Although judging from what I see around Rittenhouse Square and the pages of fashion mags these days, that opinion may once again be in the minority. Gross. Anyway.
Familial jokes about heritable body odor aside, I seem to have done pretty well for myself in the inherited conditions department. (Excepting the body odor. 23andMe doesn’t yet provide analysis for what we call the E Gene, for Uncle Everett, admired far and wide for his eye-wateringly terrible pitstink, but I hereby offer up my genome to the search.) When it comes to Parkinson’s, Crohn’s, Rheumatoid Arthritis, I’m all Typical to Reduced Risk. Huzzah! But there’s one great big insulin-resistant elephant in the genetic room, and that would be...
Type II Diabetes. Dun-dun-dunnnnnn!
If you’ve been here at the Modernity Ward for long, you know that the whole reason I started blogging has to do with my Polycystic Ovary Syndrome. Blah blah no periods, blah blah facial hair, INFERTILITY INFERTILITY, metformin low-carb two kids. Ta-da.
It should have come as no shock to me, with my family history of Type II Diabetes (maternal grandpa, paternal lots of people) and, oh, CONDITION THAT HAS BEEN LINKED TO DIABETES that I carry a genetically increased risk of developing Type II. Still, there was a sinking feeling in my gut when I saw it pop up in forbidding red type. It’s a lot easier to avoid thinking about the possible sequelae of insulin resistance when it’s not blaring from your monitor. I always knew it was a theoretical risk, but diabetes always seemed so far away.
Thankfully the facts are not nearly so horrifying. While on average, 21.9 out of 100 people will develop Type II Diabetes, those with my genotype develop it at a rate of 30.9 out of 100. A significant increase, statistically speaking, but not so enormous as to be a death sentence. More important, the heritability of Type II Diabetes is estimated to be about 26%. Does that mean the other 74% of the equation is within my control? Not really. While 23andMe’s explanation notes that “environmental factors” play a large role in who develops diabetes, they list the following as environmental factors:
“...obesity, gestational diabetes, giving birth to at least one baby weighing nine pounds or more, high blood pressure, abnormal cholesterol levels, physical inactivity, polycystic ovarian syndrome, other clinical conditions associated with insulin resistance, a history of impaired glucose tolerance or impaired fasting glucose, and a history of cardiovascular disease.”
Bolding mine. Those are all things I have done/had/seen on the lab sheet, and while they might play into whether I actually develop diabetes at some point, they’re not exactly independent from diabetes in the first place. I mean, they’re all facets of the same problem, with insulin and inflammation at the center, and maybe some other single factor underlying even that. So it’s not like if can just keep my cholesterol down and, you know, not have another horse baby, I’ll lessen my chances of becoming diabetic. It’s that the appearance of those bolded factors in my own life is telling me that yes indeedy, I am on the Acela to injectable insulin if I don’t watch those carbs. This applies to me. No getting around it.
And as terrifying as that is, it’s awfully useful information to have. Ass-kickingly useful.
What I suspect, and what I’d love to see some data on someday, is whether those “environmental factors” listed above ride right alongside diabetes in the genome. I keep putting “environmental factors” in quotes because the term implies something separate from the diabetes, but I think they’re all just best buddies, diabetes and bad cholesterol and PCOS, and they like to hang out together flirting with the carhops at the drive-in and drag-racing their T-birds and smoking. And I’d like some scientific confirmation on that.