Dehydroepiandrosterone, Melatonin, and Testosterone in Human Evolution

This thesis is an entirely new explanation of human (hominid) evolution and part of a new paradigm. I believe hominids evolved because of two primary changes: (1) increased production of testosterone in both sexes and (2) increased use by the brain of the pineal gland hormone, melatonin, and the adrenal gland hormones, dehydroepiandrosterone (DHEA) and the more abundant form, DHEA-sulfate (DHEAS). This explanation of human phylogeny also provides some new explanations of human ontogeny, pathology, and behavior. These ideas will be presented in a series of articles.

Relatively recent hominid fossil finds indicate that bipedal locomotion occurred early in human evolution and may have developed in an arboreal environment (National Geographic, Sept., 1995, page 38.) Bipedal walking preceded large increases in brain size by millions of years and occurred near the separation of chimpanzee and human lines. I suggest the same mechanism that produced bipedal walking eventually triggered the large increases in brain size of later hominids.

My foundation hypothesis is that DHEA is necessary for duplication and transcription of DNA. Therefore, all growth, development, maintenance, activation, and aging are dependent upon production, antagonism, or loss of production of DHEA. All tissues compete for available DHEA by "capturing" it from blood. (Serum, the liquid part of blood, is used for optimum cell duplication and gene transcription in vitro. DHEA is the major hormone found in serum.) The following chart represents the availability of DHEA during the human life-span. (It is derived from a combination of data in Adrenal Androgens, A.R. Genazzani, Raven Press, 1980.)

In the competition for DHEA among tissues, nervous tissues capture DHEA better than other tissues. "Brain tissue naturally contains 6.5 times more DHEA than is found in other tissues." (Total Health, Feb. 1994, page 42, E.R. Braverman, M.D.) This is why brains evolved; nervous tissues grow at a greater rate than other tissues. For example, in a chicken embryo, after blood vessels form a system for nutrient delivery, the brain is the first organ to develop. Since DHEA may be necessary for transcription and the brain captures more DHEA than other tissues, the brain should have the highest transcription rate. Additionally, DHEA should affect all cellular DNA, hence, it should affect mitochondrial DNA, as well as nuclear DNA. Mitochondria are the seat of metabolic activity in cells. The following quotations support my hypotheses. In the second quotation, "protein synthesis" indicates transcription has occurred.

The brain's increased ability to capture DHEA results in its growth at the expense of other organs. This explains why: "...the brain is most unusual in its pattern of accelerated growth in comparison to the other organs and to the body as a whole." (Patterns of Human Growth, B. Bogin, Cambridge University Press, 1988, page 61.) The brain's use of DHEA produces Period B of the chart above. Period B is a decline in measurable DHEA, i.e., the brain uses so much DHEA for growth and development that DHEA levels decline. At birth, DHEA is produced in extremely large amounts for early brain, and body, growth; this is Period A. (In children who succumb to SIDS, it is found that "Somatic [body] growth and brain weight were significantly greater in SIDS than controls." (Journal of Neuropathology and Experimental Neurology 1991; 50: 29.) This would reduce DHEA of Period B so low that enough is not available to maintain activation of the brainstem which controls the heart and breathing.) As the brain approaches final development, DHEA levels increase. This is the beginning of Period C; it is called adrenarche. Puberty occurs at the end of Period C. Earlier, I mentioned that DHEA is used for "activation." As the brain finishes growth and development, it starts using the extra DHEA for higher functional activity (thinking, behavior, etc.). The most pronounced behavior following adrenarche and childhood is puberty. I suggest puberty simply occurs when use of available DHEA switches from growth and development to reproductive drives.

In vitro, extremely small amounts of DHEA increase neuron differentiation and survival (Journal of Neuroscience Research 1987; 17: 225.) The neuron is the basic building block of the brain. During development in utero or postnatally, low levels of, or antagonism of, DHEA availability should adversely affect brain growth. This should occur along a continuum, i.e., in severe cases this could lead to anencephaly (lack of brain development) to less subtle forms of brain development that are exposed only by reduced DHEA availability later in life. For sake of this section, I will briefly demonstrate the connection of DHEA with two of these that cause a lot of problems and costs in our society: schizophrenia and Alzheimer's disease. (I will consider these in greater detail later in this series.)

