Mark Jacobs' Evolution and Philosophy - James Howard's Theories

An appraisal of the role of testosterone, DHEA and melatonin in human evolution

James runs his own website with lots of material to look at. Please read the latest writings and essays there. It is surprising how much is explained by how these hormones interplay. I heartily recommend reading his articles - they really are eye-openers, and it is shocking that these ideas have been given little attention in mainstream media.

Writings by James Michael Howard found on Bionet's website

(Reproduced here for fear of it going missing at some point) :-
I just found this citation that supports my theory that hominid migration was
forced.  That is, it shows, in a free-living primate, that individuals of lower
testosterone are forced away from the breeding group.

James Howard
(read my theory at on the web)

Wickings EJ, 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 increasedmost 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."

A number of posts have connected hair loss and sweat glands in the development of Homos sapiens at other newsgroups. 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. (I have posted some of my explanations of human evolution resulting from increased testosterone here, but one can read more in my article on human evolution at on the web.) 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. Rhodes L et al., "The Effects of Finasteride (Proscar) on Hair Growth, Hair Cycle Stage, and Serum Testosterone and Dihydrotestosterone in Adult Male and Female Stumptail Macaques (Macaca arctoides)" J Clin Endocrinol Metab 1994; 79: 991 "Finasteride, a 5 alpha-reductase inhibitor, was administered orally (1 mg/ 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)." 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 at my web page.) 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. Rees J and Shuster S "Pubertal Induction of Sweat Gland Activity" Clin Sci 1981; 60: 689 "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." 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. Takayasu S et al., "Activity of Testosterone 5 alpha-reductase in Various Tissues of Human Skin" J Invest Dermatol 1980; 74: 187 "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." 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. James Howard
The following is a post designed for some other newsgroups, that were dealing with the subject of a "neurochemical basis of violent behavior." Since my explanation of this is based on my theory of human evolution, I thought it should be posted here. What you will be reading about is the "secular trend." I think the secular trend is the current signal of human evolution; it is easily seen and is explanable as an increase in testosterone. (Some say the secualr trend is due to increased nutrition. If this were the case, blacks should exhibit less of the secular trend than whites; the opposite happens to be the case.) This is an introductory paragraph for the other newsgroup: 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. All, but one, failed to even acknowledge receipt. (It is very un-politically correct.) You judge for yourself. This is from 1994. "I am a theoretical biologist; my work contains an explanation of increased violence in our society. I suggest violence results directly from an increase in numbers of individuals of higher testosterone, who arrive at puberty early. increased testosterone and early puberty increase the probability of impulsive actions. The Federal Bureau of Investigation has compiled statistics which demonstrate that I am correct. Males kill more than females; blacks kill more than whites. In the remainder of this letter, I include references from hightly reputable journals (eg. Journal of the National Cancer Institute) that demonstrate the blacks produce significantly more testosterone than whites and enter puberty at an earlier age. What this boils down to is that individuals of both races, who exhibit these qualities, are more apt to resort to violence in a heated moment. This is why there is so much black on black and white on white violence; these are impulsive actions, not premeditated, thoughtful actions. These are thoughtless actions that happen quickly, without forethought. You, or your aides, are aware from interviews that many of these kids, who kill other kids, are really nice kids when they are not in a stressful, heated moment. I am aware your background is not biological, nor are the backgrounds of those whose advice you seek when confronting the increase in violence in our society. You must consider, therefore, that a major explanation of human behavior is being neglected by educators, sociologists, crimnologists, etc. Their "model" of human behavior suggests that almost all human behavior is determined by the environment. It is time a biological model is considered. I will explain how this produces violence in the remainder of this document; if you read this, you should note the same mechanism also explains increased sexuality and learning problems in our youth. That is, all of these result from a single change in our society, which is very easily produced and increases exponentially. This change increases with each generation. Not everyone is affected, but more children are affected now than in the past. Therefore, each past generation contains more who notice the change. More grandparents see it than parents. It occurs earlier in some places than others. This is why some people always see these problems in some place at some earlier time. I think the "60s" was the time it occurred in such magnitudes that it openly impacted our entire society. It is a continuing process, but usually takes more time to occur in conservative areas. My works suggests this is a major biological change that affects both the body and brain. Most grandparents and some parents have noticed the change in body size and function in children. Children are getting bigger and reaching puberty earlier. "The average age of menarche [puberty] in the female has dropped from approximately 17 years to approximately 13 years. Thus, today maturation occurs about 25% faster than it did 100 years ago." ("Sexual Dimorphism in Homo sapiens," R.L. Hall, Praeger Publishers, New York, 1982, page 279). "...children in average economic circumstances have increased in height at age five to seven by about 1 to 2 centimeters per decade. ...Most of the trend toward greater size in children reflects a more rapid maturation; only a minor part reflects a greater ultimate size." (Encyclopaedia Britannica 1984; 5: 656). My work suggests a cause of this change. The hormone, testosterone, is rising rapidly in our society. Increased testosterone increases body size, aggression, and sexuality in both sexes. (Testosterone is not "the" male hormone, men simply produce more.) People who produce more testosterone are more aggressive and sexual, therefore, on average, they ultimately