Here is more evidence that Darwinian natural selection has not stopped operating on humanity as a result of medical advances and rising living standards. Lee Ellis of Minot State University in North Dakota and his student Dan Haman have just published a research paper providing evidence that natural selection is currently selecting for fatter people.
This study sought to determine if genetic factors might be contributing to the increases in the proportions of North Americans who are obese and overweight. The body mass index (BMI) for a large sample of two generations of United States and Canadian subjects was correlated with family fertility indicators. Small but highly significant positive correlations were found between the BMIs of family members and their reproduction rates, especially in the case of women. For instance, mothers in the sample (most of whom were born in the 1940s and 50s) who were in the normal or below normal range had an average of 4·3 siblings and 3·2 children, compared with 4·8 siblings and 3·5 children for mothers who were overweight or obese. When combined with evidence from twin and adoption studies indicating that genes make substantial contributions to obesity, this study suggests that recent increases in obesity are partially the result of overweight and obese women having more children than is true for average and underweight women.
Ellis and Haman speculate that medical advances are allowing obese and diabetic women to live longer to have more children. But that does not explain why overweight women would have more children than skinny women.
So what is going on here? There are a number of possibilities.
One possibility is that one or more of the many hormones being released by fat cells are altering the brain to make women (or their spouses) either more eager or able to have children (possibly by causing them to enter puberty at an earlier stage) or more eager to find a mate or to engage in other behavior that increases reproduction. The hormones from fat cells might even be increasing fertility.
The scientific view of fat cells has changed a lot in recent years and fat cells are now seen as exerting many influences on the rest of the body. There are plenty of hormones being released by adipose fat tissue into the bloodstream. (same article here and here and here)
“When we look at fat tissue now, we see it’s not just a passive depot of fat,” says Dr. Rudolph Leibel of Columbia University. “It’s an active manufacturer of signals to other parts of the body.”
The first real inkling that fat is more than just inert blubber was the discovery 10 years ago of the substance leptin. Scientists were amazed to find that this static-looking flesh helps maintain itself by producing a chemical that regulates appetite.
Roughly 25 different signaling compounds — with names like resistin and adiponectin — are now known to be made by fat cells, Leibel estimates, and many more undoubtedly will be found.
Another possibility is that the obesity is a side effect of a higher fat diet that also boosts hormones and thereby makes girls more fertile or eager to have sex or to have children. This is plausible because a higher fat diet in adolescence raises sex hormones and causes other endocrine changes.
Joanne F. Dorgan, Ph.D., of the Fox Chase Cancer Center in Philadelphia, and her colleagues conducted a study ancillary to the Dietary Intervention Study in Children to examine whether diet influences sex hormone levels during adolescence. The study involved 286 girls ages 8 to 10 who were randomly assigned to a low-fat dietary intervention group or to a group receiving usual care (e.g., educational materials available to the public). The researchers measured blood sex hormone levels at the start of the study and 1, 3, 5, and 7 years later.
After 5 years, girls in the intervention group had 29.8% lower estradiol, 30.2% lower non-sex hormone binding globulin-bound estradiol, 20.7% lower estrone, and 28.7% lower estrone sulfate levels during the first half of their menstrual cycles, and 27.2% higher testosterone levels during the second half of their menstrual cycles,compared with girls in the usual care group. After 7 years, girls in the intervention group had half the progesterone levels during the second half of their menstrual cycles as did girls in the usual care group.
All those hormonal differences must be having some effects on the brain and on the reproductive organs.
Another related possibility comes from the fact that the leptin hormone acts early in life to change the brain to lower inhibition from eating and might also lower the inhibition against having sex. This is just speculation on my part of course. But it is at least plausible.
Another possibility is that obesity is negatively correlated with intelligence and that it is lower intelligence that is responsible for the higher fertility. Of course there are quite smart fat people and plenty of dumb skinny people. But it seems likely that smarter people are, again on average, doing a better job than dumber people of consciously choosing foods and restricting foods in order to manage their weight. Well, if that is the case then selection for obesity may be coming as a side-effect of the existing selective pressures that are obviously selecting against higher levels of intelligence. My guess is that this possibility explains part of the difference in fertility between overweight and skinny people. However, the difference in fertility as a function of educational attainment (which is a decent though not perfect proxy for IQ) appears smaller than the difference as a function of weight. So IQ is probably only one contributing factor.
Another possibility is that overweight people have lower expectations about what they can achieve in looking for a mate and therefore they more quickly decide someone they have found is good enough to settle for. Therefore they start having children sooner and have more children than those who hold out for better mates. Skinnier people probably (and again on average) believe they have a wider selection of choices and may be willing to wait longer to hold out for a still better choice. The delay that comes from waiting may cause them to delay reproduction and therefore reduce the number of children that women in particular can hope to have. Some women wait so long that by the time they are ready to try for a kid they are not even able to start a pregnancy.
Update: Are obese people less bright to begin with? Does lower intelligence cause the risk of obesity to increase? Also, does the direction of causation also run in the opposite direction? Does the presence of obesity cause intellectual abilities to decay? Some researchers think obesity appears to interfere with cognitive function.
Elias, a member of the Statistics and Consulting Unit of BU’s Department of Mathematics and Statistics, and his co-investigators at the Framingham Heart Study are the first to show that long-term, early-onset obesity is an independent risk factor to cognitive dysfunction. This knowledge should help inform physician–patient decisions to treat this physical condition.
Analyses of these data by the researchers found that the combination of obesity and hypertension showed a statistically significant association with the cognitive functioning of men, but not of women. Among late middle-aged and elderly men, obesity and hypertension were associated with lowered cognitive functioning. Among all men, the effects of obesity and hypertension were found to be cumulative, with cognitive functioning lowered more when both conditions were present than when one or neither was a factor. The researchers speculated that obesity and hypertension may have similar physiological “paths” by which they affect cognitive functioning and that the different distribution of fat on men and women may help to explain the adverse effects of obesity in men compared to women.
Stay skinny for your brain. Stay skinny for your heart. Do it to reduce the odds of getting cancer too.
|Share |||Randall Parker, 2004 October 24 05:33 PM Trends, Human Evolution|