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2018 Diabetes Canada Guidelines - Medications for Type 2 Diabetes

>> Monday, April 16, 2018



It can seem daunting to consider that in the treatment of type 2 diabetes, there are now 9 classes of medications available that lower blood sugars (and several different medications within each of these classes).  Which medications to choose, and in which order, are driven by data surrounding efficacy, safety, and ability to prevent cardiovascular events (one of the major diabetes complications we are aiming to prevent).  Over the last few years, we have seen several diabetes medications emerge that reduce the risk of cardiovascular events, and with this information, we are seeing more of an algorithm emerge that guides clinicians on which order to consider these different medications.

The 2018 Diabetes Canada Clinical Practice Guidelines Pharmacotherapy chapter now provides an algorithm that not only takes into account cardiovascular risk protection, but also prioritizes the diabetes medications that do not cause two unwanted side effects that are cause by some types of diabetes medications: weight gain, and low blood sugars (hypoglycemia).

This chapter is excellent, comprehensive, (necessarily) big and the list of key messages is long - I encourage patients to read the Key Messages for People With Diabetes, and clinicians to read the entire chapter, but here are some of the highlights:

1.  In people with type 2 diabetes with A1C less than 1.5% above the individual patient's target, glucose lowering medication should be added if targets are not reached with healthy lifestyle interventions within 3 months.

2.  In people with type 2 diabetes with A1C 1.5% or more above the patient's target, medication should be initiated concomitantly with healthy behavior interventions, and consideration could be given to initiating combination therapy with 2 medications.

(note that the old guidelines used an A1C of 8.5% as the cutoffs above. The new wording reflects that the A1C target, though usually 7% or less,  can be different from one person to the next - more on this here.)


3. Insulin should be started immediately if there is syptomatic hyperglycemia or metabolic decompensation.  In the absence of metabolic decompensation, metformin is still the first choice of medication in people with new type 2 diabetes.

4.  Target diabetes control should be achieved within 3-6 months.


5.  In people with cardiovascular disease in whom A1C targets are not achieved, a medication with cardiovascular benefit should be added to existing therapy: empagliflozin, liraglutide; or canagliflozin (with a lower grade and level of evidence for canagliflozin).

6.   In people without cardiovascular disease who are not at glycemic targets, DPP4 inhibitors, GLP1 receptor agonists, and/or SGLT2 inhibitors should be considered as add on medication over sulfonylureas, meglitinides, insulin and thiazolidinedones, if lower risk of hypoglycemia and/or weight gain are priorities. (Grade A, Level 1A evidence)

7.  In people who are on insulin who are not at blood sugar targets, adding a GLP1 receptor agonist, DPP4 inhibitor, or SGLT2 inhibitor may be considered before adding or intensifying mealtime insulin therapy, with less weight gain and comparable or lower hypoglycaemia risk.


8.  Newer basal insulins (degludec and U-300 glargine) may be considered over U-100 glargine to reduce overall and overnight hypoglycaemia.


This chapter now includes an excellent table (see table 1 here) that lists the effect of diabetes medications on A1C, weight, cardiovascular outcomes, and other therapeutic considerations as well.




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www.drsue.ca © 2018



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2018 Diabetes Canada Guidelines Are Out!

>> Monday, April 9, 2018



The Diabetes Canada (formerly Canadian Diabetes Association) Guidelines are issued in full every 5 years.   As a coauthor of the Weight Management Chapter, I can tell you that these Guidelines have truly been a labor of love for all of us - more than two years with several rounds of evidence review, drafting, re-drafting as new data comes out.... and this is what makes our guidelines one of the most respected diabetes documents in the world!

The 2018 Guidelines are exciting, with a number of substantial changes from the 2013 edition in terms of approach, rigour of methodology, and recommendations.

