[NOTE: This is a combination Science Made Simple article and editorial, expressing my opinion.]
This past Wednesday March 24, 2021, Dr. James Muecke, a South Australia ophthalmologist who was the 2020 Australian of the Year, posted on Facebook that Diabetes Australia reworded their webpage from ”Type 2 diabetes is a progressive condition” to ”Type 2 diabetes is often a progressive condition” — wording that Dr. Muecke calls;
“a small, but significant change that will give some degree of hope to the 280 Australians diagnosed [with type 2 diabetes] every day“.
Diabetes Australia’s change in phraseology occurred shortly after Diabetes Victoria removed the words ”Type 2 diabetes is a progressive condition” entirely from its Type 2 Diabetes webpage — replacing it with nothing. This, Dr. Muecke said;
“gives tremendous hope to patients that their newly diagnosed condition can potentially be put into remission.”
I was curious what Diabetes Canada’s web site said and was saddened to discover that it stated that “Type 2 diabetes is a progressive, life-long disease“.
Diabetes Canada: “Type 2 diabetes is a progressive, lifelong disease” (https://guidelines.diabetes.ca/docs/patient-resources/type-2-diabetes-the-basics.pdf)
We don’t tell people diagnosed with cancer they have “a progressive, lifelong disease” — but speak to them instead about treatment options and the possibility of remission. While some types of cancer are incurable and untreatable, in general people diagnosed with cancer are not told they have a “progressive, lifelong disease”. Why are people with type 2 diabetes told this?
I think calling type 2 diabetes a progressive, lifelong disease is a vestige from before there was evidence that it could be put into remission. I think we need to change our terminology to reflect that it is now possible.
In February 2018, one year data from Virta Health’s outpatient study using a ketogenic diet intervention demonstrated that reversal of type 2 diabetes symptoms is sustainable over the long term — with HbA1c level at baseline being 7.6% ± 1.5% being reduced by 1.0% and the percentage of individuals with a HvA1C of <6.5% was 56% [1].
Virta Health’s 2-year data indicated that there were improvements in body weight and that improved blood sugar control was also largely sustained, and that significant metabolic markers and health improvements occurred while using a ketogenic approach in an outpatient setting, over the usual care model approach [2]. On average after one year, participants in the intervention (ketogenic) group lowered HbA1c from 7.7% to 6.3% and at two years, HbA1C of participants in the intervention group increased slightly to 6.7%. By comparison, HbA1C of the usual care control group was 7.5% at baseline, 7.6% at one-year, and 7.9% at two years.
Even a 2019 study using an calorie-restricted diet found that “remission of type 2 diabetes within 1-year can be achieved at a cost below the annual cost of diabetes, including complications“ [3] .
There is no cure for diabetes — at least not yet, but there are three documented ways to put type 2 diabetes into remission;
a ketogenic diet [1,2]
a low calorie energy deficit diet [4,5,6]
bariatric surgery (especially use of the roux en Y procedure) [7,8]
Since there is evidence that both a well-designed ketogenic diet and a well-designed calorie-restricted diet put type 2 diabetes into remission (i.e. maintaining blood glucose below the diabetes cut-offs), we need to stop referring to type 2 diabetes as “a progressive, lifelong disease” — as if it is always the case.
It can be a progressive, lifelong disease for those who would rather not make the significant dietary and lifestyle changes that are required to put it into remission (and as I outline in this article, this is a valid choice, too!)
People can choose to live WITH diabetes or to seek remission FROM it — but they deserve to know that remission is possible.
More Info?
If you would like more information about how I can support you in aiming to put type 2 diabetes into remission, please let me know.
Hallberg, S.J., McKenzie, A.L., Williams, P.T. 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 Ther9, 583—612 (2018). https://doi.org/10.1007/s13300-018-0373-9
Athinarayanan SJ, Adams RN, Hallberg SJ, McKenzie AL, Bhanpuri NH, Campbell WW, Volek JS, Phinney SD, McCarter JP. 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. Front Endocrinol (Lausanne). 2019 Jun 5;10:348. doi: 10.3389/fendo.2019.00348. PMID: 31231311; PMCID: PMC6561315.
