How To Treat High Dhea Levels In Females

29.06.2023 Chukwudi Eze 0 Comments

Natural Treatments for Elevated DHEA — POYNOR HEALTH Natural Treatments for Elevated DHEA Dehydroepiandrosterone (DHEA) is the principal human C-19 steroid. DHEA has very low androgenic potency but serves as the major direct or indirect precursor for most sex steroids. DHEA is secreted by the adrenal gland and production is at least partly controlled by adrenocorticotropic hormone (ACTH). The bulk of DHEA is secreted as a 3-sulfoconjugate dehydroepiandrosterone sulfate (DHEAS). Both hormones are albumin bound, but DHEAS binding is much tighter. As a result, circulating concentrations of DHEAS are much higher (>100-fold) compared to DHEA. In most clinical situations, DHEA and DHEAS results can be used interchangeably. In gonads and several other tissues, most notably skin, steroid sulfatases can convert DHEAS back to DHEA, which can then be metabolized to stronger androgens and to estrogens. Within weeks after birth, DHEA/DHEAS levels fall by 80% or more and remain low until the onset of adrenarche at age 7 or 8 in girls and age 8 or 9 in boys. Adrenarche is a poorly understood phenomenon, peculiar to higher primates, that is characterized by a gradual rise in adrenal androgen production. It precedes puberty but is not casually linked to it. Early adrenarche is not associated with early puberty or with any reduction in final height or overt androgenization. However, girls with early adrenarche may be at increased risk of polycystic ovarian syndrome as adults. Following adrenarche, DHEA/DHEAS levels increase until the age of 20 to a maximum roughly comparable to that observed at birth. Levels then decline over the next 40 to 60 years to around 20% of peak levels. Elevated DHEA/DHEAS levels can cause signs or symptoms of hyperandrogenism in women. High levels may be due to PCOS, congenital adrenal hyperplasia, insulin, stress, elevated prolactin, alcohol and certain medications like ADD medications, Xanax and Wellbutrin. Most mild-to-moderate elevations in DHEAS levels are of unknown origin. However, pronounced elevations of DHEA/DHEAS may be indicative of androgen-producing adrenal tumors. In small children, congenital adrenal hyperplasia (CAH) due to 3 beta-hydroxysteroid dehydrogenase deficiency is associated with excessive DHEA/DHEAS production. Lesser elevations may be observed in 21-hydroxylase deficiency (the most common form of CAH) and 11 beta-hydroxylase deficiency. Origins of lower elevations of DHEA and DHEA-s include:

Chronic daily stress PTSD PCOS Elevated prolactin Non-classical adrenal hyperplasia

Symptoms of elevated DHEA include:

High DHEA can cause symptoms of androgen excess including oily skin, acne, sleep problems, headaches and mood disturbances. In some cases, highly androgenic people may show high levels of both DHEA or testosterone without negative clinical consequence. Symptoms include:

Difficulty in controlling weight Acne or oily skin Excess hair growth all over the body (hirsutism). Male patterned baldness Generalized fatigue or low energy Irritability, anger or depression (and other changes in mood) Infertility Changes to your voice (a deeper voice in women) Changes to muscle structure (increase in muscle mass) Aggressive behavior Reduction in breast size Known history of PCOS Recent history of stress

Management of elevated DHEA:

High DHEA can be managed with blood sugar balancing lifestyle, stress reduction and in appropriate cases Ashwagandha and other supplements. If possible find and eliminate the source of stress Manage stress Consider supplementing with the adrenal adaptogen Ashwagandha has been shown to reduce enzyme production in individuals with adrenal hyperplasia. Ashwagandha has also been shown to help balance cortisol levels which is also helpful if stress is worsening your DHEA. Dosing500mg per day but note that some people may need up to 2,000mg per day. Consider further supplementation to improve adrenal function such as:

Alpha Lipoic Acid Phosphatidyl Serine A dose of 200 mg of phosphatidylserine/phosphatidic acid complex per day may help to normalize ACTH and serum cortisol secretion in chronically-stressed individuals.800 mg of phosphatidylserine per day blunted the stress-induced activation of the HPA axis. L-Theanine : Found in green tea, L-theanine has been found in mice to protect normal ACTH secretion in the presence of stress via modulation of the HPA axis. Hypericum perforatum : In patients with PCOS who also display symptoms of depression or anxiety related to stressors, St John’s wort has been found to attenuate the plasma increases of ACTH.20 As women with PCOS are at increased risk for depression and anxiety, Melatonin When administered at bedtime in patients who are deficient in this hormone or who have sleep disorders, melatonin may help reduce ACTH stimulation of the adrenal gland. Rhodiola rosea : The active ingredient in rhodiola, salidroside, has been found in animals to attenuate CRH expression in the hypothalamus and significantly reduce the levels of cortisol, thereby improving depressive symptoms and regulating the HPA axis. Schizandra chinensis : This herb is often used in Traditional Chinese Medicine for the treatment of stress. A 2007 study found that schizandra was an effective protector against stress-related increases in cortisol, protein kinase, and nitric oxide in rabbits. Lavandula officinalis : Inhalation of the vapor of lavender oil has been found to decrease plasma ACTH levels25 and reduce self-reported anxiety. Some adaptogenic herbs may increase serum androgens, it is important to consider contraindications before prescribing commonly used adaptogen formulas.

Lifestyle

It’s important to not overlook the benefits of stress reduction via lifestyle modifications, including meditation, deep breathing, visualization and other mindfulness activities. Quality sleep Reduce refines carbohydrates and sugars Restorative exercise

Gut Repair

There exists an important connection between the gut and the HPA axis. Probiotics that improve intestinal permeability have been found to attenuate the response of the HPA axis to stress. It’s also known that cortisol increases intestinal permeability through mast cell-dependent mechanisms; as such, women with PCOS who make excessive adrenal steroids may be at increased risk.

Anti-androgen Therapeutics

Many significant clinical problems related to excess adrenal androgens occur due to their conversion to testosterone or DHT. Anti-androgen therapies may be particularly beneficial for women with androgen-related hirsutism, acne, androgenetic alopecia, and androgen-related menstrual irregularities, who wish to avoid the side effects of conventional approaches such as spironolactone or finasteride. Spearmint Tea : At a dosage of 1 cup BID, spearmint tea has been shown in 2 studies to have anti-androgenic properties. Over a 30-day period, spearmint tea brought about a significant reduction in free and total testosterone levels in a group of 42 women with confirmed PCOS and hirsutism.30 Glycerrhiza glabra : Licorice was found in a 2004 trial to significantly decrease testosterone levels in healthy female patients after 1 month of treatment. The study concluded that licorice may exert its anti-androgenic action through blocking 17-hydroxysteroid dehydrogenase and 17-20 lyase. The glycyrrhizin and glycyrrhetic acid constituents of licorice have significant anti-androgen effects, which may be helpful in reducing androgenic symptoms in women with PCOS. Paeonia lactiflora : Peony is another popular anti-androgenic herb. It is often combined with Glycyrrhiza glabra in a ratio of 1:1 in Traditional Chinese Medicine for the treatment of PCOS. Studies have found that this combination is able to decrease the production of testosterone without altering the production of androstenedione and estradiol. Camellia sinensis : For patients with androgenetic alopecia, hirsutism, or acne, Camellia sinensis (green tea) may be of benefit. Epigallocatechins in green tea are 5α-reductase inhibitors, which decrease the production of DHT. As green tea can also increase sex hormone-binding globulin, it can be helpful in patients with elevated free androgens. Serenoa repens : Saw palmetto is a well-known plant-derived anti-androgen. By moderately inhibiting the enzyme 5α-reductase, saw palmetto shows promise in the treatment of androgenetic alopecia. Ganoderma lucidum : Among its many health benefits, reishi mushroom exerts a significant anti-androgenic action.38 Research suggests that its triterpenoid fraction in an ethanol extract is able to inhibit both type 1 and type 2 5α-reductase.39 In addition, it appears to suppress the growth of cells that are stimulated by testosterone itself, suggesting that it may also have a role to play as an androgen receptor blocker. Rosmarinus officinalis : As a topical therapy for androgenetic alopecia, rosemary leaf extract was found in a 2013 study to improve hair regrowth in mice with androgen-induced hair-growth interruption. The extract showed inhibitor activity upwards of 82.4% in inhibiting 5α-reductase, and also decreased the binding of DHT to androgen receptors.

High DHEA levels can be a very serious indicator of deeper problems, thus it is necessary to assure that possible origins of elevated levels are properly evaluated.

High DHEA levels in females are often associated with PCOS. High levels of DHEA are associated with a higher risk of breast cancer. High DHEA levels in females also may indicate an adrenal gland tumor or overactive adrenal glands High DHEA levels in females also seem to be associated with Cushing’s syndrome

: Natural Treatments for Elevated DHEA — POYNOR HEALTH

What happens if DHEA is high in females?

Why do I need a DHEA sulfate test? – You may need this test if you have symptoms of high levels or low levels of DHEA sulfate (DHEAS). Men may not have any symptoms of high levels of DHEAS. Symptoms of high levels of DHEAS in women and girls may include:

Excess body and facial hair growth
Deepening of voice
Menstrual irregularities
Acne
Increased muscularity
Hair loss at the top of the head

Babies may also need testing if they have genitals that are not clearly male or female in appearance (ambiguous genitalia). Boys may need this test if they have signs of early puberty. Symptoms of low levels of DHEAS may include the following signs of an adrenal gland disorder:

Unexplained weight loss
Nausea and vomiting
Dizziness
Dehydration
Craving for salt

Other symptoms of low DHEAS are related to aging and may include:

Decreased sex drive
Erectile dysfunction in men
Thinning of vaginal tissues in women

Should I be worried if my DHEA levels are high?

What does it mean to have high DHEAS levels? – High levels of DHEAS may mean you need additional testing. They can indicate problems such as:

Polycystic ovary syndrome (PCOS),
Cancerous or noncancerous adrenal tumors, including adrenocortical carcinoma,
Congenital adrenal hyperplasia,
Ovarian cancer,

Can Dheas be treated?

Overview – Dehydroepiandrosterone (DHEA) is a hormone that your body naturally produces in the adrenal gland. DHEA helps produce other hormones, including testosterone and estrogen. Natural DHEA levels peak in early adulthood and then slowly fall as you age.

Can you have high DHEA without PCOS?

