Overcoming Pain

Why people experience chronic pain, and the power they have to de-intensify it

The Feces Thesis of Obesity

A purveyor of frottage with chocolate frosting on its lips.

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.

How to stop the rising tide of obesity? We become angry when we are told we should not drink those 32 ounce sodas. We even seem to spread obesity among those we are most friendly with, sort of a socially transmitted disease for our era: Using the Framingham Heart Study data, Harvard researchers found that obesity appears to spread in social networks, in a pattern dependent on the nature of those social ties. In their 2007 “New England Journal of Medicine” article, the authors found that friends appear to impact weight more than spouses; pairs of friends of the same sex had more influence on the weight gain of one another than did pairs of friends of the opposite sex. We are more likely to be influenced by those who resemble us. Social networking platforms and websites only reinforce this dangerous symbiosis.

Still, maybe, just maybe, our microbiome may come to the rescue. In research published last year in “Science,” it was shown that microbial communities from the gut can transmit lean or obese traits. Certain bacteria, for example, have been observed at increased levels in the microbiota of thin individuals, and were in turn found to play a protective role against increased fat accumulation in lab animals.

Perhaps instead of tummy tucks we will one day be flocking to the doctor for fecal transplants.

Mark Borigini, M.D., is a board-certified rheumatologist who has devoted his career to treating illnesses that cause chronic pain and disability.

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