Correlated genetic and non-shared environmental influences account for the co-morbidity between female sexual dysfunctions.

BACKGROUND: Previous studies have shown moderate heritability for female orgasm. So far, however, no study has addressed the pattern of genetic and environmental influences on diverse sexual dysfunctions in women, nor how genetic and environmental factors contribute to the associations between them. METHOD: The sample was drawn from the Genetics of Sex and Aggression (GSA) sample and consisted of 6, 446 female twins (aged 18-43 years) and 1994 female siblings (aged 18-49 years). The participants responded to the Female Sexual Function Index (FSFI), either by post or online. RESULTS: Model fitting analyses indicated that individual differences on all six subdomains of the FSFI (desire, arousal, lubrication, orgasm, satisfaction, and pain) were primarily due to non-shared (individual-specific) environmental influences. Genetic influences were modest but significant, whereas shared environmental influences were not significant. A correlated factors model including additive and non-additive genetic and non-shared environmental effects proved to have the best fit and suggested that both correlated additive and non-additive genetic factors and unique environmental factors underlie the co-occurrence of the sexual function problems. CONCLUSIONS: The findings suggest that female sexual dysfunctions are separate entities with some shared aetiology. They also indicate that there is a genetic susceptibility for sexual dysfunctions. The unique experiences of each individual are, however, the main factors determining if, and which, dysfunction develops.

Evidence for a genetic etiology to ejaculatory dysfunction.

A number of theoretical approaches to understanding the etiology of ejaculatory dysfunction have been proposed, but no study has yet found conclusive evidence that premature (PE) or delayed (DE) ejaculation is under genetic control. We conducted twin model fitting analyses on different indicator variables of ejaculatory function on a population-based sample of 3946 twins and their siblings (age 18-48; mean=29.9 years) to investigate genetic, shared environmental and unique environmental effects on PE and DE. A significant moderate genetic effect (28%) was found for PE. No clear-cut familial effect could be detected for DE. Significant associations between ejaculatory function and age were detected, but effects of age were generally very weak. The findings from the present study provide useful information regarding the etiology and understanding of ejaculatory dysfunction.

Recreational use of erectile dysfunction medication may decrease confidence in ability to gain and hold erections in young males.

We aimed to estimate the frequency of recreational use of erectile dysfunction medication (EDM) and to identify any adverse effects on confidence in gaining and holding erections resulting from such use. In addition, we explored differences in erectile function and sexual behavior between recreational and medicinal users of EDM to control for the possibility of recreational users having but not admitting erectile dysfunction. A subset from the Genetics of Sex and Aggression population-based sample of 4428 males with a mean age of 29.51 (s.d.=6.77) years provided information on their use of EDM, erectile function during first intercourse and currently, sexual behavior and confidence in their ability to gain and hold erections. There were 2.6% (n=115) recreational and 0.9% (n=39) medicinal users of EDM. Recreational users had currently significantly lower confidence in their erectile ability than non-users even though they had significantly better erectile function and significantly more unrestricted sexual behavior as well as had more confidence when initiating sexual activity. More frequent use of EDM was associated with significantly less confidence in erectile ability among the recreational users. We conclude that recreational users of EDM may be vulnerable for becoming psychologically dependent on pharmacologically induced erection.

The role of the liver in the acute effect of alcohol on androgens in women.

The hypothalamic-pituitary-gonadal and -adrenal axes are regarded as the main sites of the actions of alcohol on steroids. In the present study the effect of alcohol (0.4-0.5 g/kg, orally) on venous plasma and urinary androgens was investigated in 21 premenopausal women using oral contraceptives as well as in 10 premenopausal nonusers. After intake of alcohol, an acute elevation in plasma testosterone, a decline in androstenedione levels, and an elevation in the ratio of testosterone to androstenedione were observed in both groups. The effects lasted throughout the period of ethanol elimination and were abolished during pretreatment with 4-methylpyrazole (10-15 mg/kg, orally). The acute effects were higher in the group using oral contraceptives than in the nonusers. The testosterone effect in plasma was reflected in the free testosterone fraction. A decline in urinary androsterone and etiocholanolone levels, the principal catabolic products of androgens, was observed during alcohol intoxication. In conclusion, the present acute effects on plasma and urinary steroid hormones seem to be explained by an inhibited catabolism mediated by the alcohol-induced change in the redox state in the liver. Our results suggests that the liver should be included as a major site in the acute endocrinological effects of alcohol on steroid hormones in women.

Lack of effect of alcohol on ethinylestradiol in premenopausal women.

An acute elevation in estradiol during alcohol intake has been reported in postmenopausal women on estrogen replacement therapy. The objective of the present study was to investigate the acute and long-term effect of alcohol on ethinylestradiol, the estrogen component found in most oral contraceptives. Nine healthy premenopausal women with regular use of an oral contraceptive containing 30 microg ethinylestradiol and 75 microg gestodene were challenged with alcohol (0.4 g/kg p.o., approximately 2-3 standard drinks) 2 h after intake of the oral contraceptive pill at menstrual cycle day 14. Blood samples were taken at 0, 2, 3, 4, 5, and 6 h from intake of alcohol. The challenge was repeated after a 7-day period of controlled alcohol intake (0.8 g/kg/day) at cycle day 21. The same experiments were carried out during placebo conditions. At day 21 an increase in the alcohol elimination rate was observed compared with day 14. No significant acute or long-term effect of alcohol on ethinylestradiol was found. The lack of an acute effect comparable to that reported for estradiol may be due to the protection of the ethinyl group at the 17-position of ethinylestradiol.