medications that you’ve been taking, inadequate dietary intake or malabsorption that has contributed to the problem.

You can find out more about the packages and hourly consultations I offer by clicking here and if you would like additional information, please send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

References

Guralnik JM, Eisenstaedt RS, Ferrucci L, Klein HG, Woodman RC. Prevalence of anemia in persons 65 years and older in the United States: evidence for a high rate of unexplained anemia. Blood. 2004;104:2263—2268
Goddard AF, James MW, McIntyre AS, Scott BB. Guidelines for the management of iron deficiency anaemia. Gut. 2011;60:1309—1316
Amy Z, Kaneshiro M, Kaunitz JD. Evaluation and
treatment of iron deficiency anemia: a gastroenterological
perspective. Dig Dis Sci. 2010;55(3):548-559.
Qamar K, Saboor M, Qudsia F, Khosa SM, Moinuddin, Usman M. Malabsorption of iron as a cause of iron deficiency anemia in postmenopausal women. Pak J Med Sci. 2015;31(2):304—308.
The ASCEND Study Collaborative Group. Effects of aspirin for primary prevention in persons with diabetes mellitus. N Engl J Med 2018; 379:1529-1539
Harvard Health Publishing, Rethinking low-dose aspirin, https://www.health.harvard.edu/heart-health/rethinking-low-dose-aspirin
Lam JR, Schneider JL, Quesenberry CP, Proton Pump Inhibitor and Histamine-2 Receptor Antagonist Use and Iron Deficiency. Gastroenterology. 2017 Mar;152(4):821-829.

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July 23, 2019March 16, 2021

Histamine Intolerance, MCAD / MCAS and How Dietary Changes Help

INTRODUCTION: In the previous article about milk intolerance related to a novel beta casein protein found in commercial cow’s milk, I mentioned both histamine intolerance and Mast Cell Activation Disorder (MCAD) — which is also called MCAS (Mast Cell Activation Syndrome). Quite a few people with these disorders reached out to me on social media, looking for articles I may have written about them and as I hadn’t yet, I decided to write this one.

Adverse reactions to food or components of food can be divided into food allergy and food intolerance.

A food allergy is an IgE antibody-mediated immune reaction and can range from mild skin itching or hives, to full-blown anaphylactic attack where a person is unable to breathe. Specific IgE-mediated antibodies can be assessed and quantified by a blood test for an allergen, or assessed via skin scratch test with a small amount of the allergen.

A food intolerance is a non-immune reaction to a food or food component that can result in a disturbance of enzymes of the gastrointestinal (GI) tract. Lactose intolerance is probably the best known food intolerance, where people have a disturbance of the enzyme lactase in the GI tract, which makes them unable to properly digest the sugar in milk.

Histamine intolerance, like tyramine intolerance is a food intolerance and while rarely life-threatening, it can makes people’s lives quite miserable.

What are Histamines

Most people know that term ‘antihistamine‘ as medications that people take when they have seasonal allergies, such as trees and grasses or ragweed (“hay fever”), but what are histamines?

Histamine is a chemical that performs many helpful functions in the body such as stimulating the production of stomach acid (via the H2 receptors), but in this context, the interest is in histamine’s role in the immune system.

As it is intended to, histamine is released in response to exposure to an allergen, in the body’s attempt to protect you against something that it perceives as a threat. If you have breathed in some pollen that you you are allergic to for example, a signal is sent to your mast cells to release histamine in the body. These histamines result in inflammation; a condition which signals the immune system to respond. That response could make you sneeze or make your nose run in order to help get rid of the offending allergen — or in cases with people with IgE mediated allergies it can be a very serious reaction that causes your blood pressure to suddenly drop very low, and you find it very difficult to breathe (anaphylaxis).

In histamine intolerance or mast cell activation disorder, histamine is either not broken down properly so it builds up in the body or is released by the mast cells inappropriately, such as when there is no allergen present. In these people, histamine becomes like gluten to a celiac, or regular milk to someone with lactase deficiency — only worse.

Some foods are high in an amino acid called histidine; which converts to histamine during digestion (via a carboxylation reaction mediated L-histidine decarboxylase).

Foods high in histamine include aged and fermented foods such as cheese, yogurt, pickled foods such as kimchi or saurkraut, and smoked fish. Other foods include dried fruit, specific vegetables, some nuts, well as alcohol.

There are also foods that are histamine-liberators, such as chocolate, milk and tomatoes (just to name a few) that need to be considered to minimize the symptoms of histamine intolerance, as well as certain food additives [1].

Finally, foods high in histidine, which is converted to histamine upon digestion, aslo need to be factored in to the diet of someone with histamine intolerance or mast cell activation disorder.

People with mastocytosis, mast cell activation disorder (MCAD) or histamine intolerance react to foods high in histadine / histamine as well as to foods that liberate histamine from mast cells. While these are separate disorders, they all involve problems with histamine.

Mastocytosis is condition where there are too many mast cells. This can be limited to just the skin or can be systemic (all over the body) and occurs due to a mutation in a specific gene.

Mast Cell Activation Disorder (MCAD) – sometimes called Mast Cell Activation Syndrome (MCAS) is where the mast cells ‘degranulate’ (spill their contents, including histamine) at an inappropriate time. That is, they release histamine when there is no allergen present.

Histamine Intolerance is where the rate of histamine accumulation in the body is greater than the rate at which histamine degrades. The analogy of histamine intolerance is that of an overflowing “bucket”.

Histamine Intolerance

Normally, histamine is stored in the mast cells, or is rapidly degraded by one of two enzymes; either by diamine oxidase (DAO) or histamine-N-methyltransferase (HNMT) upon release, so it doesn’t accumulate. Disfunction in these enzymes can

DAO primarily functions in the small intestine, ascending colon (a section of the large intestine), as well as kidney [1]. The primary function of DAO is the elimination of excess histamine, as well as controlling the amount of histamine in the body, coming from the digestive tract [1].

HNMT is primarily functions at the level of the histamine receptors themselves, where it deactivates histamine. This enzyme is active in a wide range of body tissues; but greatest in the kidney and liver, followed by the spleen, colon (large intestine), reproductive organs (prostate, ovary), spinal cord cells and parts of the lungs (bronchi, trachea).

Histamine Receptors

There are 4 types of histamine receptors that bind histamine and cause mast cells to release histamine. The binding of histamine with these receptors result in different types of allergic reactions.

from [1] Baily N, Histamine Intolerance, Igennus Healthcare Nutrition, https://www.slideshare.net/igennus/managing-histamine-intolerance-80982438

H1 Receptors

H1 receptors are primarily involved in allergic rhinitis symptoms (sneezing, blowing ones nose), broncho-constriction such as what occurs in allergy-induced asthma, as well as systemic vasodilation (enlarging of the blood vessels)[2].

H2 Receptors

H2 receptors stimulate the stomach to release HCL acid, and inhibit the body from making antibodies, as well as activate the immune system response, including T-cell proliferation and the production of cytokines[2].

H3 Receptors

H3 receptors change neurotransmitter release in the central nervous system, including serotonin and norepinephrine (noradrenaline)[2].

H4 Receptors

H4 receptors are found mostly in bone marrow and white blood cells and are also expressed in the colon (large intestine), small intestine, spleen, tonsils and trachea (wind-pipe)[2].

Symptoms of Histamine Intolerance

People with histamine intolerance display a wide variety of symptoms, affecting different parts of the body. Some people have many symptoms in different parts of the body, whereas others have a few symptoms clustered in specific parts. Those with histamine intolerance may have chronic reactions and others may have them seemingly ‘randomly’.

That said, the most frequently observed symptoms are acute (sudden) or chronic (long term) gasto-intestinal GI symptoms [2] and can easily be mistaken for ‘food poisoning’ (acute symptoms) or irritable bowel syndrome (chronic symptoms). That said, there are individuals with MCAD that have anaphylactic-type reactions.

Gastro-intestinal symptoms often take place several hours after ingestion of the offending food or food component, because the food itself has to be digested (which takes time) for its histamine to be liberated and bind with the histamine receptors.

In other cases, the reaction is faster; especially when eating aged or leftover food or other foods with high histamine content. These foods may trigger abdominal cramps or diarrhea within 15-30 minutes[2].

Other non-GI related symptoms common with histamine intolerance and mast cell activation disorder (MCAD) are skin rashes, hives (with or without itchiness), facial and chest flushing (getting red and ‘hot’ feeling), faster or slower heartbeat (arrhythmia) or low blood pressure or extreme fatigue. Some people also experience mood changes, including inattentiveness or something described as a ‘brain fog’, as well as sleep disturbances [3,4].

Getting Diagnosed

Histamine intolerance and mast cell activation disorder are difficult to diagnose, firstly because people themselves don’t think wide range of symptoms are related, so they often don’t seek medical help. Another challenge is that the very fact that the symptoms are diverse may result in them be discounted by some physicians as being related to stress/anxiety or depression.

Mast cell activation disorder (MCAD) takes on average 14 years to be diagnosed [4] and often only occurs once the person finally gets a referral to an immunologist or allergist knowledgeable in the condition. I can assist in helping people get that referral, as well as provide support once they know they have either MCAD or histamine intolerance.

You may be interested in this article about similar condition called tyramine intolerance, especially if you suffer from migraine headaches.

More Info?

If you have been diagnosed with histamine-intolerance or mast cell activation disorder (MCAD) or suspect you may have one of these, I can help.

I can assess your symptoms to see if may meet the criteria for MCAD and if so, can put together the documentation required to obtain a referral to an experienced immunologist who can either rule out or make a diagnosis. If it seems you may have histamine intolerance or you have been diagnosed as such, I can provide you with the nutrition education in making the needed dietary changes in an effort to minimize your symptoms.

To your good health!

Joy

You can follow me on:

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

Reference

Baily N, Histamine Intolerance, Igennus Healthcare Nutrition, https://www.slideshare.net/igennus/managing-histamine-intolerance-80982438
Jernigan D, Histamine Intolerance Syndrome, Hansa Center for Optimal Health, Bimed Network, https://www.marioninstitute.org/histamine-intolerance-syndrome/
Molderings GJ, Brettner S, Homann J et al, 2011, Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options, J of Hemat and Onc 4 (10)
Hamilton MJ et al, 2011, Mast cell activation syndrome: A newly recognized disorder with systemic clinical manifestations. J of Allergy and Clin Immunology Vol 28 (1), p. 147-153

July 21, 2019August 17, 2023

Milk Intolerance May be Caused by A1 Beta-Casein

Digestive issues that result from milk consumption are often attributed to lactose intolerance, but research indicates that it may be the result of an intolerance to a specific type of protein found in some types of cow’s milk; specifically A1 beta-casein.

Casein and whey are the two primary proteins found in milk, with casein accounting for ~ 80 % of the protein in milk. Approximately 30% of the protein in milk is beta-casein.

There are two variants of beta-casein; A1 and A2, however before cows were domesticated, they only produced milk that only contained the A2 form of beta-casein[1,2]. Older breeds of cows such as most Jerseys, Guernseys, Brown Swiss, Normandes, as well as most of the cows in Asia, Africa and southern Europe[2] produce milk with the A2 variant of beta-casein, as do goats, sheep, donkeys, yaks, camel and buffalo [2]. In addition, human milk contains A2 beta-casein.

It is thought that ~8,000 years ago, a single-gene mutation occurred in Holsteins which resulted in the production of the A1 beta-casein protein in this breed. This novel gene variant was passed on to other northern European breeds of cows, including Friesian, Ayrshire and British Shorthorn since Holsteins were bred with them to improve milk production[2].

Today’s Holstein breed is the most common dairy cow in the US, Canada, Australia and northern Europe and carries both A1 and A2 forms of beta casein in approximately equal amounts[2].

Milk intolerance may not always be due to lactose intolerance, but due to intolerance to milk containing A1 beta-casein.

Note: Primary lactose intolerance is a result of a lack of the enzyme lactase, which is genetic in origin. This is a permanent condition. Secondary lactose intolerance is temporary and the result of being sick with something that causes diarrhea which sloughs off the lactase from the wall of the intestine. Genuine lactose intolerance can be tested with a hydrogen breath test.

Research suggests that A1 beta-casein protein may be at the root of stomach pain and other gastrointestinal (GI) symptoms associated with consumption of milk from A1 cows and which closely resemble lactose intolerance. These symptoms are not present when consuming milk from cows that only produce A2 beta-casein. Food-derived peptides such as β-casomorphins and others are known to have different effects on the intestines, including the secretions of the stomach and pancreas, as well as gut motility [3]. Studies have found that a peptide called β-(beta) casomorphin (BCM-7) may be behind stomach pain and other symptoms associated with milk containing A1 beta-casein.

The Difference Between A1 and A2 Beta-Casein

If one thinks of proteins as chains of amino acids strung together like train-cars in a train, each one of the ‘cars’ represents a different amino acid. In the older A2 beta-casein variant, the ‘car’ which occupies the 67th position is an amino acid called proline, but in the newer A1 beta-casein variant, the amino acid in the 67th position is histidine. When milk with A1 beta-casein is digested, the histidine bond breaks, resulting is a peptide made up of 7 amino acids, called β-(beta) casomorphin-7 (BCM-7).

β-(beta) casomorphin-7 (BCM-7) is a naturally occurring opioid peptide, with a structure similar to morphine and is known to bind to opioid receptors [3]. What effect does BCM-7 have on the body as a result of binding with these opioid receptors?

A 2015 review paper cites research demonstrating that milk containing A1 beta-casein increases GI transit time (the amount of time that it takes for food to go through the GI tract) which means in slows it down, and in animal studies, increases inflammatory markers significantly more than A2 beta-casein containing milk[5]. In a small, double-blinded, randomized crossover study from 2014 with 41 subjects, it was found that participants consuming A1 beta-casein cow’s milk had significantly softer stools, more bloating and more abdominal pain than those drinking A2 beta-casein milk [6]. In another unrelated double-blind, randomized, crossover trial from 2016 with 45 Chinese participants with self-reported intolerance to cow’s milk drank 250 mL of either A1/A2 or A2 milk following each of two meals over a 14-day period. When drinking the A1 beta-casein milk, there was an increase in transit time and in GI inflammation, and a worsening of digestive discomfort [7] as well as an increase in inflammatory markers such as IgG, IgE, and IgG1. These were significantly lower in those that drank A2 milk [7].