Each chapter in the Guidelines is structured with a framework including:

Key Messages

Key Messages For People With Diabetes (this is new and awesome, and reflects that the Guidelines are intended not only for the use of health care providers, but also for people with diabetes)

Recommendations


Over the next weeks, I will be posting blogs highlighting some of the key points and changes to the guidelines, and I'll always include a link to the chapter itself if you'd like to read it in full.

Enjoy!

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www.drsue.ca © 2018




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The Easter Waftata

>> Saturday, March 31, 2018






It's always fun to play around with a new recipe on the long weekend, when there's a little extra time!

I had never heard of a Waftata, but apparently it is a recipe reincarnated from days of yore - and super easy to cook in a modern day waffle iron! I have upped the flavour factor from the original recipe, and given options below for using eggs or egg whites in the recipe.  I think there is lots of opportunity to get creative with flavour - try adding paprika or oregano for an extra twist!

Ingredients:

  • 2 large eggs (or 1/2 cup egg white)
  • 1/3 cup part skim ricotta cheese
  • 2 tbsp onion, finely diced
  • 1 tsp minced garlic
  • 3 tsp freshly chopped parsley
  • 1/8 tsp salt
  • 1/4 tsp ground pepper
  • 1/2 cup peeled and shredded white potato
  • 1/2 cup finely diced apple (with or without skin)




Directions:

1.   Beat eggs in a small bowl.

2.  Add ricotta, onion, garlic, parsley, pepper and salt.  Whisk well.

3.  Preheat your waffle iron.

4.  Stir potato and apple into the mixture.

5.  Spray waffle iron with non stick spray and pour mixture onto it.

6.  Close lid and bake until eggs are set and golden brown.


Makes 2 servings.  Per serving:  (with whole eggs)

  • Calories: 160
  • Carbs: 12.5g
  • Fat:  6.5g
  • Protein:  11g

If you substitute 1/2 cup egg whites for the two eggs:
  • Calories: 115
  • Carbs: 12.5g
  • Fat: 2g
  • Protein: 13g


Enjoy!

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www.drsue.ca © 2018

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How Weight Loss Affects Different Body Tissues, Fat Genes, And Inflammation

>> Monday, March 26, 2018


(this is fat tissue under a microscope)



We know that a 5-10% weight loss improves many health conditions associated with obesity.  However, it is very interesting to note that some health issues like blood sugar starts to improve with as little as 2-3% weight loss, whereas other health issues like sleep apnea require closer to 10% weight loss before we start to see improvements.  Why is this?


An eloquent study helps us to understand how different tissues in our body respond to weight loss.  This was a randomized controlled clinical trial, assigning 40 patients to a target 0%, 5%, 10%, or 15% weight loss, and then conducted an array of testing to understand the metabolic changes that occur at each of these degrees of weight loss.  Testing was extensive and included assessment of body composition, 24h blood pressure monitors, blood testing for metabolic parameters and inflammatory markers, tests of organ-specific insulin sensitivity, and even biopsies of fat tissue. Participants were weight stable for at least 3 weeks before testing was conducted.

Key findings were truly fascinating.

After a 5% percent weight loss:
  • There was a decrease blood sugar, insulin levels, triglycerides, ALT (liver test)
  • systolic blood pressure decreased (the top number), but not diastolic (bottom number)
  • NO effect on good cholesterol (HDL), bad cholesterol (LDL), glucose tolerance test (OGTT)
  • improvement in insulin sensitivity in fat, liver, skeletal muscle 
  • improvement in beta cell function (the cells in the pancreas that make insulin)

After 11% weight loss: (the 10% group ended up losing 11%)
  • continued reduction in insulin and triglycerides 
  • altered gene expression in subcutaneous fat tissue - including genes involved in fat synthesis, cholesterol flux, and inflammation
  • no additional benefit to insulin sensitivity in fat tissue or liver
  • additional improvement in insulin sensitivity in skeletal muscle
  • additional improvement in beta cell function

After 16% weight loss: (the 15% group ended up losing 16%)
  • reduction in inflammatory markers (plasma free fatty acids, CRP)
  • more marked altered gene expression in subcutaneous fat tissue - including genes involved in fat synthesis, cholesterol flux, and inflammation
  • continued reduction in insulin and triglycerides
  • no additional benefit to insulin sensitivity in fat tissue or liver
  • additional improvement in insulin sensitivity in skeletal muscle
  • additional improvement in beta cell function

So what is the BOTTOM LINE from this (rather complicated) study?   

