I suggest the findings of Cullen, et al., may be explained by testosterone levels. Testosterone levels affect the availability and use of dehydroepiandrosterone (DHEA). The useful supply of DHEA determines the life span.

It is my hypothesis that skin color is partially explained by testosterone levels ("Evolution of Skin Color in Humans," at: http://www.anthropogeny.c... ) It is also my hypothesis that mammals evolved because of selection for dehydroepiandrosterone (DHEA). "Hormones in Mammalian Evolution," Rivista di Biologia / Biology Forum 2001; 94: 177-184. If your library does not subscribe to "Rivista... ," you may read this at http://www.anthropogeny.c... ). I think testosterone was selected by evolution because it increases androgen receptors through which DHEA enters cells and affects gene activity. ("DHEA, Estradiol, Testosterone, and the Relevance of Their Ratio …The Androgen Receptor …and the Secular Trend," at: http://anthropogeny.com/A... )

I suggest increased testosterone may be higher in the lower socioeconomic levels. Increased testosterone has been connected with reduced learning ability, reduced impulse control, and sexuality. All of these reduce the ability to obtain gainful employment and participation in a society increasingly dependent upon advanced educational achievement and personal control. This would concentrate this type of individual within these levels.

Blacks and males produce more testosterone than whites and females. I suggest early, high testosterone production adversely affects availability of DHEA. High testosterone increases DHEAS, the precursor of DHEA. If DHEAS is high, DHEA is not being made. Furthermore, high, early testosterone production will result in early, low testosterone later in life. The peak of testosterone is skewed towards the early years. The consequence of the loss of testosterone later in life is reduced androgen receptors. Reduced androgen receptors result in less DHEA entering cells to stimulate gene activity. This effect of the loss of androgen receptors also occurs when DHEA naturally begins to also decline.

The combined effects of early, high testosterone followed by early, low testosterone produce negative consequences of low DHEA. I suggest this produces declines in gene activity within all tissues and reduces the life span.

Therefore, while I think testosterone levels are involved in skin color, it is the consequences of the effects of testosterone on the useful availability of DHEA that produces the findings of Cullen, et al. (It is known that in all cultures, male skin is darker than female skin.)

The link, above, regarding androgen receptors and the secular trend, and my explanation of the secular trend, just below, explain this in much better detail.

“A syndrome, the 'Secular Trend,' is occurring in America and other countries, the cause of which is often attributed to one part or another of the syndrome, itself, and more often attributed to the environment or life style. I suggest a single cause may be involved that is biological and evidence of ongoing evolution. The cause may be increased exposure to maternal testosterone within the population with time. This increase in testosterone produces a decline in dehydroepiandrosterone (DHEA) because testosterone interfere with steroid sulfatase. If the precursor of DHEA, DHEAS, is not converted to DHEA, DHEA availability is reduced. It is the reduction in DHEA that is the basis of these problems. High DHEAS is often found with high testosterone. A consequence of this is reduced availability of DHEA (just above) and an earlier decline in the production of DHEA during the life span. This produces increased morbidity during life as well as earlier mortality.

It is my hypothesis that the 'secular trend,' the increase in size and earlier puberty occurring in children, is caused by an increase in the percentage of individuals of higher testosterone. More specifically, I suggest this is due to an increase in the percentage of mothers of higher testosterone with time within the population. This exposes more fetuses to increased maternal testosterone with time within the population. This causes permanent effects in the fetus which persist throughout the life span. I suggest this is the cause of the parallel increases in morbidity occurring within the population, such as increased infection rates, obesity, hypertension, chronic obstructive pulmonary disease (COPD), cancer, breast cancer, diabetes, the metabolic syndrome, etc., including prematurity, small for gestational age, etc., including less obvious gross effects which later contribute to 'failing schools' and other adverse behavioral outcomes in children. This includes the new (August,2011) finding of Dr. Kyung Hee Kim of The College of William and Mary that 'creativity' is also declining in children. This could also explain the increase in negative pregnancy outcomes, re: the increase in the increasing 'newborn death rate' in the United States.

I have come to the conclusion that the 'increase in testosterone' may partially be due to a reduction in 'sex hormone binding globulin (SHBG)' as a number of phenomena explained by the secular trend may be based on changes in SHBG. A decrease in SHBG increases free testosterone levels. Low SHBG has been found in obese children who do not produce excessive testosterone. A number of negative phenomena which may be caused by increased testosterone are found with low SHBG and a number of positive effects of reduced SHBG exist.

It is my hypothesis that human evolution is driven by increases in testosterone ('Androgens in Human Evolution,' Rivista di Biologia / Biology Forum 2001; 94: 345-362). This was directly supported by research in 2003; see the chart of testosterone levels in humans and related great apes, upper left at www.anthropogeny.com . I suggest that periodically testosterone increases excessively and the exposure to excessive maternal testosterone causes negative and evolutionarily consequential changes to the human population. We may be experiencing this effect at this time.

I suggest this increase in testosterone in the population peaks earlier with time. This earlier peak may produce an earlier decrease in the population with aging. A number of studies reported in the medical literature have identified low testosterone as a cause of currently increasing disorders. Therefore, the secular trend may be causing increased morbidity and mortality as a result of excessive testosterone and low testosterone within the population. Therefore, earlier reductions in testosterone and DHEA could be occurring simultaneously, therefore, reducing the total positive effects of these two major androgens. This could be the explanation of the severe increase in morbidity that is occurring. Evolution is increasing earlier reproductive capacity at the expense of post-reproductive years. The curve of the peak of our androgens is being 'skewed to the left.'

As I have said before, I think women of higher testosterone drive the secular trend / human evolution. I suggest these women produce the highest percentage of premature infants. It has been reported that 'preterm boys' exhibit increased testosterone and the effects of increased testosterone compared to 'full term boys' (J Clin Endocrinol Metab 2010, 'Increased Activity of the Hypothalamic-Pituitary-Testicular Axis in Infancy Results in Increased Androgen Action in Premature Boys.,' Kuiri-Hanninen, et al., J Clin Endocrinol Metab. 2011 Jan;96(1):98-105). What this means is that the population is increasing in women of higher testosterone and this group of women may also be increasing the percentage of men of higher testosterone simultaneously. This could explain why this 'secular trend' can increase so rapidly. This mechanism could expand the percentage of these individuals within a population rapidly and drive human evolution.” www.anthropogeny.com