Gary asked me to write a follow-up post to my last entry, so here goes. I’ll also point out that I’m not a doctor, and this information is mostly my opinion based on all the research I’ve done over the years.
In terms of Type-II diabetes and obesity, here’s what the research seems to show currently (which may change as research continues):
- Type-II diabetes is caused by insulin resistance at the cellular level, which in turn increases the body’s requirement for insulin. If the pancreas can’t keep up, additional insulin is required
- At it’s core, the prime defect in obesity appears to be a relative sensitivity difference between fat cells and muscle cells. That is, fat cells become slightly more sensitive to insulin when compared to muscle cells, which ultimately causes glucose in the blood to be directed away from muscle cells and into fat cells. This leads to a condition known as internal starvation, which leads to lethargy
To treat Type-II diabetes (and indirectly obesity), you effectively have to treat the fundamental defect, which is resistance to the hormone of insulin. Here are some of the current options:
- Exercise has a very limited effect on weight, and it’s use in weight loss programs is not supported by most research. It does improve health, so with that in mind it’s not entirely a wasted effort. What does help though is resistance training, as this leads to a temporary increase in the sensitivity of muscle cells to insulin, which allows glucose to be used more efficiently
- Long ago, one of the treatments for diabetes was cinnamon. For whatever reason, it’s not used very often anymore (probably because drug companies haven’t figured out a way to monetize it). While the research is a bit confusing, many studies report about a 30% drop in insulin levels from people consuming cinnamon. Also, sugary foods sprinkled with cinnamon produce a far less dramatic spike in insulin than those same foods without it
- Since 100% of digestible carbohydrates convert to glucose in the blood, and glucose directly stimulates insulin, low carb diets are pretty much the gold standard for treating metabolic syndrome. Since approximately 50% of protein metabolizes similarly to carbohydrates, proper low carb diets are high fat diets (and low on protein), not high protein diets (as the media likes to report). Strangely enough, the amount of fat lost (as a percentage of total weight lost) in a diet is inversely proportional to the amount of carbohydrates in the diet. That is if you lose weight on a high-carb diet, most of it will actually be muscle. On a diet of almost 100% fat, nearly all the weight that is lost will be fat, and not muscle.
- Insulin is the prime driver for fat storage, and carbohydrate is the prime driver for insulin. In addition, a molecule called triacylglycerol phosphate is required to store fat — it can only be produced from dietary carbohydrate
- A drug called glucophage has been used for years to treat Type-II diabetes. It works by decreasing insulin resistance.
Like I mentioned in my last post, I recommend everyone do their own research, and check out Good Calories, Bad Calories if they have time. Obviously if you think you may be diabetic, then go to your doctor, and make sure they’re aware of any changes to your diet you may make. Strangely enough, many doctors still prescribe high carbohydrate diets as a way to control both heart disease and diabetes, something most of the current literature seems to point out can be rather harmful in many individuals.
There was an interesting exchange in Reason magazine back in 2003 about Gary Taubes’s ideas on eating, obesity, and Type II diabetes. His 2007 interview on CBC Radio’s “Quirks and Quarks” and MIT interview (with links) are good reads too.
He remains controversial. That could be because he is right, and an iconoclast who is challenging an incorrect medical-scientific orthodoxy. Or he could be wrong. While Taubes’s proposals are interesting, it’s worth noting that there are also risks with the low-carb, high-fat diets they imply, notably for colon cancer. I don’t think his conclusions are as air-tight and his book implies.
I should point out that Gary refers to the entire ideas in his book as the “alternative hypothesis”. He fully admits in the book that the hypothesis needs to be tested. Also, the colon cancer link with high fat diets has never been established in any of the research I’ve read. In fact many populations that have extremely high fat diets (such as the Inuit) are relatively cancer free. But unfortunately making sense of the vast quantities of research data is difficult.
Also, I wouldn’t hold much weight to a 2003 interview with Taubes – he fully admits in his book that about 30% (I’m guessing on the number, I forget what it was, but that’s close) of what he thought prior to writing the book ended up not being the case after he spent a great deal of time researching it (in fact, I believe he had five people helping sift through research at one point).