Discussion – This study found that patients with PCOS have metabolic and hormonal differences in relation to body mass; these findings suggest an important role for obesity in pathogenesis and clinical presentation of PCOS. It was observed that obese PCOS patients have more insulin resistance evidenced by the HOMA index than nonobese PCOS patients, as previously reported ( 15– 17). In contrast, PCOS patients with low BMI (<27 kg/m 2 ) presented increased gonadotropic dysfunction, evidenced by more circulating LH levels and increased dissociation of LH/FSH than PCOS patients with high BMI (≥27 kg/m 2 ), a finding that has been found in some ( 15) but not other previous studies ( 16– 19). This finding may be complemented by the correlation between LH and A4 in nonobese PCOS patients. This study also found that some circulating androgens may be influenced by body mass. In the present study we found no significant differences in the concentration of T among obese and nonobese PCOS patients. There are studies where basal T levels are found higher in obese than in nonobese PCOS patients ( 20– 22) and other reports where the production of T is similar between obese and nonobese PCOS patients ( 15, 18, 19). However, the basal A4 levels were found to be higher in nonobese than in obese PCOS patients, as reported in some studies ( 22, 23). In fact, the A4 levels were higher in nonobese PCOS patients than in any other group. Moreover, the frequency of hyperandrogenism by A4 was greater in low-BMI than in high-BMI PCOS patients. In contrast, other studies have found similar A4 levels in obese and nonobese PCOS patients ( 15, 18, 20). The differences in comparisons of androgen levels between obese and nonobese PCOS patients can be explained by varying inclusion criteria for PCOS, different BMI cutoff points for obesity, variable sensitivity of the methodology for androgen measurement, as well as by heterogeneous ethnic/race characteristics. It is interesting that DHEAS levels were significantly higher in nonobese PCOS patients than in obese PCOS patients with the BMI cutoff value of of 30 kg/m 2, Although frequency of increased DHEA and DHEAS separately were not significantly different between obese and nonobese PCOS patients, the frequency of hyperandrogenism by DHEA along with DHEAS was found to be higher in low-BMI PCOS patients than in high-BMI PCOS patients. In this regard, this article is conceptually consistent with a previous study ( 10), which found that patients with hyperandrogenism and higher DHEAS levels showed less BMI than those with normal DHEAS levels. To date it is unknown why some data reveal higher adrenal androgen excess in nonobese PCOS. Some previous studies have found that production of these androgens was inversely related to the degree of insulin resistance ( 31, 32). However, this study did not find any correlation between the DHEA or DHEAS levels and insulin levels or HOMA. Although some findings were found with different BMI cutoff values in this study, it is likely that low adiposity in PCOS patients is associated with increased LH levels, high A4 and DHEAS levels. The relationship between ovarian and adrenal production of DHEA and DHEAS in PCOS is controversial and not well understood ( 33). The administration of GnRH agonist to PCOS patients with adrenal androgen excess suppressed A4 and T and produced a partial decrease of DHEAS levels, showing that ovarian steroids promoted adrenal androgen excess; however, there was a maximal ACTH-stimulated incremental increase of DHEA and DHEAS during GnRH agonist administration, indicating an unaltered adrenal androgen capacity ( 34). In PCOS patients with adrenal androgen excess treated with long-term GnRH analogs, A4 and DHEA responsiveness to CRH was suppressed; however, it was restored by estradiol ( 35). PCOS patients with adrenal androgen excess presented greater A4 levels than PCOS patients without it under ACTH stimulation ( 36). Finally, PCOS patients with characteristic morphology of polycystic ovaries tended to have higher concentrations of DHEAS than PCOS patients with normal ovarian morphology ( 29). The production of DHEA and DHEAS and the relationship between the ovarian and adrenal secretion has been evaluated in other clinical situations (eg, women with oophorectomy or premature ovarian failure). Exogenous T administration produced a decrease in DHEA and an increase of DHEAS in women with oophorectomy ( 37). In women with premature ovarian failure and hypoestrogenemia, the DHEAS concentrations have been found to be decreased ( 38). However, in another study, the consecutive dexamethasone inhibition and ACTH stimulation produced lower A4 and T levels but similar DHEA levels in women with premature ovarian failure in comparison with controls with normal ovarian function ( 39). One limitation of this study is the use of AE-PCOS criteria instead of Rotterdam criteria for PCOS diagnosis. The Rotterdam criteria generate different phenotypes in PCOS with the inclusion of the "two out of three criteria for PCOS diagnosis: oligo-anovulation, hiperandrogenism, and polycystic ovaries." The difficulty of using those criteria ( 13) is they include the phenotype of oligo-anovulation and polycystic ovarian morphology without hyperandrogenism, which some studies considered to be a different disorder with another pathogenesis pathway ( 40). In the present study, which focuses in women with hyperandrogenism, we considered it pertinent to work with the AE-PCOS criteria, which establish that PCOS should be considered as a predominantly hyperandrogenic disorder ( 14). In addition, all the phenotypes of AE-PCOS are included in those of Rotterdam consensus. In contrast, not all the phenotypes of Rotterdam consensus are included in those of AE-PCOS criteria. So, we consider that the scientific findings of clinical studies performed with AE-PCOS criteria can be extrapolated with pertinent explanations to studies with Rotterdam consensus criteria, but the opposite is not reasonably possible. An additional limitation of this study, but under controversy, is the point concerning the selection of the best BMI cutoff value to define obesity. We solved this problem doing the data analysis with both BMI cutoff values. The fact that some findings observed with the BMI cutoff value of 27 kg/m 2 changed with the BMI cutoff value of 30 kg/m 2, in PCOS patients and control women, can be another clue to support 27 kg/m 2 as a better tool to detect obesity, at least in some populations ( 25). Another limitation of this study is it did not use methodology aimed at clarifying the differentiation of ovarian or adrenal source of DHEA and DHEAS hyperandrogenism. However, the main objective of this study was not to determine the origin of ovarian or adrenal hyperandrogenism, but rather the relationship of hyperandrogenism by DHEA and DHEAS levels with body mass in PCOS. In conclusion, higher A4 levels were found in nonobese PCOS patients than in obese PCOS patients, as well as a significant correlation between LH and A4 in nonobese PCOS patients, but not in obese PCOS patients. In addition, it was observed significantly higher DHEAS levels in nonobese PCOS patients than in obese PCOS patients and a greater proportion of hyperandrogenism by A4, DHEA along with DHEAS in low-BMI PCOS patients compared with high-BMI PCOS patients. These finding may point in the direction that there might be different pathways involved in the pathogenesis of PCOS. It is likely that the production of DHEA and DHEAS in PCOS patients is related to that of A4 of adrenal or ovarian origin in nonobese patients. More studies are needed to determine the etiology of adrenal androgen excess.

How can I lower my DHEA levels naturally?

Chronic daily stress PTSD PCOS Elevated prolactin Non-classical adrenal hyperplasia

Symptoms of elevated DHEA include:

Management of elevated DHEA:

Lifestyle

Gut Repair

Anti-androgen Therapeutics

You might be interested: How To Cure Gyno Naturally

High DHEA levels can be a very serious indicator of deeper problems, thus it is necessary to assure that possible origins of elevated levels are properly evaluated.

: Natural Treatments for Elevated DHEA — POYNOR HEALTH

Why is my body producing too much DHEA?

What Abnormal Results Mean – An increase in DHEA-sulfate may be due to:

A common genetic disorder called congenital adrenal hyperplasia,A tumor of the adrenal gland, which can be benign or be a cancer.A common problem in women younger than 50, called polycystic ovary syndrome, Body changes of a girl in puberty happening earlier than normal.

A decrease in DHEA sulfate may be due to:

Adrenal gland disorders that produce lower than normal amounts of adrenal hormones, including adrenal insufficiency and Addison disease The pituitary gland not producing normal amounts of its hormones ( hypopituitarism )Taking glucocorticoid medicines

DHEA levels normally decline with age in both men and women. There is no reliable evidence that taking DHEA supplements prevents aging-related conditions.

What is the root cause of high DHEA?

If your level of DHEA-S is high, it means that your body is making too much of the hormones. This excess may be related to adrenal cancer, tumors, or excess growth of adrenal hormone-producing tissue (hyperplasia). If your DHEA level is low, it may mean that your adrenal glands are not making enough hormones.

Can chronic stress cause high DHEA?

4. Discussion – To our knowledge, this is the first study to examine the adrenocortical response of plasma DHEAS to a novel stressor in rhesus monkeys. As predicted, we found that DHEAS concentrations increased in response to the initial session of chair restraint (acute stressor) in adult male rhesus monkeys.

Unlike the DHEAS response of female rhesus monkeys to blood sampling procedures where cortisol concentrations were increased from baseline at 30 min and DHEAS concentrations were increased at 90 min ( Fuller et al., 1984 ), our animals showed significant increases in both cortisol and DHEAS concentrations from baseline at 30 min (cortisol data, Ruys et al, 2004 ).

Thus, it appears that the adrenocortical response of cortisol and DHEAS to acute stress is similar, at least in this situation. In the examination of other aspects of HPA activity, we found that DHEAS concentrations (like cortisol concentrations) showed a diurnal rhythm with higher concentrations in the morning than in the evening.

Variation in plasma DHEAS concentrations across the day has been confirmed in another study of rhesus monkeys ( Goncharova et al., 2006 ). Also consistent with other studies in rhesus monkeys ( Wickings and Nieschlag, 1978 ; Koritnik et al., 1983 ), we found that DHEAS concentrations decreased in response to dexamethasone (DEX) administration.

During the first chair restraint session that followed the DEX administration (first DEX restraint session), the low dose of DEX did not fully block DHEAS secretion. DHEAS concentrations increased and “broke out” of the DEX suppression 60 min after the animals were placed in chair restraint for the first time.

During the second DEX restraint session, which was each animal’s ninth time in the restraint chair, the standard dose of DEX was more effective in keeping DHEAS from “breaking out” from DEX suppression compared to the first DEX restraint session. The DHEAS response to the DEX restraint sessions was similar to the cortisol response in these animals.

Both cortisol and DHEAS “broke out” of DEX suppression during the first DEX restraint session and both hormones remained low in the last DEX restraint session ( Ruys et al., 2004 ). The lack of a large hormonal response (for DHEAS in addition to cortisol) during the last DEX restraint session (compared to the first) provides further support for the Ruys et al.

2004) conclusion that the HPA axis was more sensitive to the negative feedback effects of glucocorticoids after a week of consecutive chair restraint. Although the adrenocortical response of cortisol and DHEAS were similar with regard to diurnal rhythm, DEX suppression, and response to acute stress, the DHEAS response was different from the cortisol response following repeated exposure to chair restraint stress in our group of adult male rhesus monkeys.

Unlike the reduced cortisol response that was observed after seven days of two hour consecutive chair restraint ( Ruys et al., 2004 ), the animals’ DHEAS response to the last consecutive restraint session was as strong as the DHEAS response to the initial restraint session.

This result was surprising given that repeated exposure to a stressor typically results in a decreased glucocorticoid response, which is what we previously observed in this group of animals where cortisol concentrations increased for the first 30 min and then did not change (overall reduction of 29.8%; Ruys et al., 2004 ).

