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Why on earth would a Dietitian suggest to avoid making New Year’s resolutions to lose weight, exercise more or eat healthier? The reason is that research indicates that half of those that make these types of health-related  New Year’s Resolutions give up just a week into the new year [1] and by the end of January, 83% will have given up [1]. A New Year’s resolution will see only 8% of people reach their goal, with 92% failing[1]. I want people succeed and since it takes approximately 66 days (that’s more than 2 months!) to create a new habit[2] having my support during the critical planning and implementing stage can make a huge difference!

Rather than making a New Year’s resolution, I recommend that people set SMART goals. Ideally if they want to lose weight during the new year, they will have done this in November and begun to implement their plan in December but it’s not too late!  Setting SMART goals in January and beginning to implement them in February works great!

What are “SMART” goals?

SMART is an acronym for goals that are specific, measurable, achievable, relevant and time-bound.

Goals that are Specific

When setting a goal, it needs to be specific.

If your goal is weight loss, then think about exactly what you are trying to accomplish in terms of how much weight in what amount of time.

If your goal is to exercise more, than decide how often you will exercise, for how long at each session , and what types of exercise you will do (weights, resistance, cardio, etc).

If your goal is to eat healthier, then define what that means to you.  Is it “clean eating”; then what is that, exactly?  If you want to eat to lower your blood sugar or cholesterol or blood pressure or to reduce your risk to specific diseases that run in your family, then you need to define it that way.

Goals that are measurable

When setting a goal it is necessary to define what is going to be used to measure whether the goal will have been met.  If the goal is weight loss, then it can be measured by a certain number of pounds or kilos lost or by a specific waist to height ratio.

If the goal is to exercise more, then it can be measured in times per week at the gym, the number of hours spent exercising each week or how many fitness classes you attend each month.

If the goal is to eat healthier, then how are you going to measure that?  It could be measured in how many times you eat fatty fish (like salmon or mackerel) in a week, or how many grams of carbohydrate you eat per day or how many servings of leafy green vegetables you eat per day.  How will you measure it?

What does success look like?

Goals that are achievable

For goals to be be successfully accomplished, they need to be realistically achievable from the beginning, otherwise people get discouraged and give up.

When it comes to setting weight loss goals, it is not uncommon for people to decide they want to lose 20 pounds in a month before a special social function, but is it achievable?

When it comes to exercising more, is it achievable to set a goal of working out an hour a day, 7 days per week or is there a different goal that is more likely to be achievable, but will still keep you progressing?

It’s the same with eating healthier; the goal needs to be achievable.  When I started my personal weight loss and health-recovery journey in March 2017, one of the goals I set was to put my Type 2 Diabetes into remission by a year. Based on the research and how I decided to eat, that was achievable. It actuality it took me 13 months to accomplish, but I was not discouraged that I didn’t actually achieve it in the time frame I planned because the goal was achievable. I was close at a year, just not “there” yet.

Goals that are relevant or realistic

For a goal to be relevant it needs to fit within a person’s broader goals.

If I have a goal to lose weight but I have a larger goal to eat with my kids, then I need to plan to make food for myself that is the same as what I make for them, with some modifications for my weight loss goals

If one of my goals is to spend more time with my kids in the evening then planning to go running each evening as a way of exercising more does not fit within my broader goals. If my goal is to buy only locally-sourced food and I want to eat mangoes as part of my plan to eat healthier, I will face challenges if I live in the northern US or Canada and it’s wintertime. We need to know our broader goals and set our individual ones in that context.

For a goal to be realistic it needs to be achievable and for this step, it is often best to consult someone that would know.

Goals that are time-bound

Setting a goal to “lose weight” is one thing.  That’s pretty generic.  Setting a goal to lose a given amount of weight in a specific amount of time means that a lot of planning and implementing needs to occur for that goal to be successfully realized.  It is the planning and implementing to achieve a specific, measurable, achievable and realistic goal in a specific time-frame that makes it successful.

A Dietitian’s Journey – SMART Goals

Back in March 2017 when I set out to restore my own health and lose weight, these were the goals that I set;

(1) blood sugar in the non-diabetic range

(2) normal blood pressure

(3) normal / ideal cholesterol levels

(4) a waist circumference in the ”at or below” recommended values of the Heart and Stroke Foundation

While they don’t appear as SMART goals, as a Dietitian I knew what the “normal range” for these was and the time-frame I set was one year.

At the one year mark, my progress report as posted on Diet Doctor on March 14, 2018:

I did reach my goal of having my waist circumference at or below the recommended values of the Heart and Stroke Foundation, but still had a way to go to get it in a healthier range based on waist to height ratio;

I have not yet reached a low-risk waist circumference (one where my waist circumference is half my height).  I still have to lose another 3 inches to lose (having already lost 8 inches!), so however many pounds I need to lose to get there, is how much longer I have to go.

I am guessing that will be in about 20-25 pounds which may take another 6 months or so, but I’m not really concerned about the time because this ”journey” is about me getting healthy and lowering my risk factors for heart attack and stroke, and any amount of time it takes is what it will take.

It took years to make myself that metabolically unhealthy and it will take time for me to get to a healthy body weight and become as metabolically well’ as possible.

(from “A Dietitian’s Journey”)

As it turned out, it was only a week ago last Monday that I finally got to a place where my waist circumference was half my height; 8 months after my first year update. That was 2 months more than I thought it would take, but only 20 pounds more that I needed to lose to accomplish it, so I was close.

Was I discouraged at 6 months when I hadn’t “arrived”?

No, because  from the beginning my goals were SMART which made them rooted in what was possible.

I was very specific as to what I wanted to accomplish, how I was going to measure success, that the goals were achievable based on the available research, were relevant to my larger life goals and were time-bound. That said, just because reaching my goals was possible did not guarantee that I would achieve all of them in the time I planned. I achieved most of them within a year, and achieved the rest with a little more patience and time.

Some final thoughts…

Instead of setting a New Year’s resolution to lose weight, exercise more or eat healthier, perhaps spend the month of January setting very specific SMART goals. At the end of January, when 83% of the people have already given up on their New Year’s resolutions to improve their health, you will about to implement your well-thought out, realistic plan and may have already engaged me, as a Dietitian or a personalized trainer to help you implement it. Now THAT is a whole lot more than wishful thinking!

1. “What specifically do I want to accomplish”
2. “How will I measure success?”
3. Is this achievable? Do I know? Where can I find out?
4. Is this goal relevant to my larger life goals?
5. What time-frame do I want to accomplish this by?

Write out what you can about each of your goal(s) and then if achieving your goal will take more than a few months or a year or more to achieve, then I’d recommend engaging a professional to support you.

When it comes to weight loss and eating healthier I can certainly help, and if your goal is to lower risk to specific types of diseases I can certainly share with you the information I have gleaned as to which types of exercise are the most helpful in that regard.

If you want to consult with me to help you set SMART goals, please click here to learn more or send me a note using the Contact Me form located on the tab above. I provide in-person services in my Coquitlam (British Columbia) office or via Distance Consultation (Skype, phone) so whether you live close or far away, I’m happy to help.

If you would like more information about my hourly services or the packages I offer, please click on the Services tab above and if you have questions about those, please send me a note using the Contact Me form and I’ll reply when I am able.

Wishing you the very best for a  healthy and happy New Year!

Joy

You can follow me at:

       https://twitter.com/lchfRD

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

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https://www.instagram.com/lchf_rd

 

Copyright ©2018 BetterByDesign Nutrition Ltd.

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

References

1. 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
2. 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.

On Monday, December 17, 2018, the American Diabetes Association released its new 2019 Standards of Medical Care in Diabetes including its Lifestyle Management Standards of Care which includes use of a low carbohydrate diet saying it may result in lower blood sugar levels and also has the potential to lower the use of blood sugar lowering medications[1] in those with Type 2 Diabetes. In support, they cite the one-year study data by Virta Health[2], as well as two other studies [3,4].

“…research indicates that low carbohydrate eating plans may result in improved glycemia and have the potential to reduce antihyperglycemic medications for individuals with type 2 diabetes…”

The new 2019 Standards of Care reflect the American Diabetes Association’s change in approach which began in 2018 to revise the guide throughout the year as new scientific evidence warrants it, rather than to wait annually to update guidelines. Towards that end, in November 2018, the American Diabetes Association launched a joint partnership with the American Heart Association to raise awareness about the increased risk of cardiovascular disease for those diagnosed with Type 2 Diabetes and in October, the American Diabetes Association in conjunction with the European Association for the Study of Diabetes (EASD) released a joint Position Statement which approved use of a low carbohydrate diet as Medical Nutrition Therapy (MNT) for adults with Type 2 Diabetes (you can read more about that here).

The American Diabetes Association’s newly released 2019 Lifestyle Management  Standards of Medical Care in Diabetes builds on this joint consensus paper released with the EASD by including use of a low carbohydrate diet in the section on Nutrition Therapy where it emphasizes a patient-centered, individualized approach based on people’s current eating patterns, personal preferences and metabolic goals;

“Evidence suggests that there is not an ideal percentage of calories from carbohydrate, protein, and fat for all people with diabetes. Therefore, macronutrient distribution should be based on an individualized  assessment of current eating patterns, preferences, and metabolic goals. Consider personal preferences (e.g., tradition, culture, religion, health beliefs and goals, economics) as well as metabolic goals when working
with individuals to determine the best eating pattern for them.”

The ADA deemphasizes a focus on specific nutrients; whether fat or carbohydrate and stresses that a variety of eating patterns are acceptable.

“Emphasis should be on healthful eating patterns containing nutrient-dense foods, with less focus on specific nutrients. A variety of eating patterns are acceptable for the management of diabetes”.

The Lifestyle Management Standards of Care underscores the importance of having a Registered Dietitian involved in the process of assessing a person’s overall nutritional status, as well designing an individualized Meal Plan for them that is tailored to their health, cooking skills, financial resources, food preferences and health goals and that is coordinated with the person’s physician who is responsible for prescribing and adjusting their medications.

“…a referral to an RD or registered dietitian nutritionist (RDN)
is essential to assess the overall nutrition status of, and to work collaboratively with, the patient to create a personalized meal plan that considers the individual’s health status, skills, resources, food preferences, and health goals to coordinate
and align with the overall treatment plan including physical activity and medication.”

They outline a few eating patterns that are examples of  healthful eating
patterns that have shown positive results in research, including the Mediterranean diet, the DASH diet, plant-based diets and add that

“low-carbohydrate eating plans may result in improved glycemia (blood sugar) and have the potential to reduce anti-hyperglycemic medications (medications to lower blood sugar) for individuals with type 2 diabetes.”

The documents emphasizes again that individualized meal planning should focus on personal preferences, needs, and goals rather than focusing on any specific macronutrient distribution.

Without citing any references, the Standards of Care state that there are challenges with the ability of people to continue to follow a low carbohydrate diet long term and as a result that it’s important to reassess people who adopt this approach.

“As 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.”

It’s unfortunate that the ADA did not have access to the very recently released two-year data from Virta Health’s study which showed a 74% retention rate in the low carb intervention.

The ADA takes the position that a low carbohydrate meal plan is not recommended for women who are pregnant or breastfeeding, people who have- or are at risk for eating disorders, or have kidney disease and that caution should be taken with those taking SGLT2 inhibitor medication* for management of Type 2 Diabetes, as there is the potential risk of a condition known as diabetic ketoacidosis (DKA).

*This article outlines the risk of SGLT2 inhibitors, as well as other medications used to treat high blood pressure and some mental health disorders that need supervision when following a low-carbohydrate diet.

Low Carbohydrate Diets for Weight Loss

The ADA’s new 2019 Lifestyle Management Standards of Care also includes use of a low carbohydrate diet in the Weight Management section of the document, which underscores the benefit in blood sugar control, blood pressure and cholesterol (lipids) of weight loss of at least 5% body weight in overweight and obese individuals and that weight loss goals of 15% body weight may be appropriate to maximize benefit.

In this section dealing with Medical Nutrition Therapy (MNT), the role of a Registered Dietitian (RD) / Registered Dietitian Nutritionist (RDN) is emphasized;

“MNT guidance from an RD/RDN with expertise in diabetes and weight management, throughout the course of a structured weight loss plan, is strongly recommended.”

The ADA’s Lifestyle Management Standards of Care indicates that studies have demonstrated that a variety of eating plans with different macronutrient composition can be used safely and effectively for 1-2 years to achieve weight loss in people with Diabetes, including the use of a low-carbohydrate diet and that no single approach has been proven to be best;

“Studies have demonstrated that a variety of eating plans, varying in macronutrient composition, can be used effectively and safely in the short term (1—2 years) to achieve weight loss in people with diabetes. This includes structured low-calorie meal plans that include meal replacements and the  Mediterranean eating pattern, as well as low-carbohydrate meal plans. However, no single approach has been proven to be consistently superior.”

It is concluded that more study is needed to know which of these dietary patterns is best when used long-term and which is best accepted by patients over a long period of time.

“more data are needed to identify and validate those meal plans that are optimal with respect to long-term outcomes as well as patient acceptability.”

In the section dealing specifically with Carbohydrates, it is indicated that for people with Type 2 Diabetes or prediabetes that low-carbohydrate eating plans show the potential to improve blood sugar control and cholesterol outcomes for up to one year, and that part of the problem in interpreting low-carbohydrate research has been due to the wide range of definitions of what “low-carbohydrate” is (i.e. <130 g of carbohydrate, <50 g carbohydrate).

Point of Interest: No where in the Lifestyle Management Standards of Medical Care in Diabetes does the American Diabetes Association define what they mean by “low carbohydrate diet”.  The fact that they cite the one-year study data from Virta Health[2] (see above) as evidence for safety and efficacy in lowering blood sugar and Diabetes medication usage when that study clearly employs a ketogenic approach is most interesting.

” 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. Part of the challenge in interpreting low-carbohydrate research has been due to the wide range of definitions for a low-carbohydrate eating plan.”

The Standards of care stated that because most people with Diabetes say they eat between 44—46% of calories as carbohydrate, and that changing people’s usual macronutrient intake usually results in them going back to how they ate before, that they recommend designing meal plans based on the person’s normal macronutrient distribution, because it is most likely to result in long-term maintenance.

“Most individuals with diabetes report a moderate intake of carbohydrate (44—46% of total calories). Efforts to modify habitual eating patterns are often unsuccessful in the long term; people generally go back to their usual macronutrient distribution. Thus, the recommended approach is to individualize meal plans to meet caloric goals with a macronutrient distribution that is more consistent with the individual’s usual intake to increase the likelihood for long-term maintenance.”

NOTE: Most people are likely to indicate they eat within the recommended range of carbohydrate intake (45-65% of calories as carbohydrate) because that is how they were counselled when they were diagnosed with Type 2 Diabetes, but stating that they should continue to eat that way because they are most likely to be compliant makes no sense. If a person realizes they are not able to meet optimal blood sugar levels eating that level of carbohydrate intake and are interested and motivated to lower it, then as healthcare professionals, we need to be equipped to support that in an evidenced-based manner.

In this section on Carbohydrates, it was emphasized that;

“…both children and adults with Diabetes are encouraged to minimize intake of refined carbohydrates and added sugars…”

and

“The consumption of sugar-sweetened beverages (including  fruit juices) and processed ”low-fat” or ”nonfat” food products with high amounts of refined grains and added sugars is strongly discouraged.”

Protein

With respect to protein intake, it was emphasized that;

(1) there isn’t any evidence to suggest that adjusting protein intake from 1—1.5 g/kg body weight/day (15—20% total calories) will improve health.

(2) research is inconclusive regarding the ideal amount of dietary protein to optimize either blood sugar control or cardiovascular disease (CVD).

(3) “some research has found successful management of type 2 diabetes with meal plans including slightly higher levels of protein (20—30%), which may contribute to increased satiety.”

Caution for those with diabetic kidney disease (i.e. urine albumin and/or reduced glomerular filtration rate) advise that dietary protein should be maintained at the recommended daily allowance of 0.8 g/kg body weight/day.

