LIFESTYLE INTERVENTIONS, TYPICALLY a combination of diet and exercise, are a universally acknowledged mainstay of type 2 diabetes treatments. These two stalwarts are often portrayed as equally beneficial, and why not?
Exercise improves weight loss efforts, although its effects are much more modest than most assume. Nevertheless, physical inactivity is an independent risk factor for more than twenty five chronic diseases, including type 2 diabetes and cardiovascular disease. Low levels of physical activity in obese subjects are a better predictor of death than cholesterol levels, smoking status, or blood pressure.
And the benefits of exercise extend far beyond simple weight loss. Exercise programs improve strength and balance, blood pressure, cholesterol, blood glucose, and insulin sensitivity, without involving medications and their potential side effects. Trained athletes have consistently lower insulin levels, and these benefits can be maintained for life, as demonstrated by many studies on older athletes. These seem like good returns for a low cost investment.
Yet results of both aerobic and resistance exercise studies in type 2 diabetes are varied. Meta-analyses show that exercise may significantly reduce A1C, without a change in body mass. This finding suggest that exercise does not need to reduce body weight to have benefits, which echoes clinical experience with patients. However, the corollary is that exercise programs have minimal effect for weight loss.
With all the proven benefits of exercise, it may surprise you to learn that I think this is not useful information. Why not? Because everybody already knows this. The benefits of exercise have been extolled relentlessly for the past 40 years. I have yet to meet a single person who has not already understood that exercise might help type 2 diabetes and heart disease. If people already know its importance, what is the point of telling them again?
The main problem has always been non-compliance. Many real issues may deter someone from embarking on an exercise program: obesity itself, joint pain, neuropathy, peripheral vascular disease, back pain, and heart disease may all combine to make exercise difficult or even unsafe.
Overall, however, I suspect the biggest issue is lack of visible results. The benefits are greatly over-hyped and exercise doesn’t work nearly as well as advertised. Weight loss is often minimal.
This is what happened to me recently. I have met one of my friends and we had a chat about hers 7 pounds weight loss in two months. She was so happy about it. I told her well done, what have you been doing? Are you go to gym? She told me that she has this aerobic classes three times a week and that she is always so exhausted after them but feels good, because she thinks that she has done so well. Then she said, tell me about you. You look different. Did you lose some weight. I said yes, actually I did lose 12 KG within the same time as you.
Well done she said. Let me guess, gym? I said NO, I just walk wherever I can and some weight lifting at home. Nothing that exhaustive like yours. Just to keep me fit. But I do something else too. All the weight loss is from low carbing and intermittent fasting. She didn’t want to hear more about it. Just the thought about it got her scared. She carry on doing her aerobic classes three times a week, with minimal weight loss and, “ ME “? Steadily losing more weight with low carb and intermittent fasting.
The lesson here is: exercise has minimal effect on weight loss, but has other health benefits.
INSULIN WILL MAKE YOU FAT
ACTUALLY, INSULIN CAN make anybody fat. How? By prescribing insulin. It won’t matter that you have willpower, or that you exercise. It won’t matter what you choose to eat. You will get fat. It’s simply a matter of enough insulin and enough time. High insulin secretion has long been associated with obesity: obese people secrete much higher levels of insulin than do those of normal weight. Also, in lean subjects, insulin levels quickly return to baseline after a meal, but in the obese, these levels remain elevated.
Insulin levels are almost 20 percent higher in obese subjects, and these elevated levels are strongly correlated to important indices such as waist circumference and waist/hip ratio. The close association between insulin levels and obesity certainly suggests—but does not prove—the causal nature of this relationship.
Insulin levels can be difficult to measure since levels fluctuate widely throughout the day in response to food. It is possible to measure an “average” level, but doing so requires multiple measurements throughout the day. Fasting insulin levels (measured after an overnight fast) are a simpler, one-step measurement. Sure enough, research reveals a close association between high fasting insulin levels and obesity, and this relationship becomes even stronger when we consider only a person’s fat mass rather than his or her total weight. In the San Antonio Heart Study, high fasting insulin was tightly correlated to weight gain over eight years of follow up.
Insulin-resistant state leads also to high fasting insulin. This relationship is not coincidental, as insulin resistance itself plays a key role in causing obesity.
INSULIN IS PRESCRIBED to lower blood glucose in both type 1 and type 2 diabetes. Virtually every patient taking insulin and every prescribing physician knows full well that weight gain is the main side effect. This is strong evidence that hyperinsulinemia, high levels of insulin in the blood, directly causes weight gain. But there is other corroborating evidence as well.
Insulinomas are rare tumors that continually secrete very high levels of insulin. These cause low blood glucose and persistent weight gain, underscoring insulin’s influence once again. Surgical removal of these tumors results in weight loss. Similarly, sulfonylureas are diabetic medications that stimulate the body to produce more of its own insulin. With insulin stimulation, weight gain is the main side effect. Although the thiazolidinedione (TZD) drug class, used to treat type 2 diabetes, does not increase insulin levels, it does increase insulin’s effect. The result? Lower blood glucose, but also weight gain.
Weight gain, however, is not inevitable consequence of treating diabetes. Currently, metformin is the most widely prescribed medication worldwide for type 2 diabetes. Rather than increasing insulin, it blocks the liver’s production of glucose (gluconeogenesis) and therefore reduces blood glucose. It successfully treats type 2 diabetes without increasing insulin and, therefore , does not lead to weight gain.
Where excessively high insulin levels lead to weight gain, excessively low insulin levels lead to weight loss. Remember, patients with untreated type 1 diabetes have pathologically low insulin levels and no matter how many calories they ingest, they cannot gain any weight. Without normal levels of insulin, these patients cannot properly use or store food energy and, untreated, they waste away and die. With the replacement of insulin, these patients gain weight once again.
Increasing insulin causes weight gain. Decreasing insulin causes weight loss. These are not merely correlations but direct causal factors. Our hormones, mostly insulin, ultimately set our body weight and level of body fat.
“Remember, obesity is a hormonal imbalance, not a caloric one.”
AS WE’VE NOW established that insulin causes obesity, our next question is: What foods causes our insulin levels to rise or to spike? The most obvious candidate is the refined carbohydrate— highly refined grains and sugars. This brings us not to a new idea, but back to a very old idea that predates even William Banting: the idea that “fattening carbohydrates” caused obesity.
Highly refined carbohydrates are the most notorious foods for raising blood sugars. High blood sugars lead to high insulin levels. High insulin levels lead to weight gain and obesity. This chain of causes and effects has become known as the carbohydrate-insulin hypothesis. The man who found himself at the center of the controversy was the infamous Dr. Robert Atkins.
In 1963, Dr. Robert Atkins was a fat man. Like William Banting 100 years before, he needed to do something. Weighing in at 224 pounds (100 kilograms), he had recently begun his cardiology practice in New York City. He had tried the conventional ways to lose weight, but had met with no success. Recalling the medical literature published by Drs. Pennington and Gordon on lowcarbohydrate diets, he decided to try the low-carbohydrate approach himself. To his amazement, it worked as advertised. Without counting calories, he shed his bothersome extra weight. He started prescribing the low-carbohydrate diet to patients and had some notable success.
In 1965, he appeared on the Tonight Show, and in 1970, was featured in Vogue. In 1972, he published his original book, Dr. Atkins’ Diet Revolution. It was an immediate bestseller and one of the fastest-selling diet books in history.