In 1985, I proposed that DHEA should be low in Alzheimer's (A Theory of the Control of the Ontogeny and Phylogeny of Homo sapiens by the Interaction of Dehydroepiandrosterone and the Amygdala, Copyright, 1985, James Michael Howard.) This was supported in The Lancet; 1989, Sept. 2, page 570 and in Biological Psychiatry 1991; 30: 688, as well as other journals. The point is that DHEA naturally begins to decline in Period E. This is the time when early Alzheimer's disease occurs, in people genetically predisposed to neuropathy during this drop in availability of DHEA. If I am correct, dementia of this type should occur in the normal population as DHEA declines in late redundancy (Period F). Depending on the individual, one might develop some form of senile dementia during old age. Therefore, it should be, and is, a common form of dementia in the normal, very old, population.

"Of those over the age of 65 years, an estimated 10.3% had probable Alzheimer's disease [AD]. The prevalence rate was strongly associated with age. Of those 65 to 74 years old, 3.0% [three] had probable AD, compared with 18.7% of those 75 to 84 years old and 47.2% of those over 85 years. Other dementing conditions were uncommon. ...These data suggest that clinically diagnosed AD is a common condition..." (Journal of the American Medical Association 1989; 262: 2551)

I also propose that schizophrenia develops as a consequence of low DHEA. Schizophrenia exhibits significantly reduced levels of DHEA (Biological Psychiatry 1973; 6: 23), and "the schizophrenic group was found to have significantly less gray matter than the control group ...in all six cortical subregions analyzed..." (Archives of General Psychiatry 1992; 49: 195.) (Neurons compose the majority of "gray matter.") Reduced DHEA reduces brain growth. Schizophrenia represents a disorder of reduced DHEA and reduced development, later exposed by antagonism of DHEA availability by the hormones, testosterone and cortisol. The point of this data is that DHEA is intimately connected to brain growth and function, and hominid brain evolution can be tied to increases in DHEA availability.

Use of DHEA by the brains of monkeys, chimpanzees, and humans generate differences in the life-span charts of DHEA that follow a pattern. Use of DHEA by the large brains of humans causes the lowest measurable levels of DHEA of Period B. Period D in humans is lower because of use of DHEA for brain function; larger brains use more. Therefore, monkeys have the least Period B and lowest Period D. Chimpanzees are between the two, but nearer to humans; the chimp is the only animal which exhibits an adrenarche similar to humans (Endocrinology 1978; 103: 2112.)

Period B occurs in the monkey, but it is so small and rapid in the scale of this chart that it cannot be seen. Since the brain reaches final growth early in the monkey, puberty is reached early.

The hominids follow a trend in development that differentiates them from chimpanzee and gorilla lines (pongids). That is, the ratio of brain size to body weight increases more in hominid evolution. This is clear in the following chart adapted from Human Evolution An Illustrated Introduction, R. Lewin, W.H. Freeman and Company, New York, 1984; after figure on page 81.

The trend of both hominids and pongids in body weight is toward increased mass. Testosterone (T) increases body mass. This suggests a shared selection pressure toward increasing T in both groups. Testosterone is extremely important to human evolution, and human males and females produce more testosterone than chimpanzee males and females, respectively (J. Repro. Fert. Supplement No. 28, The Great Apes of Africa, 1980, see Text-fig. 2 (males), page 134 and Text-fig. 5 (females), page 137). In hominids and pongids, increased testosterone produces a reproductive advantage in male access to females. Testosterone produces massiveness and aggressiveness.

