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Weight Management and Diabetes: The Debate

Updated: Jan 23

- From the desk of Dr. Brkich

If you struggle with your weight, you are not alone. Weight gain also does not occur alone and is associated with other conditions such as high blood pressure, high cholesterol, low HDL, high triglycerides, high blood glucose, and high hemoglobin A1c. These conditions are all highly interrelated and collectively form a cluster of risk factors called metabolic syndrome, which greatly raises the risk of developing diabetes, heart attack, stroke, and cancer.


Conventional medical establishments, such as the Mayo Clinic and Johns Hopkins University, acknowledge that they don’t fully understand what causes metabolic syndrome. There is general agreement that it is closely tied to insulin resistance. Johns Hopkins states on its website that “insulin resistance may be a cause of metabolic syndrome.”


Evidence is mounting that there is much more to maintaining healthy weight management and good metabolic regulation than just eating less and exercising more. Calorie restriction and exercise are always helpful, but they are not always enough for everyone. Regulating homeostatic mechanisms in the human body is multifactorial and complex. What works for one person may not work as well for another. We are all different. We have different genetics, different digestion, different microbiomes, different metabolisms, different dietary preferences, different cultural and social relationships to food, and different responses to stress, all of which can impact weight regulation and associated metabolic disorders.


What is Insulin Resistance?


Insulin’s job is to open the membranes (doors) of cells such as muscle and liver cells to allow blood glucose to enter the cells. Insulin is the key that opens the doors of the cells that take up glucose from the blood. When the cell doors open, glucose goes from the blood into the cells, where it is converted into glycogen and stored as fuel to be burned for energy. Insulin resistance occurs when the key (insulin), is no longer able to open the doors to allow glucose to enter the cells. With malfunctioning doors (membranes), the cells become functionally resistant to insulin. The keyholes of the doors somehow get plugged up, preventing the key (insulin), from opening the doors. With the doors shut, glucose builds up in the blood. High blood glucose is associated with prediabetes, Type 2 diabetes, and metabolic syndrome, all of which are associated with increased risk of the leading causes of present-day morbidity and mortality, in other words, heart attack, stroke, and cancer.


Although they are two different and distinct conditions, insulin resistance affects both Type 1 and Type 2 diabetes. High blood sugar is a hallmark of both types of diabetes. In Type 1 diabetes there is an absence or deficiency of insulin. In Type 2 diabetes, there is enough insulin, maybe even too much. In Type 1 diabetes, the insulin producing cells of the pancreas are destroyed by an autoimmune inflammatory process resulting in insulin no longer being made by the pancreas. In Type 2, the cells are resistant to one’s own insulin produced by the pancreas, whereas in Type 1, the cells are resistant to pharmaceutical hormone replacement insulin that replaces the body’s missing natural insulin.


What causes insulin resistance?


What causes the keyholes of the cell doors to malfunction and not allow the key (insulin) to work? It’s like someone stuck chewing gum into the keyholes. The key (insulin), no longer works, and blood glucose has nowhere to go. Glucose floods vulnerable cells and damages tissues that cannot tolerate high glucose, such as the eyes, nerves, blood vessels, and kidneys.


The cause of insulin resistance is strongly debated. The conventional medical hypothesis postulates that insulin resistance is a result of too much dietary carbohydrates. Too much sugar from a high carbohydrate diet causes high blood sugar, which leads not only to diabetes, but all the conditions falling under the umbrella of metabolic syndrome, including weight gain. This view is championed by prominent medical doctors and scientists such as Dr. Stephen Phiney, MD, Ph.D., professor of Medicine Emeritus at the University of California-Davis, Dr. Jeff Volek, Ph.D., RD, and Dr. Sarah Hallberg DO, MS. They are founders and directors of Virta Health, claiming to be the first clinically proven treatment to safely and sustainably reverse type 2 diabetes without medications or surgery through a ketogenic diet that is high in fat, moderate in protein, and low in carbohydrates. Dr. Stephen Sinatra, M.D., a highly respected integrative cardiologist, was a supporter of this view until his untimely passing in 2022. Dr. Sarah Hallberg, who also passed away, lives on through her TEDxPurdueU video on YouTube entitledReversing Type 2 diabetes starts with ignoring the guidelines” Dr. Jason Fung, MD, is a Canadian nephrologist (kidney specialist), and author of the New York Times best seller, “The Diabetes Code: Prevent and Reverse Type 2 Diabetes Naturally Dr. Fung has numerous YouTube videos promoting the benefits of a high fat, low carbohydrate, ketogenic diet for reversing diabetes and losing weight.


