Praesent rutrum sapien ac felis. Phasellus elementum dolor quis turpis. Vestibulum nec mi vitae pede tincidunt nonummy. Vestibulum facilisis mollis neque. Sed orci. Cum sociis natoque penatibus et magnis dis parturient montes, nascetur ridiculus mus. Sed euismod magna a nibh.raesent rutrum sapien ac felis. Phasellus elementum dolor quis turpis. Vestibulum nec mi vitae pede tincidunt nonummy. Vestibulum facilisis mollis neque. Sed orci. Cum sociis natoque penatibus et magnis dis parturient montes, nascetur ridiculus mus. Sed euismod magna a nibh.

Cortisol is usually referred to as the “stress hormone” as it is involved in response to stress and anxiety Its primary function is to increase blood sugar and stores of sugar in the liver as glycogen, and also suppresses the immune system. Various synthetic forms of cortisol are used to treat a variety of different illnesses. The most well-known of these is a natural metabolic intermediary of cortisol called hydrocortisone.

Effects

In normal release, cortisol has widespread actions which help restore homeostasis after stress. bCortisol raises blood sugar by converting protein into sugar and counteracting insulin. Collagen. Cortisol causing loss of colagen thus accelerating aging of the skin and joints. Gastric secretion. Cortisol stimulates gastric acid secretion which can cause stomach ulcers and heartburns.

Cortisol also acts as an anti-diuretic hormone and causes water retention.

  • Immune system
    Cortisol weakens the activity of the immune system
  • Bone metabolism
    It lowers bone formation thus favoring development of osteoporosis in the long term.
  • Memory
    It cooperates with epinephrine (adrenaline) to create memories of short-term emotional events; this is the proposed mechanism for storage of flash bulb memories, and may originate as a means to remember what to avoid in the future. However, long-term exposure to cortisol results in impaired learning.

Additional Effects

  • It increases blood pressure. In the absence of cortisol, dangerous drop in blood pressure occurs. .
  • It allows for the kidneys to produce diluted urine.
  • It shuts down the reproductive system, resulting in an increase for the chance of miscarriage and, in some cases, temporary infertility. Fertility returns after cortisol levels are reduced back to normal levels
  • It has anti-inflammatory effects
  • It stimulates hepatic detoxification
  • There are potential links between cortisol, appetite and obesity

Factor affecting cortisol levels

Factors generally reducing cortisol levels

  • Magnesium supplementation decreases serum cortisol levels after aerobic exercise but not in resistance training.
  • Omega 3 fatty acids, in a dose dependent manner (but not significantly) can lower cortisol release influenced by mental stress Omega 6 fatty acids, on the other hand, acts inversely
  • Music therapy can reduce cortisol levels in certain situations.
  • Massage therapy can reduce cortisol.
  • Laughing and the experience of humour can lower cortisol levels.
  • One study by a Japanese cosmetics company has asserted that makeup reduces cortisol levels in a mental stress situation.
  • Soy derived Phosphatidylserine interacts with cortisol but the right dosage is still unclear.
  • Vitamin C may slightly blunt cortisol release in response to a mental stressor.
  • Black tea may speed up recovery from a high cortisol condition.
  • Maca Root Powder is also known to reduce cortisol levels and restore the adrenal glands to health (needs reference)

Factors generally increasing cortisol levels

  • Caffeine may increase cortisol levels.
  • Sleep deprivation increases cortisol levels.
  • Intense or prolonged physical exercise stimulate cortisol release in order to increase gluconeogenesis and maintain blood glucose. Proper nutrition and high-level conditioning can help stabilize cortisol release.
  • Low Estrogen and melatonin supplementation increases cortisol levels in postmenopausal women.
  • Burnout is associated with higher cortisol levels.
  • Severe trauma or stress events can elevate cortisol levels in the blood for prolonged periods.
  • Subcutaneous fat regenerates cortisol from cortisone.
  • Anorexia nervosa increases cortisol levels.
  • The serotonin receptor gene 5HTR2C is associated with increased cortisol production in men.
  • Some formulations of combined oral contraceptive pills increase cortisol levels in young women who perform whole-body resistance exercise training.
  • Commuting increases cortisol levels, related to the length of the trip, the amount of effort involved and the predictability of the trip

Estradiol (E2 or 17β-estradiol) (also oestradiol) is a sex hormone. Estradiol is the predominant sex hormone present in females; however, it is present in males, although at lower levels, as well. It represents the major estrogen in humans. Estradiol has not only a critical impact on reproductive and sexual functioning, but also affects other organs including the bones.

Production

During the reproductive years, most estradiol in women is produced by the granulosa cells of the ovaries. Smaller amounts of estradiol are also produced by the adrenal cortex, and (in men), by the testes. Estradiol is produced not only in the gonads: In both sexes, precursor hormones, to be specific testosterone, are converted by aromatization to estradiol. In particular, fat cells are active to convert precursors to estradiol, and will continue to do so even after menopause. Estradiol is also produced in the brain and in arterial walls.

Mechanism of action

Estradiol binds well to both estrogen receptors, ERα, and ERβ, in contrast to certain other estrogens, notably medications that preferentially act on one of these receptors. These medications are called selective estrogen receptor modulators, or SERMs.

Estradiol is the most potent naturally-occurring estrogen.
Recently there has been speculation about the membrane estrogen receptor ERX.
.
In the normal menstrual cycle, estradiol levels measure typically

Effects

Female reproduction
In the female, estradiol acts as a growth hormone for tissue of the reproductive organs, supporting the lining of the vagina, the cervical glands, the endometrium, and the lining of the fallopian tubes. It enhances growth of the myometrium. Estradiol appears necessary to maintain oocytes in the ovary. During the menstrual cycle, estradiol that is produced by the growing follicle triggers, via a positive feedback system, the hypothalamic-pituitary events that lead to the luteinizing hormone surge, inducing ovulation. In the luteal phase estradiol, in conjunction with progesterone, prepares the endometrium for implantation. During pregnancy, estradiol increases due to placental production. In baboons, blocking of estrogen production leads to pregnancy loss, suggesting that estradiol has a role in the maintenance of pregnancy. Research is investigating the role of estrogens in the process of initiation of labor.

Sexual development

The development of secondary sex characteristics in women is driven by estrogens, to be specific, estradiol. These changes are initiated at the time of puberty, most enhanced during the reproductive years, and become less pronounced with declining estradiol support after the menopause. Thus, estradiol enhances breast development, and is responsible for changes in the body shape, affecting bones, joints, fat deposition. Fat structure and skin composition are modified by estradiol.

