Increasing Obesity in Americans
James Michael Howard, Fayetteville, Arkansas, U.S.A.
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.