make more babies than those who produce less testosterone. (People who produce less testosterone can better control their sexual activity; over a period of time, they will produce fewer children.) Ultimately, the percentage of high testosterone people, of both sexes, increases at the expense of low testosterone people. This changes the averages of everything affected by testosterone. This is why our kids are biggfer, more sexual, and more aggressive than in the past. The mechanism is simple: higher testosterone boys and girls reach sexual maturity faster, increase their numbers faster, and their offspring are even earlier and more sexual. People seeking sexual gratification are simply more likely to engage each other. Sexual activity is so common today that no "stigma" is attached; in fact, there appears to be a negative stigma attached to those who do not indulge. Prior to puberty, the brain grows more rapidly than the body; it is a competition which the brain wins in infancy and early childhood. Because of this brain-body competition, puberty is delayed until the brain is almost finished in development. Near puberty, however, testosterone increases the body's competitive edge for growth and development which continues into adulthood. "The weight of the brain [in humans] reaches 90% of adult size by age six and virtually 100% by age 12, yet body growth continues to age 18 and beyone (note that brain growth is nearly finished before reproductive maturity every begins)." ("Patterns of Human Growth," Cambridge University Press, 1988, pages 60-61). The advanced frontal lobes of the brain develop last and control formal thinking, i.e., higher math, proper language (syntax), and the ability to form meaningfully predictive ideas (hypotheses). This is Piaget's final stage of human thought development. This stage of brain development is directly dependent on final development of the frontal lobes "from about age 11 to 14," (Science 1987; 236: 1110). I suggest early puberty interferes with this important final development of the frontal lobes. For example, it was reported that standardized test scores of 13- and 17- year-olds of 1986 are lower than those of 1970, whereas the scores of 9- year-old children have remained relatively equal (Science 1988; 241: 1751). I suggest this decline is the effect of puberty, which, in this country, on average, is now occurring between age 9 and 13. Our children are, on average, losing the ability to handle math and English. More importantly, our children are losing the ability to form meaningfully predictive ideas that help control their impulses. "What are the consequences of my actions?" Without the function of the frontal lobes, symbolized by this question, kids cannot predict the consequences of, or control, their behaviors (impulses). Violent acts and sexual activity in children and teenagers are actions of impulse. These impulses are initiated by the primitive part of our brains, which testosterone mainly affects. Children are reaching puberty earlier with each generation, and early puberty arrests final development of the brain. This means that, on average, our advanced brain is increasingly underdeveloped with each generation. This is why so many children cannot control their sexual or aggressive impulses. It is fact that, on average, the behaviors mentioned above, occur in higher incidence in the black population. That is, on average, black children have more problems with math and English, score lower on standardized tests, exhibit more aggressive and sexual impulse activity, and experience family disintegration more than white children. The reason, I suggest, is that, on average, blacks, as a group, produce more testosterone than whites, as a group. (Take note of the journal source of the following quotation.) "This report gives the results of assays of circulating steroid hormone levels in white and black college students in Los Angeles, CA. Mean testosterone levels in blacks were 19% higher than whites, and free testosterone levels were 21% higher. Both these differences were statistically significant. Adjustment by analysis of covariance for time of sampling, age, weight, alcohol use, cigarette smoking, and use of prescription drugs somewhat reduced the differences. After these adjustments were made, blacks had a 15% higher testosterone level and a 13% higher free testosterone level." (Journal of the National Cancer Institute 1986; 76: 45). The study, above, was of college students. If I am correct that testosterone adversely affects learning, then those blacks who are unable to meet requirements for college admission, or even complete high school, may produce more testosterone, on average. The should exhibit even less impulse control; this may be why there are so many black on black murders in ghettos. This was not a common occurrence in black communities in the depression. Testosterone is increasing over time. I have suggested that increases in testosterone in our society are causing the overall problems, i.e., increases intestosterone are causing problems for both blacks and whites. Therefore, the rate of teenage births should be higher in blacks than whites but increased in both, compared to other advanced coutnries. This is the case. "The rate of teenage births is especially high in the black population. An international comparison around 1980 revealed that the black U.S. teenage fertility rate was 2.3 times the white and 3.2 times the average of 30 advanced countries. The contrast is even greater among the youngest teenagers; blacks under 18 years of age had a rate in 1980 that was more than three times that of whites. Nonetheless, even white teenage birthrates were 40% higher than the average for other advanced countries." (Science 1986; 234: 554). Not only do blacks, as a group, produce more testosterone, which I have suggested, increases the onset of puberty, they do, in fact, reach puberty earlier than whites as a group. "Black youths are known to enter into puberty at a younder chronological age than white yourth." (American Journal of Diseases of Children 1991; 145: 142). Again, it is my hypothesis that the violence, sexuality, and learning problems of our youth result from increased testosterone and early puberty in those affected. High testosterone and early puberty adversely affects development of the part of the brain which controls impulsive behaviors, i.e., the advanced forebrain. This combination should generate these problems, and they should be exacerbated in areas wheere high sexuality rapidly brings high testosterone males and females together. The result is an extremely rapid increase in high testosterone, early puberty, and their combined effects on impulse control. As people of lower testosterone are literally driven away, the problem becomes more concentrated. Impulsive acts also become concentrated; this is why there is so much black on black and white on white violence." James Howard