Male reproduction

The effect of estradiol (and estrogens) upon male reproduction is complex. Estradiol is produced in the Sertoli cells of the testes. There is evidence that estradiol is to prevent apoptosis of male sperm cells. Several studies have noted that sperm counts have been declining in many parts of the world and it has been

postulated that this may be related to estrogen exposure in the environment. Suppression of estradiol production in a
subpopulation of subfertile men may improve the semen analysis.

Males with sex chromosome genetic conditions such as Klinefelters Syndrome will have a higher level of estradiol.

Bone

There is ample evidence that estradiol has a profound effect on bone. Individuals without estradiol (or other estrogens) will become tall and eunuchoid as epiphysieal closure is delayed or may not take place. Bone structure is affected resulting in early osteopenia and osteoporosis. Also, women past menopause experience an accelerated loss of bone mass due to a relative estrogen deficiency.

Liver

Estradiol has complex effects on the liver. It can lead to cholestasis. It affects the production of multiple proteins including lipoproteins, binding proteins, and proteins responsible for blood clotting.

Brain

Estrogen is considered to play a significant role in women’s mental health, with links suggested between the hormone, mood and well-being. Sudden drops or fluctuations in, or long periods of sustained low levels of estrogen may be correlated with significant mood-lowering. Clinical recovery from depression postpartum, perimenopause, and postmenopause was shown to be effective after levels of estrogen were stabilized and/or restored.[7][8]

Blood vessels

Estrogen affects certain blood vessels. Improvement in arterial blood flow has been demonstrated in coronary arteries.  Estrogen softens the arterioscletic plaques and this is why there is slight increase in heart attacks in the beginning of estrogen supplementation in women over 60.

Oncogene

Estrogen is suspected to activate certain oncogenes, as it supports certain cancers, notably breast cancer and cancer of the uterine lining. In addition, there are several benign gynecologic conditions that are dependent on estrogen, such as endometriosis, leiomyomata uteri, and uterine bleeding..

Pregnancy

The effect of estradiol, together with estrone and estriol, in pregnancy is less clear. They may promote uterine blood flow, myometrial growth, sitmulate breast growth and at term, promote cervical softening and expression of myometrial oxytocin receptors.

Role in sex differentiation of the brain

One of the fascinating twists to mammalian sex differentiation is that estradiol is one of the two active metabolites of testosterone in males (the other being dihydrotestosterone), and since fetuses of both sexes are exposed to similarly high levels of maternal estradiol, this source cannot have a significant impact on prenatal sex differentiation. Estradiol cannot be transferred readily from the circulation into the brain, whereas testosterone can; thus sex differentiation can be caused by the testosterone in the brain of most male mammals, including humans, aromatizing in significant amounts into estradiol. There is also now evidence that the programming of adult male sexual behavior in animals is largely dependent on estradiol produced in the central nervous system during prenatal life and early infancy from testosterone.[10] However, it is not yet known whether this process plays a minimal or significant part in human sexual behaviors although evidence from other mammals tends to indicate that it does.

Recently, it was discovered that volumes of sexually dimorphic brain structures in phenotypical males changed to approximate those of typical female brain structures when exposed to estradiol over a period of months.[12] This would suggest that estradiol has a significant part to play in sex differentiation of the brain, both pre-natal and throughout life.

Estradiol medication

Oral preparations are not necessarily predictably absorbed and subject to a first pass through the liver, where they can be metabolized and also initiate unwanted side-effects. Thus, alternative routes of administration that bypass the liver before primary target organs are hit have been developed. Transdermal and transvaginal routes are not subject to the initial liver passage.

Hormone replacement therapy

If severe side-effects of low levels of estradiol in a woman’s blood are experienced (commonly at the beginning of menopause or after oophorectomy), hormone replacement therapy may be prescribed. Estrogen therapy may be used in treatment of infertility in women when there is a need to develop sperm-friendly cervical mucus or an appropriate uterine lining.

Growth hormone (GH) is a protein-based poly-peptide hormone. It stimulates growth and cell reproduction and regeneration in humans and other animals. It is synthesized, stored, and secreted in the anterior pituitary gland. Growth hormone is used clinically to treat children’s growth disorders and adult growth hormone deficiency. In recent years, replacement therapies with human growth hormones (hGH) have become popular in the battle against aging and weight management. Reported effects on GH deficient patients (but not on healthy people) include decreased body fat, increased muscle mass, increased bone density, increased energy levels, improved skin tone and texture, increased sexual function and improved immune system function. At this time hGH is still considered a very complex hormone and many of its functions are still unknown. Despite marked structural similarities between growth hormone from different species, only human and primate growth hormones have significant effects in humans.

Stimulators of GH secretion include:

  • sex hormones o increased androgen secretion during puberty (in males from testis and in females from adrenal cortex) o estrogen
  • clonidine and L-DOPA by stimulating GHRH release
  • low blood sugar, arginine and propranolol by inhibiting somatostatin release
  • deep sleep
  • fasting
  • vigorous exercise

Inhibitors of GH secretion include:

  • high blood sugar
  • Costisol , prednisone
  • dihydrotestosterone

In addition to control by endogenous and stimulus processes, a number of foreign compounds (xenobiotics such as drugs and endocrine disruptors) are known to influence GH secretion and function.[14]

Secretion patterns

HGH is synthesized and secreted from the anterior pituitary gland in a pulsatile manner throughout the day; surges of secretion occur at 3- to 5-hour intervals.[2] The plasma concentration of GH during these peaks may range from 5 to even 45 ng/mL. The largest and most predictable of these GH peaks occurs about an hour after onset of sleep. Otherwise there is wide variation between days and individuals. Nearly fifty percent of HGH secretion occurs during the third and fourth REM sleep stages. Between the peaks, basal GH levels are low, usually less than 5 ng/mL for most of the day and night. Additional analysis of the pulsatile profile of GH described in all cases less than 1 ng/ml for basal levels while maximum peaks were situated around 10-20 ng/mL. A number of factors are known to affect HGH secretion, such as age, gender, diet, exercise, stress, and other hormones. Young adolescents secrete HGH at the rate of about 700 μg/day, while healthy adults secrete HGH at the rate of about 400 μg/day. In addition to increasing height in children and adolescents, growth hormone has many other effects on the body:

  • Increases calcium retention, and strengthens and increases the mineralization of bone
  • Increases muscle mass through sarcomere hyperplasia
  • Promotes lipolysis
  • Increases protein synthesis
  • Stimulates the growth of all internal organs excluding the brain
  • Plays a role in fuel homeostasis
  • Reduces liver uptake of glucose
  • Promotes gluconeogenesis in the liver[22]
  • Contributes to the maintenance and function of pancreatic islets
  • Stimulates the immune system

Excesses

The most common disease of GH excess is a pituitary tumor composed of somatotroph cells of the anterior pituitary. These somatotroph adenomas are benign and grow slowly, gradually producing more and more GH. For years, the principal clinical problems are those of GH excess. Eventually the adenoma may become large enough to cause headaches, impair vision by pressure on the optic nerves, or cause deficiency of other pituitary hormones by displacement. Prolonged GH excess thickens the bones of the jaw, fingers and toes. Resulting heaviness of the jaw and increased size of digits is referred to as acromegaly. Accompanying problems can include sweating, pressure on nerves (e.g., carpal tunnel syndrome), muscle weakness, excess sex hormone binding globulin (SHBG), insulin resistance or even a rare form of type 2 diabetes, and reduced sexual function. GH-secreting tumors are typically recognized in the fifth decade of life. It is extremely rare for such a tumor to occur in childhood, but, when it does, the excessive GH can cause excessive growth, traditionally referred to as pituitary gigantism. Surgical removal is the usual treatment for GH-producing tumors. In some circumstances, focused radiation or a GH antagonist such as pegvisomant may be employed to shrink the tumor or block function. Other drugs like octreotide (somatostatin agonist) and bromocriptine (dopamine agonist) can be used to block GH secretion because both somatostatin and dopamine negatively inhibit GHRH-mediated GH release from the anterior pituitary.

Deficiencies

Main article: Growth hormone deficiency The effects of growth hormone deficiency vary depending on the age at which they occur. In children, growth failure and short stature are the major manifestations of GH deficiency, with common causes including genetic conditions and congenital malformations. It can also cause delayed sexual maturity. In adults, deficiency is rare, with the most common cause a pituitary adenoma, and others including a continuation of a childhood problem, other structural lesions or trauma, and very rarely idiopathic GHD. Adults with GHD present with non-specific problems including truncal obesity with a relative decrease in muscle mass and, in many instances, decreased energy and quality of life. Diagnosis of GH deficiency involves a multiple-step diagnostic process, usually culminating in GH stimulation tests to see if the patient’s pituitary gland will release a pulse of GH when provoked by various stimuli. Treatment with exogenous GH is indicated only in limited circumstances, and needs regular monitoring due to the frequency and severity of side-effects. GH is used as replacement therapy in adults with GH deficiency of either childhood-onset (after completing growth phase) or adult-onset (usually as a result of an acquired pituitary tumor). In these patients, benefits have variably included reduced fat mass, increased lean mass, increased bone density, improved lipid profile, reduced cardiovascular risk factors, and improved psychosocial well-being.

Therapeutic use

Main article: Growth hormone treatment Treatments unrelated to deficiency GH can be used to treat conditions that produce short stature but are not related to deficiencies in GH. . GH can also be used for conditions that do not cause short stature. Typically, growth hormone treatment for conditions unrelated to stature is controversial and experimental. GH has been used for remission of multiple sclerosis, to reverse the effects of aging in older adults (see below), to enhance weight loss in obesity, as well as fibromyalgia, heart failure, Crohn’s disease and ulcerative colitis, burns and bodybuilding or athletic enhancement.

Anti-aging agent

Claims for GH as an anti-aging treatment date back to 1990 when the New England Journal of Medicine published a study wherein GH was used to treat 12 men over 60. At the conclusion of the study, all the men showed statistically significant increases in lean body mass and bone mineral, while the control group did not. The authors of the study noted that these improvements were the opposite of the changes that would normally occur over a 10- to 20-year aging period. Despite the fact the authors at no time claimed that GH had reversed the aging process itself, their results were misinterpreted as indicating that GH is an effective anti-aging agent. A Stanford University School of Medicine survey of clinical studies on the subject published in early 2007 showed that the application of GH on healthy elderly patients increased muscle by about 2 kg and decreased body fat by the same amount. However, these were the only positive effects from taking GH. No other critical factors were affected, such as bone density, cholesterol levels, lipid measurements, maximal oxygen consumption, or any other factor that would indicate increased fitness. Researchers also did not discover any gain in muscle strength, which led them to believe that GH merely let the body store more water in the muscles rather than increase muscle growth. This would explain the increase in lean body mass.

Athletic enhancement

Main article: HGH treatment for athletic enhancement Athletes in many sports use human growth hormone to enhance their athletic performance. Some recent studies have not been able to support claims that human growth hormone can improve the athletic performance of professional male athletes.

Side-effects

Main article: HGH controversies There is theoretical concern that HGH treatment may increase the risks of diabetes, especially in those with other predispositions treated with higher doses. If used for training, growth at a young age (25 or less) can cause severe symptoms. One survey of adults that had been treated with replacement cadaver GH (which has not been used anywhere in the world since 1985) during childhood showed a mildly increased incidence of colon cancer and prostate cancer, but linkage with the GH treatment was not established. Regular application of extra GH may show several negative side-effects such as joint swelling, joint pain, carpal tunnel syndrome, and an increased risk of diabetes. Other side effects can include less sleep needed after dosing. This is common initially and decreases in effect after habitual use of GH.

Melatonin is a naturally occurring compound found in animals, plants, and microbes In animals, circulating levels of melatonin vary in a daily cycle, thereby regulating the circadian rhythms of several biological functions. Many biological effects of melatonin are produced through activation of melatonin receptors, while others are due to its role as a pervasive and powerful antioxidant, with a particular role in the protection of nuclear and mitochondrial DNA.[7]

Melatonin in plants has multiple roles including regulation of the photoperiod, in plant defense responses, and as a scavenger of reactive oxygen species.

As early as 1917, it was known that an extract of cow pineal glands lightened frog skin. Dermatology professor Aaron B. Lerner and colleagues at Yale University, in the hope that a substance from the pineal might be useful in treating skin diseases, isolated and named the hormone melatonin in 1958.

Melatonin is secreted in darkness in both day-active (diurnal) and night-active (nocturnal) animals.

Melatonin may also be produced by a variety of peripheral cells such as bone marrow cells, lymphocytes and epithelial cells. Usually, the melatonin concentration in these cells is much higher than that found in the blood but it does not seem to be regulated by the photoperiod.