Another piece of evidence that there was a change in the HPA axis across the week of consecutive chair restraint comes from morning basal samples collected prior to chair restraint and two more times following the first and last day of consecutive chair restraint.

DHEAS concentrations on the morning after the first day of restraint were no different from pre-restraint samples.
After a week of chair restraint, DHEAS concentrations on the morning after the last day of restraint were higher than pre-restraint samples.
Unlike DHEAS, basal cortisol concentrations were higher the morning after the first consecutive session of chair restraint but no different from pre-restraint morning samples on the morning following the last session of restraint ( Ruys et al, 2004 ).

It is unclear why an increase in DHEAS concentrations was not observed on the morning after the initial chair restraint session as it was for cortisol. DHEAS concentrations increased in response to both the first and the last chair restraint sessions, but basal DHEAS concentrations were only higher on the morning after the last day of consecutive chair restraint, suggesting that the DHEAS response (unlike the cortisol response) was still activated after a week of chair restraint.

Physical restraint of monkeys in specially designed chairs is a routine procedure in many laboratories where experimental protocols require animals to sit in place for sustained periods or require close contact between animals and humans.
Animals quickly submit to the procedure of being placed in restraint and show substantial reductions in behavioral agitation.

Most investigators have relied on such behavioral changes as indicators of habituation to the chairing procedure. However, behavior is not necessarily an indicator of underlying physiological processes ( Ruys et al., 2004 ). In Ruys et al (2004), we argued that the reduction in cortisol could be due to either (1) psychological habituation to the stressor or (2) physiological adaptation to avoid sustained high levels of circulating glucocorticoids.

In psychological habituation, the cortisol response is reduced when chair restraint is no longer perceived as a “stressor” and subsequently, the HPA response is reduced. In physiological adaptation, the animal still perceives chair restraint as a stressor, but the body has adapted physiologically in order to avoid sustained high levels of circulating glucocorticoids, which can be cytotoxic.

When the animals were re-exposed to the chair restraint procedure following a six-month absence, they showed a full glucocorticoid response (and remained behaviorally similar to the last session of consecutive chair restraint). Given these findings, the diminished glucocorticoid response observed on the last day of consecutive chair restraint was reasoned to be due to physiological adaptation, rather than psychological habituation ( Ruys et al., 2004 ).

Our current investigation examining the adrenocortical response of DHEAS demonstrates that part of the HPA axis still responding to the chair restraint and, therefore, chairing is still perceived by the animal as “stressful.” The dissociation between cortisol and DHEAS concentrations has been documented under conditions of chronic illness ( Parker et al., 1985 ), as well as during aging, surgery and fasting ( Maninger et al., 2009 ).

However, this pattern is typically characterized by an increase in cortisol and a decrease in DHEAS concentrations. In contrast to this pattern shown in chronic illness, we found that the cortisol response was reduced following a chronic laboratory stressor (repeated chair restraint), while the DHEAS response was sustained after repeated exposure to the stressor.

Thus, we observed a decrease in cortisol responsiveness and a sustained increase in DHEAS responsiveness. Scientists have been searching for decades for another pituitary secretagogue for DHEAS and other adrenal androgens, but so far, none has been found, although many modulators have been proposed ( Parker and Odell, 1980 ).

More recently, there has been research investigating interactions between the adrenal cortex and adrenal medulla ( Ehrhart-Bornstein and Bornstein, 2008 ). A local CRH/ACTH system has been found in the adrenal medulla ( Vrezas et al., 2003 ), which may help explain why an increase in DHEAS is observed in response to acute and chronic stress, since the zona reticularis is closest in proximity to the adrenal medulla.

Unlike the high sustained glucocorticoid output that is often predicted for individuals experiencing chronic stress, our animals showed a reduced cortisol response following repeated exposure to the stressor ( Ruys et al., 2004 ).
A reduction in cortisol concentrations also has been observed in other studies from our laboratory on chronic social stress in squirrel monkeys and rhesus monkeys ( Mendoza et al., 2000 ).

Because one of the primary functions of cortisol is to terminate the stress response ( Munck et al., 1984 ), the negative effects of chronic stress may be due to cortisol levels that are too low and unable to suppress and terminate the stress response.

While DHEA(S) may buffer the effects of high cortisol, it is unclear if DHEA(S) modulates instances where chronic stress is accompanied by low basal cortisol concentrations or a lack of cortisol responsiveness.
This cortisol response was observed in our monkeys exposed to repeated chair restraint ( Ruys et al., 2004 ), and has been observed in people with post-traumatic stress disorder (PTSD) ( Yehuda, 2001 ).

High DHEA(S) responses to ACTH have been speculated to be salutary in people with PTSD ( Rasmusson et al., 2004 ), yet little research has been done on the stress-responsiveness of DHEAS. Our animals showed a sustained increase in DHEAS in response to both acute and chronic stress.

Interestingly, the physiology of our monkeys exposed to repeated chair restraint is similar to people with PTSD, which is characterized by low cortisol concentrations, increased DHEA or DHEAS concentrations, and increased sensitivity to glucocorticoid feedback ( Yehuda, 2001 ; Yehuda et al., 2006 ).

What role DHEA(S) is playing with regard to PTSD is still unclear, but repeated stress studies in rhesus monkeys may be helpful in understanding whether alterations in DHEA(S) are associated with pathology or adaptation.

How long does it take to lower DHEAS?

DHEAS is a biomarker that is particularly important in women’s health and physiology. DHEAS is an abundant molecule in the body that decreases naturally as women age. While it garners limited attention in health-related media, becoming informed about your own DHEAS levels using InsideTracker may help you optimize your muscle and bone health, sexual function, fitness performance, and longevity. Dehydroepiandrosterone-sulfate, or DHEAS, is the form of the molecule dehydroepiandrosterone (DHEA) that is naturally modified in the body so it can be stored in the blood. DHEA is synthesized from cholesterol and stored as DHEAS until it is needed to make different steroid sex hormones, including estradiol and testosterone, as well as other sex steroid precursor molecules.

These hormones are crucial in maintaining energy, muscle and bone health, and sexual function in both men and women. Estrogen, testosterone, and other important sex hormones are produced by the gonads—the testes in men and the ovaries in women. In men, the testes continue to release testosterone and the other sex steroids at rates that decline slowly but steadily as they age.

In contrast, when women reach menopause the ovaries completely cease to produce sex hormones such as estrogen. The hormonal fluctuations of menopause thus lead to a variety of physiological changes, and at this time, DHEAS becomes the only source of the essential sex hormones in women.

DHEAS is produced by the adrenal cortex of the kidney, a set of glands that produce a class of hormones called corticosteroids. Other examples of these corticosteroids include cortisol, which is involved in immunit y and responding to stress, and the mineralocorticoids, which are involved in regulating blood pressure.

Of the molecules produced by the adrenal cortex, DHEAS is found in highest concentration in blood serum. However, scientists do not yet completely understand how it works or if it has functions aside from being a precursor for the sex steroids. What scientists do know is that in both women and in men, DHEAS levels increase from early childhood until they peak again during age 20-30. Lower levels of DHEAS are associated with higher risk of conditions such as diminished immunity, increased risk of cardiovascular disease and stroke, and unstable blood sugar levels. Measuring levels of DHEAS is also used as a clinical indicator of different conditions related to pituitary and adrenal function.

Low levels of DHEAS in the blood are linked to decreased pituitary and adrenal function, which can cause many health problems for women, including weakness and fatigue, difficulty in controlling weight, menstrual irregularity, and infertility. High DHEAS levels are associated with overactive adrenal glands, polycystic ovary syndrome, and early puberty.

These conditions can also lead to difficulty in controlling weight, menstrual irregularity, and infertility. Additional symptoms in women with overactive pituitary and adrenal glands include acne and excess hair growth all over the body (hirsutism). Because DHEAS levels change with both chronological age and with disorders that have serious implications for women’s health, keeping track of your DHEAS levels is a great tool to optimize your overall health in relation to your age.

You can measure your DHEAS levels with InsideTracker which assesses DHEAS along with other biomarkers, such as C-reactive protein, that are important indicators of longevity and physiological health. If your DHEAS levels are not optimized, InsideTracker provides diet, exercise, and lifestyle interventions to help you optimize its levels and maximize your fitness and wellness.

For example, research has shown that regular moderate cardiovascular activity, such as briskly jogging for 30 minutes, and performing resistance exercises such as squats can increase DHEAS levels over time for women of all ages and activity levels. Making simple changes to your diet based on your current habits—like eating more healthy animal protein if you do not frequently eat meat, or eating less processed meat if your diet is already rich in meat sources—can boost your DHEAS levels. The “S” in DHEAS stands for the sulfate group (one Sulfur and four Oxygen atoms) that is added to DHEA. Without this sulfate group, DHEA is not very soluble in the blood because it is a lipid, meaning that it does not mix or dissolve in blood (similar to the way water and oil do not mix with each other).

The sulfate group facilitates the storage and transport of DHEAS in the blood. This is why there is approximately 1000 times more DHEAS than there is DHEA in the blood, which makes it easier to measure DHEAS levels. However, DHEA is actually the form that is eventually converted into testosterone, estradiol, and other important molecules.

When DHEA is needed, specific enzymes remove the sulfate from DHEAS, converting it back into its active state. Because DHEA and DHEAS are freely interconverted, measuring DHEAS levels is a reliable indicator of the amount of active DHEA in the body that is available to make other hormones.

Furthermore, research has shown that DHEAS levels in the blood are more stable throughout the day than DHEAS levels. This yields more consistent measurements in a person over time, so changes in DHEAS levels represent changes in health, rather than typical daily fluctuations. DHEA supplements are readily available, particularly in the United States.

Unfortunately, the quality of these supplements is not well standardized, meaning that the ingredients listed in the supplement may differ from its actual contents. Many studies have investigated the effects of increasing DHEAS levels by taking DHEA supplements from external sources (in other words, from sources that are outside of your body’s natural means of producing more DHEAS), but when taken together, the data that is currently available does not show that DHEA supplements are an effective way to improve your health and wellbeing.

Plus, most of these studies take place for less than a year- too short in duration to investigate the long-term impacts of these supplements. Current research findings indicate that DHEAS is not toxic, but there is not enough data about the effects of DHEA supplements on health after long term use to know if DHEA supplementation causes more harm than good in the long run.

For now, it is safer to stick to natural methods of boosting your body’s DHEAS levels through modifications to diet and exercise that will increase DHEAS and improve your overall health and performance. DHEAS is an essential precursor of important sex steroid hormones, particularly for women, that naturally declines with age.