Testosterone will increase in a group, because it increases sexual opportunity. Aggressive, high T males force less aggressive, less massive males away from females. Over time, therefore, T increases in hominids and pongids; this is the driving force that causes all lines in the chart above to move to the right, i.e., increased size. This is supported in the fossil record; early Australopithecines were smaller: "...it is notable that the more ancient Australopithecines had thin skull bones and only modest protuberances on his cranium" (Encyclopædia Britannica 1984; 8: 1033.) Eventually, extremely massive males, such as Australopithecus robustus and A. boisei, were produced. These species became extinct without contributing to the hominid line; too much testosterone is a bad thing.

The "pushing" of lower testosterone males away from the group can be seen in living primates. Here is an example from Wickings E.J. et al., "Testicular Function, Secondary Sexual Development, and Social Status in Male Mandrills (Mandrillus sphinx)" Physiology & Behavior 1992; 52: 909.

"Positive correlations between dominance rank and plasma testosterone levels have been described for adult males of several primate species in captivity, but the relevance of such observations to free-ranging animals is unclear. CIRMF in Gabon maintains a breeding group of 45 mandrills in a six hectare, naturally rainforested enclosure. This study describes correlations between dominance rank (in agonistic encounters), levels of plasma testosterone, testicular volume, body weight, and development of secondary sexual characteristics (red and blue sexual skin on the muzzle and rump areas) in male mandrills under semifree ranging conditions. Two morphological and social variants of adult male mandrill were identified. Large-rumped or fatted adult males (n = 3) remained in the social group and exhibited maximal development of sexual skin coloration as well as large testicular size and highest plasma testosterone levels. By contrast, slimmer-rumped or nonfatted males (n = 3) lived a peripheral or solitary existence and these exhibited less development of their secondary sexual coloration and had smaller testes and lower plasma testosterone levels. Longitudinal studies of gonadal development in these six males revealed that testicular volumes and plasma testosterone levels increased most rapidly during pubertal development (4-5 years of age) in the three animals which proceeded to the fatted condition. These included the highest ranking, group-associated male which exhibited the most intense sexual skin coloration and had higher testosterone levels, although this was not correlated with testicular volume. This study shows that in the male mandrill social factors and reproductive development are interrelated."

All lines in the chart above also move upward, i.e., all groups show an increase in brain size. This is also partly due to increasing testosterone. I suggest T acts by increasing the uptake of DHEA in testosterone-target tissues. That is, T increases the uptake of DHEA for transcription of T-activated genes. The brain is full of T receptors used for capturing T. Therefore, increases in T will increase the supply of DHEA to the brain. T receptors are located in the cerebral cortex, but mainly in subcortical regions of the brain. This means that increases in T will only increase brain size by a limited amount over time. However, this effect of T does occur in humans. Males are exposed to T in utero and for a few months postnatally. The result is a slightly increased head circumference in males at birth and at the end of the first year (Sexual Dimorphism in Homo sapiens A Question of Size, R.L. Hall, Praeger Publishers, New York, 1982, page 281.) However, significant increases in hominid brain size depend on another mechanism of increasing the availability of DHEA.

DHEA increases resting metabolism; more heat from dietary intake. Therefore, increased DHEA allows migration into colder environments.

"There is growing clinical and experimental evidence that dehydroepiandrosterone ...plays an important regulatory role in intermediary metabolism by inhibiting the storage of dietary energy as fat. For instance, one of the predominant features associated with a DHEA deficiency in humans is obesity. ...Recently it has been reported that these inhibitory effects of DHEA on adiposity can be attributed to an increase in resting metabolism." (Journal of Nutrition 1987; 117: 1287)

Migrating groups of low testosterone would have an advantage in colder climates only if they produced increased DHEA. That is, they could produce more heat from scarce calories. Increased DHEA increases brain growth and development, hence, groups of higher DHEA forced northward should, on average, exhibit increased cranial size. In Asia, northern groups of Homo erectus have larger brains than southern groups.