Hominids and Teeth ...yes, testosterone I have suggested to this group that the cause of hominid evolution is increases in testosterone. I have explained this and given a number of demonstrations of how increases in testosterone cause the various characteristics of Homo. This group has been discussing increased tooth enamel in hominids. Therefore, this post is designed to demonstrate that this characteristic is, also, due to the increases in testosterone. First, I want to explain, again, that I think testosterone has increased relatively continuously to produce Homo sapiens sapiens. We have not reached the size in teeth, etc., characteristic of some some earlier hominids, such as the robust Australopithecines, that, I think, exemplify extremes of testosterone. Our brains produce many testosterone receptors that literally absorb testosterone at the expense of other organs, such as teeth. Therefore, our teeth are not as large as these robust characters, because their brains were small. (I have explained the relationship of the brain to tooth size earlier in this group.) Once a "feed and breed" situation is established, testosterone will increase to the point that it reaches too high levels. I have explained, also at this group, that too high testosterone increases infection rates, increases infant mortality, and reduces sperm counts, all of which will lead to extinction, especially in the environment of the extinct "high testosterone" hominids. The point is that this increase in testosterone follows a cycle. When a lot of food it present, it makes the increase in testosterone occur faster. I have explained that I think this is currently occurring in the U.S. It can be seen in changes in tooth enamel, currently in the U.S., and I think this is due to increases in testosterone. A lot of the posts to this newsgroup agree with the hypothesis that extremes in diet caused the pronounced tooth size and thick enamel of the early hominids. The argument is that a grainy, fibrous diet resulted in this increase in tooth size. In the following quotation, please note that "enamel hypoplasia" is currently being reduced in Cleveland, Ohio. That is, tooth enamel is increasing in thickness. If the current hypothesis is correct, this would mean that the diet in Cleveland, Ohio, is increasing in grain and fiber. While there is a current movement to increase fiber in our diet, the study was done in 1978, long before this trend. I suggest that the diet covered during this study changed from relatively free of fiber to very free of fiber. (The investigators offer an explanation, and it may be the answer if the robust Australopithecines had "improved nutritional conditions" and few "childhood diseases.") I think this increase in tooth enamel thickness in Cleveland, Ohio, is due to the secular trend, i.e., an increase in testosterone. El-Najjar MY et al., "Prevalence and Possible Etiology of Dental Enamal Hypoplasia" Am J Phys Anthropol 1978; 48: 185 "Two hundred black and white adult human skeletons and 200 living black and white children from the greater Cleveland area were examined for evidence of enamel hypoplasia. Enamel hypoplasia, present in varying expressings (pits, lines and grooves), was found to be more prevalent in both skeletal samples, than in the living groups. In the majority of cases, sex differences between white and black males and females through time and space are highly significant for all tooth catagories. Regardless of the mechanisms behind it, prevalence of enamel hypoplasia for both white and black group has significantly declined through time. No evidence suggesting specific etiologies responsible for enamel hypoplasia can be found. In the majority of previously published reports, the etiology is still idiopathic. The reduction in the prevalence of enamel hypoplasia in the groups examined through time may be related to improved nutritional conditions and the elimination or decline of childhood diseases that have been implicated in this condition." The literature is sometimes not certain whether the increase in hominid tooth characteristic is due to increased enamel or increased dentin, or both. In the following quotations, the general direction is in the same for increases in either, or both, enamel and dentin in maleness and individuals of increased testosterone. This quotation demonstrates that enamel and dentin are both increased in "47,XXY males. Alvesalo L et al., "Enamel Thickness in 47, XXY Males' Permanent Teeth" Ann Hum Biol 1985; 12: 421 "Enamel thickness of the maxillary permanent central incisors and canines in 14 47,XYY males, their male and female relatives and population-control males and females were determined from radiographs. The results indicated, although not fully unambiguously, that the thickness of enamel and that of 'dentin' (distance between mesial and distal dentino-enamel junctions) are increased in the teeth of 47,XYY males compared with normal controls." Individuals of the 47, XXY genotype produce more testosterone than normal genotypes. Schiavi RC et al., "Pituirary-gonadal Function in XYY and XXY Men Identified in a Population Survey" Clin Endocrinol (Oxf) 1978; 9: 233 "The XYY men had significantly higher plasma concentrations of LH, FSH and testosteroe than matched controls." In a normal population the dentin is "significantly thicker" in males than females. Stroud JL et al., "Sexual Dimorphism in Mesiodistal Dentin and Enamel Thickness" Dentosmzxillofac Radiol 1994; 23: 169 "The results showed significant sex differences (p<0.01) in mesiodistal diameter favouring mles over females. Dimorphism was more pronounced for the molars than premolars. Enamel thickness, which is 0.4-0.7 mm greater for the molars than premolars, shows no significant sex differences. Dentin is significantly thicker in males than females, and is 3.5-4.0 mm thicker in molars than premolars. It is concluded that sexual dimorphism in mesiodistal tooth sizes is due to differences in dentin thickness and not enamel thickness." I suggest that the increased enamel and/or dentin in the teeth of hominids is due to the increased testosterone in hominids. (The teeth of Neandertal are produced by a variation of this mechanism, caused by increased testosterone and DHEA in Neandertals.) James Howard