Having DHEAS levels outside of the optimal range for your age is associated with a variety of chronic conditions that can be prevented by making simple changes to exercise routine and diet. DHEAS is not typically included during standard blood draws. InsideTracker offers DHEAS analysis for women as part of the Ultimate, Foundation, and InnerAge 2.0 plans,

References Quiroga MF, Angerami MT, Santucci N, Ameri D, Francos JL, Wallach J, Sued O, Cahn P, Salomon H, Bottasso O. ” Dynamics of adrenal steroids are related to variations in Th1 and Treg populations during Mycobacterium tuberculosis infection in HIV positive persons,” PLoS ONE 7:3 (2012): e33061.

Sanders JL, Boudreau RM, Cappola AR, Arnold AM, Robbins J, Cushman M, Newman AB. ” Cardiovascular disease is associated with greater incident dehydroepiandrosterone sulfate decline in the oldest old: the cardiovascular health study all stars study,” Journal of the American Geriatric Society 58:3 (2010): 421-426 Jiménez MC, Sun Q, Schürks M, Chiuve S, Hu FB, Manson JE, Rexrode KM.

” Low dehydroepiandrosterone sulfate is associated with increased risk of ischemic stroke among women,” Stroke; a journal of cerebral circulation 44:7 (2013): 1784-9 Liu L, Wang M, Yang X, Bi M, Na L, Niu Y, Li Y, Sun C. ” Fasting Serum Lipid and Dehydroepiandrosterone sulfate as important metabolites for detecting isolated postchallenge diabetes: serum metabolomics via ultra high performance LC-MS,” Clinical Chemistry 59:9 (2013): 1333-48 Karelis AD, Fex A, Filion ME, Adlercreutz H, Aubertin-Leheudre M.

” Comparisons of sex hormonal and metabolic profiles between omnivores and vegetarians in pre and post menopausal women,” British Journal of Nutrition 104:2 (2010): 222-6 Mattei J, Noel SE, Tucker KL. ” A meat, processed meat, and french fries dietary pattern is associated w high allostatic load in older Puerto Rican adults,” Journal of the American Diet Association 111:10 (2011) 1498-506 Izawa S, Saito K, Shirotsuki K, Sugaya N, Nomura S.

” Effects of prolonged stress on salivary cortisol and dehydroepiandrosterone: a study of a 2wk teaching practice ” – Psychoneuroendocrinology 37:6 (2012) 852-8 Lennartsson AK, Theorell T, Rockwood AL, Kushnir MM, Jonsdottir IH. ” Perceived stress at work is assocated with lower levels of DHEAS,” PLoS ONE 8:8 (2013) e72460 Hammer, F.

What are symptoms of DHEA?

DHEA ( dehydroepiandrosterone ) is a hormone that’s naturally produced by the adrenal glands. Levels of DHEA naturally drop after age 30. Some people take DHEA supplements in the hopes that DHEA will have health benefits and prevent some illnesses. However, the evidence is mixed.

A number of studies have found that DHEA supplements may help people with depression, obesity, lupus, and adrenal insufficiency.
DHEA may also improve skin in older people and help treat osteoporosis, vaginal atrophy, erectile dysfunction, and some psychological conditions.
But study results are mixed and often contradictory.

Low DHEA levels are associated with aging and a number of diseases, such as anorexia, type 2 diabetes, and HIV. In older men, having low levels of DHEA is also associated with a higher chance of death. However, it’s not clear that using DHEA supplements will help lower the risks of getting any diseases.

DHEA is used by some people who want to “reverse” aging and boost immunity, cognitive function, and muscle strength. For now, studies don’t back up these uses. DHEA has been studied as a treatment for other conditions, ranging from cardiovascular disease to menopause to Alzheimer’s. The results have been unclear.

There are no food sources of DHEA. Wild yams contain a substance similar to DHEA that is used to make DHEA in the laboratory. The body manufactures DHEA naturally in the adrenal glands.

Risks. Using high doses of DHEA may not be safe. People who have heart problems, liver disease, diabetes, high cholesterol, thyroid problems, polycystic ovary syndrome, and a history of clotting problems should not use DHEA. DHEA may increase the risk of some cancers that are affected by hormones, like cancers of the breast, ovaries, and prostate, Side effects. Most side effects are mild, like headache, fatigue, insomnia, and congestion. Because DHEA affects hormone levels, it can cause other symptoms. Women may have abnormal periods, acne, or mood changes. They might also take on masculine characteristics, such as facial hair or a deeper voice. Men might develop more breast tissue, high blood pressure, and other problems. Interactions. If you take any medications regularly, talk to your doctor before you start using DHEA supplements. They could interact with blood thinners, anticonvulsants, hormone therapy, and drugs for diabetes and heart or liver problems.

Because DHEA is a powerful hormone, it is not recommended for children or for women who are pregnant or breastfeeding,

Can DHEA cause anxiety?

Footnotes – 1 Results of this linear regression were consistent when menarche status was entered as a predictor instead of PDS total scores. A significant regression equation was found, F (3, 283) = 7.29, p <,001, with an R 2 of,07. Higher DHEA ( β =,26, t (285) = 3.12, p <,01) was associated with greater SCARED scores. However, testosterone concentrations ( β = −.07, t (285) = −.90, p =,37) and menarche status ( β =,10, t (285) = 1.53, p =,13) were not independently associated with SCARED scores. Thus, greater DHEA was associated with increased anxiety symptoms even when controlling for testosterone concentrations and menarche status.2 Results of this linear regression were consistent when menarche status was entered as a predictor instead of PDS total scores. A significant regression equation was found, F (3, 279) = 4.40, p <,01, with an R 2 of,05. Higher DHEA ( β =,26, t (285) = 3.03, p <,01) was associated with greater anxiety symptom counts. However, testosterone concentrations ( β = −.07, t (285) = −.83, p =,41) and menarche status ( β = −.01, t (285) = −.22, p =,83) were not independently associated with anxiety symptom counts. Thus, greater DHEA was associated with increased anxiety symptom counts even when controlling for testosterone concentrations and menarche status.3 When individuals with a sole anxiety disorder of specific phobia were removed from both the "anxiety" and "no anxiety" groups, the association between anxiety disorder status and DHEA remained significant ( r (254)=,15, p <,05).4 Results of this logistic regression were consistent when menarche status was entered as a predictor instead of PDS scores. Greater DHEA was significantly associated with the presence of an anxiety disorder (odds ratio = 1.01, 95% CI = 1.00–1.01, p < 0.05). However, anxiety disorder status was not associated with menarche status (odds ratio =,94, 95% CI =,43–2.00, p = 0.84).5 When participant age was substituted for PDS scores in the regressions predicting SCARED total scores, anxiety disorder status, and anxiety symptom counts, DHEA remained a significant predictor (all p s <,05) of SCARED scores, anxiety disorder status, and anxiety symptom counts, while age was not significantly associated with SCARED scores, anxiety disorder status, or anxiety symptom counts (all p s >,10). Publisher’s Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

What does DHEA do to ovaries?

Conclusions – In the US and Western Europe, women above the age of 38 years and young women with premature ovarian aging and diminished ovarian reserve represent currently a sizable group of infertile patients. A low cost and potentially effective clinical approach such as DHEA supplementation is quite attractive as an adjuvant before ART, with an increase in spontaneous conceptions. In a recent online survey by IVF Worldwide, 25.8 % of respondents (representing 196 centers in 45 countries performing 124,700 ART cycles) used DHEA in their poor responder patients, 97 % of them about 3 months before stimulation start, As mentioned above, DHEA assumes a role in improving the pregnancy rate in young women with premature diminished ovarian reserve as well as decreasing the age related aneuploidy and eventually miscarriage rate in older women with age related diminished ovarian reserve. It is important to note however that all the above studies suffer from improper design, low number of enrolled subjects, and lack of truly randomized trials. Of note, Gleicher and Barad attempted to do two randomized trials but the trials had to be terminated for poor recruitment as prospective women refused to be randomized to the placebo arm. We believe that DHEA supplementation is an emerging concept in improving oocyte/ embryo yields and possibly oocyte quality by affecting the follicular environment. Much remains to be answered however, such as who does and who does not benefit from DHEA supplementation, what is the appropriate (and maximal) dose and duration, best delivery system, whether an altered sex ratio is present, and whether DHEA is of any use in women with undetectable AMH levels (<0.16 ng/ml). Based on the above studies, DHEA supplementation seems to improve the ovarian environment where follicle maturation takes place, and appears to function by acting on the androgen receptors that are expressed on the granulosa cells and ovarian stroma, resulting in increasing antral follicle counts and AMH levels, and therefore ovarian reserve. While the criticism of the dearth of studies and lack of adequately powered randomized prospective placebo-controlled trials is valid, we agree with Gleicher and Barad that these studies will be extremely hard if not impossible to perform, While DHEA's use is considered experimental, until (and if) such studies are published, and considering the absence of significant side effects, the low cost, and the increase in spontaneous pregnancies, we suggest that utilization of DHEA in suitable, consented, and well informed patients may improve ovarian reserve, response to ovarian stimulation, and potentially pregnancy outcome.

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Can DHEA cause ovarian cysts?

Abstract – Exogenous dehydroepiandrosterone (DHEA) produces ovarian cysts and atretic follicles in mice. We sought to test the hypothesis that the abnormal follicular development found after DHEA administration in mice results from aberrant ovarian apoptosis. DHEA was injected subcutaneouly for 15 days. Controls received an equivalent volume of vehicle. Follicle size was measured, and the proportion of ovarian follicles containing apoptotis was assessed by in situ end-labeling of DNA. DHEA resulted in a greater proportion of follicles with evidence of apoptosis (62.4% in the DHEA group vs.53.0% in the vehicle group ; p = 0.031). DHEA also produced larger follicles (mean diameter: 234.7um +/- 24.6um in the DHEA group vs.204.6um +/- 11.4um in the vehicle group; p 500um while only one of the mice in the vehicle group contained a follicle > 500um in diameter (p < 0.001). We conclude that DHEA administration results in increased ovarian apoptosis and in larger follicle size, thereby producing a characteristic cystic and atretic appearance in the mouse ovary. This may be the mechanism by which androgens cause ovarian cyst formation.

Does high DHEA cause weight gain?

DHEA may increase the production of the male hormone testosterone. Women should be aware of the risk of developing signs of masculinization. These include loss of hair on the head, deepening of the voice, growth of hair on the face, weight gain around the waist, or acne.

Can exercise lower DHEA?