Addendum (July 22, 2019): *there has been some anecdotal evidence that people with arthritis do considerably better when they do not consume casein (see Arthritis Foundation website).

In a large scale 2017 randomized cross-over design follow-up study, 600 adult who reported lactose intolerance and digestive discomfort following milk consumption were assigned over a 7-day period to consume either 300 mL of conventional milk containing both A1 and A2 beta casein, or only A2 milk. Results indicated digestive symptoms were markedly reduced after consuming A2 milk versus conventional milk [8].

Healthcare professionals have often assumed (without giving people hydrogen breath tests to confirm it) that people with GI symptoms related to consuming dairy products have lactose intolerance, when it is possible that the symptoms could be related to intolerance of A1 beta-casein.

Concerning to those with histamine-intolerance, including those with Mast Cell Activation Disorder (MCAD) who need to lower their intake of histadine-containing foods and histamine-liberators [9] may unknowingly be adversely affected by milk commonly available in the US, Canada, Australia and northern Europe that contains A1 beta-casein, as when it is digested it produces betacasomorphin-7 (BCM-7), a potent histamine liberator. The most well-known Histamine Intolerance Food Compatibility List from the Swiss Histamine Intolerance Group (SIGHI) lists milk as producing a low reaction — perhaps because the milk available in Central Europe, as in southern Europe, contains A2 beta casein, and not A1 beta-casein as in North America, Australia and northern Europe [10]. Those with histamine-intolerance in the US and Canada, for example and other countries with A1 beta-casein in dairy need to be aware that the milk and the hard cheeses listed as being “well-tolerated, no symptoms expected at usual intake” does not apply to the milk and cheese available to them.

Final Thoughts…

While much research has yet to be done to determine the extent that A1 beta-casein proteins impact human health, those with suspected lactose intolerance who continue to have symptoms while consuming lactose-free milk and low-lactose products such as yogurt and hard cheese, should try eliminating milk produced at ordinary large-scale dairies that have milk containing both A1 and A2 beta-casein to see if their symptoms improve. As a substitute, they could use goat milk or buffalo milk, or find small, local dairies that use “heritage herd” cows, such as specific species of Jerseys, Guernseys, Brown Swiss, and Normandes that only produce milk with A2 beta-casein.

Note: My tried and true recipe for making homemade goat or A2 yogurt in an oven or crock-pot using a temperature controller, as well as turning it into thick Greek yogurt is posted here.

Those with histamine-intolerance in the US, Canada and Australia might feel better avoiding milk, cheese, and yogurt from conventional dairies, as these contain A1 beta-casein, which are high histamine liberators. After a period of dairy avoidance to enable mast cells to calm, dairy products from “heritage herd” cows can then be trialed.

NOTE: Butter and full-fat (whipping) cream are entirely fat, and as such do not contain either A1 or A2 beta-casein proteins. These would be fine to consume regardless of which dairy they were from.

More Info?

If you have food allergies or food intolerances, including what you thought was lactose intolerance, or have been diagnosed with histamine-intolerance or Mast-Cell Activation Disorder (MCAD), I can help.

You can find out more about the packages and hourly consultations I offer under the Services tab or by clicking here. If you would like further information, please send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

References

Ware M, Metropulos M, Medical News Today, A2 milk: What you need to know, July 25, 2017, https://www.medicalnewstoday.com/articles/318577.php
Pasin G. A2 milk facts. California Dairy Research Foundation website. http://cdrf.org/2017/02/09/a2-milk-facts/. Published February 9, 2017.
European Food Safety Authority. Review of the potential health impact of β-casomorphins and related peptides. EFSA J. 2009;7(2):1-107.
Kurek M, Przybilla B, Hermann K, A naturally occurring opioid peptide from cow’s milk, beta-casomorphine-7, is a direct histamine releaser in man, Int Arch Allergy Immunol. 1992;97(2):115-20.
Pal S, Woodford K, Kukuljan S, Ho S. Milk intolerance, beta-casein and lactose. Nutrients. 2015;7(9):7285-7297.
Ho S, Woodford K, Kukuljan S, Pal S. Comparative effects of A1 versus A2 beta-casein on gastrointestinal measures: a blinded randomised cross-over pilot study. Eur J Clin Nutr. 2014;68(9):994-1000.
Jianqin S, Leiming X, Lu X, Yelland GW, Ni J, Clarke AJ. Effects of milk containing only A2 beta casein versus milk containing both A1 and A2 beta casein proteins on gastrointestinal physiology, symptoms of discomfort, and cognitive behavior of people with self-reported intolerance to traditional cows’ milk. Nutr J. 2016;15:35
He M, Sun J, Jiang ZQ et al, Effects of cow’s milk beta-casein variants on symptoms of milk intolerance in Chinese adults: a multicentre, randomised controlled study. Nutr J. 2017 Oct 25;16(1):72.
Molderings GJ, Brettner S, Homann J, Afrin LB. Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options. J Hematol Oncol. 2011;4:10. Published 2011 Mar 22. doi:10.1186/1756-8722-4-10
Lamprecht H, Swiss Interest Group Histamine Intolerance (SIGHI), Histamine Intolerance Food Compatibility List, wwww.mastzellaktivierung.info & www.histaminintoleranz.ch

This article is based in part on material by Judith C. Thalheimer, RD, LDN, Is A2 Milk the Game-Changer for Dairy Intolerance?Today’s Dietitian, Vol. 19, No. 10, P. 26

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July 19, 2019July 19, 2019

Arthritis is Not a Normal Part of Aging – it’s a degenerative joint disease

Many people mistakenly believe that arthritis is a normal part of the aging process, but many older adults never get it and most of the people that are diagnosed with it are under the age of 65 years old. In fact, 2/3 of those diagnosed are not seniors, and some include children.

US statistics report that almost 1/4 ( 22.7%) adults have doctor-diagnosed arthritis — with significantly higher age-adjusted prevalence in women (23.5%) than in men (18.1%). While arthritis is not a normal part of aging, the likelihood of getting a diagnosis increases with age[1]. Only 7.3% of adults aged 18 to 44 years have been diagnosed arthritis, almost 50% (49.7%) of adults aged 65 years of age have been diagnosed[1].

There are different types of arthritis, including osteoarthritis (OA), rheumatoid arthritis (RA), ankylosing spondylitis, gout, and juvenile arthritis. More on each of these, below.

Osteoarthritis (OA)

Osteoarthritis (OA) is the most common form of arthritis and is a degenerative joint disease that results from a breakdown of the cartilage within a joint. This breakdown results in the bone actually changing, or remodeling in order to try and accommodate the lack of cartilage. The bone does this by producing bone overgrowth called osteophytes, or ‘bone spurs’. An osteophyte is a smooth, bony deposit that grows slowly over time, and often has no symptoms but can be painful if they impinge on nerves or affect the movement of the joint. It most commonly occurs in the hands, hips, and knees and changes usually develop slowly, and get worse over time. OA can cause stiffness, swelling and pain and in some cases it results in some people are no longer able to do daily tasks.

Rheumatoid Arthritis (RA)

Rheumatoid arthritis (RA) an autoimmune and inflammatory disease where the body’s immune system attacks healthy cells in the body, resulting in inflammation and painful swelling. It mainly attacks the joints in the hands, wrists, and knees, and often many joints at once. In a joint with RA, the lining of the joint becomes inflamed, causing damage to joint tissue and this damage is what results in chronic pain, difficulty with mobility and joint deformity.

Ankylosing Spondylitis (AS)

Ankylosing spondylitis (AS) is the most common form of a group of inflammatory arthritis called spondyloarthritis and is an autoimmune disease, which means it is caused by the body’s immune system attacking healthy tissue. AS leads to rigidity of the spine, and the sacroiliac (SI) joints which attach the pelvis (hips) to the base of the spine. Ankylosing’ means “fusing” and spondylitis’ means “inflammation of the spine”. AS

Gout

Gout is a form of inflammatory arthritis that usually affects one joint at a time, (often the big toe joint. In this form, symptoms wax and wane, with times where there are symptoms being known as ‘flares’. Gout is associated with high levels of uric acid, which can also contribute to kidney stones, so controlling the level of uric acid through diet may be part of treatment. This includes keeping levels of purine-containing foods constant (not eliminating them). Repeated bouts of gout can lead to ‘gouty arthritis’; a worsening form of arthritis.

Juvenile (childhood) Arthritis

The most common type of childhood arthritis is ‘juvenile idiopathic arthritis’ (JIA), which is also known as juvenile rheumatoid arthritis (J-RA) which can cause permanent physical damage to joints and make it hard for the child to do everyday tasks such as walking, or even getting dressed by themselves.

Arthritis, Other Conditions and Quality of Life

Arthritis in adults is more common in people with other chronic health conditions, including;

– 31% of those with arthritis are obese
– 47% of those with arthritis have diabetes
and
– 49% have heart disease [1].

This isn’t all that surprising given that all of these conditions are linked to different types of systemic inflammation.

Having any of these other chronic conditions â — along with arthritis makes it all the more difficult for people to enjoy life. The pain associated with arthritis may be a barrier to physical activity for those with heart disease[1] and those who are overweight or obese already struggle with having little energy to be active and the pain of arthritis only makes that more difficult [2].

That said, physical activity â — whether it is simple aerobic activity like walking or swimming or strength / resistance training can benefit all of those conditions, so reducing the pain in arthritis is an important key to being able to be active, and have a much improved quality of life.

Reducing Inflammation – the role of an Anti-inflammatory Protocol

Many people when they get diagnosed with arthritis want to know if there is an “arthritis diet”. There is no diet specific to people diagnosed with arthritis, except perhaps a diet that lowers uric acid in those with gout, however eating in such a way as to lower inflammation can help a great deal!

I have offered an Anti-Inflammatory Protocol Package for close to ten years and recently completely updated the materials that I used to teach it, as well as the 27 pages of handouts I provide, in light of the most current research.

The goal of the Anti-Inflammatory Protocol is simple; to reduce stiffness and pain by lowering inflammation. It is divided into 3 sessions of an hour each and covers everything from the components of foods that contribute to inflammation; from grains and seed oils, to otherwise ‘healthy’ foods and even that may make symptoms worse and why, as well as those that are fine to use. I provide teaching on “nightshades” and the reasons why these should be limited and provide a list of fruits, vegetables and spices are in this family. I teach about the effect of alcohol and sugar alcohols used as sugar-substitutes and their effect on inflammation, as well as different gums and thickeners that are commonly used in many food products and that can contribute to inflammation.

My purpose in offering this package is to help those diagnosed with arthritis (and other inflammatory conditions) to improve their quality of life.

As well, I understand what it’s like to live with osteoarthritis (which I was diagnosed with in my 20’s) and the need to reduce symptoms, through diet whenever possible.

More Info?

You can find out more about the Anti-Inflammatory Protocol Package that I offer by clicking here and if you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

References

Barbour KE, Helmick CG, Boring MA, Brady TJ. Vital signs: prevalence of doctor-diagnosed arthritis and arthritis-attributable activity limitation — United States, 2013—2015. Morb Mortal Wkly Rep. 2017;66:246—253. DOI: http://dx.doi.org/10.15585/mmwr.mm6609e1External.
Hootman JM, Murphy LB, Helmick CG, Barbour KE. Arthritis as a potential barrier to physical activity among adults with obesity—United States, 2007 and 2009. Morb Mortal Wkly Rep. 2011;60(19):614—618. PubMed PMID: 21597454

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July 17, 2019July 17, 2019

Three Ways to Put Type 2 Diabetes into Remission

According to the scientific literature to date, there are three ways of putting type 2 diabetes into remission, but an article that was widely circulated on social media earlier this week implied that a ketogenic diet ‘cures’ type 2 diabetes.

The article was titled “What If They Cured Diabetes and No One Noticed?”[1] and said;

“So you’d think that if someone figured out a way to reverse this horrible disease, there would be big bold headlines in 72-point type. You’d think the medical community, politicians and popular press would be shouting it from the rooftops.

Guess what? Someone did. Yet it appears no one noticed.

The cure was simple — so simple, in fact, that it involved no medication, no expensive surgery and no weird alternative supplements or treatments.

What was this miracle intervention? Diet. Specifically, the ketogenic diet.”

The author is entitled to hold the above opinion and to express it, however in my opinion, a ketogenic diet does not “reverse diabetes” — it does not “cure” it. It is one of three scientifically documented ways to put the disease into remission. More on that below.

The distinction between “reversing diabetes” and “reversing the symptoms of diabetes” is very important, and more than a matter of semantics. In an article I posted last year titled The Difference Between Reversal and Remission of Type 2 Diabetes, I wrote that;

“Reversal” of a disease implies that whatever was causing it is now gone and is synonymous with using the term ”cured”. In the case of someone with Type 2 Diabetes, reversal would mean that the person can now eat a standard diet and still maintain normal blood sugar levels. But does that actually occur? Or are blood sugar levels normal only while eating a diet that is appropriate for someone who is Diabetic, such as a low carbohydrate or ketogenic diet, or while taking medications such as Metformin?

If blood sugar is only normal while eating a therapeutic diet or taking medication then this is not reversal of the disease process, but remission of symptoms.”

I believe that claiming that a keto diet ‘cures diabetes’ or ‘reverses the disease’ does the public a disservice:

Firstly, it implies that there is simple, free ‘cure’ that will work for everybody. As I outline below; some people are able to achieve partial or complete remission of their symptoms following a keto diet, and others are not.

Secondly, it implies that there is a simple, free ‘cure’ available, but that it is being ‘withheld’ for some reason — either because doctors don’t know about or are afraid what colleagues might think, or because the agricultural and pharmaceutical industries have ‘big bucks to lose’ by people limiting their intake of bread, pasta and insulin.

There is no question that physicians (and all clinicians) need to be selective about recommending a keto diet for their patients / clients and to be able to document from the literature that it is safe, effective and best clinical practice for the condition for which it is recommended, and appropriate for the individual.

While falling markets for specific types of food products and drugs certainly have an impact on the economics of both the agricultural industry and pharmaceutic industry, it comes across like a ‘conspiracy theory’ to imply there is a ‘cure’ available out there, but that the public is being ‘denied’ access to it by “big food” and “big pharma”.