Xin Y, Davies A, McCombie L, Briggs A, Messow CM, Grieve E, Leslie WS, Taylor R, Lean MEJ. Type 2 diabetes remission: economic evaluation of the DiRECT/Counterweight-Plus weight management programme within a primary care randomized controlled trial. Diabet Med. 2019 Aug;36(8):1003-1012. doi: 10.1111/dme.13981. PMID: 31026353.
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
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.
In November 2018, the American Association of Clinical Endocrinologists (AACE) released a Position Statement [1] which identified four separate disease stages associated with an abnormal glucose response, including Type 2 Diabetes;
Stage 1: Insulin Resistance
Stage 2: Prediabetes
Stage 3: Type 2 Diabetes
Stage 4: Vascular Complications — including retinopathy, nephropathy and neuropathy
Long before blood sugar becomes abnormal in the stage known as prediabetes, the progression to type 2 diabetes has already begun in the form of insulin resistance — and identifying insulin resistance at this stage (while blood glucose is still normal) enables people to implement dietary changes to avoid the progression to pre-diabetes, and type 2 diabetes.
Discovering insulin resistance in those who lack the more obvious outward signs can be especially helpful — including those who appear slim, but who may have visceral or ectopic fat (so-called TOFIs, “thin on the outside, fat on the inside”), or those who may have undetected hyperinsulinemia due to their abnormal response to dietary carbohydrate. Some people that fall in this category may include those with a significant family history of type 2 diabetes, or previous gestational diabetes, even though they currently appear healthy.
The Homeostatic Model Assessment (HOMA-IR) is a test that uses a simultaneous fasting blood glucose test and fasting insulin test to accurately estimate the degree of insulin resistance (IR) and β-cell function (the cells of the pancreas that produce insulin). Alternatively, HOMA-IR can also be determined from a simultaneous fasting blood glucose test and a fasting C-peptide test [2]. C-peptide is released in proportion to insulin, so it can be used to estimate insulin.
The Homeostatic Model Assessment (HOMA) equations have been widely used in research to estimate insulin resistance and the two equations which use fasting blood levels of insulin and glucose are as follows, with HOMA-IR used to assess insulin resistance and HOMA-B used to assess pancreatic β—cell (beta-cell) function [3,9].
HOMA-IR= (glucose in mmol/L x insulin in mIU/mL)/22.5
HOMA-B= (20 x insulin in mIU/mL)/(glucose in mmol/L – 3.5)
Individual results are best compared to local population cut off values for HOMA1-IR [3] (1985) or the updated HOMA2-IR* [4] (1998).
HOMA2-IR* is easily and accurately calculated using the online HOMA2 calculator released by the Diabetes Trials Unit, University of Oxford available at http://www.dtu.ox.ac.uk/homacalculator/index.php.
The original HOMA1-IR equation proposed by Matthews in 1985 [3] was widely used due to its simplicity, however it was not always reliable because it did not consider the variations in the glucose resistance of peripheral tissue and liver, or increases in the insulin secretion curve for blood glucose concentrations above 10 mmol/L (180 mg/dL), or the effect of circulating levels of pro-insulin. [5]. The updated HOMA2-IR computer model [6] mentioned above and available from Oxford University has been used since 1998 and corrects for these — and estimates both insulin resistance and β-cell function.
Cut-off for insulin resistance using the original Matthews values (1985) [3] for HOMA-IR = 2.7
Insulin sensitive is considered less than 1.0
Healthy is considered 0.5-1.4
Above 1.8 is early insulin resistance
Above 2.7 is considered significant insulin resistance
Cuff-off values for insulin resistance using the HOMA2-IR calculator (1998) [6] is HOMA2-IR = 1.8. Three population based studies found the same or very close cut-offs applied, including a 2009 Brazilian study [6] which found HOMA2-IR =1.8, a 2014 Venezuelan study [7] which found HOMA2-IR= 2.0 and a 2014 Iranian study [8] which found HOMA2-IR =1.8.
