Obesity no longer ‘belongs’ to the endocrinologist, nor occupies the lofty patient-free realm of public health officials. It is now dripping sweat on the rheumatologist, making the ride on the subway that much more uncomfortable as it presses up against my body, a purveyor of frottage with chocolate frosting on its lips. Obesity is inflammation, and its folds are falling all over me.
And maybe it would not be so bad—except that inflammation can mean chronic pain.
Animal studies have shown that knocking out the genes for tumor necrosis factor-alpha, or the receptors for tumor necrosis factor-alpha, protects mice from insulin resistance. Large fat cells are able to activate the immune system, producing inflammatory biochemicals such as interleukin-6, and tumor necrosis factor-alpha. Too much in the way of saturated fatty acids can trigger a variety of inflammatory pathways, and cause fat to be deposited in a different organs. Of course, there are ‘good’ lipid components, the prime example being the omega-3 fatty acids, which have ant-inflammatory and anti-diabetes properties. But there are too many ‘bad’ lipids.
So, if obesity has a certain degree of responsibility for inflammation, does it follow that starvation can be used as an anti-inflammatory? As summarized nicely in a 2005 article in “Nature Reviews Molecular Cell Biology,” calorie restriction is indeed the only dietary intervention proven to extend the lifespan of a variety of life forms, from yeast to worms to flies to rodents, and likely humans. Interestingly, before the development of corticosteroids in the late 1940s, starvation was prescribed as treatment for some autoimmune illnesses; and three-quarters of a century later, in an article in the “Journal of Immunology” in 2012, we learn that regulatory T cells—beneficial in lupus—are expanded as a result of fasting.