Finally, it implies that if people are unable to ‘reverse their diabetes’ and get ‘cured’ following a keto diet, that it is their fault; they mustn’t have done it properly. Even if we substitute the terms and say instead “put their diabetes into remission” or “reverse the symptoms of diabetes”, it is unreasonable and unfair to assume that everyone will be successful in doing so, and if they aren’t, the responsibility falls on them.

There is no “one-sized-fits-all-diet” that is good for everybody, nor is there a “better” dietary means to achieve remission of type 2 diabetes. As I will elaborate on below, there are 3 ways to put the symptoms of type 2 diabetes into remission, with two of them being dietary, and some might prefer one over the other for a variety of reasons. The one that they want to adopt and ‘stick with’ will be the one that will work best for them.

Virta Health Data

The on-going study from the Virta Health has had over 200 adults ranging in age from 46-62 years of age in the intervention group following a ketogenic diet for the last two years, so far. At the one year mark, participants in the ketogenic diet group lowered their glycated hemoglobin (HbA1c) to 6.3% (from 7.7% at the beginning of the study) — with 60% of them putting their type 2 diabetes into remission based on HbA1C levels >=6.5% (American Diabetes Association and Diabetes Canada guidelines). HbA1C rose slightly to 6.7% at two years. The keto group did considerably better than the ‘usual care group’ whose average HbA1C actually rose to 7.6% at one-year (from 7.5% at the beginning of the study), and rose again to 7.9% at two years [3].

Fasting blood glucose of the intervention group following a keto diet increased slightly from 127 mg/dl (7.0 mmol/L) at one year to 134 mg/dl (7.4 mmol/l) at two years, which was considerably better than the usual care group, whose fasting blood glucose was 160 mg/dl (8.9 mmol/L) at one-year and 172 mg/dl (9.5 mmol/L) at two years [3].

The data so far demonstrates that a well-designed keto diet can be a very effective means of reversing the symptoms of type 2 diabetes, and that it is more effective than what was ‘standard care’ (prior to the new ADA guidelines), but it is by no means a ‘cure’.

Dr. Stephen Phinney and the research team at Virta Health have written on the Virta Health website [3];

“A well-formulated ketogenic diet can not only prevent and slow down progression of type-2 diabetes, it can actually resolve all the signs and symptoms in many patients, in effect reversing the disease as long as the carbohydrate restriction is maintained.” [2]

That is, the Virta researchers state that a well-designed keto diet can resolve the signs and symptoms of the disease in many people, which “in effect” (i.e. ‘is like’) reversing the disease — as long as the carbohydrate restriction is maintained. They don’t promote the diet as a ‘cure’, but as an effective treatment, which it is.

There is no question that Virta’s results are impressive — so much so that their studies have been included in the reference list of the American Diabetes Association’s (ADA) new Consensus Report of April 18, 2019, where the ADA included adopted the use of both a low carb and very low carb (ketogenic) diet (20-50 g of carbs per day) as one of the management methods for both type 1 and type 2 diabetes in adults. You can read more about that here.

In fact, the ADA said in that report that;

”Reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia*’

* blood sugar

…but a keto diet is not a ‘cure’ for type 2 diabetes.

At this present time, there is no cure for diabetes. There are, however three documented ways to put type 2 diabetes into remission;

a low calorie energy deficit diet [4,5,6]
bariatric surgery (especially use of the roux en Y procedure) [7,8]
a ketogenic diet [3]

Final Thoughts…

I believe that based on what has been published to date, it is fair to say that a well-designed ketogenic diet can;

prevent progression to type 2 diabetes, when adopted early in pre-diabetes
slow down progression of type 2 diabetes
resolve the signs and symptoms of the type 2 diabetes
serve in effect like reversing the disease, provided carbohydrate restriction is maintained

…but to claim that a keto diet ‘cures’ type 2 diabetes is simply incorrect.

A ketogenic diet is a safe and effective option for those wanting to put the symptoms of type 2 diabetes into remission. So is a calorie restricted diet. The primary difference is in a calorie restricted diet, calories are drastically reduced in order to lose weight and feeling hungry is simply a side-effect that people come to expect. In a low carb or ketogenic diet, calories end up being substantially reduced as an inadvertent result of targeting protein and vegetables and adding sufficient healthy fat that comes along with that protein, or that are added to the vegetables to make them more interesting, while limiting carbohydrates. One isn’t better than the other; it is what is better suited to each individual.

More Info?

If you would like more information on using diet to seek to put the symptoms of type 2 diabetes into remission or for weight loss, I’d be glad to help.

You can learn more about my services under the Services tab or in the Shop.

If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

References

Steel, P, “What If They Cured Diabetes and No One Noticed? – if the ketogenic diet can reverse diabetes, why isn’t your doctor recommending it?”, The Startup, July 13 2019, https://medium.com/swlh/what-if-they-cured-diabetes-and-no-one-noticed-keto-diet-ketogenic-virta-study-d49c195bf8f5
Phinney S and the Virta Team, Can a ketogenic diet reverse type 2 diabetes? https://blog.virtahealth.com/ketogenic-diet-reverse-type-2-diabetes/
Athinarayanan SJ, Adams RN, Hallberg SJ et al, Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-year Non-randomized Clinical Trial. preprint first posted online Nov. 28, 2018;doi: http://dx.doi.org/10.1101/476275.
Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia2011;54:2506-14. doi:10.1007/s00125-011-2204-7 pmid:21656330
Steven S, Hollingsworth KG, Al-Mrabeh A, et al. Very low-calorie diet and 6 months of weight stability in type 2 diabetes: pathophysiological changes in responders and nonresponders. Diabetes Care2016;39:808-15. doi:10.2337/dc15-1942 pmid:27002059
Lean ME, Leslie WS, Barnes AC, et al. Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. Lancet2018;391:541-51.
Cummings DE, Rubino F (2018) Metabolic surgery for the treatment of type 2 diabetes in obese individuals. Diabetologia 61(2):257—264.
Madsen, L.R., Baggesen, L.M., Richelsen, B. et al. Effect of Roux-en-Y gastric bypass surgery on diabetes remission and complications in individuals with type 2 diabetes: a Danish population-based matched cohort study, Diabetologia (2019) 62: 611. https://doi.org/10.1007/s00125-019-4816-2

July 14, 2019July 15, 2019

Trouble-shooting Ongoing Constipation on a Low Carb Diet

Constipation is one of the most common problems that people face, with between 2 and 28% of the population in Western countries reporting having this [1-3]. In 2007 in the United States, 19.4% of people reported problems with chronic constipation[4] and in Canada between 15% and 27% of people reported having sought health care support for chronic constipation in 2001 [5].

Defining Constipation

The term “constipation” means different things to different people. For some it simply means they don’t pass their stools (feces) often enough, and for others it means that when they do, their stools are hard, difficult to pass, may cause lower abdominal discomfort, or feel like they “still have to go” afterwards (incomplete evacuation).

What is considered a ‘normal range’ in the number of bowel movements per week varies considerably; from anywhere from 3 – 21 times per week, provided the stools are soft and easy to pass, but not loose or unformed.

For some people, having bowel movements 3 times per week may be normal, as long as their stools aren’t hard, dry or compact and there is no abdominal discomfort. For others, 3 times per day (21 times per week) may also be considered fine, provided the stools aren’t unusually loose. There are many factors that can contribute to chronic constipation; including some medications that people take, inadequate fiber or the wrong kind of fiber, insufficient hydration (not drinking enough water, especially when its hotter out, or exercising), high levels of estrogen and progesterone when a woman is pregnant, or disorders such as Irritable Bowel Syndrome (IBS) and diverticulosis.

The Causes of Chronic Constipation

People often think (or are told) that if they are constipated, they just need to eat more fiber, but in some cases increasing fiber from certain sources such as grains may make the problem worse. For example, some people are wheat sensitive, but not gluten-intolerant (i.e. not Celiac). That is, they are sensitive to wheat only, but not rye or barley (which also contain gluten). Others have something called non-celiac gluten sensitivity which resolves when gluten is eliminated from the diet, yet don’t test positive for Celiac disease. These people feel better when they avoid grain-based carbs, and may opt instead for eating nutritiously-dense starchy vegetables, such as winter squash or yam, for instance. Since a low-carb diet is non-grain-based, people who experience chronic constipation due to wheat intolerance or non-celiac gluten sensitivity will start to feel considerably better eating this way. The problem may be that for those with non-celiac gluten sensitivity, other sources of gluten, such as those found in malt vinegar or low carb beer may continue to cause them symptoms.

Many people who try a “low-carb” or “keto” diet on their own often complain of being constipated and this may be for a number of other reasons. They may be taking a medication that causes constipation as a side-effect, they may not don’t drink enough water, or it may be the result of something else.

Inadequate Hydration

I would estimate that ~80% of the people that I assess in my office have observable signs that they are aren’t drinking enough water, so this is something I would recommend most people to consider as a possible contributor to chronic constipation.

The idea that everybody needs to drink “8 glass of water per day” is a fallacy; everyone’s need for water is different. A good rule of thumb to know if you are dehydrated is just to look in the mirror. If your lips are dry and wrinkled, then you probably should aim to increase your water intake. When your lips are plump and without deep lines, you’ve probably had sufficient amount. Water is best, as coffee and tea act as a mild diuretic. They won’t dehydrate you, but you will pass the water contained in them more rapidly.

If you don’t really like plain water, a Sodastream® that enables you to make carbonated water at home may be the answer. My clients know that there is always a bottle of it on my desk, as that is how I make sure to drink enough water. A twist of lime or lemon makes a nice treat too!

What about Getting Enough Fiber?

In Canada, dietary recommendations for dietary fiber intake varies with age and gender. Men under the age of 50 years are recommended to take in 38 gm / day of dietary fiber, and men over 50 years to take in 30 gm / day. Women under 50 years old are recommended to take in 25 gm of fiber per day and over 50 years, 21 gm per day [6].

In the US, fiber intake recommendations from the Institute of Medicine range from 19 grams to 38 grams per day, depending on gender and age [7].

While people generally think of “healthy whole grains” as good sources of fiber, many are not. For example, medium grain brown rice only has 3.4 g of fiber per 100 g, whereas wild rice (which is actually a grass and not a grain) has 6.2 g of fiber per 100 g [8]. Many vegetables and fruit such as avocado and berries are excellent sources. More on that below.

Two Kinds of Fiber — soluble and insoluble

There are two kinds of fiber; insoluble and soluble.

Insoluble fiber is what most people think about when they think of ”roughage” needed to form stool and prevent constipation. It helps form the bulk of the stool. Insoluble fiber is naturally present in the outside of grains, such as whole grain wheat and the outside of oats and is also found in fruit, legumes (or pulses) such as dried beans, lentils, or peas, some vegetables, and in nuts and seeds. Many of these are eaten on a low carb diet and can provide the recommended amount of fiber (more on that below).

Soluble fiber forms a gel’ in the intestine and binds with fatty acids. It slows stomach emptying and helps to make people feel fuller for longer, as well as slow the rate that blood sugar rises, after eating. Soluble fiber absorbs water in the gut, and helps to form a pliable stool. Soluble fiber is found on the inside of certain grains, such as oats, chia seeds or psyillium, as well as the inside of certain kinds of fruit such as apple and pear.

For those eating a low carb diet, getting enough fiber is not that difficult. Here are a few examples of the fiber content of foods that can be eaten;

Avocado — Surprisingly, avocado which is an excellent source of vegetable fat, is also high in fiber, having more than 10 gm fiber per cup (250 ml). Avocado grown in Florida which are the bright green, smooth-skinned variety have more insoluble fiber than California avocado, which are the smaller, darker green, dimpled variety.
Berries — Berries such as blackberries and raspberries are an excellent source of antioxidants, but also have 8 gm fiber per cup (250 ml).
Coconut — Fresh coconut meat has 6 gm of net carbs per 100 grams of coconut, but also packs a whopping 9 gms of fiber and is a very rich source of fat (33 gms per 100 gm coconut). It can be purchased peeled, grated and sold frozen in many ethnic stores or in the ethnic section of regular grocery stores.
Artichoke — Artichoke is a low-carbohydrate vegetable that is delicious boiled and it’s leaves dipped in seasoned butter. Surprisingly, one medium artichoke has over 10 gm of fiber.
Okra — Okra, or lady fingers’ is a staple vegetable in the South Asian diet and is commonly eaten in the Southern US. Just one cup of okra contains more than 8 gm of fiber.
Brussels Sprouts — These low-carb cruciferous vegetables are not just for Thanksgiving and Christmas dinner. Split and grilled on the BBQ with garlic, they are a sweet, nutty addition to any meal, packing almost 8 gm of fiber per cup.
Turnip — Turnip, the small white vegetable with a hint of purple is not to be confused with the pale beige, larger rutabaga. Turnip contains almost 10 gm of fiber per cup. It is delicious pickled with salt and one beet and is commonly eaten with Middle Eastern food.

Irritable Bowel Syndrome (IBS) and Diverticulosis

Unfortunately, in addition to the fact that 20-30% of people in the US and Canada experience chronic constipation, approximately 10-15% of the population have Irritable Bowel Syndrome (IBS) [9].

IBS is a functional disorder of the gastrointestinal (GI) tract â — which means there is no structural or biological abnormality that can be measured on routine diagnostic tests. These people often experience chronic constipation, sometimes alternating with bouts of diarrhea, as often experience abdominal pain and bloating, as well. You can read more about IBS here. As mentioned in the linked article, many people with IBS feel considerably better when they adopt a low-carb diet because they are no longer eating many of the foods that underlie their symptoms such as grains, milk and fruit, other than berries. Unfortunately, even after adopting a low carb diet about 15- 20% of those diagnosed with IBS still have residual symptoms. I have years of experiencing working with those with IBS and offer a package as well as a one-hour teaching session that can help.