Melatonin is also synthesized by various plants, such as rice, and ingested melatonin has been shown to be capable of reaching and binding to melatonin binding sites in the brains of mammals.

History

Melatonin is related to the mechanism by which some amphibians and reptiles change the color of their skin and, indeed, it was in this connection the substance first was discovered. McCord and Allen discovered that extract of the pineal glands of cows lightened frog skin, while Aaron B. Lerner is credited for naming the hormone and for defining its chemical structure in 1958. In the mid-70s Lynch et al. demonstrated that also in humans the production of melatonin exhibits a circadian rhythm.

Distribution in the mammalian body

Melatonin produced in the pineal gland, which is outside of the blood-brain barrier, acts as an endocrine hormone since it is released into the blood. By contrast, melatonin produced by the retina and the gastrointestinal (GI) tract acts as a paracrine hormone.

Roles in non-human animals

Circadian rhythm

In humans, melatonin is produced by the pineal gland, a gland about the size of a pea, located in the center of the brain but outside the blood-brain barrier. The melatonin signal forms part of the system that regulates the sleep-wake cycle by chemically causing drowsiness and lowering the body temperature, but it is the central nervous system that controls the daily cycle in most components of the paracrine and endocrine systems rather than the melatonin signal (as was once postulated).

Light dependence

Production of melatonin by the pineal gland is inhibited by light and permitted by darkness. For this reason melatonin has been called “the hormone of darkness” and its onset each evening is called the Dim-Light Melatonin Onset (DLMO). Secretion of melatonin as well as its level in the blood, peaks in the middle of the night, and gradually falls during the second half of the night, with normal variations in timing according to an individual’s chronotype.

Until recent history, humans in temperate climates were exposed to only about six hours of daylight in the winter. In the modern world, artificial lighting reduces darkness exposure to typically eight or fewer hours per day all year round. Even low light levels inhibit melatonin production to some extent, but over-illumination can create significant reduction in melatonin production. Since it is principally blue light that suppresses melatonin wearing glasses that block blue light in the hours before bedtime may avoid melatonin loss. Use of blue-blocking goggles the last hours before bedtime has also been advised for people who need to adjust to an earlier bedtime, as melatonin promotes sleepiness.

Antioxidant

Besides its function as synchronizer of the biological clock, melatonin also exerts a powerful antioxidant activity. The discovery of melatonin as an antioxidant was made in 1993. In many lower life forms, it serves only this purpose. Melatonin is an antioxidant that can easily cross cell membranes and the blood-brain barrier. Melatonin is a direct scavenger of OH, O2−, and NO. Unlike other antioxidants, melatonin does not undergo redox cycling, the ability of a molecule to undergo reduction and oxidation repeatedly. Redox cycling may allow other antioxidants (such as vitamin C) to regain their antioxidant properties. Melatonin, on the other hand, once oxidized, cannot be reduced to its former state because it forms several stable end-products upon reacting with free radicals. Therefore, it has been referred to as a terminal (or suicidal) antioxidant.[34]

In animal models, melatonin has been demonstrated to prevent the damage to DNA by some carcinogens, stopping the mechanism by which they cause cancer. It also has been found to be effective in protecting against brain injury caused by ROS release in experimental hypoxic brain damage in newborn rats. Melatonin’s antioxidant activity may reduce damage caused by some types of Parkinson’s disease, may play a role in preventing cardiac arrhythmia and may increase longevity; it has been shown to increase the average life span of mice by 20% in some studies.

Immune system

While it is known that melatonin interacts with the immune system, the details of those interactions are unclear. There have been few trials designed to judge the effectiveness of melatonin in disease treatment. In preclinical studies, melatonin may enhance cytokine production, and by doing this counteract acquired immunodeficiences. Some studies also suggest that melatonin might be useful fighting infectious disease including viral, such as HIV, and bacterial infections, and potentially in the treatment of cancer.

Dreaming

Some supplemental melatonin users report an increase in vivid dreaming. Extremely high doses of melatonin (50 mg) dramatically increased REM sleep time and dream activity in both people with and without narcolepsy. Many psychoactive drugs, such as cannabis and lysergic acid diethylamide (LSD), increase melatonin synthesis.] It has been suggested that nonpolar (lipid-soluble) indolic hallucinogenic drugs emulate melatonin activity in the awakened state and that both act on the same areas of the brain.

Current and potential medical indications

Melatonin has been studied for the treatment of cancer, immune disorders, cardiovascular diseases, depression, seasonal affective disorder (SAD), circadian rhythm sleep disorders and sexual dysfunction.

Taken 30 to 90 minutes before bedtime, melatonin supplementation acts as a mild hypnotic. It causes melatonin levels in the blood to rise earlier than the brain’s own production accomplishes.

Preventing ischemic damage

Melatonin has been shown to reduce tissue damage in rats due to ischemia in both the brain and the heart; however, this has not been tested in humans.

Learning, memory and Alzheimer’s

Melatonin receptors appear to be important in mechanisms of learning and memory in mice, and melatonin can alter electrophysiological processes associated with memory, such as long-term potentiation (LTP). There is published evidence that melatonin may be useful in Alzheimer’s disease.

Studies in rats suggest that melatonin may be effective for treating Alzheimer’s disease.

Fertility

A research team in Italy has found that melatonin supplementation in the evening in perimenopausal women produces an improvement in thyroid function and gonadotropin levels, as well as restoring fertility and menstruation and preventing the depression associated with the menopause.

Headaches

Several clinical studies indicate that supplementation with melatonin is an effective preventive treatment for migraines and cluster headaches.

Cancer

A systematic review of unblinded clinical trials involving a total of 643 cancer patients using melatonin found a reduced incidence of death. Another clinical trial is due to be completed in 2012. Melatonin levels at night are reduced to 50% by exposure to a low-level incandescent bulb for only 39 minutes, and it has been shown that women with the brightest bedrooms have an increased risk for breast cancer. Reduced melatonin production has been proposed as a likely factor in the significantly higher cancer rates in night workers.

Gallbladder stones

Melatonin presence in the gallbladder has many protective properties, such as converting cholesterol to bile, preventing oxidative stress, and increasing the mobility of gallstones from the gallbladder. It also decreases the amount of cholesterol produced in the gallbladder by regulating the cholesterol that passes through the intestinal wall. In guinea pigs, melatonin administration restored normal function by reducing inflammation after induced Cholecystitis, whether administered before or after onset of inflammation. Relatively speaking, concentration of melatonin in the bile is 2–3 times higher than the otherwise very low daytime melatonin levels in the blood across many diurnal mammals, including humans.

