By Jason Poquette,
A recently published article in the Journal of the American Medical Association (JAMA) has gotten people talking about low carbohydrate diets and insulin resistance again. Entitled “The Carbohydrate-Insulin Model of Obesity. Beyond Calories In, Calories Out,” the article seeks to explain our obesity epidemic which continues to grow in spite of education around calories and exercise. While Massachusetts actually has one of the lowest obesity rates in the nation, this is still a problem we must face. Nearly 38% of all adults in our country are clinically obese.
I remember sitting in lectures on obesity years ago. The message was almost always the same: Simply burn more calories than you consume. Easy, right? But these older models of weight loss never seemed to factor in the metabolic changes that have already occurred in many people due to our generally high-carbohydrate diets. The old approach just isn’t working for many people. More recent research has focused on the detrimental impact that our overly sugary diet has produced. Regular spikes in insulin, leading to insulin-resistant cells, has programed our bodies to store more fat, reduce energy and increase appetites. Not good.
Criticism of the “energy model” (calories in vs. calories out) has existed for years. The obesity expert Julius Bauer said back in 1941 “The current energy theory of obesity, which considers only an imbalance between intake of food and expenditure of energy, is unsatisfactory.”
Weight loss can be a touchy subject. What works for one person doesn’t seem to work for others. But it is my opinion that much of our problem today can be linked to insulin resistance that has resulted from our sugar-rich diets. I’m not suggesting this is everyone’s problem. If you exercise more and cut back your calories, and the weight starts dropping, you probably are not insulin resistant. For many people, however, this doesn’t work.
The physiology of insulin resistance is complicated. Insulin resistance means your cells are not responding normally to insulin any more. Insulin is a hormone secreted from the pancreas which triggers cells to take glucose from the blood and use it for energy. With insulin resistance the cells stop listening. As a result, the pancreas secretes even more insulin, but blood sugar remains elevated and the excess insulin triggers more fat storage.
How can you know if you are insulin resistant? Classic symptoms include persistent hunger, lethargy and weight gain around the middle (belly fat) area. Your doctor can order a variety of tests including an A1C, fasting blood glucose or glucose tolerance test as well. A surprising fact is that skin tags (little dermatological lesions) have been associated with greater risk for insulin resistance.
So what should you do? If typical dieting approaches have not worked for you I strongly recommend talking to your doctor about insulin resistance. A popular dietary strategy to consider is a “ketogenic” diet in which patients eat a very low carbohydrate diet, shifting most of their calories to healthy fats and protein. This results in fewer blood-sugar spikes and lower insulin levels, as well as a shifting to the use of “ketones” for fuel, rather than glucose (a process known as ketosis).
The authors of the Carbohydrate-Insulin Model article are not suggesting that insulin alone explains all of our obesity problems. They admit that no single “dietary factor can fully explain variations in body weight among individuals and populations.” Still, it is worth a discussion with your doctor.
I think the JAMA article has done us a favor, if only to consider some alternative possibilities and approaches to treating obesity. A focus on carbohydrates and insulin may not solve every weight loss problem, but for some people it could be just what the doctor ordered.