Another common problem is diverticulosis, which an estimated 50% of those over 50 years of age have. Diverticulosis is where your colon (large intestine) has small ”pockets” in it called diverticula, which can cause a number of symptoms including chronic constipation. Like those with IBS, many people with diverticulosis feel much better when they adopt a low-carb diet because they are no longer eating foods such as wheat, dairy products with lactose or high fructose fruit that used to contribute to their symptoms. The problem is that many of the low carb vegetables that are low in carbs and may be rich in fiber also may be contributing to their symptoms. So many of my clients have recently been diagnosed with diverticulosis, that I have recently added a one-hour teaching session that can be added to the end of a Complete Assessment Package, or taken as a stand-alone session to help.

Final Thoughts

In trouble-shooting constipation, I recommend that people ensure they are adequately hydrated, and that they remember to drink extra water when it’s hot out or when they’ve been ill.

Eating wide variety of low-carb veggies, including those listed above that are known to be high in fiber is also good. For those on a moderate low-carb diet (not a ketogenic diet), small amounts of yam or winter squash are other ways to get added nutrients and fiber.

Berries are a wonderful source of nutrients and anti-oxidants, can be enjoyed by those on a low-carb diet and are a wonderful source of fiber! Strawberries have 3g of fiber per cup and blackberries and raspberries have a whopping 8 g of fiber per cup, with blueberries paling in comparison with a mere 2.4 g of fiber (and are higher in carbs, too).

Of course, exercise as simple as a daily walk can often help people move their bowels and many people swear by their morning cup of coffee!

For those doing all of the things above and still experiencing chronic constipation, it may be time to rule out other possible causes such as Celiac disease, or non-celiac gluten sensitivity, IBS, or diverticulosis.

I can help.

More Info?

If you would like more information about how I can help in this regard, you can find the various services I offer related to Food Sensitivities / Food Allergies, Celiac Disease, IBS and Diverticulosis under the Services tab, and in the Shop.

If you have questions please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

References

Higgins PDR, Johanson JF, Epidemiology of constipation in North America: a systematic review, The American Journal of Gastroenterology 99(4); 750—759, 2004.
Corazziari E, Definition and epidemiology of functional gastrointestinal disorders, Best Practice and Research: Clinical Gastroenterology, 18 (4); 613—631, 2004.
Harris LA, Prevalence and ramifications of chronic constipation, Managed Care Interface, 18 (8); 23—30, 2005.
Johanson JF, Kralstein J, Chronic constipation: a survey of the patient perspective, Alimentary Pharmacology and Therapeutics, 25(5); 599—608, 2007.
Pare P, Ferrazzi S, Thompson WG et al, An epidemiological survey of constipation in Canada: definitions, rates, demographics, and predictors of health care seeking, The American Journal of Gastroenterology, 96(11); 3130—3137, 2001.
Health Canada, Fiber, https://www.canada.ca/en/health-canada/ services/ nutrients/fibre.html
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes: Energy, Carbohydrates, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids. Washington, DC: National Academies Press; 2005
Source: US Department of Agriculture, Agricultural Research Service. 2014. USDA National Nutrient Database for Standard Reference, Release 27. Nutrient Data Laboratory Home Page, http://www.ars.usda.gov/ba/bhnrc/ndl.
Foundation for Gastrointestinal Disorders (IFFGD), https://www.aboutibs.org/facts-about-ibs/statistics.html

July 12, 2019April 23, 2021

What is IBS and Why Do Symptoms Improve on a Low Carb Diet?

Quite a few physicians that I know that recommend a low-carb diet to their patients have mentioned to me that those who had previously been diagnosed with Irritable Bowel Syndrome (IBS) and who suffered for years reported significant improvements within a short time of adopting the dietary changes and have asked me why. That is the topic of this article.

Prior to expanding my Dietetic practice to include this low carb division a little over 4 years ago, my main focus was on helping people who were dealing with food allergies and food sensitivities; including Celiac disease, Mast Cell activation disorder (MCAD) / histamine intolerance, fructose intolerance and Irritable Bowel Syndrome For many of my clients, it was the gastrointestinal (GI) symptoms that caused them to seek out my help in the first place.

What is IBS?

I have often thought of Irritable Bowel Syndrome (IBS) as the diagnosis that people receive when all the other possible options have been ruled out. For the most part, by the time people are told that they have IBS, they already know for sure that they don’t have Celiac disease or inflammatory Bowel Disease (IBD) such as Ulcerative Colitis or Crohn’s, and they don’t have diverticulosis â —as each of those diagnoses are confirmed after a colonoscopy and/or a biopsy, and are often supported with underlying blood test results.

What makes IBS different is that it is a functional GI disorder â — which means there is no structural or biological abnormality that can be measured on routine diagnostic tests.

Of course a person experiencing a bout of diarrhea or constipation, or abdominal pain does not mean that person has a GI disorder or disease. Those symptoms could be the result of a virus, bacteria, food-borne illness (“food poisoning”) or food sensitivities. Once these have been ruled out, if the symptoms recur over and over again over time, then investigation as to what else it could be is often begun.

How is IBS Diagnosed?

While many of the symptoms of IBS and Celiac disease can be quite similar, including diarrhea and abdominal pain and bloating, there are very specific indicators that a person may have Celiac disease that clinicians such as myself notice as evidence to request further testing. The first stage in ruling out Celiac disease is an ordinary blood test looking for an antibody to gluten. If that comes back positive, then the person is referred to a Gastroenterologist for an endoscopy. If the blood test is negative, the next step may be for the person to be scheduled for a colonoscopy.

A colonoscopy which is where the inside of the large intestine (colon) is examined using a flexible probe about 1/2″ in diameter that’s fitted with a light and telescopic camera at one end and endoscopy is where a fine, flexible probe fitted with a light and telescopic camera is inserted via the mouth to view the esophagus, stomach and the upper part of the small intestine.

Celiac disease will be ruled out or confirmed using endoscopy, as the upper small intestine is where the damage to the villi (little hair-like projections on the wall that increase the surface area in order to help absorb nutrients from food) will be visible, or not.

A colonoscopy enables the Gastroenterologist to see what the lining of walls of the colon look like and to look for physiological signs of diverticulosis (little bulges or “pouches” in the colon) or signs of inflammation and damage consistent with Inflammatory Bowel Disease (IBD), such as Ulcerative Colitis or Crohn’s and to rule out colon cancer.

If the endoscopy and colonscopy come back normal, the person is often told that their symptoms of diarrhea or constipation (or both alternating), flatulence (“gas”), bloating, abdominal pain or cramping, mucous in the stool is Irritable Bowel Syndrome (IBS).

Prevalence of IBS

According to the International Foundation for Gastrointestinal Disorders (IFFGD), approximately 10-15% of the population have IBS; with 40% having a mild form, 35% having a moderate form, and 25% having severe IBS. While many people think of IBS as being a woman’s health issue, 35% to 40% of people with IBS are men and 60-65% are women [1].

IBS is so common, that it is estimated that 12% of all visits to primary care providers (family doctors) is related to symptoms of IBS [1].

Physicians will sometimes suggest their patients try following a “low-FODMAP diet” but since IBS is so common, there are many different diets called by this name that differ significantly. Even if the doctor provides guidance as to which low-FODMAP diet they should follow, people often eliminate a whole host of foods and wind up eating a very limited diet, with no way of knowing which food they stopped eating actually helped.

Why Eating a Low-Carbohydrate Diet often Improves IBS Symptoms?

A low-FODMAP diet eliminates sources of very specific carbohydrates that are fermented by the gut bacteria and that result in the increased gas production that underlies the classic IBS symptoms of abdominal pain and bloating, and the water flooding into the intestine in response to these fermented carbohydrate is what causes the very common symptom of diarrhea. The constipation results when the contractions of the colon are impaired, resulting in the stool sitting longer in the colon resulting in more and more of the water being re-absorbed.

When people eat a low-carb diet, they either eliminate or greatly reduce sources of fructose (the sugar found in fruit and many processed foods, especially processed condiments like ketchup) and significantly reduce one of the key sources of fructans (inulin) found in wheat; which is a highly fermentable carbohydrate. Galactans, another fermentable carbohydrate found in beans, lentils and legumes such as soy is also eliminated or greatly reduced — which is why people with IBS feel so much better after beginning eating a low-carb diet!

Before I taught a low-carbohydrate approach, I used to have people take the IBS Package before the Complete Assessment Package, so we could find out what foods underlie their unpleasant symptoms and eliminate them before I designed their Meal Plan. Now, if they are planning to adopt a lower carb lifestyle anyway, then I recommend they don’t take the IBS Package, as it may not be necessary. I recommend focus on them adopting a diet that greatly reduces the sources of the fermentable carbohydrates mentioned above, plus a few more that I tell them about and see how they feel. If their symptoms are gone, then there is no reason for them to take the IBS Package! If however, they are feeling quite a bit better, but still have residual symptoms, then I suggest they take the IBS Package so that we can systematically determine what other non-FODMAP foods are contributing to them feeling unwell.

More Info?

If you would like more information about the IBS Package, you can find that under Services tab of my affiliate website, BetterByDesign Nutrition Ltd. and if you’re interested in the low-FODMAP teaching, you can find that in the Shop on that site.

Of course, if you have questions please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

References

Foundation for Gastrointestinal Disorders (IFFGD), https://www.aboutibs.org/facts-about-ibs/statistics.html

July 11, 2019July 16, 2019

Have You Been Diagnosed with Diverticulosis?

Have you recently been told by your General Practitioner (CP) or gastroenterologist that you have “diverticulosis” and wonder how you should be eating differently to keep it from getting worse?

What is “diverticulosis”?

Diverticulosis is where your colon (large intestine) has small “pockets” in it called diverticula which can cause a number of symptoms or in some people, no symptoms at all.

Diverticula can vary in number from one to literally hundreds. Generally, diverticula increase in number and size over time and range in size from 0.5-1 cm (0.2-0.4 inch) in diameter to 2 cm (0.8 inch)[1]. Diverticulosis occurs in about 5% of adults younger than forty years old, but rise to at least 50% of those older than sixty, with 65% of those who older than 85 having diverticulosis[1].

These little pouches were once thought to be cause by a diet that was too low in fiber[1] which caused the stools to move too slowly though the colon, resulting in constipation. Based on this “fiber hypothesis”, the remedy was thought to be to eat a diet high in fiber; including whole grain bread, unprocessed wheat bran, porridge and fruit. For the last 50 years or so, increased fiber intake has been the recommendation for treatment of diverticulosis, including by the GI Society of Canada and the American Gastrolenterology Association recommends at least 25 g of fiber per day[2,3]. It was thought that increased fiber would increase the volume of the stool and thus require less straining to move the bowels and prevent weakening of the bowel wall, reducing the occurrence of these “pouches”. Unfortunately, several recent studies have shed doubt on the “fiber hypothesis” [4-8].

Not only did a 2012 study find no association between a low fiber diet and diverticulosis [9], the study found that increasing total fiber intake in the form of grains, insoluble fiber and soluble fiber actually increased the prevalence of diverticulosis!

“People with the lowest fiber intake were 30% less likely to develop diverticula than people whose diets included the most fiber.” [9]

Subsequent studies have either found no association between the amount of fiber intake and diverticulosis [10] or that there was no association between diverticulosis and constipation symptoms [11].

These findings left researchers and clinicians with little evidence for continuing to recommend a high fiber diet in diverticulosis, but no alternative options.

ADDENDUM (July 17 2019): There are a number of hypotheses as to what causes diverticulosis with many thinking it could be related to colonic aging weakening of the smooth muscle bands, motor dysfunction, increased luminal pressure, as well of lack of dietary fiber.

Eating foods with soluble and insoluble fiber and drinking sufficient fluid is good, however the source of that fiber is now thought to be important, as I will outline below.

Logical Hypothesis for Diverticulosis

A recent hypothesis is that the increased pressure in the colon that resulted from the intake of so much fiber; particularly the types of fiber that are easily fermented by gut bacteria is what weakens the colon wall, resulting in these ‘pockets’ or diverticula.

What seemed to add credibility to this hypothesis is that historically (prior to WWII) diverticula were seen in a specific region of the colon (proximal colon) in people in Asian countries, with the condition only affecting the right side. This has been explained by the high prevalence of lactose intolerance (inability to digest the sugar in milk and dairy) which exists in Asians. As well, the incidence of this right-sided diverticulosis has been lowest in European populations, where lactose intolerance is very low [12]. Similarly, in Western countries, most of the diverticula are on the left side of the colon, which is thought to be associated with the higher ingestion of wheat, compared historically to Asian countries [12].

Both lactose and the fructans in wheat are carbohydrates that are easily fermented by gut microbes and which results in high amounts of water being drawn into the colon, resulting in increasing pressure on the colon wall from the gas produced by the microbes, possibly leading to the creation of these diverticula.

Of interest, consumption of wheat in Japan and in South Korea has increased considerably since WWII and there is now a considerably higher incidence of left colon diverticula now being observed there, as well [12].

Use of a low-FODMAP Diet in diverticulosis

FODMAPS is an acronym for fermentable oligosaccharides, disaccharides, monosaccharides and polyols (sugar alcohols) which are the specific types of carbohydrate that are fermented by the gut bacteria, resulting in increased gas production, abdominal pain, bloating and either diarrhea and constipation or a combination of both. These are very similar symptoms as are observed in Irritable Bowel (IBS) Syndrome and a low-FODMAP diet has long been used to minimize the symptoms in IBS, and is now being used to reduce the same symptoms in diverticulosis.

It is thought that use of a low-FODMAP diet in those with diverticulosis may reduce the occurrence of diverticulitis; which is painful inflammation of these diverticula that often requires medical treatment ranging from antibiotics and pain medication, to bowel resection as is common in Inflammatory Bowel Disease (IBD), such as Ulcerative Colitis and Crohn’s disease.

I offer a Diverticulosis Option for those who want to have specific nutrition education to help them reduce their symptoms and lower the likelihood of their disease progressing to diverticulitis.

Even if you are already following a low-carbohydrate diet and not eating wheat, foods with lactose or fruit, it’s important to know that there are a number of low carbohydrate vegetables that also contain some of these fermentable carbohydrates, as do many of the sugar alcohols many people following a low carb diets use. Reducing the intake of these specific vegetables and sticking to sweeteners that are low FODMAP can greatly help!