Skin color ...perhaps testosterone I have suggested that testosterone is directly involved in hominid evolution and have posted a number of messages here to support my theory of hominid evolution. Besides my general explanation, these have included the loss of hair, enamel thickness, increased sweat glands, etc., includinding a demonstration of my mechanism currently affecting the U.S. population. A number of posts have recently been discussing the skin color aspect of hominid evolution. I considered applying my theory of DHEA/testosterone to this some time back, but was unsatisfied with the directness of the support I found. However, since my posts regarding the characteristics, mentioned above, support my theory well, I thought it is time to post the connection of testosterone and skin color since it fits the pattern of hominid characteristics directly affected by testosterone. Since many have ignored my posts and a number have indicated that they do not read them throroughly, I will put the following citation in context. I have suggested that the rise in testosterone in hominids is the mechanism that drives the population of hominids into new territories. That is, I suggest that in a breed and feed situation, testosterone rises and males of low testosterone are driven away from the group. I suggest this eventually resulted in the effects of testosterone, melatonin, and DHEA that resulted in increased brain size. This means that hominids that stayed in Africa should have the highest testosterone levels, while those that were driven out have less testosterone. (Black males produce significantly more testosterone than white males; citation in some of my past posts.) This mechanism of low testosterone individuals being pushed away from the group should occur in each location where populations of hominids reside. That is, the rise in testosterone will occur in every population. This is what continued to push the hominids throughout the world. The testosterone levels should be less with distance from Africa. (This is a generality since I think this occurs in cycles and may increase in populations that are "ice-, ocean-, and landloced" so that testosterone is increased dramatically. This testosterone, and increased DHEA and melatonin, I suggest, resulted in Neandertal.) To return to the point of skin color, it is testosterone that is of importance again. The following quotation demonstrates that testosterone and ultraviolet light (UVL) act synergistically to stimulate epidermal melanin production. That is, the more testosterone one has, the more one will produce melanin. This means that hominids that were driven away from the equator may have been lighter skinned, because they produced less testosterone. During the posts regarding light colored skin at, it was reported that Eskimos have darker skin than would be expected if the vitamin D theory of lighter skin is the only explanation. I suggest the Eskimos may be an example of a "position-locked" group that produces more testosterone. The increased testosterone in this group may be why they have darker skin than would be expected. Glimcher ME, et al., "Organ Culture of Mammalian Skin and the Effects of Ultraviolet Light and Testosterone on Melanocyte Morphology and Function," Journal of Experimental Zoology 1978; 204: 229 "Scrotal skin of black Long-Evans rats and human thigh skin were maintained in vitro as organ cultures for as long as 14 days, and examined histologically using the comined skin splitting and Dopa techniques. Selected rat skin cultures received testosterone in the culture medium and/or irradiated with ultraviolet light (290-320 nm UVL). With increased time in culture, scrotal melanocytes round up and there is an increase in epidermal pigmentation. Human skin behaves similarly; after eight days in vitro human melanocytes also become rounded, but remain strongly Dopa-positive. Addition of exogenous testosterone to cultured rat skin maintains dendritic morphology of melanocytes, but cell body size is still reduced. UVL irradiation stimulates melanocytes in rat skin cultures, maintaining their dendritic morphology and increasing epidermal and dermal pigmentation. Cultured skin receiving both UVL and testosterone illustrates a synergistic effect." The decreased skin pigmentation of groups living away from the equator may be due to decreased testosterone. I suggest this further supports my theory of hominid evolution. James Howard
ahimoe at (Albert Himoe) wrote: >In article <557c3n$bg2 at>, James Howard >(phis at writes: >> That is, I suggest that in a >> breed and feed situation, testosterone rises and males of low testosterone are >> driven away from the group. I suggest this eventually resulted in the effects >> of testosterone, melatonin, and DHEA that resulted in increased brain size. >> This means that hominids that stayed in Africa should have the highest >> testosterone levels, while those that were driven out have less testosterone. >Then why do the hominids in Africa have the smallest brain size? Or, >do you means that the losers colonized the world, and the winners >brains shrank? >-- >Albert Himoe >email: ahimoe at James Howard responds: Thank you for your question. I will attempt to answer your question as briefly as possible; I refer you to my relatively brief explanation of this at on the web. For sake of brevity here, you will find citations supporting this explanation in my article there. (If you try to reach my website, please be patient; I have been unable to reach it for days.) My work suggests that the hormones, melatonin and DHEA, as well as testosterone, are involved in increases in brain size. However, for melatonin and DHEA to exert effects, they have to be increased. DHEA is known to increase metabolism; it does this by stimulating mitochondria. Hominids that there driven away from the equator and into colder environments would have an increased survival rate if they produced increased DHEA. In vitro, DHEA stimulates neuronal survival and differentiation. Hominds that produced more DHEA could survive colder environments and produce bigger brains. My work also suggests that melatonin acts in a cycle that stimulates DHEA. Melatonin production increases as light decreases. Hence, movement away from the equator will stimulate both melatonin and DHEA. This will increase the brain size in hominids forced away from the equator. The brain is full of testosterone receptors. It is my theory that testosterone stimulates use of DHEA for "testosterone target tissues." That is, I think testosterone stimulates the absorption of DHEA. (My basic principle is that DHEA optimizes transcription and replication of DNA.) Hence, increases in testosterone will increase use of DHEA for the brain and increase its size. Humans, therefore most likely hominids, produce more testosterone than chimps. I suggest this is why hominid brain size increased in Africa. The brains of the early hominids were larger, but not significantly larger, as that found in later hominids. The hominids that remained in Africa did not have the effects of DHEA and melatonin to stimulate brain growth. Hence, the increase in testosterone of these groups affected their brains only slightly, but the increased testosterone directly affected their bodies. You see, the body is also full of testosterone receptors. Now, my work suggests all tissue compete for DHEA. The brain competes with the body. In this group, the brain did not increase in size to a large extent so the increases in testosterone affected the body in increased amounts. I suggest this is why the robust Australopithecines developed. Their brains did increase in size, but their bodies increased much moreso. Hominids that were driven