I propose melatonin is directly involved in DHEA production. This may be the mechanism of significant increases in brain size found in northern hominids. These two hormones are directly linked to each other in the sleep- wake cycle; one affects production of the other during this cycle. DHEA is used during the day to activate consciousness and is literally "used up." We get tired at the end of the day. This loss of DHEA stimulation allows the pineal gland to release melatonin, synthesized earlier. This large release of melatonin starts the first slow wave sleep of the night. Melatonin triggers this sleep by slowing release of prolactin, which is known to specifically stimulate DHEAS. During the night, melatonin is also used up; then a large release of prolactin triggers the large morning release of DHEAS that triggers awakening. I suggest this cycle is necessary for growth. (In the case of SIDS, it may be that these children produce too much melatonin. This would reduce DHEA to dangerously low levels during sleep. Melatonin is also low in schizophrenia.)

Sunlight directly affects melatonin production, i.e., decreased sunlight increases melatonin. Migration of hominids northward increases melatonin and its effect on growth. (Migration of hominids southward from the equator would produce the same effect.) I suggest melatonin is directly involved with DHEA in brain growth. The following chart demonstrates the connection of melatonin and DHEA. The time of greatest melatonin production is also the time of greatest use of DHEA for brain growth (Period B).

I suggest increasing testosterone levels began a series of changes that resulted in bipedal walking. The mechanism involves redirection of DHEA for use by T-target tissues at the expense of other tissues. That is, as T increased, anatomical structures were merely "remodeled" by increases in DHEA for T-target tissues, while other tissues changed due to decreasing availability of DHEA. No mutations would be required for this effect to occur. Many differences between males and females occur as a result of differences in testosterone. Increases in T during millions of years could produce differences in the fossil record.

Bipedal locomotion occurred millions of years prior to any significant increases in brain size. However, in the early hominid line, Australopithecus, some increase in brain size is found. This is the testosterone effect on brain size, mentioned above. Along with this small brain increase are changes which I attribute to remodeling caused by T. When compared to pongids, Australopithecine canine teeth are nonprojecting and reduced in size, their foramen magnum opens downward, and they are bipedal. In Australopithecines, changes in the size and structure of the brain, induced by testosterone in utero, could change the angle of the foramen magnum due to plasticity in the developing skull. Taken together, these produce bipedal walking and a shift away from teeth as weapons to hands as weapons of aggression. These anatomical and functional changes are a consequence of increasing testosterone.

Teeth are sensitive to DHEA availability. Nature does not often reduce large, projecting canine teeth, very well adapted as offensive weapons. I suggest reductions in size, or projection, of teeth result from reduced DHEA availability. This reduction in teeth size directly parallels increases in brain capacity. Chimpanzees have smaller brains, therefore, they produce more available DHEA, and they have much larger, projecting teeth. Reduced teeth size is a consequence of competition between teeth and brain.

The possible connection of teeth and use of DHEA by the brain is clearer in modern humans. There are two times of high production of DHEA, Period A and C/D; these are also the times of the two dentitions in humans. During growth of the "permanent" dentition, front teeth develop during the final stages of brain growth. This competition causes the front teeth to be small; as the process of brain growth finishes, the size of the teeth increases. The very large molars develop during a time when ample DHEA is present for growth. We lose our teeth during DHEA decline of redundancy.

It is known that testosterone increases sex drive in males and females. Since modern human females have sex throughout their cycle while chimpanzees are limited to estrus, I suggest the difference results from the increased T in modern women. Therefore, female hominids of increased T had a selection advantage in reproduction. They increase the probability of male attention throughout their cycles, and, therefore, increase their reproduction rate. As the population of higher T female hominids increased, their size would increase and the male-female difference would decrease.

"Another correlate of brain size is a decrease in male- female body size difference. Sexual dimorphism remained marked in the pithecanthropines [now called Homo erectus], but it is reduced from its Australopithecine extreme. The reduction in dimorphism was not caused by a decrease in male size and robustness, but rather an increase in female size." (The Stages of Human Evolution and Cultural Origins, 3rd. ed., G.L. Brace, Prentice-Hall, 1968, page 93)

As testosterone increases in females, the effect of estrogen declines in proportion. Estradiol in female humans and chimpanzees is about equal, however, female chimpanzees announce sexual receptivity with an extreme estrus display. Therefore, I suggest increases in T in hominids reduced estrus displays, while, at the same time increasing sex drive. Human female pubic and axillary hair is due primarily to adrenal androgens, primarily DHEA. Since chimps produce more DHEA and hair than humans, I suggest our relative lack of hair results from the T-target tissue competition. That is, our hair is reduced because of reduced DHEA.

