The results of a recent animal study have shown that obesity may result from chronically high insulin levels, not the other way around. These findings challenge the widespread view among doctors that rising insulin levels are a secondary consequence of obesity and insulin resistance.
The new study, at the University of British Columbia, showed that genetically modified mice with persistently low insulin levels didn’t gain weight even when being allowed unrestricted access to a high-fat diet. This suggests that circulating insulin itself drives obesity in mammals. In addition to staying slim, the low insulin mice also had lower levels of inflammation and less fat in their livers than normal controls.
These results are consistent with clinical studies showing that long-term insulin use by people with diabetes promotes weight gain. They also back up what people like Dr Robert Atkins were saying 20 years ago – that too much insulin promotes fat storage and stops your body from breaking down fat, so that you can’t help but pile on the pounds.
Another important finding from this research was that low levels of circulating insulin appeared to “re-programme” the animals’ fat cells so that they stopped accumulating more fat and started to burn it instead. It is already known that some of the hormones produced by fat cells can act to improve insulin sensitivity, suppress appetite, enhance metabolic rate and increase physical activity. It seems that, in the absence of abnormally high insulin levels, the body’s own complex mechanisms for regulating weight start to re-appear.
So, if we now have the insulin/obesity horse and cart the right way round, what causes high insulin levels? No prizes for guessing that the main culprit is dietary glucose, which constitutes 50 per cent of sucrose, or table sugar. Fructose, the other half of sucrose, doesn’t affect insulin levels at all, but has its own ways of causing havoc in the body (see Real Diabetes Truth 27 December 2012)! Some amino acids also trigger insulin release, because insulin is needed to get amino acids into muscle cells, but they provoke a much weaker insulin response than glucose.
Our body’s mechanisms for regulating blood sugar, insulin and body weight developed millions of years ago, when man’s early ancestors were roaming the plains of Africa. Since then, our diet has changed dramatically. The main difference is in the amount of glucose that we consume in the form of refined sugar. Getting closer to the “cave man diet”, by eating only foods with a low glycaemic load (GL) that don’t overstimulate insulin production is the main tool we have for keeping insulin levels in check.
Like sugar, stress can also raise your insulin level
The other thing that is different in modern societies is the chronic stress that most of us live with. Our stress response was designed to be activated by acute events, like the sudden appearance of a predator. It readies the body for “fight or flight” by raising the levels of both blood sugar (by converting glycogen stored in the liver into glucose) and insulin, so that the muscles are charged with the fuel they need for strenuous action. Now, of course, our stress response is kicked off by a million daily pressures and frustrations, so that it is constantly switched on. It used to be thought that stress raises insulin levels simply as a result of increased blood sugar, but new research at the Karolinska Institute in Sweden has demonstrated how the autonomic nervous system, which regulates our “fight or flight” response, also directly controls insulin secretion from the beta-cells in the pancreas.
If you have normal insulin function and are not injecting insulin, then ensuring that your insulin levels remain low could help you to stay slim or lose weight without cutting your intake of calories. Keeping to a low GL diet and avoiding all foods with added sugar is the most effective way of doing this. In addition, any form of enjoyable, moderate exercise, preferably outside in natural surroundings, will help you to switch off your stress response and reduce insulin release.
If you have type 1 diabetes, in which the immune system’s T-cells attack the pancreatic beta-cells, your problem will be too little naturally-produced insulin, rather than too much. But what if your T-cells could be “re-trained”, so that they left your pancreas alone and allowed it to do its job again? That is the intriguing prospect raised by the latest research and will be the subject of my next blog post.
Wishing you the best of health,
PhD DHD Nutritionist
for Real Diabetes Truth
Bear in mind we are not addressing anyone’s personal situation and you should rely on this for informational purposes only. Please consult with your own physician before acting on any recommendations contained herein.
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2. Rabe K, Lehrke M, Parhofer KG, Broedl UC. Adipokines and insulin resistance. Mol Med. 2008; 14(11-12):741-751.
3. Rodriguez-Diaz R, Speier S, Molano RD, Formoso A, Gans I, Abdulreda MH, Cabrera O, Molina J, Fachado A, Ricordi C, Leibiger I, Pileggi A, Berggren PO, Caicedo A. Noninvasive in vivo model demonstrating the effects of autonomic innervation on pancreatic islet function. Proc Natl Acad Sci U S A. 2012; 109(52):21456-21461.
Category: Diet and Exercise