Increasing Obesity in Americans
Copyrightã 1997 by James Michael Howard.
The AP (Washington) reported that "The percentage of overweight Americans has increased by about a third in the last 20 years, and more hefty adults are on the way because more then 25 percent of today's children are overweight or obese, says obesity researcher James O. Hill. 'The trend will continue. There is no indication that it will turn around. Actually, it seems to be getting worse,' said Hill, the director of the Colorado Clinical Nutrition Research Unit at the University of Colorado. ...Hill blames the environment: Americans have too much food available, social situations encourage overeating ...and technology has made it possible to avoid exercise." This may be the reason, but I want to suggest another explanation, a biological explanation.
My work suggests human evolution is the result of increased testosterone in our species. Human males and females produce more testosterone than chimpanzee males and females, respectively. Furthermore, my work suggests testosterone increases periodically in civilizations. That is, where food and shelter are beneficial, people of higher testosterone will increase rapidly, compared to low testosterone people. They are more sexual and impulsive; they make more babies. They are bigger and reach puberty earlier; this is known as the secular trend. The secular trend is not due to better food. Black girls reach puberty much earlier than white girls, and there is no support that black girls eat better than white girls. We are currently witnessing an increase in testosterone in America.
Increased testosterone affects obesity in the following manner. About a year ago, a major discovery was made in obesity research. That is, the "obesity gene," called "ob," was found, and its product, leptin, was found to reduce appetite. The more leptin one has, the less appetite they have. Defective obesity genes did not produce the proper amounts of leptin. If one has low leptin, the appetite is not satisfied. A direct connection of testosterone and leptin was first reported in 1997. "Hypogonadal patients [those who produce little testosterone] had significantly higher leptin serum levels" (Clin. Endocrinol. (Oxf) 1997; 47: 237). This means that low testosterone increases leptin production, and high testosterone reduces leptin. The conclusion of another study of this connection is that "Testosterone possesses an inhibitory effect on adipocyte ob gene transcription." (Eur. J. Clin. Invest. 1997; 27: 1016). Another report "...suggests that testosterone decreases leptin levels..." (J. Clin. Endocrinol. Metab. 1998; 83: 1091). The experiment that confirms these correlations was done on children with delayed puberty. Treatment with testosterone was found to reduce leptin levels in these children (J. Clin. Endocrinol. Metab. 1997; 82: 3213).
Nature has done its own experiments with testosterone and leptin levels in humans. Black men produce significantly more testosterone than white men (J National Cancer Institute 1986; 76: 45), and black women produce more testosterone than white women (J. Clin. Endocrin. Metab. 1996; 81: 1108). Blacks have a higher rate of obesity than whites (Int. J. Obes. Relat. Metab. Disord. 1998; 22: 236). A recent report confirms the connection of testosterone and leptin when black boys are compared to white boys. There were lower leptin concentrations in black boys compared to white boys; girls' leptin levels were, on average, 2.15 times those of boys; and there was a strong inverse relationship of serum testosterone levels with serum leptin levels in boys. (Horm. Res. 1998; 49: 240).
I suggest that the numbers of people who are higher testosterone is increasing faster than those of lower testosterone. Therefore, the numbers of people who produce less leptin are increasing. These people experience less appetite control, and, therefore, eat more. It is not strictly the environment that is causing the increase in obesity in America. It is a change in the population that is causing the increase in obesity.