(My main page is www.anthropogeny.com.  Everything here that is mine: Copyright 2009, James Michael Howard, Fayetteville, Arkansas, U.S.A.)

Common Mechanism in Consciousness, Dreaming, Positive Symptoms of Schizophrenia, Hallucinations, Near- Death Experiences, etc

It is my hypothesis that sleep and consciousness are controlled by levels of melatonin and DHEA (http://www.anthropogeny.com/Sleep%20and%20SIDS.htm ).  The effects of this mechanism control our circadian rhythms and our relationship with the environment and the self.  More specifically, these control the activity of the forebrain.  They turn it on and off.  When we sleep, activity of the forebrain declines and the ratio of lower brain activity increases.  The input of the midbrain increases and is interpreted by a forebrain which is not fully active.  This is dreaming, a time when DHEA availability is reduced, overall.  Activity of both systems is reduced.  As forebrain activity is reduced, momentarily, the availability of DHEA is increased for the midbrain; this is the “dream.”  The ratio of use of DHEA by these competing systems determines their activity.  As DHEA begins to increase at morning, the forebrain, again, becomes active.

When we are conscious, the forebrain and the middle / hind brain are all activated.  While this is occurring, the forebrain controls interpretation of the input and output systems.  While active, the forebrain sequesters DHEA at the expense of the midbrain.  The activity of the midbrain does not penetrate our conscious activity without examination and analysis.  When active, the forebrain brings relevant association areas into decisions and interpretation.

It is also my hypothesis that schizophrenia represents a situation whereby activity of the forebrain is diminished (http://www.anthropogeny.com/Schizophrenia.htm ).  DHEA levels have been found to be low and high in schizophrenia.  Low levels probably are connected with “negative” symptoms of schizophrenia, thus, producing reduced brain activity concerned with self-awareness.  High levels of DHEA may indicate further use of DHEA by the forebrain, therefore, increasing availability of DHEA for the midbrain.  This allows midbrain activities to penetrate the “consciousness” during inattention of the forebrain.  I suggest this is how “positive” symptoms of schizophrenia are produced, that is, hallucinations.  That is, hallucinations are the product of an over stimulated midbrain without proper interpretation.

It is also my hypothesis that death occurs when DHEA declines to very low levels.  Specifically, I suggest death occurs when there is insufficient DHEA to support activity in the brainstem.  Prior to death, the declines of DHEA reach a point when forebrain activity declines, just as it does in sleep and in schizophrenia.  At some point in this decline, the activities of the midbrain, momentarily, become stronger as the ratio of forebrain to midbrain activities change.   Association areas come into action in relevant and irrelevant connections to the dying person producing hallucinations, just as in schizophrenia and dreaming. 

Differences in the relative activity of the forebrain and the midbrain produce differences that are interpreted as consciousness, dreaming, or hallucinating.  I suggest the same mechanism is responsible for all of these.

 


Why Phthalates may be Connected with Cancer and other Negative Outcomes of Phthalate Ingestion

It is my hypothesis that low DHEA may trigger breast cancer, as well as other cancers (Annals of Internal Medicine 2005; 142: 471-472).  It is known that phthalates inhibit sulfotransferase, therefore reducing conversion of the precursor, DHEAS, to the active molecule, DHEA (Environ Health Perspect. 2007 Dec;115 Suppl 1:51-4).  Reducing conversion of DHEAS to DHEA produces low DHEA.  Since I think all tissues rely on sufficient levels of DHEA for optimal function, I suggest that the negative findings of phthalate ingestion may result from this reduction converstion of DHEAS to DHEA.


New Support for my Explanation of Homosexuality

It is my hypothesis that low maternal DHEA produces homosexuality (http://www.anthropogeny.com/Etiology%20of%20Male%20Homosexuality%20and%20Current%20Rise%20of%20Male%20Homo.htm  ).  An article was recently published that says: "These data, although based on a small sample, suggest that prenatal exposure to antiandrogenic phthalates may be associated with less male-typical play behaviour in boys." (International Journal of Andrology 2009: "Prenatal phthalate exposure and reduced masculine play in boys," Swan, et al.).  The usual explanation is that phthalates reduce testosterone.