Use of HOMA-IR to Assess Insulin Resistance and β-cell Function in the Individual
HOMA-IR has been used to assess Insulin Resistance (IR) and β-cell function as a one-off measures in individuals in >150 epidemiological studies of subjects of various ethnic origins, with varying degrees of glucose tolerance [9].
In the Mexico City Study which used single glucose-insulin pairs (not the mean of three samples at 5-min intervals) [10], β-cell function and insulin resistance were assessed using HOMA-IR in ~1500 Mexicans with normal or impaired glucose tolerance (IGT). Subjects were followed up for 3.5 years for the incidence of diabetes and to examine any possible relationship with baseline β-cell function and IR. At 3.5 years, ~4.5% of subjects with normal glucose tolerance at baseline and ~23.5% with impaired glucose tolerance at baseline had progressed to type 2 diabetes. That is, the development of diabetes was associated with higher HOMA-IR at baseline.
The use of HOMA-IR on an individual basis enables clinicians to quantify both the degree of insulin sensitivity and β-cell function on assessment — before the person makes any dietary changes. Once the individual understands the significance of their HOMA-IR results, it can provide significant motivation for them to make dietary changes in order to prevent the progression toward abnormal glucose tolerance, or type 2 diabetes. When HOMA-IR is repeated 6 months into dietary changes, it provides significant feedback to the individual regarding the effectiveness of dietary changes, and the motivation to continue.
”HOMA-IR can be used to track changes in insulin sensitivity and β-cell function longitudinally in individuals. The model can also be used in individuals to indicate whether reduced insulin sensitivity or β-cell failure predominates[10].
Assessing HOMA2-IR is the reason I may request a simultaneous fasting blood glucose and fasting insulin from those that come to me and who have insulin resistance and/or hyperinsulinemia. My goal is to find out even when blood sugar results are still normal in order find out if their pancreas is working too hard in order to keep them that way.
More Info?
If you would like more information about how I can support you in meeting your health and nutrition goals, please have a look around my web page.
Note: In British Columbia, family MDs may decline to order the fasting insulin test for the investigation of insulin resistance as the BC government does not authorize payment for that use, but many physicians will if they feel it is clinically warranted. Alternatively, a fasting C-peptide test can be ordered without restriction and can be used to determine HOMA2-IR using the Oxford calculator.
Crofts, C., Understanding and Diagnosing Hyperinsulinemia. 2015, AUT University: Auckland, New Zealand. p. 205.
Matthews, D. R; Hosker, J. P; Rudenski, A. S; Naylor, B. A; Treacher, D. F; Turner, R. C; “•Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man”–; Diabetologia; July, 1985; Volume 28, Number 7: Pp 412-419
Levy JC, Matthews DR, Hermans MP. Correct homeostasis model assessment (HOMA) evaluation uses the computer program. Diabetes Care. 1998;21:2191—2192
Song YS, Hwang Y-C, Ahn H-Y, Comparison of the Usefulness of the Updated Homeostasis Model Assessment (HOMA2) with the Original HOMA1 in the Prediction of Type 2 Diabetes Mellitus in Koreans, Diabetes Metab J. 2016 Aug; 40(4): 318—325
Geloneze B, Vasques AC, Stabe CF et al, HOMA1-IR and HOMA2-IR indexes in identifying insulin resistance and metabolic syndrome: Brazilian Metabolic Syndrome Study (BRAMS), Arq Bras Endocrinol Metabol. 2009 Mar;53(2):281-7
Bermíºdez V, Rojas J, Martínez MS et al, Epidemiologic Behavior and Estimation of an Optimal Cut-Off Point for Homeostasis Model Assessment-2 Insulin Resistance: A Report from a Venezuelan Population, Int Sch Res Notices. 2014 Oct 29;2014:616271
Tohidi M, Ghasemi A, Hadaegh F, Age- and sex-specific reference values for fasting serum insulin levels and insulin resistance/sensitivity indices in healthy Iranian adults: Tehran Lipid and Glucose Study, Clin Biochem. 2014 Apr;47(6):432-8
Haffner SM, Kennedy E, Gonzalez C, Stern MP, Miettinen H: A prospective analysis of the HOMA model: the Mexico City Diabetes Study. Diabetes Care 19:1138—1141, 1996
LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only. The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything you have read or heard in our content.