Fats

The Standards of Care acknowledged that the ideal amount of dietary fat for individuals with diabetes is controversial and underscored that the National Academy of Medicine has defined an acceptable macronutrient distribution for total fat for all adults to be 20—35% of total calorie intake. They stated that the type of fats consumed are more important than the total amount of fat when looking at metabolic goals and cardiovascular (CVD) risk and recommended that the percentage of total calories from saturated fats be limited. It was recommended that people with Diabetes follow the same guidelines as the general population when it comes to intakes of saturated fat, dietary cholesterol and trans fat and they recommended a focus on eating polyunsaturated and monounsaturated fats for improved glycemic  (blood sugar) control and blood lipids (cholesterol) and that there does not seem to be a CVD benefit of supplementing with omega-3 polyunsaturated fatty acids.

Other Points of Interest

It is interesting that the Lifestyle Management Standards of Care indicated that the literature concerning Glycemic Index (GI) and Glycemic Load (GL) in individuals with Diabetes often yields conflicting results and that “studies longer than 12 weeks report no significant influence of glycemic index or glycemic load independent of weight loss on A1C”.

Conclusion

The American Diabetes Associations 2019 Lifestyle Management Standards of Medical Care in Diabetes emphasis on a patient-centered, individualized approach is under-girded by an acknowledgment that based on the current evidence, a low-carbohydrate diet is both safe and effective used as Medical Nutrition Therapy for up to two years in adults in order to lower blood sugar, reduce Diabetes medication usage and support weight loss.

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I’m a Registered Dietitian that has years of experience working with non-insulin dependent individuals with Type 2 Diabetes. I can assess your overall nutritional status, review your personal and family medical background and lifestyle habits and create a individualized Meal Plan just for you that considers your health status, cooking skills, food preferences, resources as well as your health and weight goals. I even offer a single package (the Complete Assessment Package) that will do just that.

I provide in-person services in my Coquitlam (British Columbia) office as well as via Distance Consultation (Skype, long distance) for those outside of the Lower Mainland area.

You can find out more about the hourly consultations and packages I offer by clicking on the Services tab above and if you have questions, feel free to send me a note using the Contact Me form, and I will reply as soon as I am able.

To your good health!

Joy

You can follow me at:

       https://twitter.com/lchfRD

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

          https://plus.google.com/+JoyYKiddieMScRD

https://www.instagram.com/lchf_rd

 

Copyright ©2018 BetterByDesign Nutrition Ltd.

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

References

1. American Diabetes Association, Lifestyle Management Standards of Medical Care in Diabetes – 2019. Available at: http://care.diabetesjournals.org/content/42/Supplement_1. Accessed: Dec. 17, 2018.
2. 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
3. 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
4. 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

Some speak of having “reversed” Type 2 Diabetes (T2D) as a result of dietary changes whereas others refer to having achieved “remission”. What is the difference and why is the distinction important?

What is meant by Type 2 Diabetes “reversal”

“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.

We do see Type 2 Diabetes reversal in a majority of T2D patients who have undergone a specific kind of gastric bypass surgery called Roux-en-Y; with 85% having achieving normal blood sugar levels within weeks of having the surgery, without taking any blood sugar lowering medications or following any special diet[1]. The mechanism that is thought to make Type 2 Diabetes reversal possible with this type of surgery are (a) that the operation results in more of the incretin hormone GIP being released in the upper part of the gut (duodemum, proximal jejunum) which results in less insulin resistance [2,3] or (b) that the presence of food in lower gut (terminal ilium, colon) stimulates the lower incretin hormone GLP-1, which results in more insulin being secreted [3], which lowers blood sugar levels.

Is Type 2 Diabetes “reversal” possible with diet alone?

It is currently believed that T2D may be reversible by non-surgical intervention if diagnosed very early on in the progression of the disease.

One matter that needs to be overcome is that both the mass and function of the β-cells of the pancreas that produce insulin are thought to be reduced by 50% by the time someone is diagnosed with Type 2 Diabetes [5]. Furthermore, the β-cells are thought to continue to deteriorate the longer a person has Type 2 Diabetes.

It is unknown for how long or at what stage T2D becomes irreversible [6].

What is meant by Type 2 Diabetes “remission”

There is evidence that indicates that weight loss of ~15 kg (33 pounds) can result in remission of Type 2 Diabetes symptoms and that β-cell function can be restored  to some degree either by (a) dormant β-cells being reactivated through a variety of means or (b) by existing β-cells functioning better [6].

Type 2 Diabetes “reversal” defined

In 2009, the American Diabetes Association defined Type 2 Diabetes partial remission, complete remission and prolonged remission as follows;

Remission is defined as being able to maintain blood sugar below the Diabetic range without currently taking medications to lower blood sugar and remission can classified as either partial, complete or prolonged.

Partial remission is having blood sugar that does not meet the classification for Type 2 Diabetes; i.e. either HbA1C < 6.5% and/or fasting blood glucose 5.5 – 6.9 mmol/l (100—125 mg/dl) for at least 1 year while not taking any medications to lower blood glucose.

Complete remission is a return to normal glucose values i.e. HbA1C <6.0%, and/or fasting blood glucose < 5.6 mmol/L (100 mg/dl) for at least 1 year while not taking any medications to lower blood glucose.

Prolonged remission is a return to normal glucose values (i.e.
HbA1C <6.0%, and/or fasting blood glucose < 5.6 mmol/L (100 mg/dl) for at least 5 years while not taking any medications to lower blood glucose.

Remission can be achieved after bariatric surgery such as the Roux-en-Y procedure outlined above or with dietary and lifestyle changes such as a low-carbohydrate or ketogenic diet, weight loss and exercise.

According the American Diabetes Association, people who are able to achieve normal blood sugar through diet, weight loss and exercise but also take blood sugar lowering medication such as Metformin do not meet the criteria for either partial remission or complete remission.*

Those who have achieved normal blood sugar levels as a result of following a low-carbohydrate or ketogenic diet and are also taking the medication Metformin are sometimes referred to in published studies as having “reversed” their Type 2 Diabetes.  I think this is problematic because clearly if these people go back to eating a standard diet again, their blood sugar would not remain normal. As well, in some well-designed ketogenic diet studies subjects are allowed to use Metformin but no other blood sugar-reducing medication, but based on the American Diabetes Association definition the use of Metformin which helps regulate blood sugar (largely via reducing gluconeogenesis of the liver and making the muscles less insulin resistant) precludes these cases from being referred to as either partial remission or complete remission*.

Don’t get me wrong; having normal blood sugar (and insulin) levels as the result of a well-designed low carbohydrate or ketogenic diet with or without the use of Metformin enables people to reap significant health benefits and lower their risk of the chronic diseases related to hyperglycemia (high blood sugar) and hyperinsulinemia (high circulating levels of insulin) but it’s not reversal unless the people can then eat a standard diet without an abnormal glucose response.  It is normal glycemic control achieved through diet with or without the use of Metformin. Perhaps a term such as “partial remission with Metformin support” would be a more accurate descriptor.

Some final thoughts…

I think it’s important what terms we use.

There are genuine cases of Type 2 Diabetes “reversal” and we should use that term for those who can now eat a standard diet and maintain normal blood sugar levels, without the use of any medication or diet.

There are also genuine cases of “partial remission” or “complete remission” according to the American Diabetes Association definition that are a result of dietary and lifestyle changes and these terms should be reserved for cases where the defined criteria is met.

There are also genuine cases of “partial remission with Metformin support” that have been achieved as the result of people implementing dietary and lifestyle changes plus the use of Metformin that should be acknowledged and celebrated, but calling these either “Type 2 Diabetes reversal” or “Type 2 Diabetes remission” is confusing, at best.

Yes, Type 2 Diabetes a) reversal, b) partial remission and complete remission as well as c) partial remission with Metformin support are all possible. It may well be that people such as myself who had been Type 2 Diabetic for many, many years can eventually transition to genuine partial remission with eventual discontinuation of Metformin. That is my hope, at any rate!  The bottom line is that maintaining normal blood glucose levels and normal circulating levels of insulin is necessary in order to put the symptoms of Type 2 Diabetes into remission, as well as to reduce the risks to the chronic diseases associated with high blood sugar and insulin levels — and for that there are well-designed dietary and lifestyle changes. This is where I can help.

If you have Type 2 Diabetes or have been diagnosed as being pre-diabetic (which is the final stage before a diagnosis, not a ”warning sign” — more about that here) and would like to work toward putting your symptoms into remission, then please send me a note using the Contact Me form above to find out more about how I can help.

I offer both in-person and Distance Consultation services (via Skype or long distance phone) and would be glad to help you get started as well as support you as you achieve your health and weight loss goals.

To yours and my good health!

Joy

You can follow me at:

       https://twitter.com/lchfRD

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

          https://plus.google.com/+JoyYKiddieMScRD

https://www.instagram.com/lchf_rd

 

Copyright ©2018 BetterByDesign Nutrition Ltd.

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

References

1. Xiong, S. W., Cao, J., Liu, X. M., Deng, X. M., Liu, Z., & Zhang, F. T. (2015). Effect of Modified Roux-en-Y Gastric Bypass Surgery on GLP-1, GIP in Patients with Type 2 Diabetes Mellitus. Gastroenterology research and practice, 2015, 625196.
2. Schauer P. R., Kashyap S. R., Wolski K., et al. Bariatric surgery versus intensive medical therapy in obese patients with diabetes. The New England Journal of Medicine. 2012;366(17):1567—1576
3. Lee W. J., Chong K., Ser K. H., et al. Gastric bypass vs sleeve gastrectomy for type 2 diabetes mellitus: a randomized controlled trial. Archives of Surgery. 2011;146(2):143—148.
4. Laferrí¨re B., Heshka S., Wang K., et al. Incretin levels and effect are markedly enhanced 1 month after Roux-en-Y gastric bypass surgery in obese patients with type 2 diabetes. Diabetes Care. 2007;30(7):1709—1716
5. Taylor R. Banting Memorial lecture 2012: reversing the twin cycles of type 2 diabetes. Diabet Med. 2013;30:267-275
6. Watson J., Can Diet Reverse Type 2 Diabetes? December 12, 2018 https://www.medscape.com/viewarticles/905409_print

In the previous article titled When Normal Fasting Blood Glucose Results Aren’t Necessarily “Fine” I explained how normal results on a fasting blood glucose (FBG) test may simply mask ‘silent Diabetes’ and that even when fasting blood glucose is normal and results from a 2-hour Oral Glucose Tolerance Test (2-hr OGTT) do not indicate glucose intolerance, a person can still have a very abnormal blood sugar response after they eat refined carbohydrates. These spikes’ can be seen between 30 minutes and 60 minutes on 2-hour glucose curves and are reflected by equally abnormal insulin curves. Chronically high circulating levels of insulin (called hyperinsulinemia) result from these blood sugar ‘spikes’ that occur every time the person eats carbohydrate-based foods, which is usually every few hours, for meals and snacks.

Insulin is released in order to take the excess sugar resulting from the digestion of carbs and move it out of the blood and into the cells and even though these people’s blood glucose returns to below the impaired glucose tolerance range by 2 hours, the abnormal glucose response particularly between 30 and 60 minutes drives hyperinsulinemia (chronically high levels of insulin) and is made worse by insulin resistance (which is the ignoring of insulin’s signal by the cells).  It is this hyperinsulinemia and insulin resistance that are the essence of carbohydrate intolerance; ; the varying degrees to which people can tolerate carbohydrate without their blood sugar spiking. It is not unlike other food intolerances such lactose intolerance or gluten intolerance which also reflect the body’s inability to handle specific types of carbohydrate in large quantities.

It is the hyperinsulinemia, rather than the high levels of blood sugar that puts people at risk for the serious chronic diseases of cardiovascular disease (heart attack and stroke), high cholesterol and high blood pressure[1] that people usually associate with type 2 diabetes. High blood sugar does have risks of course, including loss of vision, chronic kidney disease and amputation of limbs but if high blood sugar (hyperglycemia) is the “tip of the iceberg”, then high circulating levels of insulin (hyperinsulinemia) is the bigger part of the iceberg that can’t be seen. We can’t see it simply because it is rarely, if ever measured.

Most concerning is that based on a large-scale 2016 study which looked at the blood glucose response and circulating insulin responses from almost 4000 men aged 20 years and older and 3800 women aged 45 years or older during a 5-hour Oral Glucose Tolerance Test, 53% had normal glucose tolerance (normal fasting blood sugar and did not have impaired glucose tolerance (IGT) at 2 hours after the glucose load) but of these people, 75% had abnormal blood sugar results between 30 minutes and 60 minutes (two points in time that are not normally looked at in a standard 2-hour Oral Glucose Tolerance Test (2-hr OGTT).

A normal blood glucose curve represents Carbohydrate Tolerance, and there are 3 Stages of Carbohydrate Intolerance — early, advanced, and severe, with the final stage being a diagnosis of type 2 diabetes (T2D).

Hyperinsulinemia combined with insulin resistance form the heart of Carbohydrate Intolerance.

Insulin Resistance

In the early stages of Carbohydrate Intolerance, receptors in the liver and muscle cells begin to stop responding properly to insulin’s signal. This is called insulin resistance. Insulin resistance can be compared to someone hearing a noise such as their neighbour playing music, but after a while their brain ”tunes out” the noise.  Even if the neighbour gradually turns up the volume of the music, the person’s brain compensates by further tuning out the increased noise. This is what happens with the body when it becomes insulin resistant. It no longer responds to insulin’s signal. To compensate for insulin resistance, the β-cells of the pancreas begin producing and releasing more and more insulin resulting in hyperinsulinemia, which is too much insulin in the blood.

Normal Insulin Response

The β-cells of the pancreas of healthy people are constantly making insulin and storing most of it until these cells receive the signal that food containing carbohydrate has been eaten. β-cells also constantly release small amounts of insulin in very small pulses called basal insulin. This basal insulin allows the body to use blood sugar for energy even when the person hasn’t eaten for several hours or longer. The remainder of the insulin stored in the β-cells is only released when blood sugar rises after the person eats foods containing carbohydrate and this insulin is released in two phases; the first-phase insulin response occurs as soon as the person begins to eat and peaks within 30 minutes and can be seen at 30 minutes on the graph below. The amount of the first-phase insulin release is based on how much insulin the body is used to needing each time the person eats. Provided a carbohydrate tolerant person eats approximately the same amount of carbohydrate-based food at each meal day to day, the amount of insulin in the first-phase insulin response will be enough to move the excess glucose from the food into the cells, returning blood sugar to its normal range of ~100 mg/dl (5.5 mmol/L). If there is not enough insulin in the first-phase insulin response, the β-cells will release a smaller amount of insulin within an hour to an hour and a half after the person began to eat.

Below is the Carbohydrate Tolerance curve (i.e. normal glucose curve). The solid black line is unlabeled and is shown along with its corresponding normal insulin curve (dashed line). The insulin response more or less mirrors the glucose response; as glucose rises in the blood, insulin is released mainly as a first-phase insulin response, which results in the blood glucose level falling.

In 990 people with normal glucose tolerance and normal insulin tolerance (i.e. with curves like the one above), mean fasting insulin = 48.6 pmol/L, which is equivalent to 7 uU/ml / 7 mU/L [SD = 5 mU/L]. Therefore the normal range for fasting insulin 2-12 uU/ml.

Early Carbohydrate Intolerance

Below is the Early Carbohydrate Intolerance curve and the solid black line (glucose) is shown along with its corresponding abnormal insulin curve (dashed line). As glucose rises in the blood even more insulin is released; initially as a first-phase insulin release and then as a second-phase insulin release.  This results in blood glucose level falling but not to baseline (fasting level) by 2 hours afterwards. Notice too that the fall is not as a straight line, but there are two peaks in the glucose curve, before it falls.

It is insulin resistance of the liver and muscle cells which results in the β-cells of the pancreas making more insulin and as can be seen from the graph below it takes more insulin to move the same amount of glucose (carbohydrate) into the cell.

Advanced Carbohydrate Intolerance

By the time people have progressed to Advanced Carbohydrate Intolerance, the first-phase insulin response won’t produce enough insulin be able to clear the extra blood glucose after a carbohydrate load and even the second-phase insulin response won’t be enough to overcome the insulin resistance of the cells. At this point, the β-cells of the pancreas are unable to make enough insulin to clear the excess glucose from the blood and blood glucose rises well above the normal high peak of 126 mg/dl (7.0 mmol/L).  What is also apparent is that even with all the insulin release, blood sugar levels begin rising sooner and rise to much higher levels.

