Models of Sexual Response in Humans

Sexual behavior is crucial in life, yet comparatively little is known about the mechanisms in the sexual response in humans. A lot of theories and models have been developed to explain about the process of the sexual response in humans. The first model of sexual function was described by Masters and Johnson, defined the four-phase model (phases of excitation, plateau, orgasm and resolution). Helen Kaplan proposed a slightly different model of human sexual response by adding the conception of the desire phase. Some years later, a new model of circular sexual response pattern was described by Whipple and Brash-McGreer, who acknowledged the cyclic nature of women's sexual response. Basson presented an alternative model of women's normative sexual function, which featured a responsive form of desire in women's sexual response. Bancroft developed a new theoretical model, the Dual Control Model, which postulates sexual response and arousal is ultimately determined by the balance between the sexual activation or excitation system and the sexual inhibition system. The Sexual Tipping Point is a model created by Perelman, suggesting that a sexual response is determined by a balance between excitatory or inhibitory factors that may be psychological, organic, psychosocial, or cultural. A comprehensive understanding of sexual response and function is of paramount importance for the psychiatrist to study sex, offer counseling to the patient on sex, and practice sex therapy. In this literature, models of sexual response would be reviewed to understand the knowledge of the sexual functioning in humans.

CYP2D6 P34S Polymorphism and Outcomes of Escitalopram Treatment in Koreans with Major Depression

OBJECTIVE: Cytochrome P450 (CYP) enzymatic activity, which is influenced by CYP genetic polymorphism, is known to affect the inter-individual variation in the efficacy and tolerability of antidepressants in major depressive disorder (MDD). Escitalopram is metabolized by CYP2D6, and recent studies have reported a correlation between clinical outcomes and CYP2D6 genetic polymorphism. The purpose of this study was to determine the relationship between the CYP2D6 P34S polymorphism (C188T, rs1065852) and the efficacy of escitalopram treatment in Korean patients with MDD. METHODS: A total of 94 patients diagnosed with MDD were recruited for the study and their symptoms were evaluated using the 21-item Hamilton Depression Rating scale (HAMD-21). The association between the CYP2D6 P34S polymorphism and the clinical outcomes (remission and response) was investigated after 1, 2, 4, 8, and 12 weeks of escitalopram treatment using multiple logistic regression analysis and chi2 test. RESULTS: The proportion of P allele carriers (PP, PS) in remission status was greater than that of S allele homozygotes (SS) after 8 and 12 weeks of escitalopram treatment. Similarly, P allele carriers exhibited a greater treatment response after 8 and 12 weeks of escitalopram treatment than S allele homozygotes. CONCLUSION: Our results suggest that the P allele of the CYP2D6 P34S polymorphism is a favorable factor in escitalopram treatment for MDD, and that the CYP2D6 P34S polymorphism may be a good genetic marker for predicting escitalopram treatment outcomes.