As I just said, I think low maternal DHEA is the cause.  It is known that phthalates inhibit sulfotransferase, therefore reducing conversion of the precursor, DHEAS, to the active molecule, DHEA (Environ Health Perspect. 2007 Dec;115 Suppl 1:51-4).  Reducing conversion of DHEAS to DHEA produces low DHEA.  I suggest the foregoing supports my explanation of how homosexuality forms.


Risks of daily aspirin may outweigh the benefits, November 4, 2009

Drug Ther Bull. 2009 Nov;47(11):122-5.
Aspirin for primary prevention of cardiovascular disease? 


Cardiovascular disease (CVD) is a leading cause of mortality.1 For example, in 2000, it accounted directly for around 2 million deaths in the European Union.2 Worldwide, many people take aspirin daily in the belief that doing so helps to prevent CVD. This approach is established for the secondary prevention of recurrent vascular events.1,3,4,5 However, there has been some uncertainty about the place of aspirin for the primary prevention of cardiovascular events.6 In particular, there have been doubts about whether any benefits of aspirin in people with no history of CVD outweigh the risks (e.g. the fact that long-term low-dose aspirin therapy almost doubles the likelihood of gastrointestinal haemorrhage).7,8 Here we consider the place of low-dose aspirin in primary prevention of CVD.

I suggest the reason aspirin is useful in some pathologies is that aspirin reduces testosterone.  I think it is testosterone that is the culprit, that is, testosterone exacerbates pathologies.  If interested: http://www.anthropogeny.com/Aspirin.htm .  In the case above, gastrointestinal bleeding is considered to be a problem if this causes problems worse than the protective effect of aspirin.  I suggest this becomes a problem when the aspirin causes testosterone to become too low.  While I could not find direct support, I did find this: " It is concluded that endogenous testosterone plays an aggressive role in the pathogenesis of ethanol-induced gastric erosions in rats." (Acta Physiol Hung.1992;80(1-4):289-92).



November 5, 2009, the American Institute for Cancer Research that excess body fat is causing cancer.  I say that excessive testosterone is causing increased body fat and cancers and that this increase is due to an increase in the percentage of individuals of higher testosterone with time within the population.  It is my hypothesis that the "secular trend," the increase in size and earlier puberty occurring in children, is caused by an increase in the percentage of individuals of higher testosterone with time within the population.  I think this is why cancer and obesity, diabetes, etc. are increasing within many populations. 

NEUROLOGY 2009;73:1359-1366 

Diabetes is associated with a slower rate of cognitive decline in Alzheimer disease

This is my explanation:

"It is known that sex hormone binding globulin levels are low in type 2
diabetes in both sexes (N Engl J Med. 2009 Sep 17;361(12):1152-63). It is
also known that testosterone is an 'endogenous neuroprotective factor' in
Alzheimer's disease (Front Neuroendocrinol. 2009 Jul;30(2):239-5).

The findings of Sanz, et al., may be explained by increased available, free
testosterone."

Neurology rejected this.

Possible Reason for Poorer Health per Health Care Dollar in the United States.

It is my hypothesis that the "secular trend," the increase in size and earlier puberty in children is caused by an increase in the percentage of individuals of higher testosterone within the population over time.  The driving force is an increase in women of higher testosterone within the population over time.  This exposes their fetuses to higher levels of testosterone in utero.  I suggest this increase in testosterone is the cause of the current increases in diabetes, obesity, infections, low birth weight and preterm babies, breast cancer and other cancers, etc within the population over time.  Different races also produce different levels of testosterone.  It is known that black women produce more testosterone than white women.  I also think lower socioeconomic levels are characterized by higher levels of testosterone.  For example, blacks and the poor exhibit disproportionately high levels of HIV as well as the other problems mentioned above.  Many of these problems, especially the differences between races, are used to measure the competence of medical care in different countries.