Abstract – Dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) are hormones produced by the adrenal cortex that decline in concentration with age. Decreased DHEA levels are associated with age-related disease and oxidative stress but might be increased in younger adults by exercise. Studies are presented assessing the response of DHEA and DHEAS to varied-intensity exercise in older age. DHEA increased significantly in young adults (14.5 +/- 6.1 ng/ml rising to 21.1 +/- 7.5 ng/ml; p <,01), whereas DHEAS decreased significantly (2.56 +/- 1.11 microg/ml falling to 1.90 +/- 0.8 microg/ml; p <,05), after submaximal exercise. DHEA and DHEAS levels were significantly lower in older adults than in younger adults (p <,01), and there was no observed response of either hormone to exercise in older adults. Lipoprotein protein carbonylation is presented as a measure of oxidative status and significantly decreased in younger adults postexercise. Participants with higher DHEA postexercise had lower LDL protein carbonyl concentrations (Pearson's coefficient -.409, p <,05).

How do I stop DHEA from converting to estrogen?

Hypothesis Dehydroepiandrosterone sulfate (dhea-s) causes a proliferation of estrogen receptor (er)–positive breast cancer cells, even with tamoxifen citrate blockade. the er antagonist ici 182 780 (fulvestrant) will more effectively stop the proliferative effect of dhea-s on breast cancer cells.

Design Examination of in vitro breast cancer cell growth in the presence of fulvestrant and dhea-s.
Setting Surgical oncology research laboratory.
Interventions The er-positive and er-negative breast cancer cells were pretreated with fulvestrant and stimulated with 900 µg/dl (22.8 µmol/l) of dhea-s.
Main outcome measures Assays using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, thiazolyl blue, were performed on the third, fifth, and seventh days poststimulation and permitted the calculation of growth percent change.

Results The er-positive and progesterone receptor–positive cells demonstrated universal proliferation of 107% by day 7 when treated with fulvestrant, regardless of the dose. the er-negative and progesterone receptor–negative cells demonstrated growth inhibition.

Conclusions The dhea-s circumvented fulvestrant inhibition and caused er-positive breast cancer cell growth. BReast cancer remains a major epidemiological concern, with estimates that the disease will have affected 5 million women in the last decade.1 Although endocrine therapy has been clinically available for the past century and has proven beneficial for many patients, disease progression still occurs.

There are 3 mechanisms by which antiestrogen therapy for hormone-sensitive breast cancer may be implemented. the source of the estrogens may be ablated, the estrogen receptor (er) may be blocked with antagonists, or the conversion of estrogens from precursors may be blocked with aromatase inhibitors.

Currently, most patients receive tamoxifen citrate, an antagonist that competitively inhibits the binding of estrogen to its receptor.
Whereas tamoxifen achieves antitumor effects via antagonism of the er, the drug also retains partial to full agonist properties depending on the target organ and species.2 – 4 Although beneficial to bone density and serum lipid profiles, er agonistic properties are thought to be responsible for the increase in endometrial cancers reported among tamoxifen users.2, 5 Of concern is the fact that this agonistic effect may be largely responsible for tamoxifen resistance and subsequent disease progression.6 Fulvestrant (ici 182 780) is a pure er antagonist.7, 8 It has been shown in in vitro studies to down-regulate the er 3 and has recently been approved as a second-line hormonal therapy.9 In vitro studies have also demonstrated that some breast cancer cell lines resistant to tamoxifen retain their sensitivity to fulvestrant, indicating that the drug has a role in the treatment of cancers that progress during adjuvant tamoxifen therapy.10 Because it lacks estrogen agonist properties, adverse effect profiles appear limited with no increased risk of endometrial thickening or thrombogenicity.

however, the beneficial effects found in the lipid levels and bone density patterns of tamoxifen users are not seen with fulvestrant therapy. Current therapeutic approaches have focused chiefly on estrogens and their effects on breast cancer growth, but the role that estrogen precursors play in cellular proliferation has not been fully explored.

We previously demonstrated that high levels of dehydroepiandrosterone sulfate (dhea-s), a steroid precursor of 75% to 100% of the estrogens in women, is a risk factor for disease progression in women with stage iv breast cancer treated with third-generation aromatase inhibitors.11 We reported that er-positive cell lines proliferated when exposed to dhea-s in vitro.

the conversion of dhea-s into estrogens was prevented with the use of anastrozole, demonstrating the specificity of this compound. we subsequently reported that high dhea-s levels are a risk factor for disease progression in women treated with adjuvant tamoxifen therapy.

concomitant in vitro studies demonstrated that dhea-s used the er and induced cell proliferation even in the presence of tamoxifen. we speculated that because tamoxifen is a competitive inhibitor of the er, sufficient quantities of dhea-s were able to overcome its inhibitory blockade.12 On the basis of these studies and suppositions, we hypothesized that blockade of the er by the pure antagonist fulvestrant could ameliorate dhea-s–induced proliferation of hormone-sensitive breast cancer cells.

therefore, in vitro studies were undertaken in which cells were cultured with high levels of dhea-s. fulvestrant was used as the er blocker to further delineate the ability of dhea-s to induce cellular proliferation. We obtained er-positive and progesterone receptor(pr)–positive (t-47d) and er-negative and pr-negative (hcc1937) cell lines from atcc (rockville, md).

cells were plated onto 96-well plates in triplicate at a concentration of 1 × 10 4 cells per well. they were then grown in type-specific hormone-depleted media composed of phenol red–free rpmi (gibco/life technologies, east syracuse, ny), 5% dextran charcoal-treated fetal bovine serum (hyclone, logan, utah), 1% sodium pyruvate, and 0.5% gentamicin sulfate (gibco brl, rockville), either with (t-47d) or without (hcc1937) 1% insulin (gibco brl), at 37°c with 5% carbon dioxide.

After 5 days of incubation in hormone-depleted media and following 4 hours of pretreatment with 100µm anastrozole (astrazeneca, wilmington, del), cells were stimulated with 900 µg/dl (22.8 umol/l) of dhea-s (sigma, st louis, mo). cells with only anastrozole and the vehicle were maintained in tandem.

Parallel cultures were pretreated with 100µm anastrozole and fulvestrant (ici 182 780; astrazeneca) at concentrations ranging from 10µm to 0.0001nm prior to stimulation with 900 µg/dl (22.8 µmol/l) of dhea-s.
Wells containing the vehicle, anastrozole, and fulvestrant but no dhea-s were again maintained as controls.

Cell proliferation was determined using an assay (sigma) performed on poststimulation days 1, 3, and 5. this assay, which counts only living cells, is a rapid colorimetric assay composed of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, thiazolyl blue.13 A microplate reader (mrx; dynatech technologies, chantilly, va) recorded optical density readings of each plate at a wavelength of 570 nm.

growth or inhibition was reported as growth percent change of the dhea-s–treated cells vs those grown in the vehicle, anastrozole, and fulvestrant. statistical significance of differences in growth between various cell cultures was determined using a 2-tailed t test. ENzyme immunoassay for estrogens The t-47d cells were plated and cultured and subjected to pretreatment, blockade, and dhea-s stimulation, as mentioned previously.

cells were lysed with ripa buffer (150nm sodium chloride, 50nm tris-hydrochloride, 1% nonidet p-40 (roche, basel, switzerland), 0.5% sodium deoxycholate, 1% sodium dodecyl sulfate, and 1 tablet of protease inhibitor (complete mini; roche). after the lysates were pelleted, the resultant cell suspensions were collected and purified using a ym-10 micron filter (millipore, bedford, mass).

estradiol enzyme immunoassays (alpco diagnostics, windham, nh) were performed and read using a microplate reader (mrx; dynatech technologies) at 450 nm. ENzyme immunoassay for intracellular estrogen levels Immunoassays performed on t-47d cells demonstrated that negligible levels of estradiol were detected in all cells treated with dhea-s and anastrozole.

this indicates that, when present, anastrozole provides effective blockade of the conversion of dhea-s into estrogens. EFfects of dhea-s stimulation When er-positive t-47d cells were stimulated with 900 µg/dl (22.8 umol/l) of dhea-s while blocking the dhea-s conversion to estrogens with anastrozole, cell growth was 41% higher than that achieved with cells exposed only to the vehicle and anastrozole.

The er-negative hcc1937 cell lines failed to exhibit growth in identical conditions (growth, −5%) ( Figure 1 ).
Growth of t-47d cells was inhibited by fulvestrant treatment at all concentrations, ranging from 0.0001nm to 10µm.
However, no concentration of fulvestrant within this range prevented cell proliferation when er-positive t-47d cells were exposed to 900 µg/dl (22.8 umol/l) of dhea-s and anastrozole.

cell cultures containing fulvestrant concentrations of 0.0001nm to 0.001nm exhibited a mean growth increase 26% higher than controls. cell cultures with concentrations of 0.1nm to 10nm exhibited an average cell proliferation of 32%, whereas those with fulvestrant concentrations between 0.1µm and 10µm resulted in an average cell proliferation of 39% ( Figure 2 ).

The er-negative hcc1937 cell line was unaffected by exposure to fulvestrant blockade.
In identical experimental conditions, hcc1937 cells demonstrated no proliferation.
Growth inhibition was similar to that seen in cultures treated only with dhea-s and anastrozole (−5%).
That dhea-s induces the proliferation of t-47d cells even in the presence of fulvestrant is graphically depicted in Figure 3,

with all cultures undergoing fulvestrant blockade, there was no significant difference in growth on day 3 between cells stimulated with dhea-s and those that were not ( P =,73). in the presence of dhea-s, there was a 34% increase in cell growth on day 5 ( P =,04) and a 107% increase on day 7 ( P =,02) compared with controls on the same days.

Our previous studies demonstrated that dhea-s stimulates the growth of er-positive breast cancer cells 11 and that competitive tamoxifen blockade of the er may be circumvented by sufficient quantities of dhea-s.12 In this study, the competitive blockade of the er provided by fulvestrant failed to prevent dhea-s–induced proliferation of er-positive breast cancer cells.

Having shown in our studies that high levels of serum dhea-s may function as an agonist er ligand and that this may contribute to treatment failure during tamoxifen therapy, we hypothesized that fulvestrant, as a pure antagonist of the er, would be more useful for blocking the effects of dhea-s.

This study demonstrated that dhea-s induced cell proliferation even in the presence of a pure er antagonist, fulvestrant.
Contrary to our expectations, at no concentration of fulvestrant was growth inhibited.
Because the immunoassay results demonstrated no conversion of estradiol from dhea-s, it is likely that the dhea-s was responsible for the proliferation of er-positive cells.

Our results indicate that dhea-s induces cellular proliferation in the presence of multiple agents and in a variety of settings. in environments where the estrogen concentration is low, such as after menopause or during third-generation aromatase inhibitor therapy, dhea-s may function as a ligand for the er and thereby induce cellular proliferation.