As testosterone increased in hominid females, along with upright locomotion and reduced hair, competition among females must have increased, especially with increased sex drive. I suggest this produced a selection pressure for development of the breast as a primary sexual attractive device; the same mechanism that produced the estrus display in chimpanzees. We are the only group of mammals that use the breast as a sexual display. Breast development is directly tied to the abundant form of DHEA, called DHEA sulfate, from which DHEA is made.

"A significant positive correlation was observed between DHA-S [DHEA sulfate], body weight and each stage of breast development before and after onset of menarche." (Acta Obstet. Gynaecol. Jpn. 1988; 40: 561)

The human breast display is directly related to sexual maturity, i.e., ovarian function. The ovaries are connected to DHEAS production: "Our data show that premature ovarian failure and ovariectomy in young as well as postmenopausal subjects precipitate an earlier decline in DS [DHEAS] levels" (Journal of Clinical Endocrinology and Metabolism 1982; 54: 1069.)

Human DNA and chimpanzee DNA differ by only 1.2%. This difference has taken six million years to produce. The DNA of archaic Homo sapiens, H. erectus, and even Australopithecus must have been even more similar to ours. Hominid evolution is a pattern change more than a genetic change. I suggest it results from changes in hormone production and their effects on gene regulation. Some genes have increased activity, while others have decreased activity. These have produced significant physical and behavioral changes over time.

Human evolution relies on simple changes in hormone production, that result from basic behaviors that we see everyday. Human evolution is viable and unyielding today, and affects every aspect of our lives. In the next part of this series, I will explain how this mechanism applies to contemporary society. This will be followed by a number of articles concerning other hypotheses.

A number of newsgroup posts have connected hair loss and sweat glands in the development of Homo sapiens. Often these explanations deal with temperature. Since I think human evolution is mainly the result of the increased testosterone in us, I must be able to show that hair loss is due to increased testosterone and that sweat glands are a target tissue for testosterone. We have less hair and more sweat glands.

If I am correct that we produce less hair because of more testosterone, then reducing testosterone should increase the amount of hair growth. This has been done in the stumptail macaque. In the following quotation, note that "finasteride, a 5 alpha-reductase inhibitor," significantly increases hair growth. Finasteride reduces the effects of testosterone. That is, 5-alpha-reductase produces 5-alpha-dihydrotestosterone from testosterone in "testosterone target tissues." If this enzyme product of testosterone is reduced, hair growth increases.

"Finasteride, a 5 alpha-reductase inhibitor, was administered orally (1 mg/kg.day) for 6 months to six male and five female stumptail macaques. Vehicle was given to five male and five female animals over the same period of time. Hair weights in a defined 1-in.2 area of frontal scalp were measured periodically every 1-2 months, and serum was collected for measurement of testosterone and dihydrotestosterone. In addition, scalp biopsies were taken before and 6 months after treatment to evaluate the micromorphometry of hair follicles. Results showed that both male and female serum dihydrotestosterone levels were significantly reduced (60-70%) by finasteride treatment. Both males and females showed statistically significant increases in mean hair weight over the treatment period compared to controls (P = 0.034). In addition, there was a statistically significant increase in mean follicle length (measured histologically in scalp biopsies) compared to baseline in the finasteride-treated animals (P = 0.028)." (J. Clin. Endocrinol. Metab. 1994; 79: 991)