I think the overall medical care and education in this country are absolutely first rate.  However, as the increase in testosterone continues, it is overwhelming the ability of health care to contend with it.  Without an understanding of what may be occurring, our health system must rely on explanations from the past, which worked very well in their time.  Many of the countries which exhibit fewer problems, based on the criteria used to compare countries, have already gone through the secular trend and women of very high testosterone have reduced fertility.  It is known that high testosterone reduces fertility.  Those countries are not producing as many offspring affected by high maternal testosterone as they did in the past.  Our problem is that we are a wealthy, young country that is being directly affected to a high degree by the effects of the secular trend.

While I think a strong case may be made for more available medical care for the poor out of simple, basic human compassion, I think the high levels of morbidity in the U.S.A. are caused by high levels of testosterone and the problem will continue, even if increased health care is provided for our under-insured, uninsured, and indigent populations.  The secular trend is causing these problems, not inadequate health care.  (An additional thought:  The same mechanism may be the reason that American education is faltering, that is, the increase in testosterone is reducing the ability to learn and the American educational system cannot keep up with the decline.  It is not the teachers' fault!)


Response to: Neurology 2009; 72: 922-927 "Weather and air pollution as triggers of severe headaches"

"Conclusions: Higher ambient temperature and, to a lesser degree, lower barometric pressure led to a transient increase in risk of headache requiring emergency department evaluation. We did not find clear association of air pollutants with risk, but cannot exclude effects of air pollution of the magnitude previously observed for stroke and other cardiovascular events."

My response to the journal: "Melatonin is low in individuals who exhibit migraines.  It is my hypothesis that low melatonin triggers a high response of DHEA periodically in these individuals and it is this increase in DHEA that causes the migraines.

Increased ambient temperature reduces melatonin.  I suggest the findings of Mukamal, et al., may be explained by reduced melatonin during times of increased ambient temperature."

I do not know of any research regarding the effects of barometric pressure on melatonin or DHEA.  You may read my explanation of the connection of melatonin and DHEA with migraine, just below.


DHEA, Migraine and Epilepsy

Copyright 1997 by James Michael Howard.

 

My theory suggests all tissues of the body depend on the "melatonin-DHEA cycle." I think this cycle is necessary for growth, development, and function during childhood and adolescence and maintenance and function of the adult. I look for disturbances of this cycle to help explain pathology. Migraine headaches and epilepsy may result from malfunctions in melatonin (MLT) and DHEA. Prior to my explanation, increased MLT in epilepsy and reduced MLT in migraines has been discovered. However, according to a medical literature search (medline), no one has addressed any connection of DHEA with migraines or epilepsy.

The main connection of low MLT in migraines is found in the female cycle. MLT "increases significantly from the follicular to the luteal phase" in normal women’s cycles (Cephalalgia 1995; 15: 136); another study found that MLT is significantly reduced throughout the cycle in women with migraines. This second study also found that MLT is decreased during headaches (Caphalalgia 1994; 14: 205). I have read anecdotal remarks on the internet that some women have increased migraines during the second part of their cycles (luteal phase). MLT begins a steep decrease just prior to puberty, and declines rapidly thereafter. Since, "migraine occurs most commonly in men and women aged 25-55 years" (Neurology 1994; 34 Suppl. 2: 6), I suggest that this is a time when MLT reaches critically low levels in susceptible people. Low MLT is somehow connected to migraines, but, I suggest, the levels of DHEA have to be examined to fully explain it.