1. A 5% weight loss has important benefits to our health, primarily related to a decrease in our body's resistance to insulin.  

2. Further weight loss continues to improve our body's insulin resistance (particularly in muscle), with additional improvements in our metabolic health.  

3.  At 11% weight loss, we start to see changes in how our fat tissue expresses genes, in favour of better health.

4.  At 16% weight loss, there is a decrease in inflammation in our bodies, and a more marked change in fat tissue gene expression.

While a smaller degree of weight loss (even just 2-3% based on other studies) has a very important impact on our metabolic health, the changes in inflammation and fat gene expression seen at over 10% weight loss may well be what it takes to see benefits in other medical conditions associated with obesity, such as obstructive sleep apnea and arthritis.


Follow me on twitter! @drsuepedersen

www.drsue.ca © 2018




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How Your Diet Influences Where You Lose Fat

>> Monday, March 19, 2018




In weight management, our goal is to improve overall health.  In a perfect world, it would be preferable if we could melt away the fat around and inside the internal organs (called 'visceral fat') rather than the fat under the skin, as it is this visceral fat that contributes most to health complications of obesity such as diabetes, high blood pressure, and metabolic syndrome.

A recent study suggests that what we eat actually can help us to target this visceral fat.

The CENTRAL study, published in the journal Circulation, randomized 278 sedentary adults with either abdominal obesity or high cholesterol to follow either the Mediterranean diet versus a low fat diet for 18 months.  Six months into the trial, participants were also randomized to follow an exercise program or not. They used MRI scans to evaluate fat under the skin, fat around the organs, fat in the liver, pancreas, and even around the heart.

At the end of the 18 month study, weight loss was the same between all four groups (Mediterranean vs low fat diets, with or without exercise) at -3.2%.   However, where fat was lost from, and how this influenced health, was different between groups:


  • People on the Mediterranean diet lost more fat from the liver, pancreas, and around the heart. 
  • Exercise with either diet had a greater effect on reducing visceral fat. 
Whether or not total body weight was lost: 
  • Losing visceral fat and/or liver fat improved cholesterol.
  • Losing fat deep under the skin improved insulin sensitivity.
  • Losing fat just under the skin had no effect on health and reduced levels of leptin (a hormone that tells our brains that we feel full). 
The findings that the Mediterranean diet preferentially reduces the more dangerous visceral fat may explain why it is the only diet that has been convincingly found to prevent cardiovascular events.  

These results also show us that it's not about numbers on the scale, as this does not reflect the important changes going on with fat deposit patterns inside. 



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www.drsue.ca © 2018

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Why Short Term Weight Gain Can Be Easier to Lose Than Long Term Weight

>> Monday, March 12, 2018





No weight gained is easy to lose, but - have you ever wonder how Hollywood's actors can gain weight for a movie role, and the next thing you know, they are back at their usual weight for their next photo shoot?  While one may think that it’s simply the superstar access to personal chefs and trainers that gets actors back in shape, there is actually a physiologic basis that can make it less difficult to shed a quick/temporary/intentional weight gain than excess weight that has been present for the long term.

As discussed in a recent Scientific Statement on Obesity Pathogenesis by the Endocrine Society, obesity is associated with inflammation in various tissues, including muscle, fat tissue, vascular system, and liver, and this inflammation appears to be a consequence of chronic obesity.    There is also inflammation in the hunger/fullness centre of the brain, called the hypothalamus.

