On page 20 of the book by Professor Traci Mann that we reviewed last week it says “..that genes account for 70 percent of the variation in people’s weight..the role genes play in height (is) about 80%.” Where do numbers like this come from and what do they mean?
Before anybody was paying attention, Gregor Mendel figured out how single genes work. He showed that one or two or more alternative genes determined whether peas would be tall or short. We can predict what the pea plant’s height will be knowing the parents’ heights and we know which gene they got by knowing the height of the pea plant. There are genes like the leptin gene that follow the Mendelian rules for obesity. But height and weight in humans and lots of other creatures depends usually on many genes each following Mendel’s rules. That makes height and weight take a continuous distribution of values that draws a bell-shaped curve. For those things we need a different way to assign the contribution of genes – the attributable risk of genes to the size of people.
One way to get at this is find a sample of people, both of whose parents are obese and subtract their rate of obesity from the rate in an equal sample of people whose parents are not obese and divide by the total group of both samples and multiply by 100 to get the attributable risk percent of having two obese parents. That is one form of measuring the genetic contribution to obesity.
Another way is to draw a graph of the weights of fathers or the average between both parents’ weights on one axis and the weights of their individual kids on the other. Then you draw a regression line that best fits all the points on the graph. The slope of that line is the regression coefficient or correlation coefficient. If it is zero that means the points of parent-kids weights is not related and totally random. If it is 1 then they match perfectly and kids’ weights are one hundred percent correlated to parents’ weight.
An even more exact way is to do that for twins and compare the regression coefficient of weights of identical twins’ who have 100% of the same genes to that of fraternal twins who share 50% of their genes. Then by subtracting the regression coefficient for identical twins from that for fraternal twins times two we can make the genetic contribution number.
All these methods result in different numbers and there are other adjustments to how they make these numbers. Now that we know how they make these numbers, what do they mean? When we say that genes account for 80% of the variation in height does that mean that 20% is due to the environment? That is the usual interpretation but how might the environment cause 20% of the variation and how many inches is that? How could you change somebody’s height? You could starve them during their growth spurts or give them growth hormone or cut off part of their legs. It’s really hard to imagine. In the case of weight what if both parents and all the brothers and sisters are skinny but you are obese. Is that the environment, are you a mutation? We also know that it is almost impossible to increase or decrease your weight significantly and permanently. We have a set point that must be controlled by genes somehow. Maybe what this means is that big variation from the mean is genetic and small variation from the mean is environmental but I don’t know what the math for that specific contention would be.
So for all intents and purposes obesity. especially higher degrees of it, is 100% genetic.
None of this discussion (and also not Tracy Mann’s book) addresses fat science conundrum number one – How did we get so much fatter in one generation, too fast for genes to change, if obesity is genetic?
John DiTraglia M.D. is a Pediatrician in Portsmouth. He can be reached by e-mail- firstname.lastname@example.org or phone-354-6605.