With ongoing high intake of carbohydrate every few hours, especially refined and processed carbohydrate such as bread, pasta and rice which are broken down quickly to glucose, the amount of insulin that must be released from the β-cells of the pancreas to handle a steady intake of carbohydrate-based foods increases substantially.  The dashed black line on the graph below shows the insulin curve of Advanced Carbohydrate Intolerance. While the Early Carbohydrate Intolerance glucose curve (above) doesn’t look significantly different then the Advanced Carbohydrate Intolerance curve (below), it’s easy to see that the insulin curves are very different.

The hyperinsulinemia (high levels of circulating insulin) present in Advanced Carbohydrate Intolerance is what makes these two states different.

Most concerning is these people had normal fasting blood sugar and 2-hour postprandial blood sugar which did not indicate that they had impaired glucose tolerance.  On a 2-hr OGTT, these folks would be told they were not pre-diabetic and would assume that everything was find — yet they had both an abnormal glucose response between 30 minutes and 60 minutes and abnormally high levels of insulin which accompanies it.

This high insulin response occurs every time these people eat significant amounts of refined carbohydrate and puts them at increased risk of the chronic diseases associated with chronic hyperinsulinemia including heart attack and stroke, hypertension (high blood pressure), elevated cholesterol and triglycerides, non-alcoholic fatty liver (NAFLD), Poly Cystic Ovarian Syndrome (PCOS), Alzheimer’s disease and other forms of dementia, as well as certain forms of cancer including breast and colon cancer [1].

A standard 2-hour OGTT would not show the significant abnormality in terms of how the body is able (or rather, not able) to process carbohydrate because standard blood tests do not test either glucose or insulin at 30 and 60 minutes.  It’s not that there aren’t abnormalities, it is just that they are not measured!

 Severe Carbohydrate Intolerance

As Carbohydrate Intolerance progresses, some people’s glucose-insulin curves look like the ones below. Blood sugar levels don’t rise as high, but the β-cells of the pancreas are producing less insulin and releasing it much later. They have no idea, because their fasting blood sugar is still normal.

Type 2 Diabetes

Type 2 Diabetes (T2D) is the final stage of Carbohydrate Intolerance and is the natural outcome of a person continuing to eat a diet high in carbohydrate-containing foods when their body is unable to tolerate it. Too often this is the natural outcome of people following Dietary Guidelines (US or Canadian) which are designed for a healthy population, not people who are metabolically unwell. The problem is most people think they are healthy because they have normal blood glucose tests, and their metabolic dysfunction is never diagnosed. No one is looking for it.

The Dietary Guidelines recommend that people eat 45-65% of their dietary intake as carbohydrate and people in both countries dutifully eat considerable amounts of carbohydrate in the form of bread, cereal, rice and pasta, as well as fruit, milk and sweetened yogurt and starchy vegetables such as peas, corn and potato. Not knowing their body has become carbohydrate intolerant, this chronically high intake of carbs continues to put strain on their pancreas, until udder the pressure of the combination of hyperinsulinemia and insulin resistance, their β-cells burn out, resulting in Type 2 Diabetes.

Some Final Thoughts…

It has been said that type 2 diabetes is a ”chronic, progressive disease”, but does it doesn’t have to be this way! It can be stopped LONG before fasting blood sugars become abnormal.

Diagnosing hyperinsulinemia is simple and can be done with existing standard lab tests; namely a 2-hour Oral Glucose Tolerance test with an extra glucose assessor and extra insulin assessor at 30 minutes and 60 minutes. When patients request this test because they are at high risk, too many are told that it is “a waste of healthcare dollars” when quite literally they could be spared the scourge of type 2 diabetes by having the changes in insulin and glucose response diagnosed in the 20 years before standard blood sugar begins show abnormalities [2].

NOTE (March 9, 2021): Some family medicine doctors won’t order tests to assess insulin along with glucose in order to “save healthcare system dollars” — but instead will send their patient to an endocrinologist which costs the system ~$300 before any tests are run. Why? In parts of Canada, if audited, family medicine physicians have to re-pay for preventative tests (which are deemed “unnecessary”) . Self-paying for these tests is an option to consider.

It’s time to think about ways to implement dietary changes and lab testing procedures that will prevent Carbohydrate Intolerance and from developing the abnormal glucose and insulin responses and the host of metabolic diseases that go along with them.

In fact, it is long overdue.

If you would like my help in lowering your risk to developing type 2 diabetes and the chronic disease risks associated with hyperinsulinemia, or reversing their symptoms, then please send me a note using the Contact Me form, on the tab above.

To your good health!

Joy

You can follow me at:

https://twitter.com/lchfRD

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

 

References

1. Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.
2. Sagesaka H, S.Y., Someya Y, et al, Type 2 Diabetes: When Does It Start? Journal of the Endocrine Society, 2018. 2(5): p. 476-484.

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Copyright ©2018 BetterByDesign Nutrition Ltd.

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

 

INTRODUCTION: When people have a fasting blood glucose test and the results come back normal they’re told (or assume) that everything’s fine. But is it? Certainly, a fasting blood glucose test is the least expensive test to find out if someone is already pre-diabetic, but for those wanting to avoid becoming diabetic and to lower their risk of the other chronic disease associated with type 2 diabetes and high levels of circulating insulin (called hyperinsulinemia) noticing abnormalities in how we process carbohydrates is essential and these changes are estimated to take place a decade before our fasting blood sugar begins to become abnormal.

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Our bodies have to maintain the glucose (sugar) in our blood at or below 5.5 mmol/L (100 mg/dl) but each time we eat or drink something other than water or clear tea or coffee, our blood sugar rises as our body breaks down the carbohydrate in the food from starch and complex sugars to glucose, a simple sugar.  Eating causes hormones in our gut, called incretin hormones to send a signal to our pancreas to release insulin, which moves the excess glucose out of our blood and into our cells. When everything is working properly, our blood sugar falls back down to a normal level within 2 hours after we eat.

If we’re healthy and don’t snack after supper, our blood sugar falls to a lower level overnight but that too is maintained in a tightly regulated range between 3.3 mmol/l (60 mg/dl) and 5.5 mmol/l (100 mg/dl). During the night and as we approach morning, our body will break down our stored fat for energy and convert it to glucose in a process called gluconeogenesis.

When we have a fasting blood glucose test, it measures our blood sugar after we’ve fasted overnight and when we’re healthy, the results will be between 3.3-5.5 mmol/L (60-100 mg/dl). If it is higher than 5.5 mmol/l (100 mg/dl) but less than 6.9 mmol/L (125 mg/dl) we are diagnosed with impaired fasting glucose, but what if it’s normal? Is a normal fasting blood glucose test result enough to say that we’re not at risk for Type 2 Diabetes? No, because a fasting blood glucose doesn’t tell us anything about how our body responds when we eat!

A 2 hour Oral Glucose Tolerance Test (2 hr-OGTT) may be requested for people whose fasting blood glucose is impaired (higher than 5.5 mmol/L) in order to see if it returns to normal after they consume a specific amount of glucose (sugar).

If their blood sugar returns to normal (less than 5.5 mmol/L) 2 hours after drinking a beverage containing 75 g of glucose (100 g if they’re pregnant) then the diagnoses remains impaired fasting glucose because it is only abnormal when fasting. However, if the results are greater than 7.8 mmol/L (140 mg/dl) but below 11.0 mmol/L (200 mg/dl), then they are diagnosed with impaired glucose tolerance which is called “pre-diabetes”.

If the 2 hour results are greater than 11.0 mmol/L (200 mg/dl), then a diagnosis of Type 2 Diabetes is made because their fasting blood glucose is > 7.0 mmol/L (126 mg/dl) and their 2 hour blood glucose is > 11.0 mmol/L (200 mg/dl).

But what if someone’s fasting blood glucose is normal? Does this mean that everything’s fine? Not necessarily, unless we know what happens to their blood sugar after a carbohydrate load, especially after 30 minutes or 60 minutes.

A 2016 study looking at blood sugar response (and insulin response) from almost 4000 men aged 20 years or older and 3800 women aged 45 years or older who had a 5 hour Oral Glucose Tolerance Test using 100 g of glucose. The study found that 53% had normal glucose tolerance; that is, they had normal fasting blood sugar and did not have impaired glucose tolerance (IGT) 2 hours after the glucose load. Of these people with normal glucose tolerance, 75% had abnormal blood sugar results between 30 minutes and 1 hour.

Normal Blood Glucose Pattern

Based on the above study, a little less than 1000 people (990) out of the total with normal glucose tolerance (4030) had a normal glucose pattern after having 100 g of glucose (see graph below). See how the blood sugar rises to a moderate peak and then decreases steadily until it’s back to where it started from at 2 hours. This is what blood sugar is supposed to do.

Abnormal Glucose Patterns

Almost the same number of people (961) as had normal glucose curves showed early signs of carbohydrate intolerance which can be seen most noticeably between 30 and 60 minutes. These folks had normal fasting blood glucose and but after 2 hours, blood glucose did not return to baseline, but did not meet the criteria for impaired glucose tolerance. Unless someone was looking between 30 and 60 minutes, one would not know it was not normal in between. Keep in mind, this graph represents the average blood sugar response of these individuals. Rather than blood glucose going up to a moderate peak and then falling gradually, a two-stage rise in glucose can be clearly seen between 30 minutes and 60 minutes before beginning to drop. These people had normal fasting blood sugar and while their blood sugar at 2 hours was below the cutoff for impaired glucose tolerance, it was higher than at baseline.

A little more than 1200 people (1208) had the follow abnormal glucose response between 30 and 60 minutes where blood sugar actually went slightly higher at 60 minutes than at 30 minutes before beginning to fall. While these people had normal fasting blood glucose their blood glucose did not fall to baseline at 2 hours but was below the cutoffs for impaired glucose tolerance.

Slightly more than 800 people (807) had an abnormal glucose response curve shaped as follows, with normal fasting blood glucose and  2-hour postprandial blood glucose results that were higher than at baseline, but did not meet the criteria for impaired glucose tolerance. What was significant is that blood sugar was significantly higher at 60 minutes than at 30 minutes.

The Significance of These Curves

The results of this study shows that even if fasting blood glucose is totally normal AND 2 hour postprandial blood glucose does not meet the criteria for impaired glucose tolerance, it often does not return to baseline and  the blood sugar response between fasting and 2 hours is very abnormal. What can’t be seen from these graphs is what happens to the hormone insulin at the same time. This will be covered in a future article, but suffice to say that in the normal glucose response pattern, blood sugar response mirrors what is happening with insulin but in the abnormal blood glucose response insulin secretion is both much higher and lasts much longer. This is called hyperinsulinemia (high blood insulin) and contributes to many of the same health risks as Type 2 Diabetes, including cardiovascular risks (heart attack and stroke), abnormal cholesterol levels and hypertension (high blood pressure).  This is like having “silent Diabetes”.

A “Waste of Healthcare Dollars”

When a person’s clinical symptoms and risk factors warrant it, I’ll request a 2 hour Oral Glucose Tolerance Test with an extra assessor at 30 minutes (and sometimes at 60 minutes) to determine how their glucose response compares to the above curves. Since these people have normal fasting blood glucose test results, a request for an Oral Glucose Tolerance Test (with or without the extra glucose assessor) is often declined as a “waste of healthcare dollars”.

What About Glycated Hemoglobin (HbA1C)?

A glycated hemoglobin test (HbA1C) measures a form of hemoglobin that binds glucose (the sugar in the blood) and is used to identify the person’s three-month average glucose concentration because blood cells turnover (get replaced) on average every 3 months.

While having a glycated hemoglobin test and a fasting blood glucose test is better than only having fasting blood glucose, it will still miss a significant percentage of people who are able to control their sugars between meals and overnight but who have significant spikes after eating food, between 30 minutes and 60 minutes, but that return to normal by 2 hours. Since most physicians will not even requisition a HbA1C test if a person’s fasting blood glucose is normal, and even if they do that test can miss the glucose spoke that occurs between 30 minutes and 60 minutes after eating, this is the reason I sometimes resort to using a Glucose Response Simulation.

Glucose Response Simulation

A simple, if somewhat crude means of assessing glucose response under a load can be done at home using an ordinary glucometer (a meter for measuring blood sugar) such as would be used by people with Diabetes, and either a 100 g of dextrose (glucose) tablets (available at most pharmacies) or the equivalent. As part of the services I provide to my clients, I work with those that want to do this type of estimate so that they can understand whether they fall into the 75% of people that have normal fasting blood sugar and do not have impaired glucose tolerance at 2 hour postprandial, but do have an abnormal glucose response, as well as hyperinsulinemia. I explain how to prepare for the test, step by step instruction for conducting the test and then I graph and analyze the data then teach them what the results mean.

Basis for Individualizing Carbohydrate Intake

These results are very helpful as firstly they help people understand the reason for reducing their carbohydrate intake over an extended period of time, in order to restore insulin sensitivity and insulin secretion. These results also enable me in time to individualize their carbohydrate intake once they have reversed some of their metabolic response, based on their own blood sugar response to a specific carbohydrate load.  In time, some of these individuals may want to add some carbohydrate back into their diet in small quantities, so with this information, I can guide them to test a standard size serving of rice, pasta or potato compared to their own blood glucose response to 100 g of glucose.

Below are three curves that I’ve plotted from people that all used the same type of glucometer (Contour Next One) which was rated as the best in a 2017 survey (see earlier post) and a standard 100 g glucose load as dextrose tablets or equivalent to 100 g of glucose [2]. I provided each one with identical instructions on how to run this simulation and to collect the results and ensured they understood.

Example 1: The person below had a single glucose peak (similar to the early carbohydrate intolerance of the first abnormal curve, above) but blood glucose did not come back down to the fasting level even after 3 hours.

Example 2: The person below had a single glucose peak  that reached abnormally high levels and that didn’t fall continuously downward but slowed, then dipped below baseline at 2 hours and that gradually came back to baseline over the following couple of hours.

Example 3: This person had a similar initial rise as the person above, but no dip below baseline. In fact, this person’s glucose didn’t fall to baseline until almost 5 hours.

Some Final Thoughts…

An abnormal fasting blood glucose test may warrant further testing, however a normal result is frequently dismissed as being a sign that “everything’s fine”. Data from this study indicates that as many as 75% of people with normal fasting blood sugar may have abnormal glucose responses and associated hyperinsulimia and some of the same risks as someone who has already been diagnosed with Type 2 Diabetes, but they simply don’t know it.

With reliable and relatively inexpensive glucometers, as well as continuous glucose monitors (CGM) people don’t need to wonder whether they are in the minority with a normal glucose response.

Not knowing one is at risk does nothing to provide motivation to make dietary and lifestyle changes, but knowing one has an abnormal response to carbohydrate not only enables them to want to make changes, it enables them  to find out in time which carbohydrates might be able to be added back into their diet, and in what quantities.

If you have questions as to how I can help you get started in knowing your own glucose response and to lower risk factors, please send me a note using the Contact Me form located on the tab, above.

To your good health!

Joy

References

1. Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.
2. Lamar, ME et al, Jelly beans as an alternative to a fifty-gram glucose beverage for gestational diabetes screening, Am J Obstet Gynacol, 1999 Nov 18 (5 Pt 1): 1154-7

You can follow me at:

 https://twitter.com/lchfRD

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

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Copyright ©2018 BetterByDesign Nutrition Ltd.

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

 

 

 

The new joint American Diabetes Association (ADA) / European Association for the Study of Diabetes (EASD) position paper [1] published online ahead of print on October 4th now classifies a low carbohydrate diet as Medical Nutrition Therapy. in the treatment of Type 2 Diabetes in adults. What this means is these two organizations which are responsible for educating over 30 million Americans and 60 million Europeans diagnosed with Diabetes consider a low carbohydrate not only safe, but effective therapeutic treatment. This recognition comes on the heels of Diabetes Australia having just released in late August their own updated position paper designed to provide practical advice and information for people diagnosed with Diabetes who are considering adopting a low carbohydrate eating plan [2].

What is Medical Nutrition Therapy?