away from the equator, I suggest, benefitted from the increases in DHEA and melatonin. That is, their brains benefitted. As the cycle of breed and feed cycles continued, testosterone also increased. This increased the absorption of DHEA in individuals who were producing more DHEA. This combined to make for bigger individuals with bigger brains. That is, DHEA and testosterone both increased. This is how I explain Neandertal. That is, Neandertal is the result of being "position locked." The hominids that ended up in Europe became locked in place; they could not easily run from the effects of testosterone. In the severe cold, their DHEA also increased. That is, testosterone and DHEA both increased in very large amounts at the same time. If you have been following my argument, you should know that very large increases in testosterone and DHEA should produce a hominid of very large size with a very large brain. Since I have discussed the effects of testosterone on teeth in this newsgroup, I will add that this same situation should produce very large teeth. Now, I will not go into further detail at this time, but this is an explanation of Neandertal that is directly drawn from the same mechanism that produced all hominids. My theory also suggests that the brain and body compete for DHEA. The larger the brain is, the better it can compete for DHEA in the blood. (The larger the brain, the more surface there is for absorption of molecules.) Hence, as the brain became bigger, the body became smaller. The bigger brain caused the body to become more "gracile." This is why the hominid line evolved into the gracile form. James Howard
The Flynn Effect ...yes, testosterone In response to my "Current Signals of Increases in Testosterone," which explained how I think rising testosterone causes the secular trend and is affecting a number of phenomena in the U.S., I received this response: "But IQ scores are rising with the secular trend!" The author of this comment intended to show that this, real connection between IQ scores and the secular trend, refutes my theory. This increase in IQ is called the "Flynn Effect." The Flynn Effect refers to an increase in IQ that occurs along with the secular trend. However, the Flynn Effect is mainly an increase in "non-verbal tests." The overall effect is primarily due to increases in the lower half of the IQ distribution, but it also occurs in the "gifted," or those who score 1400 or more on the SAT. The Flynn Effect is a worldwide phenomon. (It occurs in all socioeconomic groups.) I suggest the Flynn Effect is due to rising testosterone. The effect is small; perhaps 15 points in two generations. In my last post, "Hominid Brain Size: Testosterone, DHEA, and Melatonin," I suggested that two kinds of increases in hominid brain size have occurred. One, that causes only slight increases in brain size, I attribute to increasing testosterone in hominids. This is the small increase noticeable in the early hominids. This is the increase I think is due mainly to the increases in testosterone that started separateing us from the other primates. The main increase in hominid brain size, I suggest, is due to the effects of the hormones, DHEA and melatonin. The effects of these two hormones, according to my theory, have to occur away from the equator, and this is where the fossil evidence, north and south, shows the main increases in brain size. The increase in testosterone will cycle through hominids, i.e., testosterone will periodically rise in humans. It will produce some dramatic effects, but one, I suggest, is a slight increase in nonverbal abilities of the brain that will cause slight increases in overall IQ scores. To explain this, I am including part of my post, "Math and English," that was posted June 13. This was generated in response to findings that "reading proficiency is down in virtually 40 states ...and significantly down in 10." The math scores were up slightly; this is the Flynn Effect in the U.S., as of April, 1996. The increase in testosteorne causes the slight increases in nonverbal abilities, while it causes decreases in verbal abilities. "It is generally accepted that the two sides of the brain (cerebral hemispheres) interact but basically perform different functions. The things we call reading and writing are usually controlled by the left half, mathematical things and spatial abilities are usually located in the right half. Because of this divergence in function, boys are, generally, but not always, better in math than girls. My work suggests a reason for this that is directly connected to the changin reading and math scores. The left hemisphrere finishes growth a little after the right. My work suggests brain growth is particularly dependent on the hormone, DHEA. (DHEA in extremely small quantities stimulates formation and growth of the brain cells primarily used in thinking, neurons.) Therefore, the left hemisphere depends on a continued supply of sufficient DHEA for final growth. All Tissues, especially the brain, compete for DHEA. The hormone, testosterone, increases use of DHEA by testosterone target tissues, which also includes parts of the brain. Boys produce more testosterone than females so there is less DHEA, on average, for left hemisphere growth. In animals studies, it has been demonstrated that testosterone actually reduces development of the left hemisphere (Behavioral and Neural Biology 1988; 49: 344). Therefore, boys, on average, have an increased ratio of right hemisphere to growth to left. The right side is used more for mathematical and spatial thinking, therefore, on average, boys out- perform girls in these areas. If you want to be a good mathematician, you might be tempted to want more testosterone. In tests of spatial and mathematical reasoning, males with high testosterone score much worse than those with low testosterone. High testosterone increases lower brain growth and development at the expense of even the right hemisphere. That is, in high testosterone, even the right hemisphere looses in the competition for DHEA. I have suggested in past letters to this paper that testosterone is rising in this society. Most people see it in the 'secular trend,' that is, boys and girls are getting bigger and reaching puberty earlier. If testosterone is rising, it not only will affect the size of our children, but it will also affect their brains. That is, as testosterone increases it will decrease the ratio of left hemisphere to right. This will be seen, on aveage, as a decline in reading ability and an increase in math abilities. In areas where testosterone is very high, reading and math scores should both decline. The thing that worries me most is that one of my references points out that 'the left hemisphere also seems to be the seat of analytical thinking...' According to the National Assessment of Educational Progress, we may be seeing a real, and in some areas already significant, decline in functions of the left hemisphere." James Howard