Melatonin is involved in the regulation of body weight, and may be helpful in treating obesity (especially when combined with calcium).

Progesterone is produced in the ovaries (specifically after ovulation in the corpus luteum), the adrenal glands (near the kidney), and, during pregnancy, in the placenta. Progesterone is also stored in adipose (fat) tissue.

  • An additional source of progesterone is milk products. They contain much progesterone because on dairy farms cows are milked during pregnancy, when the progesterone content of the milk is high. After consumption of milk products the level of bioavailable progesterone goes up.

Reproductive system

Progesterone is sometimes called the “hormone of pregnancy”, and it has many roles relating to the development of the fetus:

  • Progesterone converts the endometrium to its secretory stage to prepare the uterus for implantation. At the same time progesterone affects the vaginal epithelium and cervical mucus, making it thick and impermeable to sperm. If pregnancy does not occur, progesterone levels will decrease, leading, in the human, to menstruation. Normal menstrual bleeding is progesterone-withdrawal bleeding.
  • During implantation and gestation, progesterone appears to decrease the maternal immune response to allow for the acceptance of the pregnancy.
  • Progesterone decreases contractility of the uterine smooth muscle.[25]
  • In addition progesterone inhibits lactation during pregnancy. The fall in progesterone levels following delivery is one of the triggers for milk production.
  • A drop in progesterone levels is possibly one step that facilitates the onset of labor. The fetus metabolizes placental progesterone in the production of adrenal steroids.

Nervous system

Progesterone, like pregnenolone and dehydroepiandrosterone, belongs to the group of neurosteroids. It can be synthesized within the central nervous system and also serves as a precursor to another major neurosteroid, allopregnanolone.

Neurosteroids affect synaptic functioning, are neuroprotective, and affect myelination. They are investigated for their potential to improve memory and cognitive ability. Progesterone affects regulation of apoptotic genes.

Its effect as a neurosteroid works predominantly through the GSK-3 beta pathway, as an inhibitor. (Other GSK-3 beta inhibitors include bipolar mood stabilizers, lithium and valproic acid.)

Other systems

  • It raises epidermal growth factor-1 levels, a factor often used to induce proliferation, and used to sustain cultures, of stem cells.
  • It increases core temperature (thermogenic function) during ovulation.[27]
  • It reduces spasm and relaxes smooth muscle. Bronchi are widened and mucus regulated. (Progesterone receptors are widely present in submucosal tissue.)
  • It acts as an antiinflammatory agent and regulates the immune response.
  • It reduces gall-bladder activity.[28]
  • It normalizes blood clotting and vascular tone, zinc and copper levels, cell oxygen levels, and use of fat stores for energy.
  • It may affect gum health, increasing risk of gingivitis (gum inflammation) and tooth decay.
  • It appears to prevent endometrial cancer (involving the uterine lining) by regulating the effects of estrogen.

Testosterone is a steroid hormone from the androgen group. In mammals, testosterone is primarily secreted in the testes of males and the ovaries of females, although small amounts are also secreted by the adrenal glands. It is the principal male sex hormone and an anabolic steroid. Testosterone is evolutionarily conserved through most vertebrates, although fish make a slightly different form called 11-ketotestosterone.

In men, testosterone plays a key role in the development of male reproductive tissues such as the testis and prostate as well as promoting secondary sexual characteristics such as increased muscle and bone mass and hair growth

In addition, testosterone is essential for health and well-being] as well as preventing osteoporosis.

On average, an adult human male body produces about ten times more testosterone than an adult human female body, but females are, from a behavioral perspective (rather than from an anatomical or biological perspective), more sensitive to the hormone. However, the overall ranges for male and female are very wide, such that the ranges actually overlap at the low end and high end respectively.

Physiological effects

In general, androgens promote protein synthesis and growth of those tissues with androgen receptors. Testosterone effects can be classified as virilizing and anabolic, although the distinction is somewhat artificial, as many of the effects can be considered both. Testosterone is anabolic, meaning it builds up bone and muscle mass.

  • Anabolic effects include growth of muscle mass and strength, increased bone density and strength, and stimulation of linear growth and bone maturation.
  • Androgenic effects include maturation of the sex organs, particularly the penis and the formation of the scrotum in the fetus, and after birth (usually at puberty) a deepening of the voice, growth of the beard and axillary hair. Many of these fall into the category of male secondary sex characteristics.

Testosterone effects can also be classified by the age of usual occurrence. For postnatal effects in both males and females, these are mostly dependent on the levels and duration of circulating free testosterone.

Pre-peripubertal

Pre- Peripubertal effects are the first visible effects of rising androgen levels at the end of childhood, occurring in both boys and girls.

  • Adult-type body odour
  • Increased oiliness of skin and hair, acne
  • Pubarche (appearance of pubic hair)
  • Axillary hair
  • Growth spurt, accelerated bone maturation
  • Hair on upper lip and sideburns.

Pubertal

Pubertal effects begin to occur when androgen has been higher than normal adult female levels for months or years. In males, these are usual late pubertal effects, and occur in women after prolonged periods of heightened levels of free testosterone in the blood.

  • Enlargement of sebaceous glands. This might cause acne.
  • Phallic enlargement or clitoromegaly
  • Increased libido and frequency of erection or clitoral engorgement
  • Pubic hair extends to thighs and up toward umbilicus
  • Facial hair (sideburns, beard, moustache)
  • Loss of scalp hair (Androgenetic alopecia)
  • Chest hair, periareolar hair, perianal hair
  • Leg hair
  • Axillary hair
  • Subcutaneous fat in face decreases
  • Increased muscle strength and mass
  • Deepening of voice
  • Increase in height
  • Growth of the Adam’s apple
  • Growth of spermatogenic tissue in testicles, male fertility
  • Growth of jaw, brow, chin, nose, and remodeling of facial bone contours
  • Shoulders become broader and rib cage expands
  • Completion of bone maturation and termination of growth. This occurs indirectly via estradiol metabolites and hence more gradually in men than women.

Adult

Adult testosterone effects are more clearly demonstrable in males than in females, but are likely important to both sexes. Some of these effects may decline as testosterone levels decrease in the later decades of adult life.