Not everyone agrees with the conventional hypothesis. Other prominent medical doctors believe the exact opposite. Dr. Neil Barnard, M.D., founder of the 20,000-member Physician’s Committee for Responsible Medicine strongly argues that it is not carbohydrates or sugar that causes insulin resistance and diabetes. Prominent U.S. cardiologists such as Drs. Robert Ostfeld, M.D., Joel Kahn, M.D., and Kim Williams, M.D., a past president of the American College of Cardiology, all share Dr. Barnard’s view. They, too, believe that carbohydrates do not cause insulin resistance, metabolic syndrome, or diabetes and that carbohydrates do not make us fat. They say that eating refined carbohydrates or refined sugar is not the same as complex carbohydrates and natural sugar found in whole, unrefined foods in their natural state. Whole foods do not carry the same risks as refined or processed foods. They maintain that diabetes is not CAUSED by too much sugar or carbohydrates. That is not the same as, and is very different from, saying that diabetes CAUSES high blood sugar. This is a very subtle but crucial distinction that must first be understood as a prerequisite to fully understanding the two sides of the debate. Everyone agrees that diabetes CAUSES high blood sugar. Diabetes is, after all, defined by high blood sugar. On the surface, and only on the surface, it is hard to fathom how diabetes could NOT be caused by dietary sugar (carbohydrates).


Dr. Cyrus Khambatta Ph.D. and Robby Barbaro, who both live with Type 1 diabetes, host an online coaching program where they teach people how to reverse Type 2 diabetes and decrease insulin resistance in Type 1 diabetes. They advocate a whole food plant-based diet that is very high in carbohydrates and low in fat, which is the exact opposite of the conventional paradigm. They warn about the long-term dangers of a high fat, low carbohydrate, ketogenic diet, despite any short-term weight loss gains and improvement in blood glucose. They say that it is excess fat, not excess sugar, that is the chewing gum that clogs up the keyholes in the cells, preventing the key (insulin), from doing its work of opening the doors to the cells. Fat builds up inside muscle cells, called intramyocellular hyperlipidemia, and liver cells, called non-alcoholic hepatic steatosis, or fatty liver. They claim that it is the fat buildup inside the cells, not sugar, that is the driver of insulin resistance. Dr. Barnard and the 3 cardiologists, Drs. Ostfeld, Khan, and Kim, all agree. Dr. Khambatta also has a New York Times bestseller entitled “Mastering Diabetes,” which recommends a high carbohydrate, low-fat diet, the opposite of Dr. Jason Fung’s recommendation in his New York Times bestseller.


Who is right?


It seems counterintuitive that two opposing diets could have similar outcomes on insulin resistance, diabetes, metabolic disorders, and obesity. I do not believe that both diets are equally beneficial for long-term health. A criticism of the high fat, low-carbohydrate diet is that success is measured in outcomes that are not necessarily beneficial for long-term health and longevity. So what that you lose weight and your blood sugar goes down while you are eating lots of fat and restricting carbs? So what? You are still a diabetic even if you have normal blood sugar while you are eating no, or low, carbs. In my view, you are no longer a diabetic when you can eat normally again, without elevating your blood sugar. If you lose weight, you will, in all probability, regain it sooner or later as you start eating normally again. A high-fat, low-carb, diet has not been shown to be sustainable long term. I believe that we should be able to maintain our weight without having to diet. My definition of a good diet is one where you can eat a wide variety and diversity of healthy foods without having to restrict yourself unnecessarily. We all know people who can eat a wide range of good fats and good carbohydrates and still stay slim. When we can eat whatever, a slim person can eat and still stay slim, then we know we may be on the right track. If we have to restrict ourselves beyond what is reasonable for good health, how can that be good? We are meant to eat many different kinds of foods; the more variety and diversity the better. It has been said that our ancestors ate upwards of 600 different of foods in a year. Our present-day diversity of foods that we eat pales in comparison.


Increasing evidence is accumulating that there are factors beyond just diet alone that affect insulin resistance and its associated metabolic disorders, including weight gain. Strong evidence is continuing to emerge that a high carbohydrate, low-fat diet, due to its abundance of indigestible fibre, has the most beneficial effect on our gut microbiome. This is why plant-based diets like the Mediterranean diet, DASH diet and Ornish diet, for example, are usually at the top of the list in yearly diet rankings by US News and World Report. Conversely, it is the relative absence of fibre from diets high in fat and low in carbohydrates, like the ketogenic diet, for example, that puts them toward the bottom of the list. It is becoming better understood how it is our gut microbiome that is the final arbiter of who gains weight, no matter what they eat or don’t eat, and who stays slim, no matter what they eat or don’t eat. I believe that staying slim, no matter what healthy foods we eat, should, ideally, be our default state. Of course, that does not mean that we can eat unhealthy foods without suffering the consequences.


