It is difficult to imagine that deficiency in some gonadal hormone could account for the situational variants of hypoactive sexual desire disorder. It may also be difficult to explain the acquired variant in terms of endocrine alterations, unless we assume that the onset of these endocrine alterations coincide with the onset of hypoactive sexual desire disorder. On the contrary, an endocrine explanation may be very suitable for explaining the life-long variant. However, it is most important not to forget that hypoactive sexual desire caused by a general medical condition is excluded from the diagnosis of hypoactive sexual desire disorder. Whenever reduced sexual desire can be attributed to diseases in the endocrine glands, castration or ovariectomy or any other medical condition, another diagnosis must be given. On the contrary, the combined type accepts organismic conditions as contributing factors, acting in conjunction with unknown psychic entities.
In Chapter 5, I made clear that adequate blood concentrations of androgens are necessary for maintaining a functional central motive state in both men and women. Therefore, it is not startling that several studies have determined blood androgen concentrations in women diagnosed with hypoactive sexual desire disorder. Early studies failed to detect any difference between women reporting an adequate level of desire and those diagnosed with hypoactive desire disorder (Stuart et al., 1987; Schreiner-Engel et al., 1989). In contrast, a group of women with life-long hypoactive sexual desire disorder were found to have a lower free testosterone blood concentration than controls (Riley and Riley, 2000). This is a very interesting observation, suggesting that the life-long variant of desire disorder can be attributed to reduced reactivity of the central motive state because of insufficient androgen stimulation. Later studies have extended these findings. Premenopausal, regularly cycling women with self-reported low libido (a common clinical expression referring to low sexual motivation) were found to have lower blood testosterone concentrations than a control group judged to have normal (probably meaning average) libido (Guay, 2001). An additional study from the same group replicated these findings and expanded them to postmenopausal women. Unfortunately, no control group was used. Instead, reduced androgen concentration was defined as any concentration of free testosterone below 2pg/ml in women under 50 years of age, and as below 1.2pg/ml for women over 50 years. These values are purportedly far below the means generally reported in the literature. Results showed that 70% of the women selected because of decreased sexual desire had free testosterone concentrations below the criterion. The proportion of women with below-criterion free testosterone concentration did not differ between premenopause and menopause. It may also be noted that total testosterone and dehydroepiandrosterone sulfate were reduced in women with low desire (Guay and Jacobson, 2002). Similar data were reported in another study of women complaining of low sexual desire. In that latter study, a control group of healthy women of about the same age as the patients was included. Half of the women in each group was premenopausal and the other half was in menopause. Total testosterone, free testosterone and dehydroepiandrosterone sulfate were reduced in women with low desire compared to controls (Turna et al., 2005).
The last few studies mentioned above coincided in reporting reduced androgen concentrations in women with low desire. They also coincided in sloppy descriptions of the diagnostic criteria used for considering a woman as suffering from low sexual desire. All we are told is that their chief complaint was decreased sexual desire. In the Turna et al. (2005) study, we are also told that the women had presented symptoms for at least 6 months. Moreover, all subjects participating in that study answered the Female Sexual Function Index. Results revealed a significant difference between patients and controls, suggesting that there indeed was a difference between patients and controls with regard to sexual desire. Nevertheless, in none of the latter studies mentioned here was the diagnosis based on the criteria given in the DSM-IV or ICD-10. Among other things, we do not know if the patients suffered from acquired or life-long hypoactive sexual desire. This could be of some importance, strangely enough. Likewise, we are not told whether the disorder is generalized or situational. It appears that the clinical researchers do not realize the crucial role of a complete and correct diagnosis before taking blood samples and determining hormone concentrations.
We will now turn to some observations contradicting the notion of reduced androgen concentration in women with low sexual desire. In a study employing women with loss of libido assessed by a psychosexual counselor and a group of healthy controls of about the same age, no difference between women with low desire and the controls was found with regard to blood concentrations of total testosterone, free testosterone, sex-hormone binding globulin, estradiol, dihydrotestosterone and dehydroepiandrosterone sulfate (Nyunt et al., 2005). The criteria for being considered a patient were less clear in this study than in any of those mentioned above, strongly reducing the value of its results. Nevertheless, they coincide with results reported by van Anders et al. (2005). These researchers measured testosterone in saliva rather than in blood, but that has become a popular procedure and it may perhaps be acceptable. The patients were assessed through a careful clinical interview. No difference in saliva testosterone concentration between patients and controls was found.
The conclusion that may be drawn from the studies having assessed alterations in androgen concentrations in women suffering from low desire in comparison to women not suffering from it is uncertain. About half of the studies report no difference while the other half does. That is exactly what we should expect if results were random. The most logical conclusion here would be that there is no endocrine difference between healthy women and women with low desire. This may be true, but due to the sloppy diagnostic criteria employed in almost all studies, such a conclusion is probably unjustified with regard to hypoactive sexual desire disorder as defined by the diagnostic manuals. Perhaps the only reasonable conclusion is that self-reported low sexual desire is not necessarily associated with reduced blood androgen concentrations. Furthermore, it is impossible to determine whether the central motive state shows a reduced sensitivity to sexual incentives because of deficient stimulation by androgens or not.
The preceding discussion was limited to studies in women. Male hypoactive sexual desire disorder has attracted far less attention. So little, in fact, that there are no recent data concerning blood androgen concentrations in men complaining of low sexual desire. An old review suggested that men suffering from low desire had blood androgen concentrations within the normal range (LoPiccolo and Stock, 1986). This is not unlikely, since there are data showing that symptoms of androgen deficiency, including reduced sexual interest, appear at blood concentrations far below the normal range or at the bottom of that range. There are large, stable interindividual variations in androgen sensitivity in men. This means that some men report symptoms of deficiency only when blood androgen concentration are very low while others report such symptoms already when concentration approaches the lower normal range (Kelleher et al., 2004). A most modest relationship between scores on some obscure questionnaire evaluating sexual desire (among other things) and blood total testosterone concentration was reported in a German study (Beutel et al., 2005) of adult and old men visiting andrology clinics for evaluation of 'aging-male' symptoms, whatever that may mean. There was no correlation between free testosterone and desire. The significant correlation between total testosterone and desire was 0.188, meaning that 1.39% of the interindividual variation in desire can be attributed to variations in testosterone concentration. This figure does not seem to be particularly impressive and may justify the suggestion that low sexual desire is not a consequence of low blood androgen concentrations made by LoPiccolo and Stock (1986) some 20 years ago.
The fact that the normal variations in blood testosterone concentrations are not associated with sexual desire does in no way exclude that men suffering from hypoactive sexual desire disorder may have lower blood androgen concentrations than men not suffering from it. The lack of empirical studies in men with an appropriate diagnosis obliges me to refrain from any more tangible conclusion.
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