Even in the presence of tamoxifen or fulvestrant, when levels of dhea-s are high, it may be able to outcompete either agent for the er, thereby functioning as a ligand and inducing proliferative cell-signaling pathways.
Extensive preclinical studies suggest that er expression is down-regulated following fulvestrant treatment.3, 14 – 16 However, our results suggest that the inhibitory effect of fulvestrant is more likely due to blockade of the er than down-regulation.

if dhea-s functions as an er ligand, as our previous studies suggest, and if there were down-regulation of the er by fulvestrant, some dose of fulvestrant should have been able to block the proliferative effects of dhea-s. because this was not observed with any dose of fulvestrant, it is more likely that this drug functions chiefly through competitive blockade of the er.

We are conducting ongoing studies to identify the changes in gene expression and cellular response to dhea-s stimulation in the presence of tamoxifen or fulvestrant.
The results of this study have important clinical implications and warrant further investigation.
Our previous studies indicated that serum dhea-s levels higher than 90 µg/dl (2.28 µmol/l) are a risk factor for cancer progression among patients treated with third-generation aromatase inhibitors 11 and adjuvant tamoxifen therapy.12 The findings of this study indicate that high serum dhea-s levels are also a risk factor for disease progression in the presence of fulvestrant blockade.

this study further supports the need to monitor serum sex steroid levels, in particular dhea-s, during endocrine therapy. serially collecting these data will determine whether patients with low dhea-s levels are more likely to respond to fulvestrant and thus will define a patient population for whom this drug is best indicated.

In addition, actively lowering serum dhea-s levels may increase the number of patients who will respond to fulvestrant treatment.
The compound dhea-s is estrogenic in a low-estrogen environment; conversion to estrogens is not necessary for its activity.
It appears to compete with both tamoxifen and the pure antagonist fulvestrant for binding to the er.

given that dhea-s can stimulate the growth of breast cancer cells in the presence of multiple therapeutic agents, it may be more prudent to control dhea-s serum levels in patients with breast cancer. Corresponding author: rodney f. pommier, md, department of general surgery, oregon health and sciences university, 3181 sw sam jackson park rd, l223a, portland, or 97201 (e-mail: [email protected] ).

Accepted for publication april 5, 2002.
This study was supported in part by women’s golf clubs of the greater portland area and the oregon chapter of the order of the eastern star (portland).
This study was presented at the 74th annual meeting of the pacific coast surgical association; february 17, 2003; monterey, calif; and is published after peer review and discussion.

the discussions that follow are based on the originally submitted manuscript and not the revised manuscript. We thank astrazeneca (wilmington, del) for providing the anastrozole used in this study. Reprints: suellen toth-fejel, phd, department of general surgery, oregon health and sciences university, 3181 sw sam jackson park rd, l223a, portland, or 97201 (e-mail: [email protected] ).1.

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Surgery.2001;130 (6) 947- 953 PubMed Google Scholar Crossref 12. Calhoun KPommier RCheek J et al. The effect of high dehydroepiandrosterone-sulfate levels on tamoxifen blockade and breast cancer progression. Am j surg.2003;185411- 415 PubMed Google Scholar Crossref 13. Mosmann T Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity assays.

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Clin cancer res.2001;7 (suppl 12) 4369s- 4375s PubMed Google Scholar Roger e. alberty, md, portland, ore: When i was asked by dr pommier to comment on this paper, i thought, why me, oh lord? then i was reminded of my days in the navy when i was qualifying for submarines.

my division commander was interrogating me. i was explaining a very complicated hydraulic pump. i wasn’t doing too well. he said, “son, if you can’t do any better than that, i will call in the chaplain. you can explain it to him. if he understands what you are saying, i know you know what you are talking about.” so i come to you today as the chaplain.

if i can understand this paper, anybody can. The association of hormonal manipulation treating breast cancer goes back a long way and dates to a rather extraordinary operation in which sir percivall pott resected bilateral herniated ovaries in a young woman and noticed a change in the progression of her breast development.

over 100 years ago there were papers published on oophorectomy for treating metastatic breast cancer. after world war ii, glucocorticoids came on board and we were able to do adrenalectomies. for those of you in the audience who remember those days, some of the results were quite spectacular but unpredictable.

this paper helps explain why some people respond and some don’t. This work makes me think of a stealth bomber. you don’t see it coming, and it makes a big impact when it gets there. the literature is very recent and very scant. dr pommier’s group is one of the few in the country that is investigating dehydroepiandrosterone.

This work and other published works show that this hormone can block the effects of tamoxifen in vitro and clinically. as we see today, it works directly on estrogen receptor cells; it does not have to be converted to estrogen. i would like to emphasize that dhea-s is the only hormone in their survey of a panel of hormones that was associated with progression of disease.

In this study, fulvestrant, which permanently rebinds estrogen receptors, was unable to block the effects of dhea-s. now this is an in vitro study. evidently dhea-s can block any estrogen blockade currently available. if we are therefore to control the dhea-s, we are going to have to control the source.

I have 2 questions: (1) why in god’s name did they study this hormone in the first place? (2) will this lead to clinical work? are we going to revisit charles huggins’ works of the 1950s and 1960s when we are going back to either chemical or surgical adrenalectomy in the treatment of metastatic breast cancer? This is truly an important paper, and it is extremely timely because there is hardly anything published on this outside of pommier’s group.

Electron kebebew, md, san francisco, calif: I find your results interesting. it has been demonstrated that there are different estrogen receptor subtypes (eg, α, β). in the cell lines you studied, have you characterized the estrogen receptor subtypes? also, if it is not working through the estrogen receptor, what other alternative mechanism is it possibly working through? lastly, did you ever consider using estrogen-positive but progesterone-negative receptor cell lines? James e.

Goodnight, jr, md, phd, sacramento, calif: I have a brief question. the only way i know to block the dehydroepiandrosterone in vivo is to either take out the adrenal gland or block it with aminoglutethimide and then block the pituitary gland with hydrocortisone. is there another method in vivo to block the hormone production? Dr pommier: We have been measuring the serum sex steroid levels of estrone, estradiol, testosterone, and dhea-s in patients who have failed tamoxifen therapy for many years now.

we treated such patients with a total endocrine ablation consisting of an oophorectomy, adrenalectomy, or total adrenal suppression with aminoglutethimide, which was the first-generation aromatase inhibitor. we verified that the estrogen and the dhea sulfate levels went to zero to confirm that the endocrine ablation was in fact total.

If patients still had high dhea-s levels, then either they were not taking their aminoglutethimide or we had an incomplete adrenalectomy.
Patients would generally respond to this therapy for a few years.
When the third-generation aromatase inhibitors came out, we could substitute 4 daily doses of aminoglutethimide, 3 doses of hydrocortisone, and 1 dose of aldosterone with a single pill and avoid aminoglutethimide’s side effects of lethargy and rash, so we switched to them.

we continued to measure serum sex steroid levels in these patients, however. we were expecting the same response rates and durations that we had seen with aminoglutethimide. while some patients did respond to the new agents, some exhibited progressive disease after a short interval.

Thinking that i was seeing the emergence of hormone-insensitive disease, i biopsied some of the new tumors and found that they were all still er-positive. i then thought that perhaps the third-generation drugs did not inhibit conversion of dhea into estrogens equally well in all patients, but the sex steroid panels showed that the estrogen levels were zero in all patients; the new drugs were quite effective at preventing conversion.

as i plotted the data, i saw a clear division between the patients who were responding and those who were progressing. those responding had low dhea-s levels, generally less than 60 µg/dl. those who were progressing had dhea-s levels greater than 90 µg/dl, and the difference was highly statistically significant.

The patients with low dhea-s levels had response durations 3 times longer than those with high levels.
When we lowered the dhea-s levels in the patients who were progressing by giving them aminoglutethimide or an adrenalectomy, they all responded again.
This made me wonder what dhea-s itself could do to the estrogen receptor.

could it be estrogenic? Dr toth-fejel and i then conducted laboratory experiments on the t-47d cells, stimulating them with dhea-s but blocking the conversion of the dhea into estrogens with anastrozole. the results were that the dhea-s stimulated cellular proliferation as much as did estradiol.

Our other manuscript presented at this meeting shows, by immunofluorescence staining, that the dhea-s itself causes the estrogen receptor to translocate into the nucleus, an effect that is blocked by tamoxifen.
It also activates the map kinase pathway.
These effects are the same as those seen with estradiol.

the dhea-s itself is estrogenic. the old paradigm on which third-generation aromatase inhibitor therapy is based is that if there is no conversion of dhea-s, then there is no problem. our new paradigm is that in a low-estrogen environment, no conversion is a big problem.

The only known ways to lower high dhea-s levels are with aminoglutethimide, adrenalectomy, or high-dose steroids.
Our other data, which are in press, indicate that it may be beneficial to lower high dhea-s levels even in the adjuvant setting.
Giving high-dose steroids (which causes cushing syndrome) or doing adrenalectomies in the adjuvant setting are clearly going to be unacceptable.

we have found a way to lower dhea-s levels close to zero, with far fewer side effects. we use 2 rather than 4 doses of aminoglutethimide per day with full hydrocortisone replacement. the lethargy and rash associated with this drug are practically nonexistent with this regimen; all of our patients tolerate it very well, and their dhea-s levels are close to if not zero.

What we really need to develop is a drug that specifically blocks the production of dhea-s and leaves synthesis of adrenal cortisol and aldosterone unaffected. The t-47d cell line is er-positive, pr-positive, and androgen receptor–positive. the hcc1937 cells are er-negative, pr-negative, but androgen receptor–positive.

that was shown in our other work presented at this meeting, along with the surprising finding that dhea-s inhibited the growth of the hcc1937 cells. we think dhea does this through the androgen receptor. functionally, dhea is neither estrogen nor androgen but can be converted into either.

apparently its structure resembles the structure of either one enough that it can bind to both the estrogen receptor when estrogen levels are low or to the androgen receptor when testosterone levels are low. it triggers different responses that are specific to the profiles of receptors. We do not yet know whether dhea binds to the progesterone receptor as well, but this may be another mechanism by which it functions, especially in the presence of fulvestrant and tamoxifen.

we are beginning experiments with cells that are only pr-positive to further investigate this. alternatively, there may in fact be a specific dhea receptor. we intend to pursue that possibility.

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Does coffee lower DHEA?

Caffeine Anyone? By So what’s the scoop on caffeine? One minute someone says caffeine is good for you, and the following week you’re reading that it causes exhaustion, fatigue and addiction. It is estimated that approximately 80% of the world’s population uses caffeine on a daily basis, mainly in the form of coffee, tea, sodas and chocolate, but it is also found in some drugs, ‘decaffeinated’ coffee and tea, and energy drinks.

According to Harvard School of Public Health researchers involved in a 22-year study, the overall balance of risks and benefits of coffee consumption, are on the side of benefits.” Another study from Finland shows that middle aged people who consumed moderate amounts of coffee or tea (3–5 cups per day), were 65% less likely to develop dementia and Alzheimer’s disease by the time they reached their mid-sixties to seventies, compared with those who drank little coffee or avoided it altogether.