For a person who has been struggling with weight long term,  inflammation in these tissues causes maladaptive changes in those tissues that make them more resistant to weight loss.    It takes time for this inflammation to develop, so for a person who has had a fairly acute weight gain, it may be easier to drop pounds because they don't have this inflammation working against them.

So then you may wonder - why do some people seem to lose quickly gained weight more easily than others? (e.g. after pregnancy)?

Well, the story of the hunger/fullness centre in the brain is a little more complex.  It turns out that this inflammation may not only be a consequence of long term obesity, but may actually be present in some people before obesity develops.   Some animal studies suggest that eating a high fat diet triggers these inflammatory changes, damaging the neurons in the hypothalamus, which may then result in a disruption of sensations of hunger/fullness, lead to weight gain, plus make it harder to lose it again.

In other words, people who struggle to lose weight after a fairly quick/new weight gain may have inflammation in their hunger/fullness centre that was there before the weight gain, thus making them not only more prone to weight gain, but also making it harder to lose weight than the person without the inflammation. 


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www.drsue.ca © 2018

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The Sleeping Beauty Diet

>> Monday, March 5, 2018




I was shocked and saddened to learn about yet another potentially harmful way that some people may be trying in a desperate attempt to lose weight.

The Sleeping Beauty diet involves taking sleeping pills, with the goal of sleeping through normal waking hours to avoid eating.  Also referred to as 'narcorexia', this fad is not only ineffective, but also dangerous:


1.  While it is true that not enough sleep is associated with higher body weight, so to is too much sleep.


2.  When you are sleeping, your body's metabolism is at its slowest.  When you are awake and moving around, you burn more calories.  Thus, people who sleep more than what their body needs are putting themselves at risk of weight gain by decreasing their overall calorie burn.

3.  Sleeping at unusual hours alters the body's circadian rhythm and the normal hormonal rhythm, which can has a negative impact on health from many perspectives.  Poor sleep quality caused by messing up the body's normal daily rhythm is associated with weight gain, due to alterations in the normal rhythm of hunger/fullness hormones, and an increase in craving for unhealthy foods.

4.  Most importantly: sedation induced by sleeping pills increases the risk of all manner of dangers  and problems due to impaired brain function while under the influence - car accidents, accidents at home, mistakes at home or the workplace... need I go on.

I am so terribly saddened that people out there are so desperate to lose weight that they are literally willing to sleep their life away to do it.  Yet another powerful and compelling reason why the health care profession, and society in general, needs to uniformly accept obesity as a chronic medical condition and help people get the support and care they so desperately need.

Follow me on twitter! @drsuepedersen

www.drsue.ca © 2018

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How Do Our Gut Bacteria Contribute To Obesity... And Can We Treat Them?

>> Monday, February 26, 2018




As blogged previously, we are learning that the bacteria we carry in our intestines (called the gut microbiota) have a role in obesity.  While we still seem to have more questions than answers on this topic, a fascinating review was just published, discussing some very interesting perspectives on this topic.  Here are some key points:

1.  We know there is an association between certain types of gut bacteria and obesity.  However, which is the 'chicken' and which is the 'egg', so to speak, is not clear, and the answer may be both.  In other words, there is evidence that certain types of gut bacteria contribute to the development of obesity, while others are protective.   There is also evidence that developing obesity can change the gut bacteria in favour of those that further contribute to obesity.


2.  Several ways that gut bacteria can contribute to obesity are identified:
  • some gut bugs are better at helping us extract calories from food by fermenting otherwise indigestible fibers
  • gut bacteria can influence permeability (leakiness) of the gut lining, allowing bacterial products into the bloodstream that can trigger an obesity-promoting low grade inflammatory response 
  • short chain fatty acids produced by gut bugs may have an effect on the gut's barrier function, as well as inflammation and appetite
  • (particularly fascinating in my opinion:) gut bacteria can have an impact on the genes we express in the hunger/fullness center in the hypothalamus in our brains through effects on inflammation and nerve signalling. 