The extent to which our gut microbiome affects every aspect of our health and well-being is astonishing. Imbalances in our gut microbiome affect us more than we could ever have imagined. Every chronic degenerative or inflammatory disease that we could possibly name has its origins in a disturbance in the normal balance of microbes in our gut. Research on the human microbiome has given us new insight and understanding of what a normal healthy microbiome looks like. What we eat is important, but it may be equally important, and perhaps even more important, to properly feed our commensal resident gut bacteria. We are discovering that most of what we eat, no matter how healthy, is useless to us without the presence of our gut bacteria. Our gut bacteria are in complete control of our physical state and brain health in ways that we would never have imagined. Compelling research is constantly accumulating in support of the hypothesis that it is a deviation from the normal balance of gut microbes that is the ultimate driver of insulin resistance, metabolic syndrome, diabetes and a host of inflammatory conditions that may appear very unconnected to the gut. This should not come as a surprise. There is a saying that the more things change, the more they stay the same. Hippocrates said over 2000 years ago that all disease starts in the gut.


Here is a summary of how our gut microbiome impacts obesity, insulin resistance, diabetes and metabolic syndrome.


  • In mice, microbiota implanted from obese identical twins to slim identical twins made the slim twins obese. Similarly, microbiota implanted from slim twins to obese twins made the obese twins slim. They all ate the same food. These experiments demonstrate that it is the microbiome, not genetics, that determines our normal weight. Here is an interesting story about a fecal transplant from daughter to mother:

  • A high Firmicutes to Bacteroides bacteria ratio in the colon is associated with weight gain. Lowering Firmicutes and increasing Bacteroides is associated with weight loss.

  • Low saccharolytic fermentation by gut bacteria results in a deficiency of short-chain fatty acids such as butyrate, propionate, and acetate, which promotes weight gain and metabolic syndrome.

  • Low Akkermansia muciniphila bacteria in the gut is associated with weight gain and an increase in the size of body fat cells. Restoring Akkermansia results in weight loss and a decrease in the size of fat cells.

  • Low Bifidobacteria and Lactobacillus bacteria in the gut promote weight gain. Supplementation with strain-specific species of these bacteria induces fat-burning and weight loss.

  • Bifidobacteria in the intestinal tract makes conjugated linoleic acid (CLA) which promotes fat mobilization and fat burning.

  • Supplementing Bifidobacteria to mice fed a high-fat diet reduces body fat, total fat deposition, triglycerides, and cholesterol.

  • Bifidobacteria increase short-chain fatty acids in the gut, which promote weight loss and inhibit metabolic syndrome.

  • Lactobacillus supplementation showed benefits for weight loss in 23 studies referenced here.

  • Butyrate, a short chain fatty acid produced from gut bacterial saccharolytic fermentation of fibre from carbohydrates stimulates the release of leptin, a satiety hormone, that is our off-switch for hunger. Without leptin, it is hard to stop eating even when we are full. Gut bacteria are in charge of leptin production.

  • Lack of bacterial diversity in the gut promotes weight gain and metabolic syndrome.

  • Gut derived postbiotics derived from saccharolytic fermentation of carbohydrates improve gut barrier function, which inhibits systemic translocation of inflammatory lipopolysaccharides that promote weight gain and metabolic syndrome.

  • Intestinal dysbiosis (imbalance in the normal distribution of good and bad bacteria) is the initiating trigger for metabolic endotoxemia, which is the cause of weight gain via the release of inflammatory lipopolysaccharides into general circulation.

  • Correction of dysbiosis and intestinal permeability (leaky gut) improves leptin and ghrelin balance, the hormones of satiety and hunger, resulting in reduced hunger and increased satiety (fullness after eating), making weight easier to manage when willpower is no longer sustainable. If you have ever wondered why some people are naturally thin no matter what they eat, you now know it is more than just their genes.


Given all the factors in the gut that prevail against weight loss, it should not be a surprise that exercising more and eating less doesn’t always work for everyone. It is becoming increasingly evident from the thousands of publications per year on the human microbiome that obesity is not a choice. It is a disease, just like any other disease. As with any disease, it is a modifiable and preventable risk factor for the major killer diseases of our time, most notably heart attack, stroke, and cancer.


Please contact Dr. Brkich at the clinic if you have further questions: 250-564-1700.

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