More Info

If you would like a Meal Plan designed just for you in light of your diagnosis, as well as specific nutrition education services on how to minimize the symptoms of diverticulosis and lower the likelihood of it progressing to diverticulitis, please click on the Diverticulosis Option, under the Services tab to learn more.

If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

References

GI Society, Canadian Society of Intestinal research, https://badgut.org/information-centre/a-z-digestive-topics/diverticular-disease/
Painter NS, Diverticulosis of the Colon and Diet. Br Med J. 1969 Jun 21;2(5659):764-5.
American Gastroenterological Association. A Patient Guide: Managing Diverticulitis. Gastroenterology. 2015;149:1977—1978
Tan KY, Seow-Choen F. Fiber and colorectal diseases: separating fact from fiction. World J Gastroenterol. 2007;13:4161—4167.
Unlu C, Daniels L, Vrouenraets BC, Boermeester MA. A systematic review of high-fibre dietary therapy in diverticular disease. Int J Colorectal Dis. 2012;27:419—427.
Peery AF, Sandler RS. Diverticular disease: reconsidering conventional wisdom. Clin Gastroenterol Hepatol. 2013;11:1532—1537.
Tursi A, Papa A, Danese S. Review article: the pathophysiology and medical management of diverticulosis and diverticular disease of the colon. Aliment Pharmacol Ther. 2015;42:664—684.
Elisei W, Tursi A. Recent advances in the treatment of colonic diverticular disease and prevention of acute diverticulitis. Ann Gastroenterol. 2016;29:24—32.
Peery AF, Barrett PR, Park D, Rogers AJ, Galanko JA, Martin CF, Sandler RS. A high-fiber diet does not protect against asymptomatic diverticulosis. Gastroenterology. 2012;142:266—272
Peery AF, Sandler RS, Ahnen DJ, Galanko JA, Holm AN, Shaukat A, Mott LA, Barry EL, Fried DA, Baron JA. Constipation and a low-fiber diet are not associated with diverticulosis. Clin Gastroenterol Hepatol. 2013;11:1622—1627
Braunschmid T, Stift A, Mittlbí¶ck M, Lord A, Weiser FA, Riss S. Constipation is not associated with diverticular disease – Analysis of 976 patients. Int J Surg. 2015;19:42—45.
Uno Y, van Velkinburgh JC. Logical hypothesis: Low FODMAP diet to prevent diverticulitis. World J Gastrointest Pharmacol Ther. 2016;7(4):503—512. doi:10.4292/wjgpt.v7.i4.503

July 9, 2019July 9, 2019

Experts: WHO Draft Guidelines Excludes Key Facts and Studies

An analysis was published last week in the British Medical Journal which raised several important concerns about the World Health Organization (WHO)’s draft guidelines on fatty acids; including saturated fat.

The international group of 16 nutrition experts who wrote the paper are concerned as “many governments consider the WHO dietary guidelines to be state of the art evidence, translating them into regional and national dietary guidelines” [1].

In fact, this is exactly the case in Canada. The new Canada Food Guide that was just released on January 22, 2019 relied extensively on the WHO’s 2017 Guidelines for it’s policy regarding decreasing dietary saturated fatty acids (SFA), as indicated by the table below from pg. 5 of Health Canada’s Interim Evidence Update 2018 [2].

Pg 5 Health Canada’s Interim Evidence Update 2018 [2]

Regarding the significance of the WHO Guidelines, the authors wrote:

“These guidelines have potential health implications for billions of people, so the consistency of the science behind such recommendations and the validity of the conclusions are crucial”.

The authors state that the WHO, in their draft guidelines released in May 2018 “excluded some important aspects and studies” concerning evidence linking saturated fat intake and cardiovascular (CVD) risk.

“They [WHO] recommend reducing intake of total saturated fatty acids to less than 10% of total energy consumption and replacing with polyunsaturated fat and monounsaturated fat to reduce incidence of cardiovascular disease and related mortality. But this fails to take into account considerable evidence that the health effects vary for different saturated fatty acids and that the composition of the food in which they are found is crucially important.”[1]

The authors point out that the composition of the food in which the fatty acid is found has a substantial effect on lipid digestion, absorption, as well as the amount of emulsified fat that is found in the blood after a meal (postprandial lipemia), which “is an independent risk factor for cardiovascular disease.”[1]

The authors point out that recently there have been several meta-analyses of observational studies and randomized controlled trials (RCTs) that found that total saturated fat is NOT associated with coronary heart disease, cardiovascular disease, and all cause mortality (i.e. deaths). In addition they report that a Cochrane analysis found no significant association between reducing saturated fatty acids and total mortality, cardiovascular disease deaths, fatal and non-fatal myocardial infarction (MIs), stroke, coronary heart disease events, and coronary heart disease deaths.

Continued Reliance on Surrogate Endpoints

The authors note that the WHO draft guidelines continue, as they have in the past to (1) rely heavily on “surrogate endpoints” of the effect of dietary saturated fat intake on the level of lipid and lipoproteins in the blood — and (2) ignores the food source of the saturated fat.

They raise three key points;

1. Not all saturated fatty acids are equal; the amount and even the direction of the effects (raises or lowers) both surrogate and long term endpoints vary, depending on which fatty acid is involved.

2. Influence of the food source that the fatty acid is found in; the authors note that it has still not been determined whether any changes in blood lipoproteins translates into a lowering of cardiovascular risk and death, regardless of food source.

“Most trials included in the meta-analysis did not investigate whole food sources of saturated fat.”[1]

That is, the studies that WHO considered compared the effect of diets supplemented with fats rich in saturated fatty acids — not the effect of saturated fats in a specific food matrix.

One example of saturated fat in a whole food matrix cited in the paper is one of eggs; where there is “no association with coronary heart disease, and there is a reduced risk of stroke, and that randomized control trial data show that two eggs a day has beneficial effects on cardiovascular disease biomarkers“. (table 1, [1]).

3. Using LDL cholesterol concentration as a marker for cardiovascular disease risk. As I’ve written about in several previous articles, the authors note that the degree to which LDL particles are atherosclerotic is determined by, among other things, their size.

“Small and medium LDL particles show the strongest association with risk of cardiovascular disease, whereas large particles show no association.” [1]

in fact, the authors point out as I did in a recent article about red meat and white meat “raising cholesterol”, that a rise in serum LDL cholesterol concentration from total saturated fat consumption has been linked to a parallel increase in particle size “so it might not translate into an
increased risk of cardiovascular disease.”[1]

Excluding Observational Studies and Prospective Cohort Studies

The authors point out that the WHO draft guidelines exclude two types of studies from consideration; observational studies and prospective cohort studies because they argue that the quality of the evidence is lower than from
analyses of RCTs, and that it was not possible to assess the potential differential effects of replacing saturated fatty acids with different nutrients.

The problem with this is that (1) observational studies enable assessing the association between saturated fat and cardiovascular disease rather than simply looking at the association between surrogate endpoints” (i.e. saturated fat and LDL-c) and (2) observational studies enable examining of the actual foods that people eat, rather than just individual nutrients, as

“Longstanding evidence indicates that the food matrix is more important than its fatty acid content for predicting the effect of a food on risk of coronary heart disease.”

The authors concluded;

“A recommendation to reduce intake of total saturated fat
without considering specific fatty acids and food sources is not
evidence based; will distract from other more effective food-
based recommendations; and might cause a reduction in the
intake of nutrient dense foods that decrease the risk of
cardiovascular disease, type 2 diabetes, other serious
non-communicable diseases, malnutrition, and deficiency
diseases and could further increase vulnerability to nutrient
deficiencies in groups already at risk.

Final thoughts

This analysis adds a critical academic “voice” to the concern of limited saturated fat intake which may translate a reduction in the intake of nutrient-dense whole foods.

In fact, this was precisely the concern that I raised in my recent article about the Canada Food Guide “Snapshot” which came out at the end of June and which linked an image of ultra-processed foods with the message “limit foods high in sodium, sugars or saturated fat”. After all, meat is high in saturated fat and cheese is high in saturated fat and sodium, but are these really the types of whole, real foods that Canadians should be advised to limit?

More Info?

If you would like more information about choosing whole, real food and limiting ultra-processed foods, I can help.

You can learn more about my services under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd

References

Astrup A, Bertram HCS, Bonjour J-P et al, WHO draft guidelines on dietary saturated and trans fatty acids: time for a new approach? BMJ 2019; 366: l4137 doi: 10.1136/bmj.l4137
Health Canada. Food, Nutrients and Health: Interim Evidence Update 2018. Ottawa: Health Canada; 2019.

July 2, 2019

Focus on Limiting Ultra Processed Food Not Saturated Fat & Sodium

Note: This article is a combination of a Science Made Simple article, with the references below and an editorial which provides my opinion.

Dietary advice â — especially National Dietary Guidelines ought to give clear, consistent messages. It would seem that the new Canada Food Guide ‘snapshot’ outlined in the previous article may inadvertently cause considerable confusion as to which foods are healthy and which are not.

The new Canada Food Guide ‘snapshot’ released last week shows a photo of ultra-processed products as foods to avoid, yet the label beneath the photo reads “limit foods high in sodium, sugars or saturated fat” (see circled part of photo, below).

In fact, when the image of these processed foods is clicked on the Health Canada website, it brings the reader to a page listing the “Benefits of Limiting Highly Processed foods” and has paragraphs below for Sodium, Sugars, and Saturated Fat.

In my opinion, this conflates two issues.

Advising people to limit ultra-processed food is not the same as advising them to limit saturated fat, sodium and sugar.

There are many whole unprocessed foods and minimally processed foods such as meat, eggs, cheese, yogourt, olives and berries that have sustained humans through thousands of years of history that contain these elements and are unlikely to be responsible for our current epidemics of obesity, diabetes, hypertension and cardiovascular disease that we now face.

As mentioned in an earlier article about distinguishing between food and food-like products there is a big difference between the three categories of food as defined by the NOVA food classification system [2,3,4]. Unprocessed Foods such as meat, chicken, fish and eggs are whole, real food in their original state and Minimally Processed Foods such as cheese, yogourt or pickled and cured fish or meat or olives are foods that have been preserved in some fashion by curing, smoking or soaking in brine. Foods such as meat, eggs, cheese and olives may be high in saturated fat or sodium but have been part of the human diet for thousands of years without compelling evidence that these pose a risk to human health.

It may be helpful to recommend that people consume pickled, cured meat and fish in smaller quantities, not because these foods are high in saturated fat or sodium, but because many are now made in less traditional ways that involve the use of chemical additives.

The primary health concern that I see it is that Ultra Processed Foods is making up more than 50% of the Canadian (and American) diet and really isn’t food at all. These are manufactured products made from a combination of refined carbohydrates (including sugar) and seed oils and are convenient, hyper-palatable and cheap — and displace real food from the diet. In fact, some of the most addictive foods available to us are ultra processed foods; including breakfast cereal, muffins, pizza, cheeseburgers, French fries and fried chicken — and desserts such as chocolate, ice cream, cookies and cake, as well as the soda we wash them down with [5]. These ultra processed foods are full of “empty calories” / have little nutritional value, and full of refined fats and refined carbs. It is for this reason ultra processed should be limited — not because it is high in saturated fat and sodium.

Even though fruit as we now know it has been bred over the last 50-100 years to be hyper-sweet, for metabolically healthy people there is still no comparison between natural whole fruit such as berries or an apple, and sugary pop. One is real, whole unprocessed food and the other is ultra processed.

In my opinion, it makes good sense for Health Canada to show a photo of ultra-processed foods as they had (above)with advice to limit them — but because they are ultra processed, not because they are high in saturated fat or sodium.

Shifting the Focus off Saturated Fat Based on the Evidence

As covered in several previous article on this site, while research does indicate that dietary saturated fat raises low density lipoprotein cholesterol (LDL-cholesterol) in the blood, distinction in these studies isn’t made between the small, dense LDL sub-fraction which is atherosclerotic, and the large, fluffy LDL which is not. This recent study makes this distinction; demonstrating that saturated fat from red meat and poultry raises the large, fluffy LDL and cardio-protective HDL, but not the small dense (atherosclerotic) LDL.

Epidemiological studies that do exist provide a very mixed picture of any possible association between saturated fatty acids and cardiovascular disease (heart disease and stroke); with recent studies finding no association [6,7]. Even more compelling, the data from the Prospective Urban and Rural Epidemiological (PURE) Study which was the largest prospective epidemiological study to date involving many different countries found that dietary saturated fat was actually beneficial; with those who ate the largest amounts of saturated fat having significantly reduced death rates and that those that ate the lowest amounts of saturated fat (6-7% of calories) had increased risk of stroke [8].

In addition, according to the Canadian Heart and Stroke Foundation position statement titled ”Saturated Fat, Heart Disease and Stroke” released in September 2015 [9], different saturated fatty acids (e.g. lauric, stearic, myristic and palmitic acids) have different effects on blood cholesterol, so we can’t simply lump all saturated fats together.

Focus on Where Change is Needed

I believe that national guidelines such as Canada’s Food Guide should focus on eliminating ultra-processed foods from the diet because these form almost half of caloric intake with little nutrients and displace real, whole nourishing food from the diet.

This makes good sense.

In my opinion, the linking of ultra processed foods to saturated fat and sodium as has been done in this most recent Canada Food Guide ‘snapshot’ will end up confusing the public that things like fried chicken and cheese are both equally unhealthy because they are high in saturated fat and salt.

It would be far more helpful to highlight the benefits of whole, unprocessed foods and minimally processed foods while encouraging the public to limit ultra processed foods.

More Info?

If you would like more information about limiting ultra-processed foods, while including whole, real foods (plant-based and animal-based), I can help.

To your good health!