More than half of middle aged people have a hiatal hernia (sometimes referred to as a “hiatus hernia“), but most people are only diagnosed when their symptoms become a problem or when having medical tests for something else.
A hiatal hernia is where part of the stomach bulges up through the space (called a “hiatus”, meaning a “gap”) in the diaphragm/ abdominal wall where the esophagus normally passes.
Illustration of a hiatal hernia (“hiatus hernia”)
There are two types of hiatal hernias; the sliding type and the fixed type.
The sliding type of hiatal hernia is the more common type and occurs intermittently (i.e. from time to time), when the pressure in the abdomen increases. This increased pressure pushes part of the stomach up through the gap in the diaphragm where only the esophagus is supposed to pass, and the little bulge is caused the hiatal hernia.
The fixed type of hiatal hernia is also called a paraesophageal hiatal hernia and occurs when the opening for the esophagus in the abdominal wall is bigger than usual. The stomach, and sometimes other organs including the small intestine or colon (large intestine) may also bulge into the chest cavity through this paraesophageal hernia. Paraesophageal hernias often get worse over time, in which case surgery is required to treat the problem.
A strangulated hernia is not a type of hernia, but rather a complication in any one of a number of different types of hernias that can occur in different parts of the body — such as an inguinal hernia which can occur near the pubic bone, an umbilical hernia which occurs near the umbilicus (or “belly button”), or in a hiatal hernia in the upper part of the abdominal wall. A strangulated hernia is a serious condition where the blood supply to the stomach, intestines or other organ is being cut off because of that part of the body being forced into the small hole of the hernia, and requires immediate medical attention.
What Causes Hiatal Hernia?
A common contributing factor to development of a hiatal hernia is obesity — especially when people are carrying their weight around their middles. The presence of increased fat around their internal organs (called visceral fat), as well as the excess fat under their skin (called sub-cutaneous fat — meaning “under the skin”) contributes to increased abdominal pressure especially when they are sitting, frequently bending, or lifting heavy objects.
Other contributing factors are frequent coughing (sometimes secondary to smoking), straining due to constipation, or it may simply be hereditary.
Symptoms of a Hiatal Hernia
Hiatal hernias are usually diagnosed when people go to their doctors complaining of symptoms such as frequent heartburn, or are having a test such as a barium swallow or endoscopy, for some other reason.
Many people with hiatal hernias have no symptoms — and because of that, they don’t even know they have one! People without symptoms usually don’t require treatment — although they may be advised to lose weight — especially if they are carrying excess weight around their abdomen. If their waist-to- height ratio is greater than 0.50, this means they are carrying more weight around their middle then optimal, so reducing this is a great place to start to prevent symptoms from occurring. Reducing fat around the abdomen may reduce abdominal pressure caused by the excess fat in the belly pushing the stomach up through the hernia.
Symptoms may include heartburn, chest pain or pressure, coughing, or frequent burpingand since these symptoms may be caused by other conditions, it is important that people first see their doctor to find out the cause. In addition, many people with hiatal hernia have also been diagnosed with GERD (gastroesophageal reflux disease) and by teaching people how to make simple dietary and lifestyle changes often greatly reduces and even eliminates the symptoms of both.
Final Thoughts…
Losing weight, especially around the belly, and simple dietary and lifestyle changes can significantly improve the symptoms that result from hiatal hernia, as well as GERD which often accompany it.