3.  Can we treat obesity by changing our gut bacteria?

Knowing that some types of gut bacteria contribute to the development of obesity, the next natural question then is whether we can treat obesity by changing gut bacteria.

There is preliminary evidence that some strains of bacteria, provided as probiotic supplements, may be of benefit in weight management, but there is still much to learn in this area. There is also a lack of regulation in the supplement industry and a huge variation in what different probiotic supplements provide, so it can be hard to know what you're getting.  Some studies suggest that some fibres with prebiotic like effects may be beneficial as well.

Interestingly, metformin, which is an antidiabetic medication, has been shown to alter gut bugs in rodent studies in favour of a gut bacteria that is associated with less adiposity. (While metformin is considered to be weight neutral, some people do lose weight with it.) Also, metformin loses efficacy in animals when pretreated with antibiotics - could this be because of an alteration in gut bacteria? 

We also know that bariatric surgery changes the gut bug composition, and may play a role in the weight loss effect of surgery, by altering gut bugs in favour of those that are not so good at helping us harvest calories from food. 

Fecal transplant (yes, you read that correctly!) is also being considered as a possible treatment strategy for obesity.



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www.drsue.ca © 2018








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New Obesity Medication Approved In Canada

>> Monday, February 19, 2018





Last week, Health Canada approved a new medication for weight management in Canada. This medication is actually a combination of two medications that have been around for years, called naltrexone and bupropion.

Bupropion is an antidepressant medication (called Wellbutrin), and is also used as a smoking cessation agent (called Zyban). It works by stimulating the fullness center of our brains, thereby suppressing appetite (specifically, it increases POMC activity in the hypothalamus by inhibiting reuptake of dopamine and norepinephrine).

Naltrexone is an opioid antagonist, which has been used for many years in the treatment of alcohol dependence and prevention of relapse to opioid dependence.  Naltrexone works by preventing the fullness center of our brains from shutting itself off, further contributing to appetite suppression (specifically: POMC releases B endorphin that creates a negative feedback loop by binding to the mu opioid receptor on POMC neurons; naltrexone blocks this negative feedback loop). 

Naltrexone and bupropion are also thought to have an effect on the mesolimbic reward center of our brains as well, which may result in decreased motivation for, desire for, and sense of reward/satisfaction from tasty foods. 

The weight loss at 1year with naltrexone/bupropion (trade name is Contrave) is about 4% of body weight compared to placebo, with people continuing to take the medication through a year (i.e. excluding those who dropped out of the study) losing 8.1% body weight in combination with lifestyle modification.  With an intensive weekly behavioural modification program, people who continued the medication and lifestyle program lost 11.5% weight after a year, again about 4% more than the behavioral modification group alone, who lost 7.3% body weight.

In a study of people with type 2 diabetes, overall weight loss was 3.7% body weight (5.9% in those who completed the trial) vs 1.7% in the placebo group (2.2% in trial completers). In addition, diabetes control improved, with a 0.5% greater reduction in hemoglobin A1C (a diabetes report card test) than placebo.

The dose of naltrexone/bupropion for weight management is gradually escalated from the starting dose of one 8mg/90mg tablet once a day, to the full dose of two tablets twice per day, over about 4 weeks.

The most common side effects of naltrexone/bupropion are nausea (in 32% of people vs 7% on placebo), constipation, dizziness, vomiting, and dry mouth.  Gastrointestinal side effects tend to abate after about 4 weeks on treatment.

In terms of rare but serious side effects, there is a slightly increased risk of seizures with bupropion (0.1% of people in the weight loss studies vs 0% on placebo), so this medication should not be used in people at risk of seizures.   It is advised not to take Contrave with a high fat meal, as this increases absorption of the medication to more than what was intended.  Also, if doses are missed, they should not be taken later (just skip it completely).

Though it is an antidepression medication, bupropion can temporarily worsen depression or suicidal thoughts (there were no suicide attempts in any of the naltrexone/bupropion weight loss studies).