In the stumptail macaque, reducing the effects of testosterone increases hair. So, increases in testosterone in Homo sapiens may be the reason for reduced hair. Different areas of hair growth respond to testosterone in differing amounts. "Androgens [testosterone] stimulate hair growth in some areas, e.g., beard, but may cause regression and baldness in the scalp" [Clin. Endocrinol. (Oxf.) 1993; 39: 633.] My basic principle, of my work, is that the hormone, DHEA, is used in transcription and replication of genes. (DHEA is used to "read" genes for gene activity and copy genes for equal distribution in cell division.) I have suggested that tissues differ in their use of DHEA; this is how I explain evolution of eukaryotes and multicellularity. Therefore, tissues will require different levels of DHEA for specific gene expression. Scalp hair and beard hair are examples of this. I suggest the differentiating factor is the availability of DHEA. It has been found that the receptor for DHEA can bind dihydrotestosterone (the 5 alpha-reductase product) secondarily. That is, "Bound [3H]DHEA was displaced sensitively by DHEA and secondarily by dihydrotestosterone, but not effectively by other steroids, including DHEA sulfate" (J. Clin. Endocrinol. Metab. 1995; 80: 2993.) This means, to me, that DHEA is absorbed for growth of hair primarily, but the by-product of testosterone, dihydrotestosterone, can compete for its receptor. (This should happen at the cell surface and within the cell.) Therefore, expression of genes dependent on less DHEA will be adversely affected by the presence of dihydrotestosterone. This is why increased testosterone reduces hair over the body, but not the hair producing tissues of the face.

Hair is present from birth. Since DHEA is at its highest immediately following birth, some neonates of high DHEA should have hair at birth. However, since the brain, primarily, and body start to use so much DHEA for growth and development (gene function and replication), the DHEA falls quickly after birth and the original hair is lost. (See my chart of DHEA during the human life-span above.) This is the same reason that the deciduous teeth form early, then are lost.

I have explained, just above, that tissues differ in their dependence on DHEA. Testosterone target tissues have their testosterone target genes "turned on" by testosterone. These genes then use DHEA for transcription. Following the finalization of brain growth, DHEA begins to increase in amounts in the blood from late childhood (5-7 years); this is called adrenarche in the textbooks. (The textbooks do not have an explanation for this.) What this means to this discussion is that DHEA begins to increase from late childhood to reach a peak around 20 to twenty-five years. Since sweat gland activity really begins following puberty, I think this means that the rise in testosterone in men and women is the cause. Sweat glands are a phenomenon of testosterone, and this is an affect on gene activity.

"1. To study the difference in sweat rate between men and women the rates of cholinergic-induced sweating were measured in normal people before and after puberty and in response to androgens and anti-androgens. 2. Sweat rate in men was more than double that in women. 3. This difference did not occur in prepubertal boys and girls in whom the rate, corrected for surface area, was comparable with that in women. 4. Application or injection of androgen locally did not stimulate sweat production in the adult female. 5. Anti-androgen topically or systemically did not decrease sweat rate in men. 6. It is concluded that the rate of sweat rate in men is caused by androgen-induced gene expression at puberty and not by androgen modulation in adult life." (Clin. Sci. 1981; 60: 689)

The next quotation demonstrates that sweat glands have the highest 5 alpha-reductase activity of the entire skin, sebaceous glands have a high activity, and hair follicles have significantly less activity than the sebaceous glands. As you read this, think about the increased activity in males, that may, therefore, increase the activity of the sweat glands, which could further increase hair loss in the scalp.

"In order to know the distribution of testosterone 5 alpha-reductase activity in human skin, we developed a micro-method, in which we used 20-50 micrograms of various tissues microdissected from freeze-dried sections. The characteristics of this enzyme in the sebaceous gland are briefly described, as follows: the identified 5 alpha-reduced metabolites are 5 alpha-dihydrotestosterone, 5 alpha-androstane-3 beta, 17 beta-diol and 5 alpha-androstanedione; the optimal pH is about 7.5; and the apparent Km is approximately 2.4 x 10(-5)M. The measurement of 5 alpha-reductase activity of various components of the skin obtained from 7 men and 5 women revealed that the sweat gland (probably apocrine) in the axillary skin possessed the highest activity of 5 alpha-reductase: the value was nearly 400 pmoles/mg dry weight/hr in the standardized condition. The sebaceous gland also showed a high activity of 85-261 pmoles/mg/hr. The hair follicles exhibited a significantly lower activity than the sebaceous gland. The enzyme activity was negligible in the epidermis, while it was detected in the dermis though the values determined were variable probably because of contamination with other components such as sweat glands and hair follicles. Thus, the present study demonstrates that the 5 alpha-reductase activity is mainly located in the apocrine sweat gland and sebaceous gland. This suggests that 5 alpha-reduction of testosterone is an important step in mediating the action of androgens in these tissues." (J. Invest. Dermatol. 1980; 74: 187)