More Info?
I provide nutrition education for reducing the symptoms of hiatal hernia which can be taken as a one-hour stand alone session, or at reduced cost as an add-on option for those taking the Complete Assessment Package. You can read more about that here.
Ashwell M, Mayhew L, Richardson J, Rickayzen B (2014) Waist-to-Height Ratio Is More Predictive of Years of Life Lost than Body Mass Index. PLoS ONE 9(9)
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.
When people come to me because they think they may be allergic to certain foods, the first thing I ask is if they have an allergy to any trees or grasses. This may seem like a strange question but some people who are allergic to tree or grass pollen may have symptoms when eating certain foods because the pollen of the tree or grass is similar to the pollen that forms the fruit or vegetable and the body recognizes the similarity. This is known as cross-reactivity.
A person who is allergic to a tree or grass pollen reacts to the food — not because they are allergic to the food itself, but because they are allergic to a pollen from a tree or grass that has similar protein sequences. If a person has never been tested for environmental allergies (pollens, for example) or for food allergies, the first place I get started is to recommend that their doctor have them tested by an allergist.
What is a Food Allergy?
An allergy is an immune-system mediated reaction which results in the body producing specific allergen IgE antibodies to the substance they are allergic to (the allergen). When people are exposed to the substance they are allergic to, the specific IgE antibody binds with their mast cells (a type of white blood cell that is part of the immune system) which result in the release histamine which causes the symptoms of an allergic reaction, which most often are sneezing, itching, difficulty breathing, or other symptoms. A true allergy is always involve IgE antibodies therefore food sensitivity tests based on IgG antibodies commonly performed by naturopaths do not diagnose food allergy.
Each IgE antibody is specific to one type of allergen, but some types of environmental substances (such as pollen or grass) or foods have several components that have protein sequences that can produce allergy. Using a food as an example, a person with a “milk allergy” may produce IgE antibodies to β-Lactoglobulin or α-Lactalbumin — two completely different proteins found in the whey fraction of milk, or they may be allergic to casein, a protein that makes up another fraction of milk. A person with a milk allergy may produce specific IgE antibodies to α-Lactalbumin but not to β-Lactoglobulin, or to casein but not the others. Or, they may allergic to all three.
Similarly, a person allergic to a tree pollen may produce IgE antibodies to only one protein in that pollen, or to several.
Oral Allergy Syndrome (OAS) – pollen allergy
Most food allergies in adults who never had food allergies as children are the result of cross-reactions between food and inhaled allergens such as pollen[1] that they are allergic to. This is this known as Oral Allergy Syndrome (OAS).
If a person has seasonal allergies in the early spring, it is most likely caused by allergies to tree pollen [2], and as many as 50%—70% of people who are allergic to birch pollen will have Oral Allergy Syndrome [3,4].
Alder is another common pollen allergen that results in OAS, as is latex found in rubber trees.
OAS reactions are most often thought of involving people’s lips, tongue or the roof of their mouth — where the cross-reacting food comes into contact with their body, but some people can also experience gastro-intestinal symptoms as a result of OAS — particularly related to birch pollen allergy[5].
It can get complicated, too.
An allergy to either birch or alder pollen can cause a Oral Allergy Syndrome to apples — but so can an allergy to apples, themselves.
How do we know if the person is reacting to apple because they are allergic to either birch or alder pollen (or both!), or because they are allergic to apples?
Only an allergist can determine that.
Since an allergist is specialized physician (MD), the costs of allergy tests done by an allergists are covered by provincial health plans
Once I’ve assessed someone, if I think they may be experiencing either food allergy of oral allergy syndrome, I will recommend that they speak to their doctor about being referred to an allergist for testing.
Once a person has been tested, the allergist’s office faxes me their report (with their permission, of course) and then person returns to me for teaching. If they have tested positive to foods or to pollens, I teach them how to avoid coming into contact with foods they are allergic to, as well as which foods may result in cross-reactions because they are allergic to specific pollens.