Contrave should not be used in people who are on opioid pain medications.  There are also a number of other potential medication interactions that must be assessed before starting the medication.

Heart rate and blood pressure can increase slightly; what is usually seen is actually a very small decrease in blood pressure with the weight loss, but not as much blood pressure decrease as one would usually expect with the amount of weight loss seen.  A cardiovascular safety trial was begun but halted about halfway through because interim data had been released, with the concern being that this data release could impact the integrity of that trial.  Naltrexone/bupropion appeared to have cardiovascular safety at the halfway mark, but this is not sufficient data to answer the question – thus, another cardiovascular safety trial is being planned.

Note that this is not a comprehensive list of all considerations in prescribing naltrexone/bupropion – the full Canadian product monograph is available here

Naltrexone/bupropion was approved in USA in 2014 - interested readers can consult the American product monograph here.  

It is encouraging that we now have three medications in Canada that are approved for weight management.  We know that obesity is very heterogeneous (different in causes, contributors, and health consequences from person to person), and thus, the best approach will be unique to each individual.  We also know that the response to antiobesity medication differs from person to person.  The general principle is that a 5% weight loss after 3 months on treatment is the best predictor of long term success with a particular medication (though in my opinion,  maintaining weight after a significant dietary-induced weight loss with the help of medication is an important success as well).  

Disclaimer: I receive honoraria as a continuing medical education speaker and consultant from the makers of naltrexone/bupropion (Valeant). 

Follow me on twitter! @drsuepedersen

www.drsue.ca © 2018



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Exactly How Does Diabetes Medication Empagliflozin Save Lives?

>> Monday, February 12, 2018




The diabetes world was stunned and delighted in 2015 when the diabetes medication empagliflozin (Jardiance) was proven to reduce cardiovascular death by a whopping 38%.   This was an unexpected finding, as no diabetes medication had ever before been shown to decrease the risk of cardiovascular events.  The protective ability of empagliflozin starts very early, suggesting that it is not an effect on atherosclerosis (hardening of the arteries) per se, as this process takes a longer time. It has been a puzzle to understand exactly what is behind the protective abilities of empagliflozin.

A recent publication by Inzucchi and colleagues describes an analysis of the EMPA REG data to try to shed some light on this interesting question.  They conducted an exploratory mediation analysis, examining many different variables, to see which ones contributed to the CV event reduction.

They found that changes in hematocrit and hemoglobin mediated about half of the benefit of empagliflozin.  (This may be because a higher hematocrit means that there is less plasma volume, and/or increased oxygen delivery to the heart.)  Smaller mediation effects were seen for uric acid levels, fasting blood sugar, and A1C (a diabetes ‘report card’ blood test).   The combination of hematocrit, fasting blood sugar, uric acid, and protein in the urine (urine albumin:creatinine ratio) mediated most of the beneficial effect of empaglifozin.

So, we learn what we suspected - that there are multiple and complex mechanisms at play by which empagliflozin reduces cardiovascular risk. There may well be additional mechanisms at play that were not measured, or measurable, in the EMPA REG study.

Empagliflozin was the first type 2 diabetes medication that was shown to decrease the risk of cardiovascular events.  Its cousin in this class called SGLT2 inhibitors, canagliflozin (Invokana), has also been shown to protect against cardiovascular events, but canaglifozin was also found to increase the risk of amputations and bone fracture.  Two medications of a different class (GLP1 receptor agonists), called liraglutide (Victoza) and semaglutide (Ozempic) also have a protective benefit.


Disclaimer: I receive honoraria as as continuing medical education speaker and consultant from the makers of empagliflozin (Boehringer-Ingelheim and Eli Lilly), canagliflozin (Janssen), liraglutide and semaglutide (Novo Nordisk).  I am involved in research of SGLT2 inhibitors and GLP1 receptor agonists as treatments for diabetes. 