Sudden Infant Death Syndrome, Melatonin, DHEA, and Testosterone

Copyright © 1996 James Michael Howard.

The following is a compilation of three postings to newsgroups at different times regarding my idea about Sudden Infant Death Syndrome (SIDS).

Part I (August 11, 1996)

My work suggests that sudden infant death syndrome (SIDS) results from a time during sleep when melatonin is too high and this reduces DHEA so low that there is insufficient DHEA to maintain function in the brainstem. (If this interests you, you should read my theory of sleep. Part of my theory suggests melatonin increases at night, which decreases DHEA, and that increases in DHEA during sleep cause REM sleep. I think that melatonin and DHEA reciprocate during the night so that sufficient DHEA is always present to maintain function of the brainstem. As DHEA increases to maintain brainstem function at night, the increase in DHEA also activates areas other than the brainstem and this causes REM sleep.

My idea that DHEA causes REM sleep was supported in 1995. "DHEA administration induced a significant increase in rapid eye movement (REM) sleep, whereas all other sleep variables remained unchanged compared with placebo condition." (American Journal of Physiology 1995; 268: E107)

With the connection of DHEA and REM sleep in mind, consider the following quotation concerning the reduction in REM sleep that occurs as melatonin increases. Keep in mind that the time of maximum SIDS is from 2 months to six months; this is the time when melatonin starts to really increase and reduce REM sleep. Note that at 4 months, the adult pattern of significant increases in non-REM sleep begins to precede the first REM sleep. My work suggests that this is time when melatonin is exerting its most profound depression of DHEA, therefore, this should be the most deadly time for infants. (You can see my chart of DHEA and melatonin during the human life-span in my sleep article at my website.) The following will make more sense if you look at my chart and read my theory.

"Electroencephalographic studies have shown that the amount of REM sleep changes with age. While newborns spend almost 50% of their sleep time in REM, the percentage of REM sleep decreases to 30% by the age of 3 months and to 20% by the age of 6 months. In addition, newborns enter REM sleep soon after the initiation of sleep, but by the age of 4 month entry into sleep assumes the adult pattern in which a significant period of non-REM sleep precedes the onset of REM sleep. Since reduction in the amount of REM sleep is associated with cerebral maturation and since the pineal gland has been implicated both in cerebral development and in the organization of REM sleep, the pineal gland may be involved in the maturation of the adult REM sleep pattern. Prior to the age of 3 months melatonin plasma levels are low and the characteristic circadian rhythms of melatonin are absent. Thereafter, melatonin secretion increases and circadian rhythmicity of melatonin becomes apparent. Thus, the decline in the percentage of REM sleep coincides with the emergence of melatonin secretion coincident with the maturation of the pineal gland." (International Journal of Neuroscience 1992; 63: 1)

If I am correct, REM sleep should exhibit a higher activity than slow wave sleep (SWS or non-REM sleep); I think this is due to the possibility that DHEA is an activator of nervous function. "During REM sleep, brain reactivity and brain excitability thus seem to be higher than during SWS; the reactivity thresholds are lower during REM and a stimulation more readily evokes a cortical response during this stage than during SWS." (Physiology & Behavior 1990; 47: 1272.) What this means is that if melatonin rises too high and DHEA is too low, the activity caused by DHEA during sleep in the brainstem may falter and cause death. I think this is the explanation of SIDS.

Part II (September 5, 1996)

Earlier, I posted my hypothesis that SIDS occurs during a time when melatonin is high and DHEA is low. I suggested that DHEA is a stimulator of the nervous system, that melatonin reduces DHEA during sleep, and levels of DHEA that are too low will result in loss of DHEA stimulation of the brainstem. Hence, when DHEA is too low, death occurs. I want to extend this with further supporting evidence that involves epidemiological findings in SIDS.

The first place to look, given my hypothesis, is the adrenal glands, the site of DHEA production. Well, I did and the adrenal glands are normal in SIDS. "Our data revealed a normal maturation of the adrenal glands in SIDS cases." (Int. J. Legal Med. 1994; 106: 224.) I decided to look elsewhere, i.e., I decided to look at the influence of testosterone on the incidence of SIDS. More boys than girls are affected by SIDS. Additionally, I have already shown that testosterone has a negative effect in HIV infection and AIDS, so this is a logical thing, for me, to check. This where the answer lies. (You may find my hypothesis of AIDS on the index page.)

If you read my first posting on SIDS, you will remember the connection of REM sleep and DHEA. The idea is that REM sleep is a healthy sign for infants during the time of SIDS incidence. (Proper amounts of REM sleep mean proper amounts of DHEA during this time.) In the following quotation, note that there is a "lag in the maturation of REM sleep" in SIDS. This indicates to me that DHEA is in low amounts as melatonin increases in the first months of life.