If they have tested negative to food or pollen allergies and the person’s symptoms are gastro-intestinal (involving their stomach or intestines), then if they haven’t already been tested, the next thing I usually rule out is celiac disease (gluten intolerance). This is determined with a simple blood test that their family doctor can requisition.
If the person has no food or pollen allergies, doesn’t have celiac disease, and their doctor has ruled out inflammatory conditions such as Crohn’s or colitis, then very often they are diagnosed with Irritable Bowel Syndrome (IBS). Since symptoms of IBS can be significantly minimized with changes in diet, I provide them with this type of teaching.
Final Thoughts…
Spring is almost here, and if you have seasonal allergies and find yourself having more reactions to food, it may be an indication that you have Oral Allergy Syndrome.
Mogensen JE, Wimmer R, Larsen JN, et al. The major birch allergen, Bet v 1
shows affinity for a broad spectrum of physiological ligands. J Biol Chem 2002;
277: 23684-92.
8. Hoffmann-Sommergruber K, O’Riordain G, Ahorn H, et al. Molecular characterization of Dau c 1, the Bet v 1 homologous protein from carrot and its cross-reactivity with Bet and Api g 1. Clin Exp Allergy 1999; 29:840-7.
Rentzos G, Lundberg V, Stotzer PO, Pullerits T, Telemo E. Intestinal allergic inflammation in birch pollen allergic patients in relation to pollen season, IgE sensitization profile and gastrointestinal symptoms. Clin Transl Allergy. 2014;4:19. Published 2014 May 30. doi:10.1186/2045-7022-4-19
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.
Most people know that prediabetes and diabetes is having “high blood sugar” but just how much sugar is actually in the human body? And how does grazing on food, rather than eating set meals affect this?
An adult has 5 liters of blood circulating in their body at any one time. A healthy person’s body keeps the range of sugar in the blood (called ‘blood glucose’) tightly-controlled between 3.3-5.5 mmol/L (60-100 mg/dl) — that is, when they eat food with carbohydrate the body breaks it down to sugar, and insulin takes the extra sugar out of the blood and moves it into cells.
Where does it put it?
First, the body makes sure that glycogen stores are sufficient, which is the body’s “emergency supply of energy”. There’s about a day’s worth of energy (2000 calories) in our muscle and liver glycogen. Once the liver and muscle glycogen is full, the rest of the blood sugar is moved to the liver where it is converted into LDL cholesterol and triglycerides and then the rest stored in fat cells. Fat is where the sugar that we make from the food we’ve eaten goes if it is not needed right away. Fat is storage for later.
So how much sugar is there in the blood of a healthy adult?
Doing the math (see illustration below), there are only 5 grams of sugar in the entire adult human body — which is just over one teaspoon of sugar.
That’s it!
One heaping teaspoon of sugar in the entire adult body!
The amount of sugar in the blood of a healthy adult
How Do We Understand Diabetes in Terms of Blood Sugar?
How much sugar does someone with diabetes have in their blood compared to a healthy person?
Someone with a fasting plasma glucose level of 7 mmol/L (126 mg/dL) meets the diagnostic criteria for Diabetes — which is just 6.25 grams of sugar or 1 -1/4 teaspoons. That is, the difference between the amount of sugar in the blood of a healthy person and the amount of sugar in the blood of someone with Diabetes is just a quarter of a teaspoon of sugar.
That’s it!
A quarter teaspoon of sugar is such a small amount but it makes the difference between someone who is healthy and someone who has Diabetes.
The difference between the amount of sugar in the blood of a healthy person and the amount of sugar in the blood of someone with Diabetes is just a quarter of a teaspoon of sugar.
