Cross-sectional and cohort analyses of sexual response and T values are inconclusive. Either there is no correlation between T levels and sexual variables correlation with estradiol levels but not T, or a correlation of free-T with levels of sexual desire. There have been several short-term randomized controlled studies of T administration to women complaining of diminished sexual interest and satisfaction. An amended result has been found by most but not all of these trials, but the T levels produced were not clearly within the physiological range. The study with levels closest to the physiological was of oophorized women, and showed benefit only in older women receiving 300 mg/day of transdermal T, with correlated blood levels at or slightly above the normal range for premenopausal women. Of note, the correct range for postmenopausal women is unclear. A very recent study of T administration to premenopausal women did show benefit over placebo, but the free androgen index was above the upper limit for normal premenopausal women. Of major importance is the fact that these examines have been only of short duration, and, therefore, safety data are very limited. Moreover, only estrogen replete women have been studied.
Despite documented progressive loss of DHEA and DHEAS in women from late 30s onwards, the results of DHEA supplementation to improve sexual health have been conflicting.
The term androgen deficiency syndrome has been utilised recently. However, the usual criteria practiced in endocrinology for administration of a deficiency state have not been met. These include:
1. Symptoms regularly associated with low levels of the hormone;
2. Relationship of symptoms to the established biological actions of the hormone;
3. Reversal of symptoms on administration of the hormone in doses which are physiological and not pharmacological.
None of these criteria is fully met in the case of androgen deficiency syndrome . In addition, a specific level of testosterone in women, which can be considered diagnostic of androgen deficiency, has not been established.
Some of this confusion may be in part owing to problems in evaluating T, including a lack of assay specificity. Free-T is preferably measured by balance dialysis, but this is rarely available in clinical practice. Free-T correlates more closely with the biological effects of the hormone than does the total because most of the circulating T is bound to SHBG which prevents diffusion into tissues. Unluckily, the analog attempts for free-T are inaccurate. Free-T can be calculated if the total T, albumin, and SHBG are known. Nevertheless, at the low levels of T found in women, few assays of total T are reliable. Whichever assay is used, thorough validation is necessary. Another major complicating factor is that much T activity within the cell is derived 52 Basson intracellularly from ovarian adrenal precursors. This intracellular T cannot be measured. Judging T activity from evaluating testosterone metabolites is not yet standardized.
There is distinctly a clinical dilemma. Clinicians repeatedly see previously responsive women markedly distressed from their lost arousability none of their formerly useful stimuli are effective. Typically, this is of gradual onset in the late 40s or early 50s. Loss of innate sexual thoughts and fantasies is not the issue. The context of their sexual lives has not changed they speak of a sexual deadness . Accurate measures of T activity and long-term randomized controlled trials of physiological T therapy are very much needed. Clearly, this loss of arousability appertains to just a subgroup of mid-life women perhaps partially explaining the inconsistencies amongst reports of T levels of women in mid-life and older in the general population.
The free-T can be reduced by about 50% by many oral contraceptive pills and by administration of glucocorticoids. There has been little research in these areas that is helpful to clinicians.
The risks of T administration include those that are familiar, for example, greater sebum production, acne, loss of scalp hair, stimulation of facial and other body hair, as well as other potential risks including metabolic dysfunction in some women. This is based on the fact that although in the condition of polycystic ovarian syndrome, it appears that hyperinsulinemia is usually the cause of the hyperandrogenism, there are some reports of situations in which hyperandrogenism causes insulin resistance. There is also a risk that other concerns will come to light if women are given testosterone when estrogen deficient, in view of the recent withdrawal of large numbers of women from estrogen therapy owing to the results of the women's health initiative study.
Author Resource:-
David Crawford is the CEO and owner of a male impotence cause company known as Male Enhancement Group which is dedicated to researching and comparing male enhancement products in order to determine which male enhancement product is safer and more effective than other products on the market. Copyright 2010 David Crawford of how to help premature ejaculation This article may be freely distributed if this resource box stays attached.
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