Testosterone is known to increase sex drive in both males and females. This would increase the percentage of higher testosterone hominids with time. Increased testosterone would reduce hair, increase sweat glands and activity and, in the female would reduce labial displays, normally dependent upon increased estrogen to testosterone. The exposed breast, also indicative of sexual maturity, would become the primary sexual display. This combination would eventually lead to bipedalism. Other events, dependent upon the hormones DHEA and melatonin, would, much later, result in an enlarged brain.

So, you see, one does not have to resort to looking for environmental effects to account for all of these characteristics of hominids. The single mechanism of increases in testosterone, alone, will cause all of these changes. That is, increases in testosterone increase the sexual device. The sexual device is one of most important devices created by DNA for duplication.

Testosterone is the basis of violent behavior. That is, testosterone is the basis of impulsive behavior. The amount of testosterone determines the ability to control, or not, impulses. More men are imprisoned than women. Black men (at the college level) produce more testosterone than white men; more black men are imprisoned than white men. The following is a letter describing this, which has been sent to a number of U.S. congressmen and U.S. senators. You judge for yourself. This is from 1994.

Northwest Arkansas Times, Fayetteville, AR, U.S.A., May 22, 1998.

"May 18, page A3, the ... [Northwest Arkansas] Times... reported Retired Army Lt. Col. Dave Grossman's conclusions that "Like military training that reduced inhibitions to killing, television and movie violence is desensitizing the young, and doubling the murder rate every 15 years." This is not a new idea; many people have suggested the "media" causes increased violence and sex in our youth. It produces a "straw man," with which one may do lengthy, imaginary battle. My work suggests the current phenomena, and others, are the result of human evolution. That is, I think humans evolved due to increased testosterone. Human males and females produce more testosterone than male and female chimpanzees, respectively. In advantageous circumstances, testosterone levels will increase in a population. Increased testosterone increases impulsive behavior. We are witnessing an increase in testosterone in America.

This is directly supported by very strong correlative data and direct experimental evidence. In a study of "delinquent" and "control" white men and women, Banks and Dabbs found that "The delinquent group, which was characterized by flamboyant dress, drug use, and violence, had significantly higher testosterone levels than the college students did." (J. Soc. Psychol. 1996; 136: 49). Brooks and Reddon compared testosterone levels in violent and nonviolent "young offenders." They found that "The violent group had the highest level of testosterone and differed significantly from the nonviolent offenders..." (J. Clin. Psychol. 1996; 52: 475). This represents a strong correlation between high testosterone and impulsive, aggressive acts. People who do not think aggressive, impulsive acts are due to increased testosterone can simply dismiss this as coincidence.

The key experiment that directly supports testosterone as the causative agent was reported in 1997. In a study of "hypogonadal," boys, who produce little testosterone, the effects of increased testosterone become clear. Finkelstein, et al., found that "At the mid dose boys showed a 19% increase in aggressive impulses scores, a 17% increase in physical aggression against peers score, and an 18% increase in physical aggression against adults scores." (J. Clin. Endocrinol. Metab. 1997; 82: 2433). Men produce much more testosterone than women. There are many more men in prison than women.

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. Impulsive acts will increase directly proportional to the increased numbers of higher testosterone types. High testosterone should have a greater effect on a kid following puberty, because the brain is not fully developed. The greatest amount of youth violence is coming from young, male offenders. Let's look at biological factors."