In a person with type 2 diabetes, the once tightly-controlled system that is supposed to keep the range of sugar in the blood between 3.3-5.5 mmol/L (60-100 mg/dl) is “broken” — and it may get this way by them “grazing” all day long, or eating more carbohydrate than their body can handle. When someone with diabetes eats food with carbohydrate in it, their insulin is unable to take the sugar out of their blood fast enough, so the sugar stays in their blood longer than it should. Just as with a healthy person, the body of someone with type 2 diabetes takes the sugar that results from the food they’ve eaten and ‘tops up’ their liver and muscle glycogen stores, then the rest is sent to the liver where it is converted into LDL cholesterol and triglycerides, and then the rest is stored in fat cells. But what if the person is grazing all day long? The sugar just keeps on coming!
Some people have the ability to store the excess sugar in the form of fat under the skin (called sub-cutaneous fat). In this way, obesity is a way of protecting the body from this sugar overflow. Eventually though, if the constant flow of carbohydrate continues, the ability of the body to store the excess as sub-cutaneous fat is limited and then fat around the organs (called visceral fat) increases and this is what ends up contributing to type 2 diabetes and fatty liver disease. It is easy to pack away excess carbohydrate when one is grazing instead of eating, because they don’t eat enough at anyone time to feel satiated (full).
Sub-cutaneous fat (LEFT) versus visceral fat (RIGHT) – from Klí¶ting N, Fasshauer M, Dietrich A et al, Insulin-sensitive obesity, Am J Physiol Endocrinol Metab 299: E506—E515, 2010, pg. 5
The problem often is that we never get to access our fat stores because we are grazing on food with carbohydrate in it every few hours, storing the excess sugar in our fat stores. According to recent statistics, three-quarters of us lead sedentary (inactive) lives and barely get to make a dent in the energy we take in each day. We just keep getting fatter and fatter.
We eat breakfast — maybe a bowl of cereal (30 gms of carbs) or two toast (30 gms of carbs) or if we’re in a rush we grab a croissant breakfast sandwich at our favourite drive-through (30 gms of carb). Each of these contains the equivalent of a bit more than 6 teaspoons of sugar. Mid-morning, maybe we eat a fruit – say, an apple (30 gm of carbs) to hold us together until lunch — and take in another 6+ teaspoons of sugar in the process. Ifwe didn’t bring a fruit, maybe we go out for coffee and pick up an oat bar at Starbucks® (43 gms of carbs) — the equivalent of almost 10 teaspoons of sugar. The grazing continues…
At lunchtime, maybe we’ll have a sandwich (30 gm of carbs) or some leftover pasta from the night before (30 gm of carbs) or we’ll go to the food court and have a small stir-fry over rice (30 gm of carbs) — the equivalent of another 6+ teaspoons of sugar. Then, believing grazing is better than eating 3 big meals, maybe we eat another piece of fruit mid-afternoon, this time an orange (30 gms of carb) — and we’ve provided our body with the equivalent of another 6+ teaspoons of sugar.
In the scenario above, by mid afternoon (assuming we didn’t eat any fast-food or convenience foods, but only eating the food from home) we’ve eaten the equivalence of 24 teaspoons of sugar! But isn’t grazing, and eating food we bring from home supposed to be healthier?
What if we go to MacDonald®’s and eat a Big Mac® (20 g of carbs), large fries (66 g of carbs) and a large soft drink (86 g of carbs) – we’ve eaten a total of 172 g of carbs – which is equivalent to 43 teaspoons of sugar in just one meal!
In short, a healthy person will keeps moving the excess carbohydrate they eat off to their liver and will keep making triglyceride and LDL cholesterol out of it and storing the rest as fat and a person who is not insulin resistant or does not have type 2 diabetes will have normal blood sugar level, but their high carbohydrate intake can be reflected in their “cholesterol tests” (called a lipid panel) — where we may see high triglyceride results or high LDL cholesterol results or both.