Medical Nutrition Therapy (MNT) is defined as;

”nutritional diagnostic, therapy and counseling services for the purpose of disease management, which are furnished by a Registered Dietitian or nutrition professional” [3].

The American Diabetes Association and the European Association for the Study of Diabetes preface their updated position statement by saying;

“A systematic evaluation of the literature since 2014 informed new recommendations.”

That is, upon a review of the most current research, these two organizations have updated their prior position statements and now consider a low carbohydrate diet defined as < 26%* of daily calories as carbohydrate [1] is suitable for the purpose of disease management of Type 2 Diabetes in adults.

*Note: based on an 1800-2000 calorie per day diet this amount of daily carbohydrate would be less than < 113-125 g daily. In fact, the position paper concludes that carbohydrate restriction of 26—45% is ineffective.

The new joint position statement elaborates that Medical Nutrition Therapy (MNT) is made up of an education component and a support component in order to enable patients to adopt healthy eating patterns with the purpose of “managing blood glucose and cardiovascular risk factors” and “reducing the risk for Diabetes-related complications while preserving the pleasure of eating” [1].  The paper defines the two basic dimensions of MNT as diet quality and energy restriction and outlines the benefits of a low carbohydrate diet in the section on diet quality.

Furthermore, the joint consensus paper lists  under diet quality (Table 2, page 13) which is one of the aspects of Medical Nutrition Therapy, several diets considered suitable for adults with Type 2 Diabetes, including a low carbohydrate diet.

This move has far-reaching significance!

Publication of this paper indicates that the current scientific literature supports that a low carbohydrate is not only safe for use in adults, but is also effective in lowering metabolic markers of Type 2 Diabetes, as well as  delaying or eliminating the need for blood-glucose lowering medications for up to 4 years [1].

It moves a low carbohydrate diet from the realm of a popular lifestyle approach to Medical Nutrition Therapy.

Most importantly, this consensus paper means that qualified healthcare professionals throughout the USA and Europe can now recommend a low carbohydrate diet to their adult patients in order to enable them to manage their Type 2 Diabetes. This is a huge step forward from only being able to provide such a diet based on person’s individual preference to follow a low carbohydrate lifestyle.

Some final thoughts…

The American Diabetes Association, European Association for the Study of Diabetes and Diabetes Australia have collectively led the way for international Diabetes Associations the world over to re-evaluate their own treatment and dietary recommendations in light of the most current scientific evidence and update their position statements regarding the safe and effective use of low carbohydrate diets in the management of Type 2 Diabetes in adults.

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Perhaps you have wanted to follow a low carbohydrate lifestyle and have questions about how such a diet could help you manage some of your clinical conditions or lose weight. Please send me a note using the Contact Me form above and I will reply as soon as I am able.

Whether you live locally or away, I provide services in-person in my Coquitlam (British Columbia) office, as well as via Distance Consultation (Skype or phone).  You can find more information under the Services tab and in the Shop including the Intake and Service Option form to send in to get started.

To your good health!

Joy

you can follow me at:

 https://twitter.com/lchfRD

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

Copyright ©2018 BetterByDesign Nutrition Ltd.

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

References

1. Davies M.J., D’Alessio D.A., Fradkin J., et al, Management of Hyperglycemia
   in Type 2 Diabetes, 2018. A Consensus Report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD), Diabetes Care, October 2018,  https://doi.org/10.2337/dci18-0033. Click here for pdf of the full article (on affiliate web page).
2. Diabetes Australia, Low Carbohydrate Eating for People with Diabetes — Position Statement, August 2018,  https://www.diabetesqld.org.au/media-centre/2018/august/low-carb-position-statement.aspx and https://www.diabetesqld.org.au/media/583017/da-low-carb-statement-21-august-2018.pdf
3. U.S. Department of Health and Human Services: Final MNT regulations. CMS-1169-FC. Federal Register, 1 November 2001. 42 CFR Parts 405, 410, 411, 414, and 415

 

 

I was asked an interesting question recently which was “have you found the silver bullet for reducing carb cravings“? This was an interesting way to phrase something I have been asked in many different ways the last few years.

Some people have been told that it really doesn’t matter what or how much they eat as long as they only eat “real” food. Others have heard that they need to eat plenty of fat each day, and that this will keep them full and reduce cravings for carb-based foods. Some have read that what they need to do is eat mostly protein with some fat or only eat during a very small ‘eating window’.

So what is the answer?

There really isn’t a ‘silver bullet’ as much as there is the need for a well-designed low carbohydrate diet that is specific to each person’s physiological needs.

Every person has different nutrient needs based on their age, stage of life, gender and activity level. As well, each individual has different degrees of insulin resistance and hyperinsulinemia and each person’s blood sugar responds differently to a carbohydrate load (called glycemic response). Much of these depends on their specific family history, their medical history and the type of foods they normally eat. [You can read more about all three of these here.]

There isn’t a ”once-size-fits-all low carb diet”.  Based on all of the above factors, some people will do better with a higher ratio of protein to fat, whereas others need plenty of natural, healthy fats and average amount of protein. The amount and type of carbohydrate each person can tolerate will also be different. Since everyone’s needs are different, in designing a Meal Plan for someone, I start by conducting a complete nutritional assessment (personal medical history, family medical history, review of recent lab tests, dietary and lifestyle review, etc.) so that the Meal Plan that I design is tailored to their individual needs.

If there was a ‘silver bullet’ to eliminate carb cravings it would be to understand what causes them. Carb cravings are driven by several different hormones that the body produces in response to the way each person eats, as well as how much and how well they sleep, how they manage stress (or don’t), as well as any conditions or diseases that they have and any medications that they take.  All of these affect the various hormones that impact cravings for carbohydrate-based food. When I design people’s Meal Plans, I take all of these into account.

A well-designed low carbohydrate diet designed specifically for each person and taking into account the various factors that are driving their specific carbohydrate cravings is the most effective means to addressing them.

A person’s Meal Plan is not carved in stone. If a person has a fair amount of weight to lose, their Meal Plan will change once they’ve lost a significant amount of weight or if they’ve hit a plateau where they haven’t lost either weight or inches in a while.  Achieving optimal body weight is a dynamic process not a static one — as people’s needs change, so should their diet.  It’s not that a person’s Meal Plan needs to be re-designed, as much as ‘tweaked’ or ‘adjusted’ to keep them moving towards achieving their goals. This is where follow-up can be helpful.

If you have questions as to how I can help you achieve your health and nutrition goals — either by taking service in-person in my office or via Distance Consultation please send me a note using the Contact Me form above and I will be happy to reply as soon as I am able.

To your good health!

Joy

you can follow me at:

 https://twitter.com/lchfRD

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

Copyright ©2018 BetterByDesign Nutrition Ltd.

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

 

In a landmark decision yesterday the Australian Health Practitioner’s Regulation Agency (AHPRA) dropped all charges of wrong-doing against orthopedic surgeon Dr. Gary Fettke for recommending a low carb high fat lifestyle to his patients. This is great news for a physician who had tired of amputating the gangrenous limbs of patients with uncontrolled Diabetes when lifestyle changes could not only spare their limbs, but their lives. It was not only Dr. Fettke that was investigated, but the strength of the scientific evidence behind his recommendation of a low carbohydrate diet was on trial. That is the subject of this article.

It is great news that AHPRA ruled that Dr. Fettke had caused no patient harm by his recommendation of a low carb high fat (LCHF) diet:

”…no significant risks to public safety have been identified that require a regulatory response under the National Law. In the case of each of the three issues considered, there is no evidence of any actual harm and nor does the Board discern any particular risk to public health and safety moving forward. For these reasons, the Board has decided to take no further regulatory action.”

— AHPRA medical board

It is outstanding that AHPRA apologized in writing to Dr. Fettke for the 4½ years of distress caused to him by the investigative process;

“I would like to take this opportunity to apologize for the errors that were made when dealing with this notification. We recognize that these errors are likely to have compounded any distress that you experienced as a result of being the subject of this investigation. We appreciate your cooperation and engagement through the complaint management process, and the reconsideration of the previous decision.”

— AHPRA medical board

This is fantastic news and must come as a tremendous relief both to Dr. Fettke and to his family who have endured untold stress from this long ordeal.

Dr. Fettke’s exoneration comes on the heels of the results of not one, but two trials over a 4-year period against South African Professor Tim Noakes for his response to a tweet on Twitter social media from a breastfeeding mother in February 2014 where he recommended that good first foods for infant weaning are low carbohydrate high fat foods. As noted by Dr. Sarah Hallberg in a letter to the Health Professions Council of South Africa (HPCSA), low carbohydrate foods such as meat, chicken, fish and leafy green vegetables align closely with South Africa’s pediatric guidelines which advise that;

”From 6 months of age give your baby meat, chicken, fish, or egg every day as often as possible. Give your baby dark green leafy vegetables and orange coloured vegetables and fruit every day.”

—Food-based Dietary Guidelines for South Africa

In April 2017 and again in the appeal  which concluded in June of this year, Noakes was cleared of all charges of professional misconduct by the HPCSA which confirmed that his advice to the breastfeeding woman in his tweet was neither “unconventional” nor “dangerous medical advice“.

In June, Noakes’ lawyer Adam Pike said in a statement that the HPSCA’s ruling;

”preserves the right of scientists and doctors to express scientific opinions and disseminate medical information”

— Adam Pike, Professor Tim Noakes’ lawyer

Phrased another way, Noakes acted as a scientist who tweeted scientifically based information.

While it was Dr. Gary Fettke and Professor Tim Noakes that have been investigated as individuals, what was largely on trial was the scientific evidence behind their recommendation of a low carbohydrate diet. This evidence indicates that low carbohydrate diets are both safe and effective for treating obesity and for managing the symptoms of Type 2 Diabetes.

In an article I wrote in January 2018 titled A Preponderance of the Evidence, (and posted on my website dedicated to a low carb dietary approach) I documented that not only is a low carbohydrate diet for the treatment of Diabetes not new, but almost a year ago there were already many research  studies and meta-analyses published in 76 publications which spanned 18 years which involved 6,786 subjects which used a low-carb intervention — which included 32 studies of 6 months or longer and 6 studies of 2 years or longer all of which indicated that a low carbohydrate diet is safe. Not only has it been amply documented that a low carbohydrate diet is safe, but a low carbohydrate diet performed as well, if not better than competing diets in all of the above studies. Dr. Sarah Hallberg who compiled the above list is Medical Director at Indiana University Health Arnett and Virta Health Medical Director. She she pointed out in a letter to the Health Professions Council of South Africa that data available from the US government and reported in a 2015 study indicates that in 1965 (which is just prior to the beginning of the current obesity and Diabetes epidemic) Americans ate 39% of their calories as carbohydrate and 41% of their calories as fat which is considered by many nutrition researchers today to fall within the realm of a “low carbohydrate high fat diet”. Dr. Hallberg is correct. Dietary Guidelines in both the US and Canada currently recommend that the diet be 45-65% of calories as carbohydrates and that up until 2015, the US recommended a upper limit of 35% calories as fat (<30% of calories as fat in Canada). Both countries currently still recommend limiting saturated fat to <10% of calories.

Nutrition researchers today generally consider diets less than 45% of calories as carbohydrate and >35% of calories as fat to be “low carbohydrate high fat diets”, so the average American diet that was 39% carbohydrate and 41% fat in 1965 would be considered “low carb high fat” by most nutrition research studies today.

Given the much lower rates of overweight, obesity and Type 2 Diabetes in 1965 — at a time when the average American ate what is now considered a “low carb high fat diet”, should not such a macro distribution be granted “generally recognized as safe” (GRAS) standing?

For the last 40 years, the Dietary Guidelines in both the US and Canada have been counselled people to limit fat, especially saturated fat and to eat 45-65% of their calories as carbohydrate yet even a cursory look at the rates of overweight and obesity in both countries and the steadily increasing rates of Type 2 Diabetes indicates that something is terribly wrong. Clinicians (Physicians, Dietitians, Pharmacists) educated since 1977 which is the vast amount practicing in both countries (and in South Africa and Australia apparently, where Dr. Fettke and Professor Noakes are from) have all been educated within a “low fat paradigm”— where fat is vilified as the cause of cardiovascular disease and increasing carbohydrate intake is promoted as the ‘solution’ to reducing fat intake. Unless clinicians educated in this time period stayed current with the literature they simply keep teaching what they were taught; eat less fat, eat more carbs.

In the past number of years there are increasing numbers of clinicians around the world that have considered the evidence; both epidemiological and clinical studies that indicate that a low carbohydrate high fat diet not only has no adverse impact on individual health but is safe and effective for reducing overweight and obesity, as well as reducing (and in some cases reversing) the symptoms of Type 2 Diabetes. Two such clinicians are Australian orthopedic surgeon Dr. Gary Fettke and South African Professor Tim Noakes; both of whom were investigated for having recommended a low carb high fat diet which was viewed as “dangerous” and both of whom, when the scientific evidence was considered, were exonerated. To their credit both Dr. Fettke and Professor Noakes conducted themselves with integrity and transparency through the entire process and all charges of wrong-doing against them were dropped, but let’s not lose sight that it was also because of the amount and strength of the scientific evidence which indicates that a well-designed low carbohydrate high fat diet is both safe and effective for weight loss, as well as for reducing symptoms of Type 2 Diabetes.

Both men have no doubt been through a very distressing and incredibly stressful >4-year ordeal which forever changed them and their families that went through it with them, however this story is not only about them but what they believed about the safety and efficacy of a low carb diet. It was low carb high fat diets that were investigated and put on trial and the conclusion in both cases as that such a diet is neither unconventional nor dangerous.

Yes, there are other dietary options for weight-loss and targeting the reduction of symptoms of Type 2 Diabetes and diets such as the classic Mediterranean Diet or a very low-fat calorie-restricted plant-based diet are effective for those that maintain them long term. The issue is that a well-designed low carbohydrate diet is at least as effective as these and may be easier for some to stick with long term, making them more effective for those individuals. Since the scientific evidence indicates that all three of these diets are safe and to varying degrees effective for weight loss and glycemic control, it is time for clinical guidelines in both the US and Canada to be formulated to enable clinicians in both countries to offer their patients a well-designed low carbohydrate diet as an option.

Perhaps you have questions about whether a low-carbohydrate diet would be appropriate for you or wonder how medical conditions you have or medications you take may factor in? I provide both in-person services in my Coquitlam (British Columbia) office, as well as via Distance Consultation using Skype or phone and I would be happy to answer your questions and help you reach your goals. Please send me a note using the ”Contact Me” form on the tab above and will reply as soon as possible.

To your good health,

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/BBDNutrition/

Copyright ©2018 BetterByDesign Nutrition Ltd.

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

References

1. Fettke Free at Last, Foodmed.net, Sept 28 2018 (http://foodmed.net/2018/06/noakes-free-hpcsa-licks-wounds-lchf/)
2. Noakes: Top Doctors Globally call on HPCSA to Stop Prosecuting Him, Foodnet.net, February 14, 2018
3. Food-based Dietary Guidelines for South Africa, S Afr J Clin Nutr 2013;26(3)(Supplement):S1-S164
4. Noakes Free at Last, Foodmed.net, June 10 2018 (http://foodmed.net/2018/06/noakes-free-hpcsa-licks-wounds-lchf/)
5. Cohen E, Cragg M, deFonseka J et al, Statistical review of US macronutrient consumption data, 1965—2011: Americans have been following dietary guidelines, coincident with the rise in obesity, Nutrition (2015), Vol 31 (5), Pg 727-732.

There are many popular articles available on the internet, but if you are looking for researched, credible articles about a therapeutic use of Low Carbohydrate or Ketogenic Diets as well as articles with practical applications then this article is for you.

I have written 100+ “Science Made Simple” articles related specifically to this topic — most of which are posted on an affiliate website. For the most part these are articles that folks without a science background can easily understand and apply, and they are arranged by topic so that they are easy to find.