Joy

You can follow me on:

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

References

Health Canada Snapshot: https://food-guide.canada.ca/en/?utm_source=canada-ca-foodguide-en&utm_medium=vurl&utm_campaign=foodguide
Moubarac JC, Batal M, Martins AP, Claro R, Levy RB, Cannon G, et al. Processed and ultraprocessed food products: Consumption trends in Canada from 1938 to 2011. Can J Diet Pract Res. 2014 Spring;75(1):15-21.
Monteiro CA, Moubarac J-C, Cannon G., Ng SW, Popkin B. Ultra-processed products are becoming dominant in the global food system. Obes Rev. 2013
Moubarac JC. Ultra-processed foods in Canada: consumption, impact on diet quality and policy implications. Montréal: TRANSNUT, University of Montreal; December 2017Nov;14 Suppl 2:21-8. doi: 10.1111/obr.12107.
Schulte EM, Avena NM, Gearhardt AN (2015) Which Foods May be Addictive? The Roles of Processing, Fat Content and Glycemic Load. PLoS ONE 10(2); e0117959. https://doi.org/10.1371/journal.pone.0117959
Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, et al. Association of dietary, circulating and supplement fatty acids with coronary risk: A systematic review and meta-analysis. Ann Internal Medicine 2014;160:398-406.
Sri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nut 2010;91(3):535-546.
Dehghan M, Mente A, Zhang X et al, The PURE Study — Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062
Heart and Stroke Foundation of Canada, Position Statement ”Saturated Fat, Heart Disease and Stroke, September 24, 2015, https://www.heartandstroke.ca/-/media/pdf-files/canada/position-statement/saturatedfat-eng-final.ashx

June 28, 2019June 28, 2019

CFG Snapshot – conflating Ultra-Processed Food and Whole, Real Foods?

Note: This article is a combination of a Science Made Simple article with references below and an editorial which provides my opinion.

This past Monday, Health Canada released the Canada’s Food Guide “snapshot”[1] in 28 languages which is not intended to be a stand-alone resource, but to be used as a tool to guide people to the Canada’s Food Guide website.

Canada’s Food Guide includes Canada’s Dietary Guidelines[2], the healthy eating recommendations[3], and all of the other resources and information on the Canada’s Food Guide website. Links to the guidelines and healthy eating recommendations are available in the References, below.

The “Snapshot”

Canada Food Guide "Snapshot" The main message of the “snapshot” is that “healthy eating is more than the foods you eat” â — which I think is an excellent way of summarizing the guidelines and recommendations and encouraging the public to want to learn more. From that point of view, the snapshot is successful in that it is likely to guide people to the website.

The main points on the Snapshot are;

Be mindful of your eating habits
Cook more often
Enjoy your food
Eat meals with others
Use food labels
Limit foods high in sodium, sugars or saturated fat*
Be aware of food marketing

Each of these points link to the sections of Canada’s Food Guide which address those points and in my opinion are all very helpful, except for one elaborated on below.

For example, under “Be mindful of your eating habits” is and encouragement for Canadians to be aware of;

how you eat
why you eat
what you eat
when you eat
where you eat
how much you eat

Being mindful can help you:

make healthier choices more often
make positive changes to routine eating behaviours
be more conscious of the food you eat and your eating habits
create a sense of awareness around your every day eating decisions
reconnect to the eating experience by creating an awareness of your:
- feelings
- thoughts
- emotions
- behaviours

As the Snapshot re-iterates, these are factors that are “more than the food you eat” and helpful for people to keep in mind.

My only issue with the “Snapshot” is the use of the image for “Limit foods high in sodium, sugars or saturated fat“, circled below.

Snapshot with “Limit foods high in sodium, sugars or saturated fat” circled

Here is that image by itself;

What I see when I look at this image is ultra-processed food (what I refer to in a previous article about the NOVA Food Classification System as “food-like products“.

These are not whole, real food, but are creations of the food industry that are intended to displace real, whole food from the diet (you can read more about that by clicking here). These are products that are “branded assertively, packaged attractively, and marketed intensively“.

In fact, this picture shows some of the most addictive foods listed in a 2015 study including chocolate, muffins, pizza, pastry and soda pop[4].

Fifteen Most Addictive Fast Foods

If the intention is for Canadians to “limit foods high in sodium, sugars and saturated fat” (not that I think there is solid, scientific evidence that healthy individuals necessarily need do so with all sources of saturated fat and sodium), in my opinion the following photo would be a more accurate reflection of that principle;

Real, whole foods that are high in sodium, sugars or saturated fat

Cheese, eggs and meat are high in saturated fat, and cured meats are high in sodium and saturated fat, and dates are certainly very high in sugar, but are not ultra-processed foods. Are these really foods that all Canadians should limit?

Is there irrefutable scientific evidence that healthy people should limit eggs, real cheese and whole fresh meats and poultry? Is it “unhealthy” for metabolically well folks to eat dates, which are very high in sugar? Or are we conflating whole, real food with ultra-processed food?

Using the NOVA food classification (outlined in the article linked above) that foods such as cheeses, cured meats and olives or anchovies are minimally processed foods that have been processed to make them ore durable and palatable, but they are not “ultra-processed foods” akin to hot dogs, pizza and pop!

I don’t believe that it is helpful to lump “ultra-processed food” and whole, real food that are high in saturated fat, sodium and sugar, together.

In my opinion, it would far better for the image in the Snapshot to read like this;

It makes good sense to advise Canadians to limit ultra-processed foodâ because they are high in refined carbohydrates and refined fats, and low in nutrient density â — but when ultra-processed food is labelled with the advice “limit foods high in sodium, sugar or saturated fat”, whole, real foods are conflated with food-like products which displace real, whole food from the diet.

Ultra-processed food is not the same as whole, real foods high in sodium, sugars or saturated fat

More Info?

If you would like more information about limiting ultra-processed foods, while including whole, real foods that are both plant-based and animal-based, I can help.

To your good health!

Joy

You can follow me on:

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

References

Health Canada Snapshot: https://food-guide.canada.ca/en/?utm_source=canada-ca-foodguide-en&utm_medium=vurl&utm_campaign=foodguide
Health Canada, Canada’s Dietary Guidelines, https://food-guide.canada.ca/en/guidelines/
Health Canada, Healthy Eating Recommendations, https://food-guide.canada.ca/en/healthy-eating-recommendations/
Schulte EM, Avena NM, Gearhardt AN (2015) Which Foods May be Addictive? The Roles of Processing, Fat Content and Glycemic Load. PLoS ONE 10(2); e0117959. https://doi.org/10.1371/journal.pone.0117959

June 24, 2019June 24, 2019

Only Half of People Have Newer Gene that Controls High Blood Sugar

The maintenance of blood sugar is very tightly regulated; with a healthy person’s blood glucose being kept in the range from 3.3-5.5 mmol/L (60-100 mg/dl) between meals, however a new study indicates that it may be newer variant of a gene that determines how well (or not) we are able to maintain these levels.

After eating, the higher levels of blood glucose that comes from the broken-down carbohydrate-based food triggers the release of insulin by the pancreas, which in turn causes the release of a special transporter called GLUT4. The GLUT4 transporter acts like a taxi to remove excess glucose from the blood, taking it into muscle and fat tissue.

Newer Variant of an Older Gene

Between meals and with the help of a special protein (CHC22) produced by the CLTCL1 gene, the GLUT4 glucose transporter remains inside muscle and fat, so that some blood sugar will continue to circulate.

A newly published study [1] by research specialists in population genetics, evolutionary biology, ancient DNA and cell biology analyzed the human genomes to understand how the gene producing CHC22 has changed over human history [2].

By examining the genomes of 2,504 people from the global 1000 Genomes Project compared to the genomes of ancient humans, researchers found that almost half of the people in various ethnic groups have a variant of CHC22 protein that is produced by a new variant of the CLTCL1 gene that became more common as humans moved away from being hunter-gathers and began farming and raising crops. Researchers postulate that the increased consumption of carbohydrates may have been the selective force driving this genetic adaptation.

Researchers found that the newer CHC22 variant of the gene is less effective at keeping the GLUT4 glucose transporter inside muscle and fat tissue between meals, which means that the transporter can more readily clear glucose out of the blood*.

As a result, people with the newer variant of the gene will have lower blood sugar than those with the older variant of the gene.

“The older version of this genetic variant likely would have been helpful to our ancestors as it would have helped maintain higher levels of blood sugar during periods of fasting, in times when we didn’t have such easy access to carbohydrates, and this would have helped us evolve our large brains”[2] — lead author Dr Matteo Fumagalli

*Note: It’s important to keep in mind that only GLUT4 transporters are insulin-dependent. There are other glucose transporters that allow glucose into the cell that don’t involve insulin, such as the GLUT1 transporter that works on a concentration gradient. That is, the effect of this gene is not on all glucose regulation, but only glucose regulation in adipose and muscle cells that use GLUT4 transporters.

The higher carbohydrate diets that came as a result of the advent of agricultural meant that this newer variant of the gene could be advantageous, as it moves the excess blood sugar from the blood into the muscle and fat tissue and having the older variant of the gene may make people more likely to develop Diabetes and may also make worse the insulin resistance that underlies the process of developing Diabetes.

“People with the older variant (of the gene) may need to be more careful of their carb intake, but more research is needed to understand how the genetic variant we found can impact our physiology”[2] — co-author Dr. Frances Brodsky

Along with the 2015 study from Israel[3] that demonstrated substantial differences in blood glucose response between both healthy individuals and those with Diabetes predictable by their gut microbiome, this new research adds to the knowledge that multiple factors are involved with determining whether people can tolerate specific dietary carbohydrate loads.

Nutritional guidelines for maintaining healthy blood glucose levels are portrayed as universally applicable, however this new study and the 2015 Israeli study demonstrates that blood glucose varies significantly between individuals based on genetics as well as on gut microbiota composition, which necessitates the need for personalized nutrition in managing blood glucose levels.

More Info

If you are interested in a personalized approach aimed at helping you gain control of your blood sugar levels, I can help.

I offer both in-person services in my Coquitlam, British Columbia office as well as remote services via Distance Consultation. You can find more information about my packages under the Services tab or in the Shop and if you would like to learn more about how Distance Consultation services work, you can click here.

Have Questions?

If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

References

Matteo Fumagalli, Stephane M Camus, Yoan Diekmann, Alice Burke, Marine D Camus, Paul J Norman, Agnel Joseph, Laurent Abi-Rached, Andrea Benazzo, Rita Rasteiro, Iain Mathieson, Maya Topf, Peter Parham, Mark G Thomas, Frances M Brodsky. Genetic diversity of CHC22 clathrin impacts its function in glucose metabolism. eLife, 2019; 8 DOI: 10.7554/eLife.41517
University College London. “Gene mutation evolved to cope with modern high-sugar diets.” ScienceDaily. ScienceDaily, 4 June 2019, https://www.sciencedaily.com/releases/2019/06/190604084857.htm
Zeevi D, et al. Personalized nutrition by prediction of glycemic responses. Cell. 2015;163:1079—1094.
Noecker C, Borenstein E. Getting Personal About Nutrition. Trends Mol Med. 2016;22(2):83—85. doi:10.1016/j.molmed.2015.12.010

June 23, 2019June 23, 2019

Lowering LDL and Saturated Fat to Lower Risk of Cardiovascular Disease

INTRODUCTION: There much debate in the health community about the effect of dietary fat — especially saturated fat on cholesterol levels and whether there is an association between dietary saturated fat intake and cardiovascular disease.

In the first part in this two-part series titled High Cholesterol and the Risk of Cardiovascular Disease, I explained what cholesterol is, the different types of cholesterol (HDL-C, VLDL, LDL-C and triglycerides (which are not actually cholesterol), what their role is, and what “high cholesterol” is.

In this article which is Part 2 in the two-part series, I will explain the association between dietary intake of saturated fat and higher levels of total LDL, and whether reducing total LDL — whether through the use of statin medication or diet lowers the risk of cardiovascular disease.

Dietary Saturated Fat and LDL

When people are told that they have “high cholesterol”, what is meant is that they have high total LDL. They are told they have high “bad” cholesterol, with no regard that there are different sub-fractions of LDL.

It is well known that eating foods high in saturated fat can raise LDL-C (total LDL cholesterol, but as covered in Part 1 of this two-part series, the first question one should ask when told they have “high LDL cholesterol” is “which LDL? The small dense ones or the large fluffy ones?”[1].

More often than not, the clinician that breaking the ‘bad news’ to the patients has absolutely no idea that there are different sub-fractions of LDL and that it is only the small, dense ones that are atherosclerotic [1].

Furthermore, there is almost a knee-jerk reaction on the part of many clinicians to prescribe statin medication in order to lower their LDL, on the assumption that lowering LDL will lower their risk of cardiovascular disease. In fact, aggressive treatment to lower total LDL-C has been at the (pardon the pun) heart of preventative cardiology for decades.

While statin medication (e.g. Lipitor®, Crestor®, etc.) is well-documented to reduce LDL-C levels, these are only surrogate markers (not direct markers) of cardiovascular disease (CVD). The assumption of an association between high LDL levels and CVD goes back as far as Ansel Keys and the Seven Country Study, and that the Diet Heart Hypothesis (covered in several previous articles) is simply an “establish fact”. But it is?

What evidence is there that lowering total LDL with statin medication lowers one’s risk of cardiovascular disease (CVD)?

The brand new guidelines on cholesterol management issued by the American Heart Association (AHA) and American College of Cardiology (ACC) which has just been published online ahead of print[2], places a renewed focus on LDL-C as a means to assess risk. In fact, these guidelines propose that non-fasting lipids be adopted as a screen in the general population, including “non-adults” (children and youth) [2]. As has been the case for decades., this is based on the assumption that total LDL (LDL-C) is an accurate surrogate marker for elevated cardiovascular risk, but does lowering LDL-C really lower CVD?

Of particular interest, the new American Heart Association (AHA) and American College of Cardiology (ACC) guidelines state that the traditional Friedewald equation which is used to calculate total LDL (i.e. LDL-C) as covered in Part 1 of this series of articles has been “prone to inaccuracy …at low-LDL-C and high triglyceride levels“ — yet decades of statin treatment has been based on the previous “inaccurate” Friedewald equation. The new guidelines promote the use of a new Martin/Hopkins LDL-C calculation method which is said to “perform better in these settings”. The question remains ‘does lowering LDL-C lower the risk of cardiovascular disease?’.

There are 44 randomized controlled trials of drug or dietary interventions to lower total LDL ( LDL-C) published in the literature which show no benefit in lowering rates of death [3] and most did not reduce CVD events [4].

Furthermore, despite a 37% drop in LDL-C and a 130% increase in HDL-C (so-called “good cholesterol”), the ACCELERATE double-blind randomized control trial showed no significant reduction in CVD or death [3.4].