The body takes the triglycerides into very-low-density lipoprotein (VLDL) cholesterol. Think of these as “taxis” that move cholesterol, triglycerides and other lipids (fats) around the body. When the VLDL reach fat cells (called ”adipose tissue”), the triglyceride is stripped out and absorbed into fat cells. The VLDLs shrink and becomes a new, smaller, lipoprotein, which is called Low Density Lipoprotein, or LDL — the so-called bad cholesterol’. This is a misnomer, because not all LDL is harmful. LDL which is normally large and fluffy in texture is a good cholesterol (pattern A) that can become bad cholesterol (pattern B) when it becomes small and dense.
In a healthy person, LDL is not a problem because they find their way back to the liver after having done their job of delivering the TG to cells needing energy. In a person with insulin resistance however, the LDL linger a little longer than normal, and get smaller and denser, becoming what is known as “small, dense LDL” and these are the ones that put us at a risk for cardiovascular disease.
There are two important points here: (1) the only source of LDL is VLDL not the fat we take in though our diet and (2) only the “small dense LDL are “bad” cholesterol and these occur as a result of insulin resistance.
People often believe that because their blood sugar is ‘normal’ on a lab test, that there isn’t any problem, but as Dr. Joseph Kraft discovered in his 25+ years of research measuring blood glucose and insulin response in some 10,000 people, 75% of people with normal glucose levels are actually insulin resistant and are at different stages of pre-diabetes or “silent Diabetes” (what Dr. Kraft called “Diabetes in situ”).
These people (and maybe their doctors) think they are “fine” because their blood sugar seems normal. Perhaps however, their triglycerides and LDL blood tests come back high. The origin of the problem is not because they are eating too much fat, but grazing on too much carbohydrate.
The body is trying to store the excess sugar somewhere. First it stores it in glycogen, then the rest is made into triglyceride and LDL and shipped all over the body, with the rest stored as fat. The fat cells in the body keep filling up — in the muscle, in and around our organs, and some get “fatty liver disease” and some even get fat cells in their bones if their body needs a place to put it. Bone is not supposed to have fat cells it in, but the body has to store it somewhere, because the carbohydrates just keep arriving every few hours!
Think of grazing it this way;
Imagine you are at home and you hear the doorbell ring. You go to the door and there’s a package and it’s for you. You take the package, close the door and head to the kitchen table to open it. Just as you’re about to open it, the door bell rings again. You go to the door, and there’s another package — and it’s for you, again. You take the package and head back to the kitchen and set it down beside the first, when (you guessed it) the doorbell rings again. You take that package and the ones that keep arriving, finding places to put them. When the kitchen table is full, you put the packages on the floor underneath the table, but then you get a delivery of several packages. You set those down wherever there’s a spot, just in time to answer the door yet again. Package after package arrives and before you know it, you look like something out of the TV series Hoarders. You can barely move for all the boxes, and all of them are unopened.
This is what grazing on meals and snacks with carbohydrates in them every few hours is like.
We overwhelm our body’s tightly-regulated system that is supposed to maintain our blood sugar level between 3.3 and 5.5 mmol/L (60-100 mg/dl) by continually requiring it to process the equivalent of anywhere from 6 teaspoons of sugar in a bowl of cereal or two toasts to the equivalent of 43 teaspoons of sugar in a fast-food meal.
This is how the system gets “broken”.
In time, we may get Type 2 Diabetes or fatty liver disease or high triglycerides or high cholesterol or group of symptoms called Metabolic Syndrome. This is the result of the constant strain we put our bodies under by eating a steady diet of foods containing a large percentage of carbohydrate.
It is easy to see where the high rates of obesity and Diabetes have come from. We have become a nation of “hoarders”.
What’s the solution?
We stop the constant delivery of packages of carbohydrate every few hours.
We feed our body the protein and the nutrients it needs with enough fat to use as fuel (in place of carbs) and allow it to take the extra energy it needs from our “stored fat”. We finally take the fat out of storage and we do this by following a low carb high fat diet.
Klí¶ting N, Fasshauer M, Dietrich A et al, Insulin-sensitive obesity, Am J Physiol Endocrinol Metab 299: E506—E515, 2010, http://www.physiology.org/doi/10.1152/ajpendo.00586.2009
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