Current list of topics includes:

-Low Carb High Fat (LCHF) Diets

-Ketogenic (Keto) Diets

-Therapeutic Low Carb Diets

-Low Calorie / Low Fat Diets

-Diet & Food Choices

-Myths about Low Carb / Keto Diets

-Low Carb / Keto Diets & Medications

-Dietary Fat

-Carbs & Carbs with Fat

-PUFA / Industrial Seed Oils

-Effects of Food Processing on Insulin and Blood Sugar

-Insulin Resistance

-Type 2 Diabetes

-Cardiovascular Disease (CVD)

-Older Adults & Diet

-Concerns and “Warnings”

-Clinical

-Setting Health and Nutrition Goals

-Anthropometrics (Body Measurements)

-Practical Applications

-Media

-Background & History

These articles can be accessed by clicking here. You will be redirected to an affiliate website that focuses only on the therapeutic use of low carb and ketogenic diets.

Perhaps you have questions about how I can support you in following a lower-carbohydrate diet? Please feel free to send me a note using the Contact Me form located on the tab above and I will reply shortly.

I provide services both remotely via Distance Consultation (Skype, long distance phone) and in-person in my Coquitlam (British Columbia) office so whether you live near or far, I can help if this is something you are interested in.

To your good health.

Joy

You can follow me on social media at:

 https://twitter.com/lchfRD

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

Copyright ©2018 BetterByDesign Nutrition Ltd.

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

For a second week in a row dire warnings about the alleged dangers of “low carbohydrate diets” scream out from headlines across the internet.

“Low-Carb Diets Linked to Higher Risk of Premature Death”

~Newsweek August 28, 2018, 12:51 PM

“Low carbohydrate diets are unsafe and should be avoided, study suggests”

~ScienceDaily, August 28, 2018

The general public relies on journalists to thoroughly research their stories before publishing them however in the above two examples and the other incidences of reporting this story it was not indicated that (1) there was no published study (2) the story was based on researcher’s conclusions in provided materials based on an Abstract from a Poster presentation and (3) the provided materials / Abstract didn’t define the term “low carbohydrate” (# of grams of carbohydrate per day) which is central to the claims of the researchers.

The supposed link to “premature death” of a “low carbohydrate diet” were said to be part of a large study that was presented at the European Society of Cardiology (ESC) Congress 2018 in Munich, Germany, but when I went to find the journal in which the study was published so I could read it, I discovered that it’s not even been published yet.  I even checked the lead author’s Publication page on ResearchGate and could not find the published study. Furthermore, the findings were not presented as one of the more than 500 Conference sessions of research studies at the European Society of Cardiology Congress, but was one of the 4,500 Abstract presentations — not even as a talk, but as a Poster Session.

A “Poster Session” at  an academic Conference is where 100s of researchers assemble in a large hall and stand in front of a poster summarizing their research. People walk by, look at the poster and if they wish, ask questions.

Journalists wrote stories based on “materials provided to them by the European Society of Cardiology” (see story source at bottom of ScienceDaily article) which is based on the Abstract available on the website of the European Society of Cardiology’s 2018 Congress from the yet-to-be-published study by M. Mazidi  (Gothenburg, Sweden), N Katsiki (Thessaloniki, Greece), DP Mikhailidis (London, Great Britain) and M Banach (Lodz, Poland) and also published the same day (August 28, 2018) in the European Heart Journal, Volume 39 Supplemental on pages 1112-1113.

The Abstract (viewable below) is downloadable from the journal’s website and the 2018 Congress website and clearly indicates that it was a “Poster Session”.

A glaring omission from the Abstract is that it is not stated anywhere how many grams of carbohydrate per day is defined as a “low carbohydrate diet”.

The Abstract and supplied press materials claim that there is a relationship between “low carbohydrate diets” (not defined!) and death from all-causes, as well as specific death from coronary heart disease, cerebrovascular disease (stroke) and cancer and that the data analyzed was based on a representative sample of 24,825 participants of the US National Health and Nutrition Examination Survey (NHANES) from 1999 to 2010.

The researchers conclude that compared to participants with the highest carbohydrate consumption (also not defined!), those with the lowest carbohydrate intake had a 32% higher risk of all-cause death during the ~6.4-year follow-up. As well, the risk of death from coronary heart disease from “low carbohydrate”diets was 51% higher, from cerebrovascular disease (stroke) was 50% higher and from cancer was 35% higher. They furthermore state that their results were confirmed by a pooled meta-analysis of 7 prospective cohort studies with 447,506 participants and which had an average follow-up of 15.6 years which indicated that risk of death from all causes resulting from “low carbohydrate diets” was 15% higher, from cardiovascular disease was 13% higher and from cancer was 8% higher compared to high carbohydrate diets.

Wait a minute…

The researchers found risk of death from coronary heart disease and cardiovascular disease (heart attack and stroke) as ~50% higher and the pooled data of the studies they compared it to found a 13% higher incidence. Even without defining what a “low carbohydrate diet” is, a 50% increased chance of death is not comparable to a 13% increased chance of death.  Similarly, the researchers found risk of death from cancer from a “low carbohydrate diet” was 35% greater and said their findings were comparable to an 8% higher incidence in the pooled data.

The researchers (1) did not define how many grams of carbohydrate per day was considered a “low carbohydrate diet” and (2) said their data was confirmed by studies that reported very different results.

Yet, they conclude;

Our study highlighted the unfavorable effect of low carbohydrate diets (LCDs) on total- and cause- specific mortality, based on both individual data and by pooling previous cohort studies. Given the fact that LCDs may be unsafe, it would be preferable not to currently recommend these diets. Further studies to clarify the mechanisms involved in these associations and to support our findings are eagerly awaited.

Which “low carbohydrate diet” did they study? How many grams of carbohydrate per day? We don’t know because the Abstract doesn’t say and the study hasn’t yet been published.

Some Final Thoughts…

It is not responsible journalism for the media to scream headlines warning of higher risk of premature death from “low carbohydrate diets” based on supplied press materials and an Abstract of a Poster Session of an unpublished study that doesn’t even define “low carb”.

There are many studies and meta-analyses using a low-carbohydrate or ketogenic dietary intervention that span 18 years and that are outlined in detail in 76 publications involving  6,786  subjects and that include 32 studies of 6 months or longer and 6 studies of 2 years or longer that demonstrate that low carb diets of a specified number of grams of carbohydrate per day are both safe and effective. You can read more about that here.

Perhaps you have questions such as is a low-carbohydrate diet appropriate for you given your health goals, medical conditions or medications you are taking? Please feel free to send me a note using the ”Contact Me” form and I will reply as soon as possible.

I provide both in-person services in my Coquitlam (British Columbia) office as well as Distance Consultation services (via Skype / long distance phone) and I’d be happy to help you achieve your health and nutrition goals.

To our good health,

Joy

You may also want to read:
Do Low Carb Diets Shorten Lifespan – a closer look (August 23 2018)
Is Coconut Oil Pure Poison (August 24 2018)

You can follow me on Twitter and Facebook:

 https://twitter.com/lchfRD

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

Copyright ©2018 BetterByDesign Nutrition Ltd.

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

 

Reference

Mazidi M, Katsiki N, Mikhailidis DP et al, Abstract (P5409): Low carbohydrate diets and all-cause and cause-specific mortality: a population based cohort study and pooling prospective studies, European Heart Journal, Volume 39 (Supplemental), pages 1112-1113.

 

INTRODUCTION: Headlines warned people this week of the dire risks of a shorter lifespan by eating a low carbohydrate diet, but is it true?  By asking a few simple questions it’s easy to see that this newly published study cannot be used to support this claim.

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Headlines are designed to attract readers to a story, to have people talking about it on social media and sharing it, so the way a study is framed is critical. Readers need to be discerning — to ask questions about the story so they can tease apart truth from significance. What do I mean by this?

A fact can be true but really be quite meaningless, having little significance, which is often the case in these types of sensationalized reports. Let me give you an example to help explain what I mean. Let’s say there are 3 blond-haired 6 year old children and 2 red-haired 6 year old children in a room and one of the red-headed children slips on some water on the floor, falls and injures themselves, I could truthfully claim that injury rate of 6 year olds is 20% (1 in 5) but that the injury rate among red-headed children is much higher, at 50%. This is true, but is it significant? First of all the study groups were too small to make a comparison meaningful and that the child’s injury had nothing to do with them having red-hair and everything to do with the fact that there was water on the floor.

Looking at the recently published study which claimed that low carb diets could shorten lifespan[1], there are several questions we need to ask ourselves to begin to determine if the findings were meaningful such as “how was the information collected”, “how many people were in each comparison group” and “were there confounding factors” (factors that could confuse understanding the data).

How was the Information Collected

Subjects were asked to complete a 66-item semi-quantitative food frequency questionnaire (FFQ) indicating how many times in the last year they ate specific foods. The FFQ it was based on was the 61-item Harvard Food Frequency Questionnaire, a page of which appears below.

That’s right, people needed to estimate how many times in the last year they ate 1 oz of chocolate, or 1 cup of breakfast cereal or an ounce of nuts. Seriously?? How accurate would you be at adding up in your head all the 1 oz servings of chocolate that you estimated that you ate in a year. If you ate breakfast cereal in a serving size other than a cup, how would you even begin to accurately estimate how many 1 cup servings you had in an entire YEAR — including for breakfast and night time snacks? Thinking about this, one can see why FFQ data is considered very inaccurate and certainly can’t be used to estimate the percentage of carbohydrate a person has in their diet!

The first part of the study took place between 1987 and 1989 and asked ~15,000 people between the ages of 45 and 64 years living in 4 communities in the US to complete the FFQ.  The data from the second part of the study was a meta-analysis which combined the data from the first part of the study with data from 7 multi-national population studies using the same FFQ and the third part of the study took place between 1993—95.

One huge problem with this paper was that it assumed that even if people changed their diet between the first visit in 1987-1989 and the third visit in 1992-1993, that people didn’t change their diets from the third visit until the data was analyzed in 2013; a period of ~20 years. There are all sorts of reasons people change the way they eat over time including health reasons (wanting to lose weight, for example), becoming parents, changes in economic situation, getting married and having someone else doing the cooking, or taking cooking classes! Assuming people ate the same way from 1993 until 2013 makes no sense.

How Many People Were in Each Comparison Group

As with the risk of injury amongst red-headed 6 year olds in the example above, the way the groups are divided and how many people are in each group matters.

Carbohydrate ranges were broken down into 5 groups;
<30% of calories as carbohydrate
30-40% of calories as carbohydrate
40-50% of calories as carbohydrate
50-55% of calories as carbohydrate
55-65% of calories as carbohydrate
>65% of calories as carbohydrate

A major problem with how the groups were broken up was that there were only 315 people that fell in the <30% of calories as carbohydrate group compared with more than 6,000 in the 40-50% of calories as carbohydrate  group and the more than 3,000 in both the 50-55%  and 55-65% of calories as carbohydrate groups.

As with the risk of injury of being red-headed example above, the way the groups were divided and how few people were in the lowest group of carbohydrate consumption makes the higher relative risk of being in the lower carbohydrate group truthful, but meaningless.

Were There Confounding Factors?

There’s an even bigger problem with this study.

Researchers did not update the carbohydrate intake of subjects that developed heart disease, Diabetes, or stroke before the third visit. Let’s say that some people in the lowest carb intake group developed Type 2 Diabetes and went to see their public health Dietitian who recommended that they increase their carb intake to be around the recommended ~50% (45-65%)  of their dietary caloric intake, or more. If they followed that advice and developed complications and died, their death would have been attributed to them eating a “low carb diet” rather than eating 50% or more of calories as carbohydrate over the subsequent 20 years.  The same holds true with dietary changes that subjects made based on their doctor’s or Dietitian’s recommendation when they got heart disease or had a stroke.  Because the groups were so lopsided in terms of size, being diagnosed with one of these serious conditions had the most impact on the lowest carb intake group because it was comparatively much smaller.

There were other confounding factors including, as someone pointed out on Twitter, that there was no mention of analysis done on alcohol consumption in the paper, so there’s no way of knowing if higher death rates were associated with higher alcohol consumption. As well, there was a higher rate of smoking in the lower carbohydrate intake group, so were the deaths smoking-related or diet-related?

Some final thoughts…

There are many more problems with this study, outlined in depth by people such as Dr. Zoe Harbcombe but there is one glaring fact. Epidemiological studies (population studies) do not establish causation.  When properly done, the results of epidemiological studies indicate that there may be a relationship between factors that needs to be tested in a randomized control trial.

Nevertheless, researchers concluded that there was a ‘negative long-term association between life expectancy and a low carbohydrate diet’ (which they defined as a diet of <40% of calories as carbohydrate, which is not a low carbohydrate diet, but a moderate-carbohydrate intake.

How the dietary information was collected, how the comparison groups were set out and the how the subjects were distributed amongst those groups and the multiple significant confounding factors make it impossible to conclude that a low carbohydrate diet shortens lifespan.

Evidence that Low Carbohydrate Diets are Both Safe and Effective

There are many studies and meta-analyses using a low-carb intervention that span 18 years that are outlined in 76 publications involving  6,786  subjects and that include 32 studies of 6 months or longer and 6 studies of 2 years or longer that demonstrate that low carb diets are both safe and effective. You can read more about that here.

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Do you have questions about whether a low-carbohydrate diet would be appropriate for you given your health goals? Or do you wonder medical conditions you may have or medications you may take factor in? Please send me a note using the ”Contact Me” form and I’ll be happy to reply.

I provide both in-person services in my Coquitlam (British Columbia) office as well as Distance Consultation services (via Skype or long distance phone) and would be happy to help.

To our good health,

Joy

 https://twitter.com/lchfRD

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

Copyright ©2018 BetterByDesign Nutrition Ltd.

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

References

1. Seidelmann SB, Claggett B, Cheng S, et al. Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analysis. The Lancet Public Health 2018. https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(18)30135-X/fulltext
2. Harvard Food Frequency Questionnaire  https://regepi.bwh.harvard.edu/health/FFQ/files/8

INTRODUCTION: Diabetes Australia, the national body responsible for making treatment and dietary recommendations for the 1.7 million people  living with Diabetes in that country has just released a new Position Statement titled Low Carbohydrate Eating for People with Diabetes [1] said to be based on the latest evidence on the subject.  The publication is designed to provide practical advice and information for people diagnosed with Diabetes who are considering adopting a low carbohydrate eating plan and was created in response to numerous inquiries from individuals, healthcare professionals and the general public, Diabetes Australia. Since I don’t provide dietary to support to those with Type 1 Diabetes (but defer instead to someone with CDE credentials), I have limited my discussion to recommendations pertaining only to Type 2 Diabetes.

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Diabetes Australia defines low carbohydrate (“low carb”) eating patterns as those that restrict carbohydrate intake — especially processed and packaged foods and beverages including cakes, candies, chocolate, chips, ice cream and sugary drinks as well as breads, cereals, grains, potatoes, fruit and sugar. They elaborate that when people are limiting carbohydrates they eat a higher proportion of protein and fats such as those found in meat, chicken, eggs, oily fish, avocados, nuts, oils and butter and eat plenty of low carb vegetables, such as cauliflower and zucchini.

“When it comes to low carb eating, there is no particular diet or standard approach.”

Diabetes Australia reinforces that the (Australian) “Dietary Guidelines provide general healthy eating advice and are a good starting point for people wanting to improve their eating habits”, but that

“there is no one-size-fits-all approach to living well with Diabetes. Everybody is different.”

The publication makes clear that Diabetes Australia “does not promote or encourage any single diet or eating plan or any particular ‘diabetes diet'” and that “every person with Diabetes needs a personalized approach and support to have the healthiest eating plan and this may change over their lifetime with Diabetes“. They mention that in recent years, low carb eating has gained popularity with the general population and has also gained interest for people with Diabetes as “an option to help lose weight and to assist in managing blood glucose levels” — because “low carb diets are relatively easy to follow”.

In formulating their Position Statement, the organization states that they rely on “strong scientific evidence before making specific health and nutrition recommendations for people with diabetes or those at risk” and that “evidence is usually based on the National Health and Medical Research Council (NHMRC) hierarchy of evidence”[2] whose components are; 1. The evidence base, in terms of the number of studies, level of evidence and quality of studies (risk of bias), 2. The consistency of the study results, 3. The potential clinical impact of the proposed recommendation, 4. The generalisability of the body of evidence to the target population for the guideline, and 5. The applicability of the body of evidence to the Australian healthcare context. This hierarchy of evidence is said to also need to take into account “the quality of the study and the likelihood that the results have been affected by bias during its conduct; the consistency of its findings to those from other studies; the clinical impact of its results; the generalisability of the results to the population for whom the guideline is intended; and the applicability of the results to the Australian (and/or local) health care setting”.

