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| Archive : Summer
2006 |
THE CROOKED LOGIC OF TYPE 2 DIABETES:
The afflicted are often obese, but not always // Fat cells ensure survival, but can spew toxins too // A bodily defense—inflammation— only accelerates the crisis.
An Epidemic of Excess [page 2]
 By
Wendy Orent |
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Soon, the body’s fat cells are full to overflowing, and fatty acids begin leaking into the bloodstream. Excess fat may be deposited into the liver, causing a condition known as steatohepatitis (fatty liver disease), and infiltrates muscle cells, which may increase insulin resistance and even affect the functioning of the insulin-secreting cells in the pancreas. Worse, the overfilled cells serve as biochemical pumps, producing hormones and immune-system chemicals such as interleukins and tumor necrosis factor alpha. Known as pro-inflammatory cytokines, these substances are normally a critical part of the body’s response to acute infection. But in diabetics, perversely, an inflammatory response is triggered, and the body turns against itself.
Inflammation is a series of responses that evolved largely to defend the body from such acute problems as germs and injuries. If you’re attacked by a respiratory virus, you may develop a fever that produces a body temperature too high for the germs; if you sprain your ankle, the resulting inflammation helps keep your ankle immobile so healing can occur. But a steady, low level of inflammation, exactly the sort produced by overstuffed fat cells and the chemicals they pump out, is another matter. Normal fat is a necessary energy reservoir. But in diabetics, fat itself acts as a pathogen.
How could any species evolve such a response? How could fat, essential for survival, come to be an enemy? Part of the answer involves how we live today, under conditions unprecedented in our evolutionary history. Fast food and soft drinks containing massive doses of sugar confront our bodies with an excessive, energy-dense diet we’ve never before experienced. Meanwhile, we drive cars, sit in front of computers and use self-propelled lawn mowers and vacuum cleaners. The combination of supersize portions and inactivity makes us overweight and impairs our health. These conditions are, in Ewald’s words, something new to the human species.
Yet it’s hardly news that we’re getting fatter, and it’s hardly the only explanation for the explosion of type 2 diabetes. For one thing, even the constant ingestion of sugar and fat doesn’t necessarily lead to insulin resistance and diabetes. According to Dhurandhar, there is increasing evidence that mild respiratory viruses called adenoviruses may contribute to obesity, but without causing diabetes. Dhurandhar began researching this connection in his native India, where he treated more than 8,000 obese patients, some of whom, among the most overweight, seemed to have been infected with the adenovirus SMAM-1. Curiously, these patients had lower cholesterol and triglyceride levels than the rest of the group. Dhurandhar’s research team later discovered that another human adenovirus, Ad-36, promotes obesity in animals while improving insulin sensitivity by increasing the number of fat cells. With more places to store fat, lipid levels don’t go up, and without increased lipid levels and insulin resistance, even very obese people may not develop diabetes.
Yet for those, obese or not, whose fat storage is used up, diabetes poses a growing threat. What’s more, some researchers now feel that any chronic inflammation, such as periodontitis, or gum disease, may aggravate, or even help begin, the process leading to the disease (see “A Deadly Synergy,” page 35). So, stopping diabetes may mean stopping the damaging inflammatory cascade that elevates lipids and produces systemic disease. Swollen fat cells have to be prevented from discharging their contents into the bloodstream, and other factors that raise lipid levels, such as severe periodontitis, must be brought under control. |
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Photo by Age Fotostock/Superstock
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