I suggest migraines result from low MLT and increased DHEA. Women produce more DHEA from birth than men. This extra DHEA should have most effect on migraines prior to the onset of interfering sex hormones, before puberty. It has been found that "when the onset [of migraines] is below the age of puberty there is a striking predominance of women over men in a ratio of 3:1," (Headache 1994; 34: S8). It is part of my theory that the hormone, testosterone, causes DHEA to be used for "testosterone target tissues." This use of DHEA by these tissues should reduce the availability of DHEA, i.e., increased testosterone should decrease migraines. This can be seen in the fact that, following puberty, women still have more migraines and that whites have more migraines than blacks. Blacks produce more testosterone than whites. "In women, migraine prevalence was significantly higher in Caucasians (20.4%) than in African (16.2%)... A similar pattern was observed among men (8.6%, 7.2%, ...)." (Neurology 1996; 47: 52). Interestingly, my theory suggests that people of higher testosterone congregate together, as in cities, and higher DHEA/lower testosterone types tend to live apart from cities.

The prevalence of migraines also follows this pattern. "Females, whites, and individuals residing in rural counties were more likely to suffer migraine headache than their respective comparison groups." (Clinical Therapeutics 1994; 16: 855).

I have read that headaches occur when blood vessels in the brain constrict. Since I have suggested elsewhere that I think DHEA stimulates constriction of blood vessels and increases blood pressure, I suggest increased DHEA causes the constriction of blood vessels in migraine headaches. Constricting blood vessels and reduced blood flow is characteristic in migraines. "The transient neuronal excitatory wave is followed by a longer lasting ‘depressive’ wave, which involves a substantial reduction in cortical blood flow (with an active constriction of resistance vessels) and ionic changes and transmitter release into the extracellular fluid compartment." (Cephalalgia 1992; 12: 75).

I have produced a theory of sleep that explains the connection of MLT and DHEA. At its most basic, I suggest melatonin binds to neurons and shut them down. The connection with DHEA is that MLT shuts down the nerves that release the hormone, prolactin (PRL). It is also known that PRL specifically and powerfully stimulates DHEA. When MLT shuts down PRL, DHEA production is reduced and its stimulating effects on the brain are reduced. This is sleep. Now, to keep this from killing us, PRL is released in rebound to the negative effects of MLT. This cycles slowly until a large release of PRL occurs in the early morning. This large release of PRL then starts a large morning release of DHEA, which awakens us. In the quotation just above, I suggest the "excitatory wave" represents the effects of MLT, i.e., the shutdown of MLT causes nerves to rebound in response. I suggest the "depressive wave" represents the restabilization caused by a subsequent response of secreted DHEA. The increased DHEA causes the blood vessel constriction that causes the migraine headache.

With the foregoing in mind, it should be easier to explain epilepsy with the MLT - DHEA cycle. MLT is high in epileptic people. "Melatonin production in untreated patients with active epilepsy is increased and had a circadian pattern with a phase difference as compared with that of normal subjects." (Epilepsia 1995; 36: 75). In the paragraph, just above, I demonstrated how MLT can induce the production of DHEA. During the day, my sleep mechanism suggests that the larger production of DHEA is involved in inhibiting synthesis of MLT from the pineal gland (where MLT is made). This means that once DHEA is "used up" during the day, there is not enough DHEA to keep the pineal from making MLT. When MLT production occurs, the shut down of PRL occurs and DHEA is reduced to even lower levels. This is how the sleep - wake cycle occurs.

Sleep deprivation keeps MLT from being released. This has been determined. "It was found that the melatonin levels were increased after sleep deprivation..." (Sleep 1988; 11: 362). A much later study found that MLT was not increased by sleep deprivation, but that "Prolactin was higher on the post-sleep deprivation and control nights but did not rise on the deprivation night." (Journal of Pineal Research 1996; 20: 7). Sleep deprivation increases the build up of the thing that stimulates DHEA, i.e., prolactin. Since increased sleep is a consequence of sleep deprivation, I suggest MLT increases. Since it is the PRL that stimulates DHEA production, both of these studies say, essentially, the same.

There is another way of seeing this. I have suggested that DHEA stimulates the nerves that inhibit synthesis of MLT. I suggest that electroconvulsive shock exerts its effects by stimulating DHEA. In the following quotation, I suggest the reduced production of MLT is due to increased DHEA, inhibiting the pineal gland. "In ECS [chronic electroconvulsive shock]-treated rats, both pineal and serum melatonin levels after isoproterenol administration were significantly lower than those in sham-treated animals and in rats receiving subconvulsive shock." (Psychiatry Research 1994: 53: 185).

