Earlier this year, I explored the “evolution” of human dietary requirements in the last 10,000 years by examining some of the SNPs – single nucleotide polymorphisms, or variations in genetic sequences – that relate to diet and nutrition. I concluded that while certain genetic changes to the way we process certain foods have arisen in certain populations, for the most part we’re still best off eating from an ancestral, Primal spread of animals, sea creatures, and plant life. Nothing has changed on that front in my mind, but people are still understandably curious about their genetic predispositions toward various conditions, and, with the recent reduction in price for SNP sequencing from 23andMe (to $99 with no subscriptions required), as well as slightly more affordable full-on genome sequencing (~$1000) on the not so distant horizon, it’s easier than ever to actually do it.
But should you?
You hear a lot about type 2 diabetes on this and other sites in the community. It’s easy to see why: type 2 diabetes is the “lifestyle” diabetes, the preventable one, the one that “doesn’t have to happen” and that you can “fix if you just dial in the food.” All true, for the most part. Whether you’re in the camp that thinks it’s red meat or egg yolks causing it, or fatty liver from excess PUFAs and fructose, the point is that people commonly accept the idea that T2D is preventable and manageable with the right diet and lifestyle. But what about type 1 diabetes? Why don’t we hear so much about it?
I think we can all agree that a basic goal in life is the attainment of happiness, that mind state characterized by positive and pleasant thoughts and emotions. But how do we become happy? By definition, happiness requires some type of pleasure to be present. We need good feelings and good physical sensations. Furthermore, the pleasure must come first, before the happiness. Something, and I don’t care what it is, has to make you feel good before you can truly call yourself happy. As such, our behaviors and our motivations are shaped by that pleasure-seeking tendency. And that pleasure-seeking is mediated through the reward system, which has several different but interrelated components: liking, which describes the sensation of pleasure; wanting, which describes the desire to obtain the thing; and learning, the Pavlovian-esque conditioning. Basically, if we do something or expose ourselves to something (a fun social situation, a healthy food, the sun) that confers a survival and/or health benefit (improved social standing, some vital nutrient that our body needs, vitamin D production), our reward center “activates.” We like it, we want it, and we learn that having it is in our best interest.
Pretty much every feature of the human body can be found, in some form or another, on other species. Opposable thumbs? Great for building and using tools, but apes have them, too. Even the giant panda has an opposable sesamoid bone that works like a thumb. Bipedalism? Helped us avoid direct mid-afternoon sun and carry objects while moving around the environment (among other possible benefits), but plenty of other creatures walk upright, like birds and Bigfoot. The human foot? Okay, our feet are quite unique, but every other -ped has feet (just different types), and they all work well for getting around. So, what is it that makes us so different from other animals (because it’s got to be something)?
A couple weeks back, the LA Times published a piece on a geneticist’s experience with “personalized medicine.” Based on careful and constant monitoring of his sequenced DNA and around 40,000 health markers – or “omics” – over 14 months by a team of his colleagues, Stanford geneticist Michael Snyder observed in painstaking detail exactly what his body was doing during periods of sickness and health. If and when a viral infection entered the picture, Snyder and his team could watch how thousands of biomarkers responded. He could track its invasion, his body’s battle against it, and its eventual retreat. Although Snyder had no family history of diabetes, his sequenced DNA revealed he was at risk for it, so he began monitoring his blood sugar. Sure enough, a couple weeks after the viral infection, he noticed that his glucose was abnormally elevated. Analysis of his “omics” profile during the infection showed that auto-antibodies, which are often produced by the body in response to infections, had begun targeting an insulin receptor-binding protein which impaired his ability to clear glucose from the blood. Snyder was eventually diagnosed with the disease (but later fought it off with diet and meds), and though it isn’t spelled out clearly in the article, it sounds like the fallout from the viral infection may have precipitated his development of type 2 diabetes.
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