The position statement stresses that Diabetes Australia believes that;

“People with Diabetes should make their own, informed  choices about their Diabetes management (including eating plans) in consultation with their diabetes healthcare team”.

They recognize that “long-term studies can take years to be designed, conducted and published” and underscore that they will continue to review and update their advice in relation to low carb eating for people with Diabetes based on new evidence as it becomes available.

Key Points

[1] Based on two studies [3,4] the report states that “recent evidence has shown that in the short term (up to 6 months), lower carb eating can help with the management of Type 2 Diabetes but that this benefit is no longer evident after 12 months”.

NOTE:
(a) Both of the studies quoted [3,4] were not low carb studies but moderate carb studies of <45% (225g carbohydrate) per day. Low carbohydrate diets as defined by this paper are diets which provide “less than 130 g of carbohydrate daily/ less than 26% of total daily energy intake” and the paper defines a moderate carbohydrate diet as one that provides “130g—225g of carbohydrate daily/ 26%—45% of total daily energy intake”. The two quoted studies provided dietary intake of carbohydrate that were moderate carbohydrate. Neither was a low carbohydrate study.
(b) Interestingly, despite neither study being low carb, one of the quoted studies [3] found “greater weight loss at 12 months on moderate carb diets than high carb diets” — which contradicts that there was no benefit after 6 months. Even a moderate-high carb diet had benefit beyond 6 months when compared with a high carb diet!
(c) In addition, the position statement did not consider the recent publication of the 1-year study results from Virta Health [5] outlined in detail in this article.

[2] In addition to promoting weight-loss, reducing carbohydrate intake can provide health benefits that include lowered average blood glucose levels and reduced risk of heart disease such as raised cholesterol and raised blood pressure and that some benefits can be achieved independent of the amount of weight-loss achieved.

[3] All people with Diabetes who wish to follow a low carb diet should
do so in consultation with their Diabetes healthcare team.

[4] People with Diabetes who begin low carb eating should monitor their
blood glucose levels and, if necessary, talk to their doctor about the need to
adjust their Diabetes medication to reduce the risk of hypoglycaemia (low
blood glucose).

[5] People with Diabetes considering low carb eating are encouraged to seek
personalized advice from an Dietitian experienced in Diabetes management as there are some practical considerations that need to be taken into account to ensure the eating plan is safe and enjoyable, provides adequate nutrition for general health, is culturally appropriate and fits into the person’s lifestyle.

[6] People with Diabetes considering low carb eating should be aware of
possible side effects (such as tiredness, headaches and nausea) and seek
advice from their health care team if concerned.

[NOTE: I’ve never heard or read about people experiencing nausea following low carb eating, and even at the beginning of following a low carb style of eating symptoms such as tiredness and headache are easily addressed with adequate fluid and electrolytes.]

[7] Low carb eating may not be safe and is not recommended for children,
pregnant or breastfeeding women, people at risk of malnutrition, people
with kidney or liver failure, or those with a history of disordered eating or some rare metabolic conditions.

[8] All people who choose to follow a low carb eating plan should be encouraged to eat foods proven to be beneficial to good health, including whole fruit and vegetables, whole-grains*, dairy foods, nuts, legumes*, seafood, fresh meat and eggs.

[*NOTE: Depending on the amount of insulin resistance and hyperinsulinemia that someone with Type 2 Diabetes has they may or may not be able to maintain glycemic (blood sugar) control eating whole-grains and legumes. In their minimally processed forms, these may be able to be re-introduced in small quantities on an individual basis after reversal of Type 2 Diabetes symptoms and lower circulating insulin levels / reduced insulin resistance.]

[9] All people should be encouraged to limit their intake of foods that are high in energy*, carbohydrate or salt*, including processed foods such as sugary drinks, chips, cakes, biscuits, pastries and candies.

[NOTE: Unfortunately, foods that are ‘high in energy’ or ‘high in salt’ are inadequately defined in this publication. “High in energy” would be better framed as “low nutrient density foods” — which are foods high in energy relative to the amount of nutrients they contain.  Cheese for example may be energy-dense per 100 g but is also very nutrient-dense. What does “high in salt” means — high in salt for whom? 

Perhaps you have questions as to how I could help you get started on eating low carb to lower your blood sugars, reverse symptoms of Type 2 Diabetes, reduce your risk of heart disease including raised cholesterol and  blood pressure and lose weight?

Since I provide services both in-person in my Coquitlam (British Columbia) office as well as via Distance Consultation (Skype or phone), I am available to help.

Please send me a note using the Contact Me form above and I will reply as soon as I am able.

To our good health!

Joy

---

you can follow me at:

 https://twitter.com/lchfRD

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

Copyright ©2018 BetterByDesign Nutrition Ltd.

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

References

1. Diabetes Australia, Low Carbohydrate Eating for People with Diabetes – Position Statement, August 2018,  https://static.diabetesaustralia.com.au/s/fileassets/diabetes-australia/ee67e929-5ffc-411f-b286-1ca69e181d1a.pdf
2. National Health and Medical Research Council (2009), NHMRC additional levels of evidence and grades for recommendations for developers of guidelines, https://www.nhmrc.gov.au/_files_nhmrc/file/guidelines/developers/nhmrc_levels_grades_evidence_120423.pdf
3. Sainsbury E et al. Effect of dietary carbohydrate restriction
   on glycaemic control in adults with diabetes: a systematic
   review and meta-analysis. Diabetes Research and Clinical
   Practice, 2018; 139: 239-252.
4. Snorgaard O et al. Systematic review and meta-analysis
   of dietary carbohydrate restriction in patients with type 2
   diabetes. BMJ Open Diabetes Research & Care, 2017;
   5(1).
5. Hallberg, S.J., McKenzie, A.L., Williams, P.T. et al. Diabetes Ther (2018). 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.  https://doi.org/10.1007/s13300-018-0373-9

 

 

The US and Canada and much of the westernized world is in the midst of a Diabetes epidemic but this is just the tip of the iceberg when it comes the underlying metabolic disruption caused by insulin. The part of the iceberg that is visible and that people know about is hyperglycemia (elevated blood sugar) but the part that is invisible and that few are aware of  hyperinsulinemia (elevated blood insulin levels) which often precedes a diagnosis of pre-diabetes or Type 2 Diabetes by decades. It is this high circulating level of insulin that contributes to the significant risk of developing cardiovascular disease including heart attack and stroke, hypertension (high blood pressure), elevated cholesterol and triglycerides, non-alcoholic fatty liver (NAFLD), Poly Cystic Ovarian Syndrome (PCOS), Alzheimer’s disease and other forms of dementia, as well as certain forms of cancer including breast and colon / bowel cancer.

High blood sugar may or may not be a symptom of high levels of insulin levels and in the early stages of metabolic dysfunction almost 75% of people will have normal fasting blood glucose yet have abnormally high levels of circulating insulin.  As a result, these people are at increased risk of the metabolic diseases mentioned above but unlike someone already diagnosed with Type 2 Diabetes they have no idea!

High circulating levels of insulin is entirely missed by most routine lab tests because blood sugar is being monitored as the first indication that someone is becoming insulin resistant.  By the time blood glucose levels are abnormal, the β-cells of the pancreas that produce insulin are already being over-taxed to the point of exhaustion.  Physicians have ”answers” (lab test results) but oftentimes are asking the wrong questions. That is, having normal fasting blood sugar or even HbA1C (3-month blood sugar average) does not necessarily mean everything is ”fine”.  Most sobering is that by the time a person is diagnosed with Type 2 Diabetes they have already lost ~ 40% of their beta-cells mass sometimes more — cell loss which is currently thought to be unrecoverable.

The healthy human body maintains blood sugar in a tightly-regulated range between 60-100 mg/dl (3.3-5.5 mmol/L).  When a healthy person eats food containing carbohydrate — whether as the starch in bread, pasta and rice, the sugar in milk (lactose), fruit (fructose), simple table sugar (sucrose) or high fructose corn syrup in commercially prepared foods, special glucose-sensing cells in the small intestine release signalling hormones called incretin hormones in response to the presence of these carbohydrates. The incretin hormones tell the pancreas to release insulin which in turn tells the body’s cells what to do with the energy from the food we eat; either (1) burn it or (2) send it to the liver to store it, first as glycogen, and the remainder as fat (adipose tissue).  This is called fuel partitioning. When metabolic processes respond appropriately, blood sugar rises modestly after eating carbohydrate-based food but is quickly restored to its normal, tightly-regulated range soon afterwards.

Metabolic problems begin because people eat foods that contain some form of carbohydrate every few hours which results in frequent release of insulin. Glycogen levels in the muscle and liver remain close to full due to the steady supply of refined or processed carbohydrate-based food compounded by the reality that body’s cells are rarely challenged to use stored energy. In the early stages cells simply stop responding appropriately to insulin’s signal. This is called insulin resistance. Insulin resistance is the decreased ability of our cells to partition fuel. It can be compared to someone hearing a noise such as their neighbour playing music, but after a while their brain ”tunes out” the noise.  Even if the neighbour gradually turns up the volume of the music, the person’s brain compensates by further tuning out the increased noise. To compensate for insulin resistance, the β-cells of the pancreas begin producing and releasing more insulin, which results in hyperinsulinemia — too much insulin in the blood.

In the early stages the body is simply trying to keep blood sugar levels within its normally tightly regulated range by making and releasing more insulin to force the cells of the body to take up the excess glucose and burn it, but this just makes the problem worse. It is the increasingly high circulating levels of insulin that contribute to the health risks and metabolic disease listed above.

Just as high blood sugar is not necessarily associated with high circulating levels of insulin, neither is obesity.  Approximately 1/3 of insulin-resistant people are lean. A person who is obese simply makes more fat cells (adipocytes) in order to store the excess energy as sub-cutaneous fat (fat under the skin) which serves as a protective mechanism. Contrary to what most people assume, people don’t become insulin resistant because they are fat; becoming fat may be a protective response to high levels of circulating insulin. Those who are lean but insulin-resistant are thought to have a lower personal fat threshold’ than those that become overweight of obese. That is, they are limited in terms of how many new fat cells their body can make to store excess energy, so they store the excess energy in and around their organs in what’s called visceral fat.  This is where the metabolic disruption occurs.  Whether the person is obese or lean, once they have exceeded their personal fat threshold, the result is the same.

Assessing whether my clients have higher than ideal levels of insulin is as important as assessing whether they already have higher than ideal levels of blood sugar, in fact it is even more important. When people already have pre-diabetes or Type 2 Diabetes, they’ve likely been told by their doctors that they are increased cardiovascular risk and that this is a risk factor for other metabolically related conditions, including high blood pressure, fatty liver disease, Alzheimer’s and other forms of dementia and certain types of cancer. Having normal blood sugar many are told “everything is fine” when very often it is not.  These people are at risk and don’t even know it.

It is important that my clients know whether they have symptoms of hyperinsulinemia and to help them understand the factors that contribute to it. This helps people to have the motivation to make necessary dietary and lifestyle changes to reduce their disease risk and totally avoid the progression to Type 2 Diabetes, long before blood sugar levels begin to rise.

For those that already are pre-diabetic or been diagnosed as having Type 2 Diabetes, it is not too late. A carbohydrate-modified diet as well implementing very specific lifestyle changes makes the reversal of symptoms entirely possible and does not require dietary or exercise extremes.

I think that for too long we as clinicians have tackled this as an insulin problem caused by overweight and created by “eating too much and moving too little” rather than as the exact opposite; that people get overweight because of an underlying insulin problem. When we address hyperinsulinemia, weight, blood sugar, blood pressure and high cholesterol and triglycerides are corrected. There are studies documenting this (covered in previous articles) and my “A Dietitian’s Journey” tells my own sample-set-of-one story reversing Type 2 Diabetes that I had for 10 years, as well as the related conditions of high blood pressure and abnormal cholesterol and triglycerides. It can be done.

Have questions as to how I can help you either in-person in my office or via Distance Consultation? Please send me a note using the Contact Me form above and I will reply as soon as I am able.

To our good health!

Joy

you can follow me at:

 https://twitter.com/lchfRD

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

References

Reaven, G., Insulin resistance, type 2 diabetes mellitus, and cardiovascular disease: the end of the beginning. Circulation, 2005. 112(20): p. 3030-2.

Reaven, G.M., Pathophysiology of insulin resistance in human disease. Physiol Rev, 1995. 75(3): p. 473-86.

Taylor, R. and R.R. Holman, Normal weight individuals who develop type 2 diabetes: the personal fat threshold. Clin Sci (Lond), 2015. 128(7): p. 405-10.

Reaven, G., The metabolic syndrome or the insulin resistance syndrome? Different names, different concepts, and different goals. Endocrinol Metab Clin North Am, 2004. 33(2): p. 283-303.

Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.

Ludwig, D.S. and M.I. Friedman, Increasing adiposity: consequence or cause of overeating? JAMA, 2014. 311(21): p. 2167-8.

Crofts, C., Understanding and Diagnosing Hyperinsulinemia. 2015, AUT University: Auckland, New Zealand. p. 205.

Copyright ©2018 BetterByDesign Nutrition Ltd.

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

I’d heard of Alzheimer’s disease (AD) being referred to by some clinicians as ”Type 3 Diabetes” but until yesterday the link between AD and abnormalities in glucose metabolism in the brain was an academic interest. Now it’s personal. You see, yesterday I found out that my dad (90 years old) was diagnosed with Alzheimer’s disease. His once-sharp mind is no longer capable of recalling what happened yesterday or in fact what just happened. It is as though he has ”partial amnesia”.

The majority of those that are diagnosed with AD (95%) have the same form of the disease that my dad has called sporadic Alzheimer’s disease. Only 5% are diagnosed with a genetically-linked form inherited from the maternal side of the family [2].

In sporadic Alzheimer’s disease the first part of memory that is affected is the person’s unique memory of specific events (called episodic memory).

I remember three or four years ago asking my dad to recount the details of our family history from his side of the family that he often told yearly at holiday dinners — yet he couldn’t even remember their existence! I tried prompting him with parts of the story to try and trigger the memory but was met with ”I’m sorry dear, I don’t recall“.  I was dumbfounded because he told this same exact story over and over again for years, and then suddenly it was gone. From his perspective, it didn’t exist. His behaviour and other forms of memory were completely normal, so I discounted his forgetfulness to ”aging” but I now know this was the first noticeable indication that something was not working as it should.

As Healthy People Age

As healthy people age, brain cells waste away (atrophy) and are not replaced such that brain volume decreases at a rate of about 1.6% / decade after the age of 30 years old [1]. So, at 40 years old, a person is expected to have a 1.6% decrease in brain volume, at 50 years old a 3.2% decrease, and so on. At 90 years old, a healthy person would be expected to have lost a little less than 10% of their brain volume.

My maternal grandmother was healthy and lived until well over 100 years old and I can see in retrospect that the kinds of memory changes my dad was showing a few years ago (at age ~85) were not simply part of normal aging.

Changes in Alzheimer’s Disease

Over the last 30 years, there has been a lot of progress in terms of understanding changes in brain energy metabolism during AD as compared with what occurs in normal, healthy aging. Until recently, many thought that lower brain function of those developing AD led to less use of glucose by the brain, but now it is thought that it is actually the other way around; that decreased glucose uptake into the cells of the brain leads to decrease metabolism in the brain. This decrease glucose uptake into the cells of the brain are believed to be a critical part of the early development of AD and that significantly lower brain glucose metabolism may be present long before the onset of any clinically measurable mental decline in AD [2].

It is now widely believed that there is decreased glucose metabolism in the brain in those with AD. When compared with healthy aged-matched people, those with AD have ~25% more brain atrophy than would be expected for their age. This is, after correction for age-associated brain atrophy, the majority of PET scan studies conducted from 1981- until the present, show that glucose utilization by the brain is decreased by as much as ~25% in AD [2].

While healthy, normal aging is associated with some slow brain atrophy, it is not thought to be associated with decreased glucose metabolism.