I suggest that the opposite mechanism explains epilepsy. I suggest the increased melatonin found in untreated epileptics builds up and is released so that nerves are shut down. Individuals susceptible to epilepsy must have entire sections of the brain shut down so much that they "rebound" and call up a large response of DHEA. It is this rebound response that is the large area of stimulated nerves that cause the seizures. Once the brain has stimulated sufficient DHEA, then the seizure stops.

Migraine, Exercise, and DHEA


Sent January 27, 1998, to MGH Neurology Web-Forum, Headace, as a response to "Migraine and Exercise"

My explanation of migraines suggests it is triggered by too little melatonin and too high DHEA. I suggest that melatonin and DHEA act in a cycle, the purpose of which is to stimulate DHEA. It is known that exercise stimulates DHEA. Now, when you exercise, especially when you exercise vigorously, the result is a triggering of this cycle. However, this statement, from the following quotation will explain what may be happening in you, and the others who have responded: 'These results suggest that vigorous exercise training may attenuate rather than augment the secretion of pineal melatonin.' This means that vigorous exercise may actually reduce the melatonin response. You see, according to my explanation, you may be triggering this cycle with your exercise, and you may be altering the ratio of melatonin to DHEA towards DHEA. Now, this may only affect certain people who are prone to migraines, but I suggest this is the cause of your exercise-associated-migraines.

James Howard

J. Pineal. Res. 1989; 7(2): 185-194 "Melatonin response to exercise training in women"

"Previous human studies have indicated that daytime melatonin levels increase when the organism is subjected to the stress of fasting and exercise. Melatonin, epinephrine, and norepinephrine levels were measured during a mock run and in the course of treadmill exercise performed before (T-1), during (T-2), and following (T-3) a progressive conditioning (running) program. Hormonal responses to the training program were determined by comparing values at T-1 and T-3. Plasma melatonin, epinephrine, and norepinephrine levels rose significantly (P less than .01) from baseline values for each exercise intensity during all three treadmill runs. While a dose-response trend was observed in each of the norepinephrine and epinephrine trials, there appeared to be a progressive diminution of this relationship in melatonin between intensities. Further, as training progressed, the peak melatonin concentration was decreased by 52% from T-1 to T-3, while peak epinephrine and norepinephrine values diminished only 19% and 8%, respectively. These results suggest that vigorous exercise training may attenuate rather than augment the secretion of pineal melatonin. Development of a human model of pineal responsiveness to exercise may contribute to the elucidation of exercise-associated reproductive disorders."


Increase in Arch of Foot may indicate Effects of Testosterone in Human Evolution

James Michael Howard

The increase in the "arch index" from the early hominid footprints to the
later ones may indicate an increase in testosterone. I could find one
reference, not much but a little, that "Males had a significantly higher
arch index than females.." in J Am Podiatr Med Assoc. 2005
May-Jun;95(3):273-6. An increase in arch index just may indicate an
increase in testosterone when one compares the arch index of chimpanzees and
humans. Human males and females produce more testosterone than chimpanzee
males and females. James Michael Howard "Androgens in Human Evolution,"
Rivista di Biologia / Biology Forum 2001; 94: 345-362


Tibolone, Testosterone and Recurrent Breast Cancer (The Lancet Oncology 2009; 10: 103-104)

It is my hypothesis that increased testosterone may cause breast cancer, as
well as other cancers, (International Journal of Cancer 2005; 115: 497). It
has been demonstrated that tibolone increases free testosterone in women,
over and above the testosterone-like structure of tibolone ( Maturitas. 2005
Apr 11;50(4):321-30).
I suggest this report supports my hypothesis of the link between
testosterone and breast cancer in women.