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www.drsue.ca © 2018


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Ketogenic Diet - Controversies

>> Monday, February 5, 2018






Last week, the Journal of the American Medical Association (JAMA) was rather aggressively promoting an opinion article about the ketogenic diet.  I know I'm getting into some rather controversial waters here, but I feel it is important to point out some concerns that I have about this article.

A ketogenic diet is an eating plan that restricts carbohydrates to a maximum of 20-50g per day (which is very low), which causes the body to burn fat as fuel instead.  The liver converts fatty acids to ketone bodies, which serve as an energy source.  There is often a reduction in hunger on this diet, and perhaps less reduction in energy burn with weight loss.

In support of the ketogenic diet, the first piece of science that the JAMA article discusses is a meta analysis of 13 randomized controlled trials that suggested that more people lose weight and keep it off on a ketogenic diet than people on low fat diets.

A reality check on this analysis: The difference in weight between these two groups was only 0.9kg (2 lb) at one year, and when they analyzed the four studies that continued out to 2 years, there was no difference in weight between the groups at all.

The JAMA article also comments on improvements in several metabolic parameters - but in the meta analysis, the only thing that was significantly different at 2 years was a small improvement in good cholesterol (HDL).

The article goes on to discuss the potential benefits of the ketogenic diet to people with type 2 diabetes.  I am very glad to see that they point out that medications like insulin and some oral medications for diabetes can cause low blood sugars, and have to be adjusted to avoid low blood sugars.

However, nowhere do I see mention of safety issues for people on SGLT2 inhibitors [canagliflozin (Invokana), dapagliflozin (Forxiga), empagliflozin (Jardiance)] - as blogged previously, there is a low risk of diabetic ketoacidosis (DKA) with these medications, and that risk could be increased on the ketogenic diet.   Some people with type 2 diabetes who require multiple doses of insulin per day may also have quite low to absent insulin production of their own, which could be a recipe to increase the risk of DKA on the ketogenic diet.

My third concern about this article is that it suggests that the lifestyle change to a ketogenic diet may not need to be permanent, and that some people may be able to add back a limited amount of carbs.  To me, this encouragement goes against the foundation of long term successful weight management - that lifestyle changes made to manage weight should be permanent changes that can be sustained lifelong. I'm concerned that this opens the door to the yo-yo weight pattern that is consequent to trying a diet plan that is not permanent nor sustainable for many.   

Finally, they include an image of coconut oil in their article. Seriously?  As blogged previously, coconut oil is actually one of the least healthy oils you can eat.

I do appreciate that the ketogenic diet can work for some people. Avoiding carbs helps to avoid a lot of the unhealthy and quick-grab food that permeates our society, from muffins to burgers to snacks at the grocery store checkout. 

We also know that what will work for one person is very different from the next.  So while the meta analysis shows no difference in weight on the ketogenic vs low fat diet at 2 years, there will be people within each of these groups who had success, and others who did not.

I also appreciate that the authors of the JAMA article note that "this is not a do-it-yourself-diet" for both safety and efficacy reasons. 

But I do feel that their review of the ketogenic diet is overly optimistic, misses some important safety concerns in people with type 2 diabetes, and gives inappropriate hope that this diet can be a non-permanent approach, when no lifestyle change that is not permanent is unlikely to result in sustained success over the long term.

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www.drsue.ca © 2018




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A HEARTFELT WELCOME!

I am excited that you have arrived at my site, and I hope you are too - consider this the first step towards a Healthier New You!! As a medical doctor, Endocrinologist, and obesity specialist, I am absolutely passionate about helping people with weight management. Though there is certainly no magic cure for obesity, there IS a successful treatment plan out there for you - it is all about understanding the elements that contribute to your personal weight struggle, and then finding the treatment plan that suits your needs and your lifestyle. The way to finding your personal solution is to learn as much as you can about obesity: how our toxic environment has shaped us into an overweight society; the diversity of contributors to obesity; and what the treatment options out there are really all about. Knowledge Is Power!!


Are you ready to change your life? Let's begin our journey together, towards a healthier, happier you!!




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