Normal Brain Glucose Use

The brain, heart, liver and kidneys together use ~ 60% of the body’s resting metabolic energy needs and while the heart and kidneys are metabolically more active than the brain, the brain is larger. As a result, the brain uses about ¼ of the body’s total energy needs [2]. This energy is used for blood flow in the brain, use of oxygen by the brain and for glucose metabolism — but most of the glucose used by the brain is used to maintain a glucose gradient (difference) between glutamate neurons which enable communication along this neurotransmitter system.

Glucose transporters (GLUTs) bring glucose into the brain in a three-step process: (i) Transport across the blood-brain barrier (ii) transport into the brain cells (astrocytes) and (iii) transfer of the glucose into the neurons of the glutamate neurotransmitters.

When the brain is active, the Adenosine Triphosphate molecule (ATP) which is the ”currency” of energy transfer inside cells decreases, and the brain needs more glucose, so glucose uptake is stimulated by the cell. It is unknow at what point partial reduction in glucose transport begins to limit brain function in AD.

Brain Glucose Use in Alzheimer’s Disease

Alzheimer’s Disease is a neurodegenerative disease that results in progressive worsening of memory and cognitive function, as well as behavior changes and disorientation.

Even though normal healthy aging is not associated with AD. Aging itself is the main risk factor for sporadic AD, with rates ~doubling every five years after 65 years of age [3] and affecting more than 60% of people over the age of 95 years of age [4].

The brain of those with AD is marked by an accumulation of βeta-amyloid plaques between brain cells and by neurological ”tangles” within brain cells.  As mentioned earlier, there are two types of AD — familial / early onset AD and sporadic / late onset AD. The early onset type is much rarer (~5% of all AD) and is inherited from the maternal (mother’s) side of the family. Except for a different age of onset, what is seen clinically, and the progression of decreased cognitive function is not significantly different between the two types of AD. The βeta —amyloid plaques occur slowly before any change in memory or understanding become apparent. The progressive brain atrophy speeds up later in the disease process, bringing the cognitive decline frequently associated with AD.

There are also other forms of dementia besides Alzheimer’s disease, including fronto-temporal dementia and vascular dementia but these are very different from either of the two sub types of AD.

PET scan studies point to lower brain glucose metabolism in AD, with difference between normal aging subjects and those with AD being as much as ~20—25% lower in AD with most of the atrophy occurring in the region of the brain called the hippocampus, which is involved in memory processing.

Mild Cognitive Impairment (MCI)

There is intermediate stage between normal healthy aging and AD, called Mild Cognitive Impairment (MCI) which includes some decreased thinking ability (cognitive decline). When these thought process changes and memory loss are present in the elderly, but don’t significantly affect daily life or interactions it is considered to be MCI. There are a few studies of glucose metabolism in MCI which show that it is lower than in healthy aged-match controls but less than in moderate to severe AD.

As MCI progresses to AD, glucose usage decreases in additional regions of the brain (cingulate, inferior parietal lobes, temporal lobes) [2].

Nutritional Factor that Affects Glucose Metabolism

The omega-3 fatty acid found mainly in fatty fish known as Docosahexaenoic acid (DHA; 22:6ρ‰3) is known to have an important role in normal brain development. In animal studies,  supplementation with DHA was found to increase expression of the glucose transporters (GLUTs) that bring glucose into the brain and in primate studies, brain DHA concentration was found to be directly proportional to brain glucose uptake in the same region of the brain [2]. Insufficient intake of DHA and/or low levels in the hippocampus (the region of the brain initially impacted by AD) may play a role in cognitive decline in older adults.

Metabolic Factors that Affect Glucose Metabolism

While the glucose transporters (GLUTs) involved in getting glucose across the blood-brain barrier and into the brain cells (GLUT1) and across glutamate neurons (GLUT3) are not sensitive to insulin, GLUT4 which is another glucose transporter involved in memory and cognition in areas of the brain including the hippocampus are insulin-sensitive [5]. It is thought that brain insulin signaling may be defective in AD [5].

Older adults and the elderly often develop glucose intolerance which often progresses to Type 2 Diabetes then to Metabolic Syndrome which is a combination of Type 2 Diabetes, high blood pressure (hypertension), increased waist circumference (visceral obesity) and abnormal cholesterol tests (dyslipidemia).

Insulin resistance, which often comes before glucose intolerance / high blood sugar tops the list of known risk factors to cognitive decline [5, 6] and younger adults that are obese are predisposed to Metabolic Syndrome which is associated with increased risk of degenerative changes in the brain [6].

Decreased skeletal muscle mass (sarcopenia) in older adults and the elderly may contribute to the increased risk of insulin resistance associated with aging, as muscle is the main site of insulin-mediated glucose utilization in the body. In older adults, adequate dietary protein intake as well as incorporating some form of resistance training of large muscle groups may play a role in decreasing cognitive decline by increasing glucose update from the blood to the muscle where it can then be transported to areas of the brain.

Ketones: the body’s preferred alternative fuel

In healthy people that haven’t eaten in while (such as after an overnight fast or a during relatively long period of time between meals) ketone bodies (ketones) are the body’s key replacement fuel which maintains brain function. The brain even has a separate transport system for ketones which is independent of glucose transport [2].

When blood sugar levels drop over a period of several hours or even days during fasting the energy requirements of the body are dependent on the availability of two ketones — acetoacetate and β-hyydroxybutyrate for normal function.  During prolonged fasting over a period of days and in starvation up to ~60% of the human brain’s energy requirements can be met by a combination of acetoacetate and β-hydroxybutyrate [7].

The brain can convert ketones to ATP, the energy ”currency” of the cell by oxidizing ketones (converting β-hydroxybutyrate to acetoacetate, acetoacetate to acetoacetyl CoA, and acetoacetyl CoA to acetyl CoA which then is used to generate ATP).  While brain cells (astrocytes) can beta-oxidize fatty acids [8] to produce ketones, transport of fatty acids across the blood-brain barrier is too slow to make fatty acids as useful alternative as fuel for the brain.

Ketones cannot fully replace glucose as a brain fuel as a small quantity of glucose is essential for the brain, however this does not need to be supplied in the diet but can be manufactured by the liver (as well as to a lesser degree by the kidneys and the intestines) from fat or protein in a process known as gluconeogenesis (literally ”making new glucose”).

The body can make ketones from fat stores in a process called ketogenesis but first there needs to be a lowering of blood glucose, which will result in decreased blood insulin levels. This can occur during fasting, as well as by following a low-carbohydrate diet. When insulin level decreases, free fatty acids from fat cells (adipose tissue) can be freed into the blood. These long chain fatty acids are then brought to the liver where they are broken down (β-oxidized) to acetyl CoA, which are then condensed into ketones.

Use of a Therapeutic Ketogenic Diet in Alzheimer’s Disease

It is thought that in Alzheimer’s disease the combination of brain glucose insufficiency and the inadequate supply of naturally-produced ketones (which normally would naturally be produced by the body in response to low blood glucose) puts the high energy consuming areas of the brain in mild, but constant shortage of energy.

Since the brain can’t get its main fuel source which is glucose nor its preferred back- up fuel source which are ketones (because blood glucose doesn’t drop) this forces the brain to rely on a third, but inadequate source of energy — which is making glucose from fat stores or protein (gluconeogenesis).

Over time, specific regions of the brain such as the hippocampus are thought to be put in a situation of long-term chronic fuel shortage and gradually these brain cells burn out’, which leads to the brain changes seen in Alzheimer’s Disease [2].

It is thought that if brain ketone metabolism is unaffected in AD — or at least is affected less than glucose, a ketogenic diet may provide the brain with ketones it can use as an alternative fuel to glucose, enabling it to function more normally, reducing cognitive decline resulting from brain glucose insufficiency.

If you have questions about how eating a low carbohydrate diet can significantly reduce insulin resistance, a major risk factor for Alzheimer’s disease, as well as reverse symptoms of Metabolic Syndrome, please send me a note using the “Contact Me” form on this web page and I’ll be glad to reply as soon as I’m able. Remember, I provide services via Distance Consultation (via secured Skype) as well as in-person in my Coquitlam office.

To our good health!

Joy

you can follow me at:

 https://twitter.com/lchfRD

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

Copyright ©2018 BetterByDesign Nutrition Ltd.

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

 

References

1. Svennerholm, L., K. Bostrí¶m, and B. Jungbjer, Changes in weight and compositions of major membrane components of human brain during the span of adult human life of Swedes. Acta Neuropathol, 1997. 94(4): p. 345-52.
2. Cunnane, S., et al., Brain fuel metabolism, aging, and Alzheimer’s disease. Nutrition, 2011. 27(1): p. 3-20.
3. Canadian study of health and aging: study methods and prevalence of dementia. CMAJ, 1994. 150(6): p. 899-913.
4. Brayne, C., et al., Dementia before death in ageing societies–the promise of prevention and the reality. PLoS Med, 2006. 3(10): p. e397.
5. Watson, G.S. and S. Craft, Modulation of memory by insulin and glucose: neuropsychological observations in Alzheimer’s disease. Eur J Pharmacol, 2004. 490(1-3): p. 97-113.
6. Raffaitin, C., et al., Metabolic syndrome and risk for incident Alzheimer’s disease or vascular dementia: the Three-City Study. Diabetes Care, 2009. 32(1): p. 169-74.
7. Cahill, G.F., Fuel metabolism in starvation. Annu Rev Nutr, 2006. 26: p. 1-22.
8. Guzmán, M. and C. Blázquez, Is there an astrocyte-neuron ketone body shuttle? Trends Endocrinol Metab, 2001. 12(4): p. 169-73.

 

Those who are younger than 40 years old probably grew up hearing that saturated fat is ”bad” and polyunsaturated fat is ”good”, but where did we get this idea and is it true?

The process of what I call the ”vilification of fat” began when researcher Ancel Keys presented a graph at a talk at Mount Sinai Hospital in New York in January 1953 and later published it in a research paper titled Atherosclerosis: a problem in newer public health [1]. It was said to show the relationship between fat calories as a percentage of total fat” and the number of deaths from degenerative heart disease per 100,000 people’ for men between the ages of 45-49 and 55-59. The linear relationship of these data points from the Six Country Study (Japan, Italy, England & Wales, Australia, Canada and the USA) suggested that there was a strong relationship between the amount of fat calories as a percentage of dietary intake and deaths from degenerative heart disease for men aged 55-59. At the time of publication of the Six Country Study, Keys said that it was possible to only get complete data from those 6 countries [1] at the time. He concluded;

”Whether or not cholesterol etc. are involved, it must be concluded that dietary fat somehow is associated with cardiac diseases mortality, at least in middle age [1].

In Key’s mind, the total amount of dietary fat was ”somehow associated” with cardiac death in middle aged men, but he expressed doubt whether or not cholesterol was involved.

In 1957, Yerushalamy and Hilleboe [2] published data from 22 countries which showed there was no linear relationship between fat calories as a percentage of total fat” and the number of deaths from degenerative heart disease per 100,000 people’.

Keys went onto conduct what became known as the Seven Country Study which collected data on almost 13,000 men aged 40-59 from the USA, Finland, the Netherlands, Yugoslavia, Greece and Japan. Findings were only published in 1970 in the journal Circulation in several papers from separate countries [3]. Keys no longer believed that total fat was associated with heart disease but that saturated fat was the villain. Keys concluded that the average consumption of animal foods (with the exception of fish) was positively associated with 25-year heart disease death rates and that the average intake of saturated fat was strongly related to 10 and 25-year coronary heart disease death rates.

What solidified this association was that the 1970 publication on the Seven Country Study contained Keys’ 1953 graph from the Six Country Study (above) [4]. Even though it indicated a linear relationship between total fat intake and degenerative heart disease it became tied in the minds of many that this graph ”proved” that saturated fat was linked to heart disease—even though that is not what the graph shows at all.  It isn’t even about saturated fat. Keys also neglected to mention Yerushalamy and Hilleboe’s data from 22 countries showed no relationship between total fat consumption and heart disease.

The Diet Heart Hypothesis

The diet-heart hypothesis originated with Ancel Keys and is the belief that eating foods high in saturated fat contributes to heart disease. Keys believed that replacing fat from meat, butter and eggs with newly-created polyunsaturated vegetable oils such as soybean oil would reduce heart disease and deaths by lowering blood cholesterol levels.

The Sugar Industry Funding of Research Vilifying Fat

In the mid-1960’s, the Sugar Research Foundation (predecessor of the Sugar Association) wanted to offset research that had been published and that suggested that sugar was a more important a cause of heart disease and stroke from atherosclerosis than dietary fat. The Sugar Research Foundation invited Dr. Fredrick Stare and the late Dr. D. Mark Hegsted of Harvard’s School of Public Health Nutrition Department to join its scientific advisory board and then approved $6,500 in funds ($50,000 in 2016 dollars) to support a review article that would respond to the research showing the danger of sucrose [5]. Letters exchanged between the parties came to light a November 2016 article published by Kearns et al [6] which said that the Sugar Research Foundation had tasked the Harvard researchers with preparing ”a review article of the several papers which find some special metabolic peril in sucrose and, in particular, fructose [7]”.

The Sugar Industry paying researchers to blame dietary fat and vindicate sugar for heart disease seems a little like the tobacco industry having secretly funded articles demonstrating that something other than smoking was responsible for lung cancer.

In August 1967 the New England Journal of Medicine published the first review article written by Drs. Stare, Hegsted and McGandy titled ”Dietary fats, carbohydrates and atherosclerotic vascular disease” which stated;

”Since diets low in fat and high in sugar are rarely taken, we conclude that the practical significance of differences in dietary carbohydrate is minimal in comparison to those related to dietary fat and cholesterol“.

The report concluded;

”the major evidence today suggests only one avenue by which diet may affect the development and progression of atherosclerosis. This is by influencing the levels of serum lipids [fats], especially serum cholesterol.”

The Harvard researchers went on to say;

”there can be no doubt that levels of serum cholesterol can be substantially modified by manipulation of the fat and cholesterol of the diet” and that “on the basis of epidemiological, experimental and clinical evidence, that a lowering of the proportion of dietary saturated fatty acids, increasing the proportion of polyunsaturated acids and reducing the level of dietary cholesterol are the dietary changes most likely to be of benefit.”

At no point did Stare, Hegsted and McGandy disclose that they were paid by the Sugar Research Foundation for the two-part review.

A commentary in the Journal of Accountability in Research [8] summarized the significance of those articles as follows;

“Researchers were paid handsomely to critique studies that found sucrose [sugar] makes an inordinate contribution to fat metabolism and heart disease leaving only the theory that dietary fat and cholesterol was the primary contributor.”

The same Dr. Hegsted that was funded by the Sugar Industry to write the above articles vindicating sugar and vilifying dietary fat went on to work on editing the 1977 US Dietary Guidelines [9], which entrenched the vilification of fat into the US Food Pyramid for the next 40+ years. The rest, they say, is history.

The same year (1977), Canada’s Food Guide recommended that Canadians limit fat to <30% of daily calories with no more than 1/3 from saturated fat but did not specify an upper limit for dietary cholesterol. This was based on the belief that total dietary fat and saturated fat were responsible blood levels of LDL cholesterol levels and total serum cholesterol [10]. Cholesterol in general (total cholesterol) and LDL cholesterol was assumed to be tied to heart disease, so the focus was on lowering the proxy measurements of LDL cholesterol and total cholesterol.

Recommendations for the continued restriction of dietary fat continued in both the US and Canada in the 2015 revision of the Dietary Guidelines based on the enduring belief that lowering saturated fat in the diet would lower blood cholesterol levels and reduce heart disease.

The question is does it?

A 2018 study published in the journal Nutrients looked at health and nutrition data from 158 countries from 1993-2011 and found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease and that high carbohydrate consumption,  particularly as cereals and wheat was most associated with the risk of cardiovascular disease [11]. Significantly, both of these relationships held up regardless of a nation’s average national income.

These findings support those of the 2017 PURE (Prospective Urban and Rural Epidemiological) study, the largest-ever epidemiological study which recorded dietary intake of 135,000 people in 18 countries over an average of 7 1/2 years, including high-, medium- and low-income nations. The PURE study found an association between raised cholesterol and lower  cardiovascular risk and that ”higher carbohydrate intake was associated with higher risk of total mortality”. It also reported that ”total fat and individual types of fat were related to lower total mortality (death)” [12].