"The data show that risk male infants fail to demonstrate an increase in wakefulness with age and reveal a lag in the maturation of REM sleep compared to controls and female risk infants during the critical age for SIDS. Significant sex differences within the first six months of life are of particular importance because of the consistently reported higher incidence of SIDS in males than females." (Neuropediatrics 1993; 24: 8)

My idea, in SIDS and in AIDS, is that the hormone, testosterone, directs DHEA to use by "testosterone target tissues." You see, my principle hypothesis is that DHEA is required for optimal transcription and replication of DNA. Therefore, testosterone increases use of DHEA for its target tissues; they grow bigger because of this, and this is why men are bigger than girls. Men produce more testosterone. However, in a situation of limited DHEA, this can be a problem, because testosterone redirects DHEA for its target tissues. (This is why men of high testosterone to DHEA become bald.) I think the same thing occurs in SIDS. One of the main causes of SIDS, then, is a high ratio of testosterone to DHEA. The idea that testosterone is involved in SIDS has been tested in an infant primate.

"In postnatal infants, there is similarity between the time course of transient gonadal steroid secretion and the age-related incidence of sudden infant death syndrome (SIDS). The cause of death in SIDS is generally thought to be a ventilatory arrest, but the mechanism responsible for such an event remains unknown. Testosterone has been demonstrated to depress ventilatory drive and increase sleep apnea in adult men. We tested the hypothesis that the gonadal steroid testosterone depresses infant ventilatory drive during sleep. Three newborn male infant primates were gonadectomized after birth. Ventilation was observed and quantified for each animal during completely natural unencumbered sleep by plethysmography for an average of 16 wk. Ventilatory patterns were recorded, and ventilatory drive was challenged with hypercapnia and hypoxia during quiet sleep on the night before and the night after testosterone administration. Hypercapnic ventilatory drive during sleep was significantly depressed by an average of 33.6% on the night after compared with the night before testosterone administration. Depression of the response to hypercapnia after testosterone was not accompanied by any change in resting minute ventilation measured during quiet sleep. Hypoxic ventilatory drive, incidence of apneic events, and length of apnea were not different after testosterone. The effects of injecting a placebo on ventilatory patterns and drive were tested by giving the placebo to all animals on several test weeks. Placebo injections produced no significant change in any measured parameters. These results support the hypothesis that testosterone depresses hypercapnic ventilatory drive during sleep in the infant primate." (J. Appl. Physiol. 1994; 76: 1786)

Does increased testosterone cause increased SIDS in humans?

Well, I think the case is supported for male vs. female SIDS victims. SIDS is higher in "preterm" infants: "Although only 9% of infants are born at less than 36 weeks' gestation, 20% of SIDS victims are former premature infants." [Clin Pediatr (Phila) 1995; 34: 410.] Testosterone is increased in preterm infants during the time when SIDS occurs at increased frequency.

"When preterm male and full-term male infants were compared, no difference was seen in the T [testosterone] peak in the first day of life. However, the 1-3, and 60-90 days concentrations of T were 2-fold higher in the preterm group. ...The immediate postnatal peak in plasma T levels persisted longer in the preterm than in the full-term male infants." (Acta Paediatr. Scand. 1982; 71: 425)

SIDS is increased in women who smoke. I have developed a theory that suggests that the rise in testosterone of puberty triggers smoking. (You can use my name and "smoking" to find this with Dejanews.) Since I think testosterone is rising in this society, I explain the increase in smoking in young people as a result of the increase in testosterone. Women who smoke, therefore, may be women of higher testosterone. While the following investigator gives credit to "sociological factors" in addition to testosterone in adolescent smoking in (Addict. Behav. 1992; 17: 459), his first publication concerning adolescent smoking and testosterone is more to the point for this treatise. "Social and psychological variables are used to explain why young people become cigarette smokers, whereas biological factors have been virtually ignored as possible determinants of that behavior. In this study, salivary testosterone was positively associated with cigarette smoking among 201 subjects 12-14 years of age. This finding suggests that testosterone should be included in future considerations of adolescent cigarette smoking." (J. Behav. Med. 1989; 12: 425.) I think the connection of smoking and SIDS is that women who smoke are higher in testosterone. They produce children who are higher in testosterone, which increases SIDS.

If testosterone is redirecting DHEA use, where is it going?

I think the DHEA is being redirected to brain structures that are testosterone target tissues. Consider that "The Nv [volume of hypoglossal nucleus - cells per mm3] of synapses did not differ significantly between SIDS cases and controls, although the total number of synapses was greater (61%) in SIDS." (J. Neuropathol. Exp. Neurol. 1995; 54: 627.) In some songbirds, testosterone has an effect on the hypoglossal nucleus. "We find anatomical correlates for each of these attributes in the nXIIts [hypoglossal nucleus]. This nucleus is 83% larger in males than in females." (J. Comp. Neurol. 1991; 307: 65.) Earlier, this reference says "Its [the hypoglossal nucleus] neurons concentrate androgens." This means that the hypoglossal nucleus is a "testosterone target tissue."