Other studies suggest that drinking coffee reduces the risk of being affected by Parkinson’s disease, cardiovascular disease, diabetes mellitus type 2, cirrhosis of the liver, and gout. But not everyone agrees that caffeine is beneficial, and questions remain about what exactly is the cause behind its reported benefits.

There are many new studies which appear to support caffeine but if you look closely, the scientists will not say that caffeine enhances your health and long-term well-being.
They might say a particular type or part of chocolate, or caffeine is good for you.
Most of coffee’s beneficial effects against Type 2 diabetes are not due to its caffeine content but something else, since the benefits are greatest in those drinking decaffeinated coffee,

We know that the antioxidants in roast coffee – lipophic antioxidants and chlorogenic acid lactones – are playing protective roles when it comes to protecting nerve cells, but it is unclear by which mechanism this occurs in other organs of the body. Menopausal women taking estrogen, for instance, will not enjoy reduced risk of Alzheimer’s and Parkinson’s.

In fact, their risks were increased. These finding was observed by the same Harvard researchers just mentioned – yet the dangers of drinking coffee to this group of women is rarely reported in popular media. Some studies point out that coffee consumption does not raise the risk of cardiovascular disease, yet other research has shown that chronic consumption may increase aortic stiffness.

Caffeine may contribute to the development of heart disease because it increases cholesterol levels, and a chemical in the blood called ‘homocystein’, a marker for predisposition to heart attack. Unfiltered coffee, especially, can raise blood fats. Even a small amount of caffeine can be detrimental for people who are sensitive to caffeine.

There is much conflicting research around, so above all, people must be their own health advocate and investigate further into whether you are reading industry-funded or independently-funded research.
Scraping the Bottom of the Barrel Caffeine does not add energy to your system.
Instead it burns up your reserves at a quickened pace.

This forces your glands to secrete when they don’t have much left to give, leaving you feeling more tired. According to nutritional biochemist Stephen Cherniske in his book, Caffeine Blues, caffeine begins its effects by initiating uncontrolled neuron firing in your brain.

Within 5 minutes of drinking your morning coffee, this excess neuron activity triggers your pituitary gland to secrete a hormone, ACTH (adrenocorticotrophic hormone) that tells your adrenal glands to produce adrenalin, a stress hormone that prepares you for ‘flight or fight’.
Caffeine also stimulates the production of noradrenaline and reduces the calming neurotransmitter, serotonin.

How much buzz in that cup? It depends on how the coffee bean or tea leaf or product has been processed, and/or brewed. A dosage of 50 to 100 mg caffeine – typically the amount in one cup of coffee – will make you brain feel more alert, but think again – caffeine has woken you up because it has triggered a stress response and your brain perceives as external threat or danger.

• A 6 ounces cup of Percolated coffee has about 120 mg of caffeine • Black tea has about 70 mg • Green tea has about 35 mg • Brewed decaf coffee has 5 mg of caffeine • Starbucks brewed coffee has 250 mg per 8 ounces • Starbucks Latte-Mocha has 75 mg per 16 ounces • Starbucks Vanilla Grande Frappuchino with whipped cream – 18 ounces contains 430 calories, (130 from fat), 60g sugar and 115 mg caffeine. ***NOTE: 3500 CALORIES = 1 pound of FAT
• Red Bull ‘ Monster Mixxd Energy + Juice ‘ has 80 mgs caffeine
• Baking chocolate has 35 mg caffeine per ounce

• Tim Horton’s ‘large’ coffee has 140 mg caffeine. • Popular colas have around 45 mg • Mountain Dew has 54 mg Detrimental Effects of Caffeine: What could possibly be wrong with something we have been exposed to from an early age in the form of chocolate bars, cough syrups and colas? To start with, caffeine lowers production of DHEA, a hormone critical to the optimum functioning of your immune, cardiovascular, reproductive, and nervous system health.

DHEA is an anti-aging hormone and coffee consumption interferes with that process. Though milder in its effects, caffeine manipulates the same neurochemical channels that amphetamine drugs operate on. Overuse of caffeine can result in a number of symptoms including irregular heartbeat, sleeplessness, headaches, nervousness, tremors, irritability, and depression.

Vitamin and Mineral Depletion: Caffeine acts as a diuretic, dehydrating the tissues and blood vessels of your brain. This, in turn, affects short-term memory recall. Its diuretic and adrenal gland stimulating properties have been linked to iron deficiency anemia in infants.

Coffee also interferes with the absorption of supplemental iron due to the polyphenols present.
Caffeine depletes the body of B vitamins, as well – which you need for proper brain and nervous system functioning and to convert food into energy.
B1 or Thiamine deficiency especially, can cause fatigue and nervousness.

Caffeine also speeds gastric emptying, thus preventing food nutrients from being properly absorbed in your small intestine. Minerals such as calcium, magnesium, potassium, iron and zinc, are all depleted by caffeine. Caffeine’s Effect on Blood Sugar: What is happening is that as adrenaline is released, the liver begins to emit stored blood sugar, and you get a temporary ‘lift’ or mood boost.

As insulin is released, blood sugar drops below normal. While initially, caffeine may lower your blood sugar, it can lead to increased hunger or cravings for sweets later. You get a short-term boost at the expense of long-term jitters and fatigue. If you continue to drink coffee or other caffeinated beverages throughout the day, you will find yourself in a chronic state of stress throughout the day.

Indeed, many scientists have found it exacerbates mood disorders in adults and children, triggering anxiety, depression, and irritability. Who is most at risk? The metabolism of coffee depends on the state of the liver. In a healthy liver, caffeine is mostly broken down by the hepatic microsomal enzymatic system.

It can take between 3 and 12 hours to detoxify a single cup of coffee.
At-risk groups include children, teenagers, men, women, pregnant women, people with fast metabolisms, and the elderly.
In short, it affects everyone, young and old.
Because caffeine causes your stomach to produce extra hydrochloric acid, it may aggravate pre-existing conditions such as ulcers and gastroesophageal reflux disease.

Elderly individuals with a depleted enzymatic system are especially at risk – even decaffeinated coffee may cause heartburn. In men caffeine increases the risk for prostate and urinary problems. In women caffeine has been linked to fibrocystic breast disease, PMS, osteoporosis, infertility problems, miscarriage, low birth-weight infants, and menopausal problems such as ‘hot flashes’.

Caffeine, like theobromine (found in chocolate), has to be detoxified by the liver, burdening it over time.
But caffeine is not the only toxic substance in your daily brew.
Coffee contains a host of chemicals, not just caffeine,
Among them is a group of extremely toxic compounds called ‘polycyclic aromatic hydrocarbons’ (PAHs).

You might remember this word as the cancer-causing agentisolated from barbecued meat. Chemicals in your morning Cuppa: Commercial coffees contain harmful chemicals. Over 1,000 chemicals have been reported in roasted coffee; more than half of those tested (19 out of 28) are carcinogenic.

Instant coffee, for instance, has a much greater amount of acrylamide than brewed coffee. For over 20 years coffee growers have used deadly pesticides on their coffee plants – including chemicals such as Aldrin, Dieldrin, Chlordane and Heptachlor. Thus, coffee is a seemingly benign route for daily toxin consumption.

Finding out whether you are addicted to caffeine is easy. Just give up all of your caffeine sources – including soft drinks – for a couple of days and see if you feel tired, headachy, grumpy and depressed. Headaches and fatigue are the classic signs of caffeine deprivation Strategies to wean yourself off the caffeine habit: Upon arising, drink at least 2 glasses of pure water.

Once your brain cells are refreshed, you may not even feel like drinking something to ‘wake you up’.
Also: Gradually reduce the amount you are consuming, i.e., 3 cups of coffee, tea or soda per day during week 1; 2 per day during week 2; 1during week 3; and none in week 4.
Gradually replace coffee with decaf.

During week one, use half regular coffee and half decaf; week 2, use ¼ regular coffee and the rest decaf, week 3 start drinking only decaf (this is not the best strategy as even decaf contains caffeine). Whatever strategy you use, stick with it. Taking magnesium glycinate or citrate will help with headaches.

Teeccino – herbal coffee made of roasted carob, barley, chicory root, figs, dates, orange peel and almonds.
Ayurved Roast – an organic blend made with ashwagandha, shatavari, and brahmi herbs.
Roasted carob- lightly roasted carob powder has a light mocha flavour.

Yerba maté – this grassy tasting tea contains caffeine, however preliminary evidence suggests its caffeine affects muscles tissues versus the central nervous system. Know that is has a stimulating effect on both myocardial (heart muscle), as well as smooth muscle tissue.

Grain coffees (these contain ingredients such as almond, asparagus, malted barley, okra seed, potato peel, sassafras, and dandelion root).
Here’s a recipe for a roasted carob smoothie that you can try today. In a blender place:
1 cup organic almond milk (hot or cold) 1 heaping tablespoon roasted carob powder 3 pitted dates or a few drops of maple syrup to taste (can also try ¼ teaspoon stevia) 1 teaspoon pure vanilla
Optional: 5 or 6 soaked walnuts
Whizz for 30 seconds and enjoy.
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: Caffeine Anyone?

What level of DHEA indicates PCOS?

Remember that PCOS cannot be diagnosed by symptoms alone. PCOS is a very complicated endocrine disorder. Remember that PCOS cannot be diagnosed by symptoms alone. PCOS is a very complicated endocrine disorder. Blood tests to measure hormone levels, an ultrasound to look at your reproductive organs and thorough personal and family histories should be completed before a PCOS diagnosis is confirmed.

Depending on your symptoms, your physician will determine exactly which tests are necessary.
Assessing hormone levels serves two major purposes.
First of all, it helps to rule out any other problems that might be causing the symptoms.
Secondly, together with an ultrasound and personal and family histories, it helps your doctor confirm that you do have PCOS.

Most often, the following hormone levels are measured when considering a PCOS diagnosis:

Lutenizing hormone (LH)Follicle-stimulating hormone (FSH)Total and Free TestosteroneDehydroepiandrosterone sulfate (DHEAS)ProlactinAndrostenedioneProgesterone.

Other hormones that may be checked include:

estrogenthyroid stimulating hormone (TSH)

In addition, glucose, cholesterol (HDL, LDL and triglicerides) levels might also be assessed. Lutenizing Hormone (LH) and Follicle Stimulating Hormone (FSH) LH and FSH are the hormones that encourage ovulation. Both LH and FSH are secreted by the pituitary gland in the brain.

At the beginning of the cycle, LH and FSH levels usually range between about 5-20 mlU/ml. Most women have about equal amounts of LH and FSH during the early part of their cycle. However, there is a LH surge in which the amount of LH increases to about 25-40 mlU/ml 24 hours before ovulation occurs. Once the egg is released by the ovary, the LH levels goes back down.