A recent study published in the American Journal of Clinical Nutrition reports that long-term consumption of the saturated fat found in full-fat dairy products is not associated with an increased risk of cardiovascular disease (atherosclerosis, coronary artery disease, etc.) or other causes of death, and may actually be protective against heart attack and stroke [13].

This recent large-scale epidemiological data provides strong evidence that eating a diet containing saturated fat is not associated with heart disease. While eating saturated fat raises blood levels of LDL cholesterol, we now know that there is more than one type of LDL cholesterol and only the small, dense LDL cholesterol is linked to atherosclerosis. The large, fluffy LDL is protective [14].

We now know that fat was made out to be the villain in scientific reviews paid for by the sugar industry and this combined with Ancel Key’s Diet-Heart Hypothesis ended up being the impetus for the creation of an entire food industry designed to extract fat from industrial seed oils, such as soybean oil and rapeseed (Canola). These industrial seed oils are the so-called ”healthy polyunsaturated fats” that we are encouraged to eat instead of so-called ”dangerous” saturated fat, yet these industrial seed oils are only able to be produced using solvent-based chemical extraction under very high temperature. Should we be confident in industrial fats brought to us by the same industry that brought us ”trans fats”? With a lack of evidence that natural fats such as butter or cream are dangerous, perhaps eating a bit of real animal fat and plenty of natural plant-based monounsaturated fats such as olive oil is the better way to go?

For more than forty years, generations of Americans and Canadians have avoided eggs, full fat cheese and creamery butter — and done so because they have believed that saturated fat raising LDL cholesterol predisposed them to heart disease. We know much more than we did in the 1970s when the first Dietary Guidelines were created in the US (under the watchful editorial oversight of one of the researchers that had been paid by the sugar industry to vilify fat).  We now know that eating foods with saturated fat will raise LDL-cholesterol, but not all LDL-cholesterol is ”bad”[14]. Before we knew this high total LDL-cholesterol (LDL-C) was seen as a good proxy (indirect substitute) measurement for heart disease risk, but no longer.

It has been known since the early 1990s that a high TG:HDL ratio is very good estimator of coronary heart disease risk [15].

The measurement of the LDL-cholesterol particle number (LDL-P) which measures the actual number of LDL particles is a much stronger predictor of cardiovascular events than LDL-C [16] because the more particles there are, the more small, dense LDL there are.

The ratio of apolipoprotein B (apoB): apolipoprotein A (apoA) is another good estimator of cardiovascular risk. Lipoproteins are particles that transport cholesterol and triglycerides (TG) in the blood stream and are made up of apolipoproteins, phospholipids, triglycerides and cholesterol. Apolipoprotein B is an important component of many of the lipoprotein particles associated with atherosclerosis, such as chylomicrons, VLDL, IDL, LDL — with most found in LDL. Since each lipoprotein particle contains one apoB molecule, measuring apoB enables the determination of the number of lipoprotein particles that contribute to atherosclerosis and for this reason that ApoB is considered a much better predictor of cardiovascular disease risk than LDL-C [17].

In light of the recently published epidemiological evidence and much stronger proxy measurement of cardiovascular risk we must update our thinking that fat in general, or saturated fat in particular is the ”villain”. It’s not.

Perhaps you could use some help as to which fats you should eat more of and in what amounts, or on deciding on what ratio of protein to fat in your diet will best help you reach your health and weight goals? I can help.

I provide services via Distance Consultation (Skype, long distance telephone) as well as in-person in my Coquitlam office.

If you have questions on my services, please send me a note using the Contact Me form located on the tab above, and I will reply as soon as I’m able.

To our good health!

Joy

 https://twitter.com/lchfRD

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Copyright ©2018  BetterByDesign Nutrition Ltd. 

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

References

1. Keys, A., Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp N Y, 1953. 20(2): p. 118-39.
2. Yerushalamy, J. and Hilleboe HE, Fat in the diet and mortality from heart disease; a methodologic note. N Y State J Med, 1957. 57(14): p. 2343-54.
3. Coronary heart disease in seven countries. Summary. Circulation, 1970. 41(4 Suppl): p. I186-95.
4. Harcombe, Z., An examination of the randomised controlled trial and epidemiological evidence for the introduction of dietary fat recommendations in 1977 and 1983:  A systematic review and meta-analysis. 2015, University of the West of Scotland.
5. Husten, L., How Sweet: Sugar Industry Made Fat the Villain. 2016.
6. Kearns, C.E., L.A. Schmidt, and S.A. Glantz, Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. JAMA Intern Med, 2016. 176(11): p. 1680-1685.
7. McGandy, R.B., D.M. Hegsted, and F.J. Stare, Dietary fats, carbohydrates and atherosclerotic vascular disease. N Engl J Med, 1967. 277(4): p. 186-92 contd.
8. Krimsky, S., Sugar Industry Science and Heart Disease. Account Res, 2017. 24(2): p. 124-125.
9. Hegsted D.M. Introduction to the Dietary Goals for the United States. p. 17 of 130.
10. McDonald, B.E., The Canadian experience: why Canada decided against an upper limit for cholesterol. J Am Coll Nutr, 2004. 23(6 Suppl): p. 616S-620S.
11. Grasgruber, P., et al., Global Correlates of Cardiovascular Risk: A Comparison of 158 Countries. Nutrients, 2018. 10(4).
12. Dehghan, M., et al., Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet, 2017. 390(10107): p. 2050-2062.
13. de Oliveira Otto, M.C., et al., Serial measures of circulating biomarkers of dairy fat and total and cause-specific mortality in older adults: the Cardiovascular Health Study. Am J Clin Nutr, 2018.
14. 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.
15. Manninen, V., et al., Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment. Circulation, 1992. 85(1): p. 37-45.
16. Cromwell, W.C., et al., LDL Particle Number and Risk of Future Cardiovascular Disease in the Framingham Offspring Study – Implications for LDL Management. J Clin Lipidol, 2007. 1(6): p. 583-92.
17. Lamarche, B., et al., Apolipoprotein A-I and B levels and the risk of ischemic heart disease during a five-year follow-up of men in the Québec cardiovascular study. Circulation, 1996. 94(3): p. 273-8.

 

 

This week Stanford University published a study which substantiates the huge glucose spikes that “healthy” people with normal blood sugar levels experience and that Dr. Joseph Kraft began documenting 45 years ago [2,3,4] — until just before his death in 2017 [5].  To those of us that are familiar with the research of Dr. Kraft, this is a bit like the 1969 Apollo 11 lunar astronauts ‘discovering’ the existence of craters and mountains on the moon that were documented by Galileo in 1609.

Kraft called these abnormal glucose spikes along with the corresponding abnormal spikes of insulin ‘occult diabetes‘ or ‘diabetes in situ‘ [4] and used the term ‘occult diabetes’ to describe it since ‘occult’ in this context means “not accompanied by readily discernible signs or symptoms“.  It is these ‘covert’ glucose spikes that Stanford university researchers reported this week.

The Stanford Study

Stanford researchers gave 57 healthy subjects without prior diagnosis of diabetes continuous glucose monitors (CGM) that recorded their blood sugar fluctuations in their normal environment for two weeks. There were 32 women, 25 men — ranging in age from 25 to 76, with an average age of 51 years [1].

Subject’s Blood Sugar Upon Screening

Upon screening for the study, 5 of the subjects were discovered to have met criteria for having type 2 diabetes, as defined as HbA1c ≥6.5%, fasting blood glucose ≥ 126 mg/dL (7.0 mmol/L), or 2-hour glucose during 75 gram Oral Glucose Tolerance Test (OGTT) ≥ 200 mg/dL (11.1 mmol/L); 14 subjects were found to meet the criteria for prediabetes, defined as HbA1c > 5.7% and < 6.5%, fasting blood glucose 100—125 mg/dL (5.5 mmol/l-6.9 mmol/L) , or 2-hour glucose during OGTT 140—199 mg/dL (7.8-11.0 mmol/L). The remaining 38 subjects had normal blood glucose defined as fasting and 2-hour OGTT plasma glucose and HbA1c below the diagnostic thresholds for prediabetes and diabetes. Average fasting glucose was 93 mg/dL (5.2 mmol/L), 2-hour glucose 125 mg/dL (6.9 mmol/L) and HbA1c 5.4%[1].

Huge Variations in Blood Sugar Response

Researchers found that there was huge inter-individual (between individuals) and intra-individual (in the same individual at different times) variation in blood sugar response — which is exactly what a 2015 study that fitted 800 people with CGMs reported [6]. In light of only the glucose part of Kraft’s findings as well as the data from the Israeli study with a study population more than 10x the size, the Stanford findings are not ‘new’.

Using mathematical techniques including spectral clustering and dynamic time warping, researchers defined 3 clusters of glucose patterns which were said to capture 73% of the variation [1]. Based on the amount of variability in glucose levels in each cluster, researchers classified the 3 patterns as low, moderate and severe variability.

Some People had lots of Abnormal Glucose “Spikes”

The researchers found that each of the 3 patterns showed a progressive increase in both the severity and magnitude of the blood sugar fluctuations. As well, some subjects mainly stayed in the low variability range, whereas others were mostly in the moderate to severe variability range. These are basically rankings of blood sugar “spike” intensity [7].

Of significance, blood sugar in the individuals that were considered healthy fluctuated a lot more than what is normally picked up by standard ‘finger-prick’ methods of blood sugar testing and these fluctuations come in the form of “spikes’; which are rapid increases in the amount of glucose (sugar) in the blood, especially after eating specific foods — most commonly carbohydrate [7].

Dr. Michael Snyder, professor and chair of genetics at Stanford and senior author of the study said;

“There are lots of folks running around with their glucose levels spiking, and they don’t even know it. The covert spikes are a problem because high blood sugar levels, especially when prolonged can contribute to cardiovascular disease risk and a person’s tendencies to develop insulin resistance, which is a common precursor to diabetes.”

“We saw that some folks who think they’re healthy actually are misregulating glucose—sometimes at the same severity of people with diabetes—and they have no idea [7].”
~ Dr. Michael Snyder

Stanford researchers documented that abnormal glucose responses were more common than they previously thought [7], but these results come as no surprise to those of us familiar with Kraft’s research [2-5] and the findings of the 2015 study from Israel [6].

You can read more about the significance of these covert glucose and corresponding insulin spikes in this article titled When Normal Fasting Blood Glucose Results Aren’t Necessarily “Fine”.

Cornflakes For Breakfast?

The Stanford researchers conducted a sub-study in 30 subjects whose prior blood sugar tests indicated that they were “healthy” (i.e. not prediabetic or diabetic). They were fitted with continuous glucose monitors (CGMs) and alternated between 3 breakfasts; (1) a bowl of cornflakes with milk, (2) a peanut butter sandwich and (3) a protein bar.

Significantly, more than half of the “healthy” group had blood sugar spikes at the same high levels as those who were diagnosed as prediabetic or diabetic [1,7].

Dr. Michael Snyder, professor and senior author of the study said;

“We saw that 80% of our participants spiked after eating a bowl of cornflakes and milk. Make of that what you will, but my own personal belief is it’s probably not such a great thing for everyone to be eating[7].”

Ordinary Blood Tests Available to Detect These Abnormal “Spikes”

Different people respond to carbohydrate based foods differently and even the same individual can respond to the same carbohydrate-based food differently — depending on part on the degree of processing it has undergone, or whether it is eaten alone or after eating protein-containing foods (see two articles on the Perils of Food Processing for more information).

As elaborated on in a previous article titled “Are You Pushing Your Pancreas Too Hard, abnormalities in insulin, including insulin resistance and/or hyperinsulinemia begin to occur as much as 20 years before a diagnosis of Type 2 Diabetes [8]; while blood sugar results are still normal and the results of this new Stanford study underscores the need to diagnose these abnormalities by capturing the blood glucose and insulin spikes well in advance of that!

The problem is, if we only monitor people’s fasting blood glucose and glycated hemoglobin (HbA1C) as a screening tool, we can miss that someone’s pancreas is overworking by constantly producing too much insulin.

Even if a standard 2 hour Oral Glucose Tolerance Test (OGTT) is run, if a person’s blood glucose results are normal at fasting and normal at 2 hours (such as was the case in the Stanford study!), we will miss the “spike” that occurs 30 minutes to 1 hour after the glucose is consumed in those with covert glucose spikes. The way to capture those “spikes” is to run a 2 hour Oral Glucose Tolerance Test with simultaneous glucose and insulin and do the two measurements at baseline (fasting), 30 minutes / 1 hour, and at 2 hours. When we detect these “spikes”, we can implement dietary changes to avoid further β-cell damage or β-cell death whose end-result is type 2 diabetes.

The Cost of Documenting These “Spikes” – penny wise and pound foolish

For less than $130 (cost in British Columbia, Canada), a physician can order a 2-hour OGTT with both glucose and insulin measured at (a) fasting, (b) 1 hour and (2) 2 hours which will capture abnormal glucose spikes at 1 hour, as well as the underlying hyperinsulinemia.

When there are clinical reasons to suspect that a person may be insulin resistant and/or hyperinsulinemic, a blood test that assesses simultaneous glucose and insulin response to a glucose challenge can provide sufficient motivation for individuals to implement dietary changes that can prevent progression to Type 2 Diabetes.

is such a test that costs <$130 to the public healthcare system not good value when the cost per person per year of having Type 2 Diabetes in Canada ranges from $1611 to $3427 ( more about that here)?

In British Columbia, the cost of a standard 2 hour Oral Glucose Tolerance Test is $11.82 before tax and $13.36 with HST.

Each additional glucose assessment is $3.48 before tax and $3.93 after tax.

Each insulin assessment costs $32.82 before tax and $37.09 after tax, so a 2 hour Oral Glucose Tolerance Test with additional glucose assessor at 1 hour and 3 insulin assessors at fasting, 1 hour and 2 hour costs as follows;

2 hour Oral Glucose Tolerance (fasting, 2 hours)           = $  13.36  with GST
additional glucose at 1 hour                                                       = $   3.93   with GST
3 insulin assessors at fasting, 1 hour, 2 hours                   = $111.27  with GST
TOTAL                                                                                                   = $128.56 with GST

The reason often given by physicians for NOT requisition the above tests is that it is “saving healthcare system dollars”, but in those with clear risk indicators, how is it wise to ignore what can’t be detected with standard screening tests?

More Info?

If you would like more information about determining how you respond to carbohydrate containing foods and whether you are at risk for prediabetes type 2 diabetes especially if your blood sugar values appear normal on standard screening tests, 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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Copyright ©2019 BetterByDesign Nutrition Ltd.

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

References

1. Hall H, Perelman D, Breschi A, et al, 2018, Glucotypes reveal new patterns of glucose dysregulation. PLOS Biology 16(7). https://doi.org/10.1371/journal.pbio.2005143
2. Kraft JR, Glucose Insulin Tolerance. A routine Clinical Laboratory Tool Enhancing Diabetes Detection. In O.B. Hunter. Jr. (ed): Radio assay: Clinical Concepts. Skokie, IL. Professional Education Dept. G.D. Searie & Co., 1974. Pp 91-106.
3. Kraft JR, The Glucose Tolerance Examination: An Obsolete Procedure. read at the Symposium on Radioimmunioassay in Diagnostic Medicine.” Annual Convention, American Medical Association, Chicago, IL. June 26, 1974
4. Kraft JR, Detection of Diabetes Mellitus In Situ (Occult Diabetes), Laboratory Medicine, Volume 6, Issue 2, 1 February 1975, Pages 10—22, https://doi.org/10.1093/labmed/6.2.10
5. Crofts C, Schofield G, Zinn C, Wheldon M, Kraft J., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.
6. Zeevi D, Korem T, Zmora N, et al. Personalized Nutrition by Prediction of Glycemic Responses. Cell. 2015 Nov 19;163(5):1079-1094.
7. Medical Press, July 24, 2019, Diabetic-level glucose spikes seen in healthy people, study finds, https://medicalxpress.com/news/2018-07-diabetic-level-glucose-spikes-healthy-people
8. Sagesaka H, S.Y., Someya Y, et al, Type 2 Diabetes: When Does It Start? Journal of the Endocrine Society, 2018. 2(5): p. 476-484.

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