  • Libido and clitoral engorgement/penile erection frequency
  • Regulates acute HPA (Hypothalamic–pituitary–adrenal axis) response under dominance challenge.
  • Mental and physical energy
  • Maintenance of muscle trophism
  • The most recent and reliable studies have shown that testosterone does not cause or produce deleterious effects on prostate cancer. In people who have undergone testosterone deprivation therapy, testosterone increases beyond the castrate level have been shown to increase the rate of spread of an existing prostate cancer.
  • Recent studies have shown conflicting results concerning the importance of testosterone in maintaining cardiovascular health. Nevertheless, maintaining normal testosterone levels in elderly men has been shown to improve many parameters which are thought to reduce cardiovascular disease, risk such as increased lean body mass, decreased visceral fat mass, decreased total cholesterol, and glycemic control.
  • Under dominance challenge, may play a role in the regulation of the fight-or-flight response
Testosterone is necessary for normal sperm development. It activates genes in Sertoli cells, which promote differentiation of spermatogonia.
  • Studies show that falling in love decreases men’s testosterone levels while increasing women’s testosterone levels. It is speculated that these changes in testosterone result in the temporary reduction of differences in behavior between the sexes.
  • Recent studies suggest that testosterone level plays a major role in risk taking during financial decisions.
  • Fatherhood also decreases testosterone levels in men, suggesting that the resulting emotional and behavioral changes promote paternal care.
  • In animals (grouse and sand lizards), higher testosterone levels have been linked to a reduced immune system activity. Testosterone seems to have become part of the honest signaling system between potential mates in the course of evolution.

Brain

As testosterone affects the entire body (often by enlarging; men have bigger hearts, lungs, liver, etc.), the brain is also affected by this “sexual” differentiation; the enzyme aromatase converts testosterone into estradiol that is responsible for masculinization of the brain in a male mice. In humans, masculinization of the fetal brain appears, by observation of gender preference in patients with congenital diseases of androgen formation or androgen receptor function, to be associated with functional androgen receptors.

There are some differences in a male and female brain (the result of different testosterone levels), one of them being size: the male human brain is, on average, larger; however, females have more dendritic connections between brain cells This means that the effect of testosterone is a greater overall brain volume, but a decreased connection between the hemispheres.

A study conducted in 1996 found no immediate short term effects on mood or behavior from the administration of supraphysiologic doses of testosterone for 10 weeks on 43 healthy men. Another study found a correlation between testosterone and risk tolerance in career choice among women.

Literature suggests that attention, memory, and spatial ability are key cognitive functions affected by testosterone in humans. Preliminary evidence suggests that low testosterone levels may be a risk factor for cognitive decline and possibly for dementia of the Alzheimer’s type, a key argument in Life Extension Medicine for the use of testosterone in anti-aging therapies. Much of the literature, however, suggests a curvilinear or even quadratic relationship between spatial performance and circulating testosterone, where both hypo- and hypersecretion of circulating androgens have negative effects on cognition and cognitively-modulated aggressivity, as detailed above.

Contrary to what has been postulated in outdated studies and by certain sections of the media, aggressive behaviour is not typically seen in hypogonadal men who have their testosterone replaced adequately to the eugonadal/normal range. In fact, aggressive behaviour has been associated with hypogonadism and low testosterone levels and it would seem as though supraphysiological and low levels of testosterone and hypogonadism cause mood disorders and aggressive behaviour, with eugondal/normal testosterone levels being important for mental well-being. Testosterone depletion is a normal consequence of aging in men. One consequence of this is an increased risk for the development of Alzheimer’s Disease.

Environmental factors affecting testosterone levels include:

    • Loss of status or dominance in men may result in a decreased testosterone level.
    • Implicit power motivation predicts an increased testosterone release in men.
    • Aging reduces testosterone release.
    • Hypogonadism
    • Sleep (REM dream) increases nocturnal testosterone levels.
    • Resistance training increases testosterone levels, however, in older men, that increase can be avoided by protein ingestion.
    • Zinc deficiency lowers testosterone levels but over supplementation has no effect on serum testosterone.
    • Licorice. The active ingredient in licorice root, glycyrrhizinic acid has been linked to small, clinically non-significant

decreases in testosterone levels. In contrast, a more recent study found that licorice administration produced a substantial testosterone decrease in a small, female-only sample.

The bones and the brain are two important tissues in humans where the primary effect of testosterone is by way of aromatization to estradiol. In the bones, estradiol accelerates maturation of cartilage into bone, leading to closure of the epiphyses and conclusion of growth. In the central nervous system, testosterone is aromatized to estradiol. Estradiol rather than testosterone serves as the most important feedback signal to the hypothalamus (especially affecting LH secretion). In many mammals, prenatal or perinatal “masculinization” of the sexually dimorphic areas of the brain by estradiol derived from testosterone Testosterone causes the appearance of masculine traits (i.e., deepening voice, pubic and facial hairs, muscular build, etc.) Like men, women rely on testosterone to maintain libido, bone density and muscle mass throughout their lives. In men, inappropriately high levels of estrogens lower testosterone, decrease muscle mass, stunt growth in teenagers, introduce gynecomastia, increase feminine characteristics, and decrease susceptibility to prostate cancer, reduces libido and causes erectile dysfunction and can cause excessive sweating and hot flushes. However, an appropriate amount of estrogens is required in the male in order to ensure well-being, bone density, libido, erectile function, etc.Therapeutic use

There are many routes of administration for testosterone. Forms of testosterone for human administration currently available include injectable (such as testosterone cypionate or testosterone enanthate in oil), oral, buccal transdermal skin patches, and transdermal creams or gels.

In the pipeline are “roll on” methods and nasal sprays.Indications

The original and primary use of testosterone is for the treatment of males who have too little or no natural endogenous testosterone production—males with hypogonadism. Appropriate use for this purpose is legitimate hormone replacement therapy (testosterone replacement therapy [TRT]), which maintains serum testosterone levels in the normal range.

However, over the years, as with every hormone, testosterone or other anabolic steroids has also been given for many other conditions and purposes besides replacement, with variable success but higher rates of side effects or problems. Examples include infertility, lack of libido or erectile dysfunction, osteoporosis, penile enlargement, height growth, bone marrow stimulation and reversal of anemia, and even appetite stimulation. By the late 1940s testosterone was being touted as an anti-aging wonder drug (e.g., see Paul de Kruif’s The Male Hormone). Decline of testosterone production with age has led to interest in androgen replacement therapy.Testosterone strongly reduces insulin resistance, therefore it can be used as anti diabetes agent.