The DHEA and Manganese Connection with Parkinson's disease

It is my hypothesis that low DHEA and testosterone trigger Parkinson's
disease. If interested:

http://www.anthropogeny.com/Parkinson's%20DHEA%20Testosterone.htm .

A study of the effect of occupational exposure to manganese reported that
manganese reduces testosterone and prolactin (Neurotoxicology. 2007
Mar;28(2):263-9). Prolactin is a direct and specific stimulator of DHEA and
a case may be made that low prolactin may indicate that DHEA is also reduced
by manganese. A search of PubMed only produced the following regarding
manganese and DHEA: "Study of the basic elimination of
dehydroepiandrosterone in the manganese-poisoned patient," in Maroc Med.
1961 Apr;40:389-91, a journal not available to me.

Propranolol and Fear Memory

In 1985, I first suggested the "fight or flight" mechanism is controlled by
the ratio of DHEA to cortisol. This is based upon my hypothesis that
cortisol evolved to counteract the actions of DHEA. I suggest DHEA promotes
positive action while cortisol promotes the opposite. As we know, cortisol
is produced along with "fear response."

Propranolol has been proven to increase the DHEA to cortisol ratio (J
Endocrinol Invest. 1998 Mar;21(3):148-53). I suggest you, et al., have
simply increased the DHEA to cortisol ratio and reduced the fear response
and the return of fear.

New Support of theory of breast cancer... Testosterone and Breast Cancer

In 1994, I first suggested that testosterone is involved in triggering
breast cancer. I think the "secular trend," the increase in size and earlier
puberty in children that is ongoing is caused by an increase in testosterone
within the population. This is driven by increases in women of higher
testosterone. This is my explanation for why breast cancer is increasing. My
idea was published in a major journal in 2005: Annals of Internal Medicine
2005; 142: 471-472. This article contains a reference to my 1994 article.

Besides other support during the years, a new article has added additional
support: Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):169-76.


Effects of acute alcohol consumption in older and younger adults: perceived impairment versus psychomotor performance.
in J Stud Alcohol Drugs 2009; 70: 242-52

"Conclusions: These results reinforce the common knowledge that self-reported measures may not provide an accurate reflection of performance outcomes and, importantly, that older adults may be impaired even under a moderate dose of alcohol, although they may not be aware (i.e., report) of this impairment. (J. Stud. Alcohol Drugs 70: 242-252, 2009)."

My response:

J. Stud. Alcohol Drugs 70: 242-252, 2009

It is my hypothesis that all drugs of addiction increase the production of DHEA. This may involve an increase in DHEAS which then is converted to DHEA. Since DHEAS is the precursor of DHEA, I suggest it does not stimulate the way DHEA does. These drugs would first reduce brain activity by increasing DHEAS which would then increase stimulation because of conversion to DHEA. The abuser would then seek to reduce this over activity. This ultimately reduces the availability of DHEA.

Alcohol consumption has been demonstrated to increase DHEAS. I suggest it is the increase in DHEAS that produces the effects of alcohol on the brain. An increase in DHEAS reduces brain function. DHEA, the active molecule, naturally begins to decrease around age twenty, reaching very low levels in old age.

I suggest your, et al., findings may be explained by the reduction in DHEA of aging. That is, older individuals will experience more effects of alcohol consumption since their DHEA is already low and alcohol increase their ratio of DHEAS to DHEA, at the expense of functional DHEA.

Why HIV Progresses Faster in Older People

In 1985, I copyrighted my hypothesis that low DHEA increases vulnerability to the HIV (not called that at the time). The first reports of low DHEA in AIDS appeared in 1989. It soon also occurred to me that the symptoms of AIDS result from the loss of DHEA that occurs after HIV infection.

DHEA naturally begins to decline around age twenty, reaching very low levels in old age. I suggest the reason for the incidence of HIV infection and more rapid progression of AIDS in the elderly is due to their low DHEA. This connection of AIDS with onset of AIDS with age is supported: AIDS 1994 Jun;8(6):797-802.