While many women with PCOS still have LH and FSH still within the 5-20 mlU/ml range, their LH level is often two or three times that of the FSH level. For example, it is typical for women with PCOS to have an LH level of about 18 mlU/ml and a FSH level of about 6 mlU/ml (notice that both levels fall within the normal range of 5-20 mlU/ml).

This situation is called an elevated LH to FSH ratio or a ratio of 3:1. This change in the LH to FSH ratio is enough to disrupt ovulation. While this used to be considered an important aspect in diagnosing PCOS, it is now considered less useful in diagnosing PCOS, but is still helpful when looking at the overall picture.

Testosterone All women have testosterone in their bodies. There are two methods to measure testosterone levels:

Total TestosteroneFree Testosterone

Total testosterone refers to the total amount of all testosterone, including the free testosterone, in your body. The range for this is 6.0-86 ng/dl. Free testosterone refers to the amount of testosterone that is unbound and actually active in your body. This amount usually ranges from 0.7-3.6 pg/ml. Women with PCOS often have an increased level of both total testosterone and free testosterone. Furthermore, even a slight increase in testosterone in a woman’s body can suppress normal menstruation and ovulation. DHEA-S DHEA-S or dehydroepiandrosterone is another male hormone that is found in all women. DHEA-S is an androgen that is secreted by the adrenal gland. It is normal for women to have DHEA-S levels anywhere between 35-430 ug/dl. Most women with PCOS tend to have DHEA-S levels greater than 200 ug/dl. Prolactin Prolactin is a pituitary hormone that stimulates and sustains milk production in nursing mothers. Prolactin levels are usually normal in women with PCOS, generally less than 25 ng/ml. However, it is important to check for high prolactin levels in order to rule out other problems, such as a pituitary tumor, that might be causing PCOS-related symptoms. Some women with PCOS do have elevated prolactin levels, typically falling within the 25-40 ng/ml range. Androstenedione (ANDRO) ANDRO is a hormone that is produced by the ovaries and adrenal glands. Sometimes high levels of this hormone can affect estrogen and testosterone levels. Normal ANDRO levels are between 0.7 3.1 ng/ml. Progesterone Progesterone is produced by the corpus luteum after ovulation occurs. Progesterone helps to prepare the uterine lining for pregnancy. For women with PCOS, especially those who are trying to become pregnant using fertility medications, Progesterone levels are checked about 7 days after it is thought that ovulation occurred. If the Progesterone level is high (usually greater than 14 ng/ml) this means that ovulation did indeed occur and the egg was released from the ovary. If the progesterone level is low the egg was probably not released. This test is especially important because sometimes women with PCOS can have some signs that ovulation is occurring however, when the progesterone test is done, it shows that ovulation did not occur. If this happens, your body is may be producing a follicle and preparing you to ovulate, but for some reason the egg is not actually being released from the ovary. This information helps your physician possibly adjust fertility medication for the next cycle to encourage the release of the egg. Estrogen Estrogen is the female hormone that is secreted mainly by the ovaries and in small quantities by the adrenal glands. The most active estrogen in the body is called estradiol. A sufficient amount of estrogen is needed to work with progesterone to promote menstruation. Most women with PCOS are surprised to find that their estrogen levels fall within the normal range (about 25-75 pg/ml). This may be due to the fact that the high levels of insulin and testosterone found in women with PCOS are sometimes converted to estrogen. TSH TSH stands for Thyroid Stimulating Hormone and is produced by the thyroid, a gland found in the neck. Women with PCOS usually have normal TSH levels (0.4-3.8 uIU/ml). TSH is checked to rule out other problems, such as an underactive or overactive thyroid, which often cause irregular or lack of periods and anovulation. Insulin and Glucose Due to the recent research that PCOS is probably caused by insulin resistance, physicians are beginning to check glucose levels as a factor when diagnosing PCOS. Most women with polycystic ovary syndrome should have an Fasting Plasma Glucose Test and a Glucose Tolerance Test at diagnosis and periodically thereafter, depending on risk factors. A high glucose level can indicate insulin resistance, a diabetes-related condition that contributes to PCOS. Cholesterol Researchers are also beginning to notice a connection between PCOS and heart disease; therefore, some physicians may want to look at your cholesterol levels when diagnosing and treating PCOS. Women with PCOS have a greater tendency to have high cholesterol, a major risk factor for developing heart disease. Cholesterol is a fat-like substance normally used by the body for form cell membranes and certain hormones. A high cholesterol level is considered greater than 200. Also, since the levels of good (high-density lipoproteins or HDL) and bad (low-density lipoproteins or LDL) are sometimes more indicative of a woman’s risk for developing heart disease, these levels might also be assessed. Too much bad cholesterol tends to increase the risk for plaque to build up in the arteries which can lead to a heart attack. Too much good cholesterol is believed to remove the cholesterol from building up in the arteries. Women with PCOS tend to have less good cholesterol and more bad cholesterol. In addition, triglyceride levels, another component of cholesterol, tend to be high in women with PCOS which further contributes to the risk of heart disease. Even if your physician does not check your cholesterol levels when diagnosing PCOS, it is a good idea to have these levels checked periodically since women with PCOS have a greater chance of developing high cholesterol which can lead to heart disease. More About Hormone Levels It is important to remember that with all women, hormone levels can very greatly. It is also important to mention that since the “normal” ranges vary greatly for some hormones (especially since each lab sets its own “normal” values for these hormones), some women with PCOS have hormone levels that appear within the “normal” range, but still suffer from symptoms and still might have PCOS. This is especially true with Testosterone, DHEAS, and LH levels. Unfortunately, many physicians are not familiar enough with PCOS to understand that even small changes in hormone levels can cause PCOS-related symptoms. If you have a Testosterone level of >40 ng/ml, DHEAS level of >200 ug/dl or a LH level that is two or three times that of your FSH level (LH and FSH levels should be roughly equal), seek the advice of a specialist since there is still a good possibility you might have PCOS.

Does anxiety lower DHEA?

DHEA and Mood – One of the most promising benefits of DHEA that’s been studied is its effect on depression and mood. Research has found that higher DHEA levels are correlated with lower levels of anxiety and a better mood, while lower levels have been associated with anxiety, depression, Chronic Fatigue Syndrome, and clinical burnout.

Research among individuals taking antidepressants has shown that those with higher DHEA levels may experience more improvement in symptoms than those with lower DHEA levels. Studies have also shown that DHEA may benefit those with less severe depression, who are not taking antidepressant medication. The treatment response to DHEA compared to a placebo in middle aged individuals with mild, chronic depression has been found to be significant.

In middle aged and older patients with major depression, boosting DHEA levels has also been shown to lead to significant improvements in symptoms.

What’s also really interesting is that DHEA has been found to improve mood in general, including among people who are not clinically depressed, or who are experiencing mild depressive symptoms or low mood.It’s also been studied with positive results for depressed mood in other conditions including schizophrenia, Alzheimer’s, HIV/AIDS, and adrenal insufficiency.An imbalanced cortisol to DHEA ratio has actually been associated with physical changes to the brain related to depression, including a smaller volume of the hippocampus (a part of the brain involved in memory processing).

Because DHEA is a powerful hormone with so many different effects, improvements in mood are usually combined with other benefits. Some of the common reported “side benefits” of DHEA supplementation for depression and mood disorders are enhanced libido and memory.

Many people who suffer from depression or adrenal fatigue experience low sex drive and challenges with memory, and these changes can lead to a huge difference in quality of life! Anxiety, low mood, and brain fog are common symptoms of adrenal fatigue, which involves an imbalanced DHEA to cortisol ratio.

This is a great example of a situation where DHEA supplementation might be used in moderation to help someone get back on their feet. Sometimes, I work with women who are so exhausted and burned out that it’s a significant challenge for them to jump into the lifestyle changes they want to make in order to get better.

What level of DHEA indicates a tumor?

Interpretation – Elevated dehydroepiandrosterone (DHEA)/dehydroepiandrosterone sulfate (DHEAS) levels indicate increased adrenal androgen production. Mild elevations in adults are usually idiopathic, but levels 5-fold or more of the upper limit of normal can suggest the presence of an androgen-secreting adrenal tumor.

DHEA/DHEAS levels are elevated in greater than 90% of patients with such tumors.
This is particularly true for androgen-secreting adrenal carcinomas, as they have typically lost the ability to produce downstream androgens, such as testosterone.
By contrast, androgen-secreting adrenal adenomas may also produce excess testosterone and secrete lesser amounts of DHEA/DHEAS.

Patients with congenital adrenal hyperplasia (CAH) may show very high levels of DHEA/DHEAS, often 5-fold to 10-fold elevations. However, with the possible exception of 3 beta-hydroxysteroid dehydrogenase deficiency, other steroid analytes offer better diagnostic accuracy than DHEA/DHEAS measurements.

Consequently, DHEA/DHEAS testing should not be used as the primary tool for CAH diagnosis. Similarly, discovering a high DHEA/DHEAS level in an infant or child with symptoms or signs of possible CAH should prompt additional testing, as should the discovery of very high DHEA/DHEAS levels in an adult. In the latter case, adrenal tumors need to be excluded and additional adrenal steroid profile testing may assist in diagnosing nonclassical CAH.

For more information, see Steroid Pathways,

Does DHEA affect your period?

A number of studies have found that DHEA supplements may help people with depression, obesity, lupus, and adrenal insufficiency. DHEA may also improve skin in older people and help treat osteoporosis, vaginal atrophy, erectile dysfunction, and some psychological conditions. But study results are mixed and often contradictory.

DHEA is used by some people who want to “reverse” aging and boost immunity, cognitive function, and muscle strength.
For now, studies don’t back up these uses.
DHEA has been studied as a treatment for other conditions, ranging from cardiovascular disease to menopause to Alzheimer’s.
The results have been unclear.

There are no food sources of DHEA. Wild yams contain a substance similar to DHEA that is used to make DHEA in the laboratory. The body manufactures DHEA naturally in the adrenal glands.

Because DHEA is a powerful hormone, it is not recommended for children or for women who are pregnant or breastfeeding,

Is high DHEA related to PCOS?

Pooled meta-analysis – The output of the pooled meta-analysis from 33studies is illustrated in Fig 2, From the pooled data, the level of DHEA was significantly higher in PCOS patients when compared to healthy controls (Random effects, SMD = 1.15, 95% CI = 0.59–1.71, p<0.00001; Fig 2 ). Moreover heterogeneity across the studies was found to be highly significant (p<0.001, I 2 = 95%). Asymmetry of the funnel plot and results of Egger's test showed no evidence of publication bias (p = 0.17) ( Fig 3 ). Forest plot of the final 33 studies included in the meta-analysis. Funnel plot of the final studies qualified in the meta-analysis.

Chukwudi Eze