In addition, there does not appear to be a clear reduction in CVD deaths in Western European countries either as a result of using statins for prevention [5].

This begs the question as to whether using statin medication to aggressively lower LDL-C has any benefit.

A 2018 article published in Expert Review of Clinical Pharmacology concluded;

“For half a century, a high level of total cholesterol (TC) or low-density lipoprotein cholesterol (LDL-C) has been considered to be the major cause of atherosclerosis and cardiovascular disease (CVD), and statin treatment has been widely promoted for cardiovascular prevention. However, there is an increasing understanding that the mechanisms are more complicated and that statin treatment, in particular when used as primary prevention, is of doubtful benefit.” [6]

What about lowering the intake of dietary saturated fat? Does that lower the risk of cardiovascular disease?

A 2014 meta-analysis of data of 72 studies involving more than 600,000 participants from 18 countries published in the journal Annals of Internal Medicine in 2014 [7] concluded that total saturated fat; whether measured in the diet or in the bloodstream showed no association with heart disease [7].

Take away: While eating dietary fat may raise the level of total LDL cholesterol (LDL-C), lowering its intake does not show any benefit in reducing the incidence of heart disease, nor does lowering LDL-C using statin drugs.

Which LDL?

A brand new study published June 4, 2019 in the American Journal of Clinical Nutrition sheds some very helpful light [8].

The study enrolled 113 people and randomized them to either a high saturated fat diet (40% carbs, 24% protein, 35% fat; 14% saturated fat) or a low saturated fat diet (40% carbs, 24% protein, 35% fat; 7% saturated fat replaced by monounsaturated fat).

Each group changed their diet every 4 weeks from (a) a high red meat diet (mostly from beef), (b) a high white meat diet (chicken and turkey) and (c) a non-meat protein diet (legumes, nuts, grain and soy).

Researchers found that LDL cholesterol and Apolipoprotein B (explained in the first part of this article) were higher with red and white meat alike and that the increase “was due primarily to increases in large LDL particles” with no change in the small particles and no significant change in the total cholesterol to HDL ratio.

This is highly significant!

What this means is that yes, eating meat; whether it’s red meat (such as beef, lamb or goat) or white meat (such as chicken or turkey) DOES increase LDL —but it’s the large, fluffy LDL particles that are increased; the ones that are not associated with cardiovascular disease[1]!

In fact, in the paper, the researchers acknowledge;

“Large LDL particles, measured by several different methodologies, have not been associated with CVD in multiple population cohorts in contrast to the associations observed for concentrations of medium, small, and/or very small LDL… Thus, the estimated impact of red meat, white meat, and dairy-derived saturated fatty acids (SFA) on CVD risk as reflected by their effects on LDL cholesterol and ApoB concentrations may be attenuated by the lack of their effects on smaller LDL particles that are most strongly associated with CVD.

Essentially, there has been on over-reliance on total LDL cholesterol (LDL-C) as a marker of cardiovascular disease, without distinguishing the atherosclerotic small, dense LDL from the non-atherosclerotic large, fluffy LDL.

The authors conclude;

“…the impact of high intakes of red and white meat, as well as saturated fatty acid (SFA) from dairy sources, which selectively raised large LDL sub-fractions may be overestimated by reliance on LDL cholesterol, as is the case in current dietary guidelines.”

This means that eating red meat (such as beef or lamb) or white meat (such as chicken or turkey) or eating saturated fat from full-fat dairy (such as full fat milk, cheese and yogurt) are associated with increased levels of the large, fluffy LDL sub-fraction and based on multiple population studies the large, fluffy LDL subfraction has not been found to be associated with cardiovascular disease.

Simply put, this means that eating foods high in saturated fat does not raise small LDL particles (which are the atherosclerotic sub-fraction) and results in no change to the total cholesterol to HDL ratio, and increases the large, fluffy LDL-subfraction (which are NOT found to be associated with cardiovascular disease)!

While this is a small pilot study, it adds further evidence that eating saturated fat does not increase cardiovascular risk.

Note: high levels of the small, dense LDL sub-fraction is thought to be genetic, but is also associated with intake of trans fatty acids and high intake of refined carbohydrates. More on that in future articles.

More Info?

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To your good health!

Joy

You can follow me on:

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References

Lamarche, B., I. Lemieux, and J.P. Després, The small, dense LDL phenotype and the risk of coronary heart disease: epidemiology, patho-physiology and therapeutic aspects. Diabetes Metab, 1999. 25(3): p. 199-211.
Cao J, Devaraj S, Recent AHA/ACC guidelines on cholesterol management expands the role of the clinical laboratory, Clinica Chimica Acta 495 (2019) 82—84, Available online 03 April 2019.
DuBroff R. Cholesterol paradox: a correlate does not a surrogate make. Evid Based Med,2017;22(1):15—9. doi: 10.1136/ebmed-2016-110602
Demasi M, Lustig RH, Malhotra A, The cholesterol and calorie hypotheses are both dead — it is time to focus on the real culprit: insulin resistance, Clinical Pharmacist, 14 July 2017.
Vancheri F, Backlund L, Strender L et al. Time trends in statin utilisation and coronary mortality in Western European countries. BMJ Open 2016; 6(3):e010500. doi: 10.1136/bmjopen-2015-010500
Ravnskov U, de Lorgeril M, Diamond DM, et al, LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature, Expert Review of Clinical Pharmacology, 2008;11:10, 959-970, DOI: 10.1080/17512433.2018.1519391
Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis. Ann Intern Med. 2014;160:398—406. doi: 10.7326/M13-1788

June 20, 2019June 23, 2019

High Cholesterol and Risk of Cardiovascular Disease

INTRODUCTION: There is much debate in the scientific community about the effect of dietary fat — especially saturated fat on cholesterol levels and risk of cardiovascular disease. To best understand this complex topic, I have broken the subject into two articles. In this first part, I explain the different ways cholesterol values are assessed, what they are used for and what they mean. In the next part I will explain whether lowering LDL and dietary saturated fat lowers the risk of cardiovascular Disease.

What is Cholesterol?

Cholesterol is a essential structural component of all the cell membranes in the body and is used in the making of steroid hormones such as cortisol and aldosterone by the adrenal glands, sex hormones such as estrogen, testosterone and progesterone by the gonads, and is also used in the making of bile acid. Approximately 80% of cholesterol made daily by the body occurs in the liver and intestines, with the remainder being made in the adrenal glands and reproductive organs.

Different Types of Cholesterol

Triglyceride isn’t actually a type of cholesterol, but is measured on lipid panels along with cholesterol.

Triglyceride is made up of three fatty acids (hence “tri-“) attached to a glycerol molecule (also known as glycerine), which is a sugar alcohol. Some triglyceride is taken in through the diet and the rest is manufactured by the body during lipogenesis (literally meaning the ‘making of fat’). Lipogenesis is how the body stores the excess carbohydrate we eat in our diet that isn’t immediately needed for energy. Yes, excess dietary carbohydrate is stored in the body as glycogen and when glycogen stores are full, it is stored as fat.

As for cholesterol itself, there are several different types found in the blood;

high density lipoprotein (HDL)
low density lipoprotein (LDL)
very low density lipoprotein (VLDL)

Most people think of high density lipoprotein (HDL) as ”good cholesterol” and low density lipoprotein (LDL) as ”bad cholesterol” but there are actually two sub-fractions of LDL; the small, dense LDL sub-fraction which is associated with atherosclerotic plaque, and the large, fluffy LDL sub-fraction which is considered protective against cardiovascular disease[1].

This is important, because when people are told they have “high cholesterol“, this is usually implies that they have high LDL. This is often presented to them as them having a high level of “bad” cholesterol.

High Cholesterol

A couple of things need to be clarified about “high cholesterol”;

Firstly, “high LDL” cholesterol means high total LDL cholesterol. When blood tests are said to indicate “high LDL” a good question to ask is “which LDL cholesterol is high; the small dense ones or the large fluffy ones?”. More on this below.

Secondly, it is important to note that lab tests don’t actually measure total LDL but calculate it from the Friedewald formula; which (in mg/dl) is calculated by total cholesterol (TC) – HDL lipoprotein (HDL)-cholesterol – triglycerides (TGs) / 5.

When people are told that they have “high LDL” results on a blood test, they are often presented with a recommendation to begin statin medication, but does high total LDL provide sufficient information about cardiovascular risk? More on this below. The use of statin medication will be covered in the subsequent article.

Very low density lipoprotein (VLDL) is produced in the liver and the best way to understand its role is to think of it as a “taxi” which the liver makes and then release into the bloodstream to shuttle triglycerides around to the various tissues. VLDL cholesterol on blood test results isn’t actually measured either, but estimated as a percentage of the triglyceride value. High VLDL is said to be a risk for cardiovascular disease but as elaborated on below, a more accurate measure is the ratio of Apopoprotein B (the lipoprotein in VLDL) compared to the Apoprotein A (the lipoprotein in HDL).

Where does LDL come from?

Once a large amount of triglyceride has been unloaded in the tissues by the VLDL “taxi”, it becomes a new, smaller lipoprotein called low density lipoprotein, or LDL which contains mostly cholesterol and some protein.

Some LDLs are removed from the circulation by cells around the body that need the cholesterol contained in them and the rest is taken out of the circulation by the liver.

A key point here is that the only source of LDL is VLDL. This is important.

LDL is what is left once the VLDL which is made by the body has offloaded its triglyceride ‘passenger’ to the tissues.

LDL and Heart Disease

Research has often reported that elevated LDL-cholesterol is a risk factor for cardiovascular disease, including heart disease and stroke and it has been assumed that lowering LDL-cholesterol in the blood would decrease cardiovascular deaths and illness. It is this premise that lead to recommendation of treatment of high LDL with statin drugs.

One major problem is that these studies looked at total LDL which doesn’t distinguish between the small, dense sub-fractions of LDL that are atherosclerotic, and the large, fluffy ones that are not [1].

Total LDL (LDL-C) calculates (not measures!) the total content or concentration of cholesterol within all the LDL particles.

LDL particle number (LDL-P) measures the particle concentration.

Since the amount of cholesterol in each particle varies, measuring LDL-C does not necessarily reflect the actual number of particles — but an increased number of LDL particles occurs in patients with lots of small, dense particles.

Therefore, LDL-particle number (LDL-P) is a more accurate predictor of cardiovascular events than total LDL (LDL-C).

An NMR lipid profile test directly measures the number of LDL particles (as well as HDL particles). For LDL particles, a value of less than 1.000 in nmol/L is considered ideal, a value of 1000-1299 is considered moderate, a value of 1300-1599 is considered borderline high, and a value >1600 is considered high.

Apolipoprotein B:Apolipoprotein A

Apolipoprotein B (apo B) is the main lipoprotein in VLDL, and subsequently in LDL after the VLDL has offloaded its triglyceride to the tissues. ApolipoproteinB is correlated with the actual number of LDL-particles, which makes it a very good assessor of the risk of cardiovascular disease,

Apolipoprotein A (apo A) is the main lipoprotein in HDL (commonly called “good” cholesterol).

Measuring ApoB to ApoA requires special blood tests, but a proxy can be calculated by dividing triglycerides (TG) by HDL-cholesterol (HDL-C) from a standard lipid panel. Studies have found this to be a very good assessor of cardiovascular risk.

Triglyceride:HDL Ratio

In Canada (as well as Europe), values are expressed as mmol/L and the ratios are interpreted as follows [2];

TG:HDL-C < 0.87 is ideal

TG:HDL-C > 1.74 is too high

TG:HDL-C > 2.62 is much too high

In the US, values are expressed in mg/dl and the ratios are interpreted as follows [2];

TG:HDL-C < 2 is ideal

TG:HDL-C > 4 is too high

TG:HDL-C > 6 is much too high

Several studies have found that TG:HDL-C ratio also reflects particle size;

One study from 2004 reported that almost 80% of people with a TG:HDL-C ratio of greater than 3.8 (when values are expressed in mg/dl) had mostly small, dense LDL particles, indicating cardiovascular risk. This same study found that more than 80% with a TG:HDL-C ratio of less than 3.8 (when values are expressed in mg/dl) had mostly large, fluffy LDL particles, indicating lower cardiovascular risk[3].

A 2005 study [4] reported that a TG:HDL-C ratio of 3.5 or greater was highly correlated with atherosclerosis in men, as well as insulin resistance and metabolic syndrome.

A recent 2014 [5] study found that a high TG:HDL-C ratio was a strong independent predictor of cardiovascular disease, coronary heart disease and all-cause mortality both before- and after adjustment for age, smoking, BMI and blood pressure.

Based on this metric, lower cardiovascular risk would be associated with lower triglycerides, raising HDL or both.

But how?

Lowering TG:HDL-C ratio

Losing weight will lower triglycerides, however low-fat diets are not usually helpful in this regard because they are often also high in carbohydrate[2].

Decreasing intake of carbohydrates — especially fructose which is found in fruit, as well as processed products made with high fructose corn syrup has been anecdotally reported to decrease hunger, making weight loss easier. Most importantly, clinical studies using well-designed low carbohydrate diets (already covered in several previous articles) are associated with both a lowering of triglycerides and a increase in HDL.

Lowering the risk of cardiovascular disease through weight loss, along with a lowering of triglycerides and an increase in HDL is where I can help.

UPDATE (June 23, 2019): Part 2 of this article titled Lowering LDL and Saturated Fat to Lower the Risk of Cardiovascular Disease is available by clicking here.

More Info?

To your good health!

