An Explanation of Increasing Childhood and Adult Obesity Caused by a Single Mechanism

© Copyright 2015, James Michael Howard, Fayetteville, Arkansas, U.S.A.

It is my hypothesis that increasing obesity is caused by an increased percentage of women of high testosterone within the population with time. This produces two phenomena; one causes increased childhood obesity and another causes adult obesity. Testosterone is known to increase all aspects of human female sexuality; higher testosterone results in higher percentages of these women in a population with time.

In adults this causes an earlier onset of high testosterone at puberty which, correspondingly, causes an earlier decline of the natural decline of testosterone. Testosterone is known to reduce obesity. Therefore, the earlier, steeper, decline in testosterone with aging is exaggerated. This causes an earlier loss of testosterone which causes earlier and greater levels of adult obesity.

Races which produce more testosterone will exhibit this adult effect more than races which produce less testosterone. Black women produce more testosterone than Asian women, with the other races between. Obesity is higher in black men and women. (At this time, I could not find testosterone levels of childbearing age Hispanic women; their sex hormone binding globulin levels are lower than White women. This is explained below.)

High maternal testosterone affects fetuses. This is the basis of human evolution and is why it is currently ongoing and increasing rapidly at this time. (“Androgens in Human Evolution,” Rivista di Biologia / Biology Forum 2001; 94: 345-362. If your library does not subscribe to “Rivista … ,” you may find this at: .)

This effect is produced by increases in fetal androgen receptors caused by high maternal testosterone. The higher numbers of androgen receptors affect the use of the basis of growth and development, dehydroepiandrosterone (DHEA) which was involved in the evolution of mammals. (“Hormones in Mammalian Evolution,” Rivista di Biologia / Biology Forum 2001; 94: 177-184.) Testosterone increased in mammalia to produce primates (“Mitochondrial Eve,' 'Y Chromosome Adam,' Testosterone, and Human Evolution,” Rivista di Biologia / Biology Forum 2002; 95: 319-326) and increased further in the development of humans.

This important increase in DHEA in mammals increased utilization of fat, burning, which enabled mammals to transition the dark / cold which eliminated the dinosaurs. DHEA is involved in decreasing fat deposition.

High testosterone increased DHEA sulfate (DHEAS) because testosterone interferes with sulfatase activity. High testosterone is often reported with high DHEAS. DHEAS is the precursor DHEA; if DHEAS is high, DHEA is not being made. If one is high testosterone and produces adequately high DHEA, then one does not become fat. If one is high testosterone but lower DHEA, one will become fat because inadequate DHEA is available to reduce fat.

This combination of high testosterone and high DHEAS is additive. That is, DHEAS decreases sex hormone binding globulin (SHBG). Reducing SHBG increases free testosterone which reduces fat, as described above … if one has some DHEA for this process. This is a strong evolutionary selection for testosterone.

DHEAS is high in obese children. I suggest this is caused by their exposure to high maternal testosterone. This also means that SHBG is lower in obese children. Sex hormone binding globulin is lower in obese children.

To put the foregoing together, women of high testosterone produce children of high testosterone. These children produce less DHEAS as a consequence and their SHBG levels are also low. Their testosterone to DHEA, not DHEAS, level is reduced.

It is my hypothesis that evolution selected DHEA because it optimizes replication and transcription of DNA, that is, genes. Therefore, DHEA levels affect all tissues and all tissues compete for available DHEA, especially the brain. (I think evolutionary selection of DHEA produced mammalia. “Hormones in Mammalian Evolution,” Rivista di Biologia / Biology Forum 2001; 94: 177-184). DHEA naturally begins to decline around the ages of twenty to twenty-five, reaching very low levels in old age. When DHEA is low or decreasing, all tissues and genes are adversely affected according to a natural competition for available DHEA between tissues / genes.

Children are using their available DHEA for growth and development of all of their tissues. This causes a competition for DHEA and, therefore, can limit their DHEA. If a child produces so much testosterone that DHEAS is not converting to DHEA, then insufficient levels of DHEA are available to burn fat. The child becomes obese.

In support of the foregoing, it has been found that “Weight loss induced a decrease in testosterone in prepubertal children and pubertal girls pointing to a reversible increase of androgens.” ( Androgens before and after weight loss in obese children,” J Clin Endocrinol Metab. 2005 Oct;90(10):5588-95).

For sake of brevity, I will state that this high testosterone – low SHBG hypothesis may account for associated phenomena related to childhood and adult obesity.