Testosterone patches are effective at treating low libido in post-menopausal women. Low libido may also occur as a symptom or outcome of hormonal contraceptive use. Women may also use testosterone therapies to treat or prevent loss of bone density, muscle mass and to treat certain kinds of depression and low energy state. Women on testosterone therapies may experience an increase in weight without an increase in body fat due to changes in bone and muscle density. Most undesired effects of testosterone therapy in women may be controlled by hair-reduction strategies, acne prevention, etc. There is a theoretical risk that testosterone therapy may increase the risk of breast or gynaecological cancers, and further research is needed to define any such risks more clearly.

Hormone replacement therapy

Main article: Androgen replacement therapy

Testosterone levels decline gradually with age in human beings. The clinical significance of this decrease is debated (see andropause). There is disagreement about when to treat aging men with testosterone replacement therapy. The American Society of Andrology’s position is that:

“… testosterone replacement therapy in aging men is indicated when both clinical symptoms and signs suggestive of androgen deficiency and decreased testosterone levels are present.”

The American Association of Clinical Endocrinologists says:

“Hypogonadism is defined as a free testosterone level that is below the lower limit of normal for young adult control subjects. Previously, age-related decreases in free testosterone were once accepted as normal. Currently, they are not considered normal. Patients with low-normal to subnormal range testosterone levels warrant a clinical trial of testosterone.”

There isn’t total agreement on the threshold of testosterone value below which a man would be considered hypogonadal. (Currently there are no standards as to when to treat women.) Testosterone can be measured as “free” (that is, bioavailable and unbound) or more commonly, “total” (including the percentage which is chemically bound and unavailable). In the United States, male total testosterone levels below 300 ng/dL from a morning serum sample are generally considered low. However these numbers are typically not age-adjusted, but based on an average of a test group which includes elderly males with low testosterone levels Therefore a value of 300 ng/dL might be normal for a 65-year-old male, but not normal for a 30-year-old Identification of inadequate testosterone in an aging male by symptoms alone can be difficult. The signs and symptoms are non-specific, and might be confused with normal aging characteristics, such as loss of muscle mass and bone density, decreased physical endurance, decreased memory abillity and loss of libido.

Replacement therapy can take the form of injectable depots, transdermal patches and gels, subcutaneous pellets, and oral therapy. Adverse effects of testosterone supplementation include minor side effects such as acne and oily skin, and more significant complications such as increased hematocrit which can require venipuncture in order to treat, exacerbation of sleep apnea and acceleration of pre-existing prostate cancer growth in individuals who have undergone androgen deprivation. Exogenous testosterone also causes suppression of spermatogenesis and can lead to infertility.[64] It is recommended that physicians screen for prostate cancer with a digital rectal exam and PSA (prostate specific antigen) level before starting therapy, and monitor hematocrit and PSA levels closely during therapy.Benefits

Appropriate testosterone therapy can prevent or reduce the likelihood of osteoporosis, type 2 diabetes, cardio-vascular disease (CVD), obesity, depression and anxiety and the statistical risk of early mortality. Low testosterone also brings with it an increased risk for the development of Alzheimer’s Disease.

A small trial in 2005 showed mixed results.

Large scale trials to assess the efficiency and long-term safety of testosterone are still lacking.
Adverse effects

Exogenous testosterone supplementation comes with a number of health risks. Fluoxymesterone and methyltestosterone are synthetic derivatives of testosterone. In 2006 it was reported that women taking Estratest, a combination pill including estrogen and methyltestosterone, were at considerably heightened risk of breast cancer.[citation needed] That said methyltestosterone and Fluoxymesterone are no longer prescribed by physicians given their poor safety record, and testosterone replacement in men does have a very good safety record as evidenced by over sixty years of medical use in hypogonadal men.

One adverse effect that many men complain of is that of the development of gynecomastia (breasts),[citation needed] but this is something that can be prevented by appropriate choice and dosing of medication, and, in required cases, the use of ancillary medications that help lower SHBG or estradiol. Another side-effect is having difficulty urinating

The thyroid hormones, thyroxine (T4) and triiodothyronine (T3), are tyrosine-based hormones produced by the thyroid gland primarily responsible for regulation of metabolism. An important component in the synthesis of thyroid hormones is iodine. The major form of thyroid hormone in the blood is thyroxine (T4), which has a longer half life than T3. The ratio of T4 to T3 released in the blood is roughly 20 to 1. Thyroxine is converted to the active T3 (three to four times more potent than T4) within cells by deiodinases (5′-iodinase).

Circulation and Transport

Plasma transport

Most of the thyroid hormone circulating in the blood is bound to transport proteins. Only a very small fraction of the circulating hormone is free (unbound) and biologically active, hence measuring concentrations of free thyroid hormones is of great diagnostic value.

When thyroid hormone is bound, it is not active, so the amount of free T3/T4 is what is important. For this reason, measuring total thyroxine in the blood can be misleading.

Another critical diagnostic tool is measurement of the amount of thyroid-stimulating hormone (TSH) that is present.

The thyronines act on nearly every cell in the body. They act to increase the basal metabolic rate, affect protein synthesis, help regulate long bone growth (synergy with growth hormone), neuronal maturation and increase the body’s sensitivity to catecholamines (such as adrenaline) by permissiveness. The thyroid hormones are essential to proper development and differentiation of all cells of the human body. These hormones also regulate protein, fat, and carbohydrate metabolism, affecting how human cells use energetic compounds. They also stimulate vitamin metabolism. Numerous physiological and pathological stimuli influence thyroid hormone synthesis.

Thyroid hormone leads to heat generation in humans.

Both excess and deficiency of thyroxine can cause disorders.

  • Hyperthyroidism (an example is Graves Disease) is the clinical syndrome caused by an excess of circulating free thyroxine, free triiodothyronine, or both. It is a common disorder that affects approximately 2% of women and 0.2% of men. Thyrotoxicosis is often used interchangeably with hyperthyroidism, but there are subtle differences. Although thyrotoxicosis also refers to an increase in circulating thyroid hormones, it can be caused by the intake of thyroxine tablets or by an over-active thyroid, whereas hyperthyroidism refers solely to an over-active thyroid.
  • Hypothyroidism (an example is Hashimoto’s thyroiditis) is the case where there is a deficiency of thyroxine, triiodiothyronine, or both.
  • Clinical depression can sometimes be caused by hypothyroidism[3]. Some research[4] has shown that T3 is found in the junctions of synapses, and regulates the amounts and activity of serotonin, norepinephrine, and Gamma-aminobutyric acid (GABA) in the brain.