Joy

You can follow me on:

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

References

Lamarche, B., I. Lemieux, and J.P. Després, The small, dense LDL phenotype and the risk of coronary heart disease: epidemiology, patho-physiology and therapeutic aspects. Diabetes Metab, 1999. 25(3): p. 199-211.
Sigurdsson AF, The Triglyceride/HDL Cholesterol Ratio, updated January 12, 2019, https://www.docsopinion.com/2014/07/17/triglyceride-hdl-ratio/
Hanak V, Munoz J, Teague J, et al, Accuracy of the triglyceride to high-density lipoprotein cholesterol ratio for prediction of the low-density lipoprotein phenotype B, The American Journal of Cardiology, Volume 94, Issue 2, 2004, Pages 219-222, https://doi.org/10.1016/j.amjcard.2004.03.069
McLaughlin T, Reaven G, Abbasi F, et al. Is there a simple way to
identify insulin-resistant individuals at increased risk of cardiovascular
disease? Am J Cardiol. 2005;96(3):399Y404.
Vega GL, Barlow CE, Grundy SM et al, Triglyceride to High Density Lipoprotein Cholesterol Ratio is an Index of Heart Disease Mortality and of Incidence of Type 2 Diabetes Melletus in Men, Journal of Investigative Medicine & Volume 62, Number 2, February 2014

June 18, 2019November 7, 2022

Distinguishing Food from Food-like Products

INTRODUCTION: National dietary guidelines in both Canada and the US focus on the variety of foods available in each of several defined ‘food groups’ and make recommendations about “healthy eating” based on how much of particular nutrients are in specific foods. In Canada for example, foods that are rich in saturated fat, sodium or sugar are said to undermine health. This type of classification results in dishes rich in cheese and fried chicken both being deemed as unhealthy, as both are high in saturated fat and sodium.

This article outlines an internationally established way of classifying foods that is based on the degree of food processing they have undergone — which I believe provides a better framework to help people to choose which foods they should aim to eat most often.

Many of us have heard the alarming health statistics in both the US and Canada, but they are worth repeating.

Obesity has risen in Canada from < 10% in 1970-1972 to almost 15% in 1989, to over 23% in 2004 [1,2]. That is, in the early 1970s, only one in 10 people in Canada was obese and now almost 1 in 4 people in Canada are obese [3]. The prevalence of obesity among American adults is almost 40% as of 2015-6 [4].

And it’s not only adults.

As of 2015, over 10% (1 in 10) children between the ages of 5 and 17 years of age in Canada were obese[3] and that figure rises to 20% (1 in 5 kids) in the United States [4].

It’s not only obesity.

As of 2015, >25% of Canadians adults have been diagnosed with high blood pressure[3] and as of 2013, >30% of American adults have high blood pressure [5]. That’s 1 in 4 in Canada and 1 in 3 in the US [4] with hypertension; a major risk factor for heart attack and stroke.

Over 8% in Canada have been diagnosed with coronary heart disease (CHD) [3] and in the US, coronary heart disease accounts for ~13% of deaths as of 2016 [6] and over 8% of Canadians has diabetes [3] and in the US, almost 9.5% of Americans has diabetes [7].

What has changed over this time period to account for this?

Too Many Carbs?

When I first started writing articles about obesity and the increased rates of metabolic diseases ~ 4 years ago, I thought it was largely related to the increased in carbohydrate content of the diet due to changes in the national dietary guidelines that occurred in Canada and the US in 1977. To some degree there is a relationship between these, but it is not as clear-cut as I once thought.

Industrial Seed Oils (Polyunsaturated Vegetable Oil)

With further reading in the scientific literature, I came to believe that it was the inclusion of novel “seed oils” (also called “polyunsaturated vegetable oil”) including canola, soybean, corn and cottonseed oil — along with too much carbohydrate in the diet that lay at the root of obesity and metabolic disease and while this is certainly part of the story, I was still missing a vital piece of the puzzle.

Manufactured Food-like Products

As national dietary guidelines in both Canada and the US in 1977 focused on reducing dietary intake of fat — especially saturated fat, food manufacturers sought to fill the gap left by the removal of butter, cream, lard and tallow (saturated fats) from the diet, and began to manufacture products that were made up of both refined carbohydrate and industrial seed oils (“polyunsaturated vegetable oils”). The food industry heavily marketed these manufactured products and promoted them as being “low in saturated fat”, which was perceived by the general public as being equivalent to “healthy”.

Since the mid-1980s, the food supplies of high-income countries such as Canada, the US, Australia and the UK have been dominated by pre-packaged, ready-to-eat “convenience foods” [13]. In fact, the percentage of energy (calories) in the diet of Canadians of these “ultra-processed foods” rose from <25% in 1938 (when manufactured products such as Crisco and soy oil were first created) to almost 54% in 2011 (9). Similar trends have been observed worldwide (10-12).

It is my now my conviction that it has been the over-consumption of these ultra-processed “convenience foods” that are high in both refined carbohydrate and seed oils which precipitated the huge deterioration of the Western diet, and which has fueled the concurrent epidemics of obesity, diabetes and other chronic diseases, such as hypertension and coronary heart disease [8].

Hundreds of thousands of people in Canada, and millions worldwide are metabolically unwell because the bulk of the diet has centered around eating these manufactured food-like products — from our morning sweetened cereal or spreads on toast to the burger with ‘plastic cheese’ and French fries we grab in place of real food.

So how do we distinguish real food from food-like products?

The NOVA Food Classification system – defining “processed food”

From the time food is harvested to when it is eaten, most food is processed in some way. Some of this processing may be as simple as peeling and chopping it, to cooking it, but food doesn’t become “unhealthy” just because it is processed. The issue is how much it is processed.

NOVA is a food classification system developed in Brazil and used in the US, Canada and other countries around the world to define the level of food processing.

The NOVA definition of types of food processing are as follows [13]:

Minimally processed foods are defined as ”unprocessed foods altered in ways that do not add or introduce any new substance (such as fats, sugars, or salt) but often involve removal of parts of the food.” Examples of these include fresh, dry, or frozen vegetables, root vegetables, grains and legumes, fruits and nuts, and meats, fish, seafood, eggs, and milk [13]. For the most part, minimal processing is what’s involved in preparing it for eating and/or improving its palatability.

Processed foods are defined as ”foods made by adding fats, oils, sugars, salt, and other culinary ingredients to minimally processed foods to make them more durable and usually more palatable, and by various methods of preservation“. They include simple breads and cheeses; salted, pickled or cured meats, fish and seafood; and vegetables, legumes, fruits and animal foods preserved in oil, brine or syrup.

Canned fish in oil would fall in this category, as would hummus (ground chickpeas with sesame seed butter, garlic and lemon juice), as well as bacon and sausages.

These foods can be part of a healthy diet, depending on how they are prepared and used in dishes and meals [13] and how much of these are eaten at a time.

Ultra processed foods are defined as ”not modified foods, but formulations of industrial ingredients and other substances derived from foods, plus additives. They mostly contain little if any intact food. The purpose of ultra-processing is to create products that are convenient (durable, ready-to-eat, -drink or -heat), attractive (hyper- palatable), and profitable (cheap ingredients). Their effect all over the world is to displace all other food groups. They are usually branded assertively, packaged attractively, and marketed intensively.“

Foundations for Healthy Eating using Degree of Food Processing

I like to define foods as being either “everyday foods” or “sometimes foods”. The issue is how much and how often we eat them.

“Everyday Foods”

Choosing foods to make up a meal should aim to include mostly unprocessed foods (whole foods in their original state) and minimally processed foods. This is how our grand-parents and great-grandparents ate (when obesity, hypertension and diabetes rates were a fraction of what they are now!).

Another way to determine what foods to include in a meal is to eat food that your great-grandparents would recognize as food.

“Sometimes Foods”

For people who are metabolically healthy, eating “processed foods” such as breads and cheese, salted, pickled or cured foods (including meat, fish, seafood, vegetables, legumes) and whole foods preserved in oil or brine are perfectly fine to add to unprocessed foods (whole foods in their original state) and minimally processed foods to make up a meal.

For those who are already overweight or metabolically unhealthy, focusing on making up a meal of real, whole foods in their original state (i.e. unprocessed foods) and minimally processed foods is best, while limiting processed foods. How much bacon, olives, bread and cheese can be eaten really depends on a person’s metabolic health. This is where having a Meal Plan designed by a Dietitian is helpful because everybody’s needs are different.

Ultra-Processed Food

Ultra-processed food isn’t food. They are products made from a combination of refined carbohydrates (including sugar) and seed oils. These are convenient, hyper-palatable and cheap, and displace real food in the diet.

According to a 2015 study, some of the most addictive foods are in this category; including breakfast cereal, muffins, pizza, cheeseburgers, French fries and fried chicken — as are the desserts that often eaten with them including chocolate, ice cream, cookies and cake, and the soda we wash them down with. Even our favourite snacks like popcorn and chips are really nothing more than a combination of refined carbs and industrial seed oil eaten in place of real food.

Fifteen Most Addictive Fast Foods

These ultra-processed food-like products are intended to displace real food in the diet and as such are not something we should consider as components for making up a meal.

Does that mean we should never eat a slice of pizza or a cheeseburger? Of course not. But let’s be fully aware that this is not real food. It is something we eat in place of real food.

As well, there is a huge difference between a homemade burger with real melted cheddar cheese on top — sandwiched between fresh leaf lettuce and tomato, and what can be picked up at a 1000 drive-throughs in cities around the Western world.

National Food Guidelines as foundations for healthy eating

National food guidelines in both Canada and the US have traditionally categorized food based on the variety available in each food group; including grains and cereals, vegetables &/or fruit. milk and dairy, and meats and alternatives.

In the case of the new Canada Food Guide, it recently eliminated the Milk and Dairy food group and combined those foods with Protein foods. The other two food groups are now Grains and Vegetables and Fruit.

The new Guide centers it’s dietary advice around 3 “Guidelines”.

Guideline 1 of the new Canada Food Guide focuses on eating from the different food groups and stresses that Canadians should eat plant-based foods more often because they lower intake of saturated fat.

Guideline 2 of the new Canada Food Guide encourages Canadians to limit processed or prepared foods and states the reason is because they contribute excess sodium, sugar and saturated fat.

Based on this definition, dishes made with lots of cheese and fried chicken are high in saturated fat and sodium, and thus are categorize as foods that undermine healthy eating.

Does eating cheese really undermine healthy eating?

Or a rib steak?

Or milk?

As covered in previous articles I’ve written on the new Canada Food Guide, I am not convinced that there is a compelling reason to limit real, whole food simply because it is high in saturated fat.

Guideline 3 of the new Canada Food Guide encourages Canadians to learn how to prepare and cook their own food and promotes the use of nutritional food labels as a tool to help them make informed choices.

The fact is, there are no nutrition food labels on unprocessed food (real, whole foods).

Choosing Healthy Food

As I’ve said in prior articles, Canadians can use the new Canada Food Guide to make up healthy meals by focusing on the part of Guideline 1 which encourages them to eat “real, whole food” and on the part of Guideline 2 which encourages them to “limit processed or prepared foods” — and by defining “processed foods” using the NOVA category of “ultra-processed foods” given above. In this way they will be able to design meals with a wide range of healthy and interesting foods.

Defining what is healthy based on how much a food is processed makes good sense. In this way people are free to add bread and cheese, and salted, pickled or cured foods (including meat, fish, seafood, vegetables, legumes) to their unprocessed foods (whole foods in their original state) and minimally processed foods to make up an interesting and healthful meal.

Furthermore, categorizing food using the NOVA categories based on the degree of food processing avoids lumping foods made with lots of real cheese with fried chicken as those that undermine healthy eating, based on their saturated fat and sodium content.

More Info?

If you would like to have a Meal Plan designed to meet your health and nutritional needs, I can help.

To your good health!

Joy

You can follow me on:

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

References

Public Health Agency of Canada, Canadian Institute for Health Information. Obesity in Canada. A joint report from the Public Health Agency of Canada and the Canadian Institute for Health Information. Ottawa: Public Health Agency of Canada & Canadian Institute for Health Information; 2009. 62 pages.
Katzmarzyk PT. The Canadian obesity epidemic: an historical perspective. Obes Res. 2002, Jul;10(7):666-74.
Public Health Agency of Canada. Canadian Chronic Disease Indicators, Quick Stats, 2017 edition. Ottawa: Public Health Agency of Canada; 2017. 4 pages
NCHS Data Brief, Prevalence of Obesity Among Adults and Youth: United States, 2015-2016, https://www.cdc.gov/nchs/data/databriefs/db288.pdf
American Heart Association, Statistical Fact Sheet 2013 Update, High Blood Pressure, https://www.heart.org/idc/groups/heart-public/@wcm/@sop/@smd/documents/downloadable/ucm_319587.pdf
American Heart Association, Heart Disease and Stroke Statistics-2019 At-a-Glance, https://healthmetrics.heart.org/wp-content/uploads/2019/02/At-A-Glance-Heart-Disease-and-Stroke-Statistics-%E2%80%93-2019.pdf
Centers for Disease Control and Prevention, New CDC report: More than 100 million Americans have diabetes or prediabetes, https://www.cdc.gov/media/releases/2017/p0718-diabetes-report.html
Liu AG, Ford NA, Hu FB, Zelman KM, Mozaffarian D, Kris-Etherton PM. A healthy approach to dietary fats: understanding the science and taking action to reduce consumer confusion. Nutr J. 2017 Aug 30;16(1):53. doi: 10.1186/s12937-017-0271-4.
Moubarac JC, Batal M, Martins AP, Claro R, Levy RB, Cannon G, et al. Processed and ultraprocessed food products: Consumption trends in Canada from 1938 to 2011. Can J Diet Pract Res. 2014 Spring;75(1):15-21.
Monteiro CA, Moubarac J-C, Cannon G., Ng SW, Popkin B. Ultra-processed products are
becoming dominant in the global food system. Obes Rev. 2013 Nov;14 Suppl 2:21-8. doi: 10.1111/obr.12107.
Moodie R, Stuckler D, Monteiro C, Sheron N, Neal B, Thamarangsi T, et al. Profits and pandemics: prevention of harmful effects of tobacco, alcohol, and ultraprocessed food and drink industries. The Lancet. 2013 Feb 23;381(9867):670-9. doi: 10.1016/S0140-6736(12)62089-3.
Baker P, Friel S. Food systems transformations, ultra-processed food markets and the nutrition transition in Asia. Global Health. 2016 Dec 3;12(1):80.
Moubarac JC. Ultra-processed foods in Canada: consumption, impact on diet quality and policy implications. Montréal: TRANSNUT, University of Montreal; December 2017.
Schulte EM, Avena NM, Gearhardt AN (2015) Which Foods May be Addictive? The Roles of Processing, Fat Content and Glycemic Load. PLoS ONE 10(2); e0117959. https://doi.org/10.1371/journal.pone.0117959