An increase in synaptic growth in lower brain structures may cause two phenomena. Firstly, it may make these structures more "mature" in that they grow faster. This could result in shorter gestation, i.e., preterm delivery. The neonate participates in the time of delivery. These neonates would be smaller, because less time would be available for growth. "Mothers of SIDS infants give birth to smaller babies in general. SIDS infants weighed, on average 85 g less at birth than their siblings and 164 g less compared with babies in nonaffected sibships. When birth weights were standardized for gestational age, most of the weight difference between SIDS infants and siblings was due to a shorter gestational age of SIDS infants, while the difference between surviving siblings of SIDS infants and births from nonaffected sibships remained. All births in sibships with a SIDS infant were intrauterine growth retarded. This may reflect factors that contribute to SIDS risk (such as maternal smoking)." (Am. J. Epidemiol. 1995; 142: 84.)

Structures in the brainstem that have excess synapses may require more DHEA in order to maintain sufficient activity of these structures. When melatonin reduces DHEA at night, there may be insufficient DHEA to properly activate these structures. The hypoglossal nucleus is in the brainstem.

SIDS should be more prevalent in women who are higher in testosterone.

Part III (September 12, 1996)

African women produce more testosterone than white women. This is very difficult to find in current journals. I know of one group of endocrinologists who measured testosterone in African American women and European American women and found much higher levels of testosterone in the African Americans, but did, or would not, publish. The following is the best I could find.

Dada ,O.A., et al., "17 Beta-estradiol, Protesterone and Testosterone in the Normal Menstrual Cycle of Nigerians," (Int J Gynaecol Obstet 1984; 22: 151)

"Circulating blood levels of estradiol, progesterone and testosterone are reported in 17 normally menstruating Nigerian women. The pattern of secretion and the range of levels of estradiol and progesterone are similar to those reported in other ethnic groups. Testosterone levels were, in general, higher than corresponding values in Caucasian or Asian women, but were of the same order of magnitude as previously reported in Zambian African women."

This corresponds with the findings that testosterone is higher in black men, medium in Asian men, and lowest in white men. See Table II, page 888 in Lancet 1992; 339: 887-889. In a group of college men in the U.S., black men produce significantly more testosterone than white men (Journal of the National Cancer Institute 1986; 76: 45).

If I am correct that SIDS, and premature delivery, occur more in women with high testosterone, we should find this in black women. The following three quotations support this. (I could not find an author for the first, but it was found in PubMed.)

. . . "Variations in the Incidence of Sudden Infant Death Syndrome (SIDS), United States, 1980-1988," (Stat Bull Metrop Insur Co 1993; 74: 10)

"Sudden infant death syndrome (SIDS) continues to be the second leading cause of infant mortality in the United States. In 1989, 5,634 SIDS cases were recorded, resulting in a rate of 139.4 per 100,000 live births. As with total infant mortality rates, SIDS rates have been slowly declining over the years but remain disproportionately higher among black infants than white. Unlike the total infant death rates, however, the gap between the races is narrowing--SIDS death rates among black infants decreased 19 percent between 1980 and 1988, in contrast to the 4 percent drop among white infants during the same period. The black-to-white ratio dropped from 2.18:1 in 1980 to 1.83:1 in 1988. Geographic differences in SIDS rates persist, with rates being the highest in the West and Midwest regions and lowest in the Northeast. While many SIDS risk factors have been and continue to be identified, the diagnosis remains one of exclusion. The etiology continues to elude definition, and increasingly more diagnoses are being made based on autopsy reports and death scene investigations. As these diagnostic practices become more standardized, SIDS prevalence is expected to change. Whether new insights will ultimately lead to eradication, remains unknown at this time."

Denmead, D.T., et al., "Placental Pathology is Not Predictive for Sudden Infant Death Syndrome (SIDS,)" (Am J Perinatol 1987; 4: 308)

"...There were more premature and black infants found in the SIDS group compared with the general birth population, and also lower five-minute Apgar scores (P less than 0.02) compared to matched controls. Analysis of the second control group match, including infant Apgar scores, maternal hematocrit, maternal age, and complications of pregnancy and delivery, did not influence any of our conclusions. The data suggests that matching for prematurity may be important in identifying the strength of additional risk factors for SIDS, since the risk factors for SIDS and premature delivery are similar.

Shiono, P.H. and M.A. Klebanoff, "Ethnic Differences in Preterm and Very Preterm Delivery," (Am J Public Health 1986; 76: 1317)

"Ethnic differences in preterm (less than 37 weeks) and very preterm (less than 33 weeks) delivery were evaluated in a prospective cohort of 28,330 women. Blacks had the highest rate of preterm and very preterm delivery, followed by Mexican-Americans, Asians, and Whites. Adjustment for maternal age, education, marital status, employment, parity, number of previous spontaneous or induced abortions, smoking and drinking during pregnancy, infant sex, and gestational age at initiation of prenatal care resulted in the following odds ratios for preterm delivery: 1.79 (1.55-2.08) for Blacks, 1.40 (1.19-1.63) for Mexican-Americans, 1.40 (1.16-1.69) for Asians, and 1.00 for Whites. The corresponding odds ratios for very preterm delivery were 2.35 (1.72-3.22) for Blacks, 1.31 (0.88-1.94) for Mexican-Americans, 1.10 (0.67-1.83) for Asians, and 1.00 for Whites. Exclusion of cases of premature rupture of membranes, placenta previa, and abruptio placenta did not explain the large ethnic differences. Although Whites and Mexican-Americans had similar birthweight distributions, Mexican-Americans had an increased risk for preterm delivery."

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