Medical use of thyroid hormones

Both T3 and T4 are used to treat thyroid hormone deficiency (hypothyroidism). They are both absorbed well by the gut, so can be given orally. Levothyroxine, the most commonly used synthetic thyroxine form, is a stereoisomer of physiological thyroxine (t4 only), which is metabolised more slowly and hence usually only needs once-daily administration. Natural desiccated thyroid hormones, also under the commercial name Armour Thyroid, is derived from pig thyroid glands, it is a “natural” hypothyroid treatment containing 20% T3 and traces of T2, T1 and calcitonin. Also available are synthetic combinations of T3/T4 in different ratios (such as Thyrolar) and pure-T3 medications (Cytomel). Levothyroxine is usually the first course of treatment tried. Some patients feel they do better on Armour thyroid, though not all doctors like to work with it, as some believe it is harder to regulate. This is not supported by the evidence.

Thyroxine is believed to be a prohormone and a reservoir for the most active and main thyroid hormone T3. T4 is converted as required in the tissues by iodothyronine deiodinase. Deficiency of deiodinase can mimic an iodine deficiency. T3 is more active than T4 and is the final form of the hormone, though it is present in less quantity than T4.

Effect of iodine deficiency on thyroid hormone synthesis

If there is a deficiency of dietary iodine, the thyroid will not be able to make thyroid hormone. The lack of thyroid hormone will lead to decreased negative feedback on the pituitary, leading to increased production of thyroid stimulating hormone, which causes the thyroid to enlarge (goiter)endemic colloid goiter. This has the effect of increasing the thyroid’s ability to trap more iodide, compensating for the iodine deficiency and allowing it to produce adequate amounts of thyroid hormone.

Effects of thyroxine

  • Increases cardiac output
  • Increases heart rate
  • Increases ventilation rate
  • Increases basal metabolic rate
  • Potentiates the effects of catecholamines (i.e increases sympathetic activity)
  • Potentiates brain development
  • Thickens endometrium in females

What is DHEA

Other names: dehydroepiandrosterone, dehydroepiandrosterone sulfate Dehydroepiandrosterone (DHEA) is a steroid hormone that’s produced by the adrenal glands. The body converts DHEA to male and female sex hormones, such as estrogen and testosterone.

DHEA levels typically peak by the time people are in their 20s and decline with age, which is why there has been considerable interest in DHEA and its role in aging. In fact, DHEA supplements have been touted as an anti-aging hormone because lower levels of DHEA have been reported in some people with type 2 diabetes, breast cancer, heart disease, osteoporosis, AIDS, adrenal insufficiency, kidney disease and anorexia. Certain medications may also deplete DHEA, such as corticosteroids, insulin, opiates and danazol.

DHEA is manufactured naturally in the body, but DHEA supplements can also be made in a laboratory from a substance called diosgenin, found in soybeans and wild yam. Wild yam cream and supplements are often promoted as being a natural source of DHEA, but the body can’t convert wild yam to DHEA on its own — the conversion must be done in a laboratory.

DHEA supplements were taken off the U.S. market in 1985 because of concerns about false claims regarding its benefits. It became available only by prescription but was reintroduced as a nutritional supplement after the Dietary Supplement Health and Education Act was passed in 1994.

Why Do People Use DHEA Supplements

DHEA is used as an “anti-aging” hormone and for conditions in which DHEA levels have been found to be low, however, there are very few large, well-designed human studies showing that it’s effective.

  • Aging – The gradual decline in the body’s DHEA levels correlate with loss of muscle mass, decreased bone density, and a decline in immune function. A study by Mayo Clinic researchers, published in the New England Journal of Medicine, looked at the effect of DHEA supplements on markers of aging, such as muscle mass, muscle strength, fat mass, peak endurance and glucose tolerance in older men and women.The study involved 87 men and 57 women. At the end of the two-year study, participants showed no significant change in any of the markers. It’s one of the largest and longest studies on DHEA and human aging to date.
  • Depression – Clinical trials examining the effect of DHEA for depression suggest that DHEA temporarily improves symptoms of depression compared to a placebo. For example, a study sponsored by the National Institute of Mental Health investigated the use of DHEA by 46 people between the ages of 40 and 65 with major or minor depression. They took DHEA for six weeks (90 mg a day for three weeks followed by 450 mg a day for three weeks) or a placebo.Twenty three people improved while taking DHEA, compared to 13 who responded while taking the placebo. After six weeks, 14 out of 15 people taking the placebo were still depressed, compared to eight out of 14 people taking DHEA.Studies on lasting mood changes, however, have had inconsistent results. More research is needed before DHEA should be used for depression, however, because the long-term effects aren’t known.
  • Menopause – One small study found that 25 mg a day of DHEA may reduce symptoms of menopause. Levels of other hormones were affected, however, which may have adverse effects.
  • Obesity – In animal studies, DHEA has shown some promise in reducing genetic or diet-induced obesity. A study funded by the National Institutes of Health looked at the effect of DHEA (50 mg a day) compared to a placebo for weight loss in 56 overweight adults between the ages of 65 and 78. At the end of the six month study, people taking DHEA lost an average of two pounds compared to the people taking the placebo, who gained just over one pound. Although overall weight loss was minimal, results were more promising when fat loss around the abdomen was assessed. After six months, women taking DHEA lost 10% of their abdominal fat and men lost 7%. A large study involving 942 men in the Massachusetts Male Aging Study looked at men between the ages of 40 and 70, first in 1987 to 1989 and then again in 1995 to 1997. Researchers found that fat around the abdomen (called central obesity) was associated with lower DHEA levels.
  • Osteoporosis – Supplementation with DHEA has been studied to increase bone density. It is usually taken by mouth or applied as a cream to the inner thigh. DHEA hasn’t been found to be helpful for younger women and men. Some evidence sugests it might be helpful for osteoporosis in older women. More research is needed.
  • Sexual Dysfunction – Studies on the use of DHEA for erectile dysfunction in men and sexual function in men and women have been inconsistent. A one-year study involving 280 men and women found that 50 mg a day of DHEA improved libido in women over 70 but not in younger women or men. Other studies have been mixed — most have been too small to be meaningful or the treatment duration has been too short.
  • Systemic Lupus Erythematosus – Scientific evidence indicates that DHEA may enhance mental function and increase bone mass in women with systemic lupus erythematosus (SLE), an autoimmune disease affecting connective tissue. In fact, synthetic DHEA called prasterone (Prestara) is under investigation for the treatment of this condition and the prevention of loss of bone mineral density. The FDA has granted orphan drug status for the prevention of loss of bone mineral density in SLE patients taking corticosteroids.