The Fat Truth About Diabetes
There is a common misconception that eating too many carbohydrates is responsible for causing diabetes. While eating foods with refined flours and sugars may play a contributory role, it is the consumption of too much fat, mostly saturated fat from animal protein, that is the major culprit. Development of diabetes involves the complex interplay of insulin resistance from fat infiltration of muscle, liver, and pancreas; inflammation which damages the liver and pancreas; and disruption of our gut microbiome.
It is true that consuming carbohydrates will lead to elevated blood glucose (sugar) levels once insulin resistance has already developed. This is because dietary carbohydrates are broken down to glucose, and glucose can no longer make its way into muscle cells once they are saturated with fat.
The solution to this problem is not to reduce consumption of healthy carbohydrates, especially foods high in fiber. While doing this may initially keep blood sugars low in someone that has insulin resistance, it is only because carbohydrates (glucose) haven’t been ingested. This can give a patient a the false sense that his diabetes is well-controlled, but it really does not address the underlying pathology: too much fat. Here is how the process unfolds in Type II diabetics:
- Excess calorie and fat consumption leads to increase in size and number of fat cells (adipocytes). Consumption of fat is particularly bad, because it does not need to be metabolized prior to being deposited directly into fat cells (it moves straight from the lips to the hips). Saturated fats, mostly found with animal proteins, have a much greater effect than unsaturated fats.
- Fat cells begin to accumulate in areas they are not supposed to be, including the muscle, liver, and pancreas.
- Fat in the muscle prevents glucose (sugar) from entering the muscle cells (because the cells are already saturated with fat), and also disrupts insulin signaling within the cells. This results in higher blood sugar levels.
- The pancreas initially works harder to produce more insulin in order to overcome insulin resistance (trying to force glucose into the muscle). High insulin levels contribute to hunger, weight gain, and further insulin resistance, and also act as a growth factor which can promote development of cancer.
- Fatty deposits in the liver cause failure of the liver to suppress glucose production, a process which usually only occurs in situations when we are fasting. This also contributes to higher blood sugar levels.
- Growth of fat cells increases inflammatory mediators (IL-1, TNF alpha) and free fatty acids in the blood. This is one reason poorly controlled diabetics have elevated triglyceride levels seen on their cholesterol profiles.
- Inflammation and high fatty acids in the blood cause damage to the liver and the beta cells of the pancreas.
- Over time, fat infiltration and inflammation eventually lead to pancreatic failure and the inability of the pancreas to produce insulin. This results in a situation similar to what is seen in Type I diabetics (an autoimmune condition which leads to destruction of the pancreas and inability to make insulin).
Additional Adverse Consequences of a High Fat, Low Fiber Diet
- High fat, low fiber diets disrupt our gut microbiome (the trillions of bacteria living in our bowel). As a result, there is reduced production of short chain fatty acids (SCFAs) such as butyrate. Among other things, these fatty acids help to feed the cells that line our bowel and reverse insulin resistance. High fiber diets, on the other hand, nourish our healthy gut bacteria and enhance production of SCFAs. Propionate, another one of these fatty acids, relaxes the stomach and slows the rate at which glucose is absorbed, thus minimizing spikes in blood sugar levels.
- High inflammation and fatty acids reduce levels of a hormone called adiponectin, which is partially responsible for clearing triglycerides and reducing inflammation (another mechanism by which diabetics can develop high triglyceride levels).
- Fat cells produce a hormone called leptin. With more fat cells, there are high leptin levels. This is typically responsible for making us feel full, however we develop leptin resistance when levels are consistently elevated. This leads to persistent feelings of hunger and greater consumption of calories (which contributes to further obesity and insulin resistance). Leptin also promotes growth of blood vessels which can feed cancer cells.
- Inflammation can cause damage to the endothelium (inner lining of the blood vessels) which leads to vascular disease.
Nurses Health Study: Followed 84,941 nurses over 16 years. 91% of diabetes attributed to being overweight (BMI > 25 kg/m2), smoking, lack of physical activity (moderate to vigorous activity for 30 minutes 5 days a week), and diets low in fiber and omega-3 fatty acids and high in trans-fats and high-glycemic foods (refined sugars and grains).
Diabetes Prevention Program: 3,234 patients with prediabetes randomized to usual care (ADA recommendations), metformin, or exercise for 150 min/week and weight loss of 7%. Lifestyle reduced development of diabetes by 58% and metformin by 31% compared to usual care.
Neal Barnard: 22-week study comparing vegan diet to ADA diet to reverse diabetes.
Vegan: Hgb A1C dropped 1.23%, 48% reduced medications, weight loss 14 lbs, LDL decrease 21%
ADA: Hgb A1c dropped 0.38%, 23% reduced medications, weight loss 7 lbs, LDL dropped 9%
Population Studies Demonstrating an Association of Diabetes with Meat Consumption:
Nurses Health Study: 8 year follow up of 91,246 women showed association of processed meat consumption (more than 5 servings/week) and diabetes
Adventist Health Study: Those who consumed versus didn’t consume meat had a 95% high risk of developing diabetes
EPIC study: Every 5% of calories from meat consumption increased risk of diabetes by 30%
Dr. Neal Barnard’s Program for Reversing Diabetes
Dr. Joel Fuhrman, The End of Diabetes
Website: Mastering Diabetes, www.masteringdiabetes.org