2. Douglas Wile, Art of the Bedchamber: The Chinese Sexual Yoga Classics, Including Women’s Solo Meditation Texts (Albany: State University of New York Press, 1992), 9.

  3. Ibid., 140–41.

  4. Richard Burton, trans., The Perfumed Garden of Cheikh Nefzoui: A Manual of Arabian Erotology (London, UK: Kama Shastra Society of London and Benares, 886), 129–59.

  5. Leora Lightwoman, of Diamond Light Tantra, another Tantric teacher, offers caveats for the growing field of Tantric sexual healing for women. In an e-mail, she wrote:

  Tantric massage for women, including yoni massage, is a beautiful ritual to share between lovers, and practitioners such as Michael offer this opportunity to those who are not in a couple, or whose partners are not Tantrically inclined, to receive a delicious, sacred sexual and emotional offering. This is good. Tantric massage can be profound. . . . I am, however, deeply concerned about the reputation of the whole field of Tantric massage, as it is clearly not regulated. Anyone can call himself a Tantric masseur. The difference between a Tantric massage and an erotic massage can be nebulous, even to those in the field, and I would see it more as a continuum.

  She sets out what she sees as distinctions between real Tantric sexual healers and garden-variety sexual healers and cautions that the Tantric teacher should have respect for the client and should have a “sense of innocence” about the transaction.

  Also, Leora Lightwoman, interview, London, UK, July 15, 2011.

  Chapter 14: Radical Pleasure, Radical Awakening: The Vagina as Liberator

  1. Judith Horstman, The Scientific American Book of Love, Sex and the Brain: The Neuroscience of How, When, Why and Who We Love (New York: Jossey-Bass, 2012), 85.

  2. Dr. Louann Brizendine, M.D., The Female Brain (New York: Morgan Road Books, 2006), 123: “In the male brain, most emotions trigger less gut sensation and more rational thought. The typical male brain reaction to an emotion is to avoid it at all costs. . . .”

  3. Dr. Helen Fisher, The Anatomy of Love: A Natural History of Mating, Marriage and Why We Stray (New York: Ballantine Books, 1992), 182–84.

  4. The following is a description of the instrument that measures the vaginal pulse amplitude:

  Vaginal Photoplethysmography—

  Embedded in the front end of the probe is a light source that illuminates the vaginal walls. Light is reflected and diffused through the tissues of the vaginal wall and reaches a photosensitive cell surface mounted within the body of the probe. Changes in the resistance of the cell correspond to changes in the amount of back-scattered light reaching the light-sensitive surface. It is assumed that a greater back-scattered signal reflects increased blood volume in the vaginal blood vessels (Levin, 1992). Hoon et al. (1976) introduced an improved model of the vaginal photometer that substituted an infrared LED (light-emitting diode) for the incandescent light source and a phototransistor for the photocell. These innovations reduced potential artifacts associated with blood oxygenation levels, problems of hysteresis, and light history effects. The vaginal photometer is designed so that it can be easily placed by the participant. A shield can be placed on the probe’s cable so that depth of insertion and orientation of the photoreceptive surface is known and held constant (Geer, 1983; Laan, Everaerd, & Evers, 1995). The photometer yields two analyzable signals. The first is the DC signal, which is thought to provide an index of the total amount of blood (Hatch, 1979), often abbreviated as VBV (vaginal blood volume). The second is the AC signal, often abbreviated as VPA (vaginal pulse amplitude), which is thought to reflect phasic changes in the vascular walls that result from pressure changes within the vessels (Jennings et al., 1980; see Figure 11.2). Although both signals have been found to reflect responses to erotic stimuli (e.g., Geer, Morokoff, & Greenwood, 1974; e.g., Hoon, Wincze, & Hoon, 1976), their exact nature and source is unknown. Heiman et al. (2004) compared, in 12 women, VPA and genital volume changes as measured using MRI, and found no significant correlations between the two. Heiman and Maravilla (2005) suggested it may be possible that at moderate levels of arousal the vaginal probe might detect changes to vaginal tissue that do not correspond with other genital blood volume changes. (Interestingly, however, the same study reported higher correlations with subjective sexual arousal for VPA than for MRI variables.) The interpretation of the relationship between the photometer’s output and the underlying vascular mechanisms is hindered by the lack of a sound theoretical framework (Levin, 1992) and of a calibration method allowing transformation of its output in known physiological events. At present, most researchers describe their findings in relative measures, such as mm pen deflection or change in microVolts. Levin (1997) stated that one of the basic assumptions underlying use of the plethysmograph is that changes in VBV and VPA always reflect local vascular events. In his discussion of findings from studies on the effects of exercise and orgasm on VBV and VPA, however, he suggests that the signals are likely to reflect rather complex interactions between sympathetic and parasympathetic regulatory processes and between circulatory and vaginal blood pressure. However, Prause et al. (2004) found that, whereas VPA discriminated between sexual, sexually threatening, and threatening film stimuli, blood pressure (while increased during all three conditions) did not. The construct validity of VPA is better established than that of VBV. Researchers have reported high correlations between VPA and VBV, particularly with stronger sexual stimuli, but others have found low or no concordance between the two signals (Heiman, 1976; Meston and Gorzalka, 1995). VPA appears to be more sensitive to changes in stimulus intensity than VBV (Geer et al., 1974; Osborn & Pollack, 1977). VPA also corresponds more closely with subjective reports of sexual arousal than VBV (Heiman, 1977). Finally, VBV changes in response to increases in general arousal, indicating that VBV is less specific to sexual arousal than VPA (Laan, Everaerd, & Evers, 1995). Two studies have directly assessed the sensitivity and specificity of VPA (Laan et al., 1995; Prause, Cerny, & Janssen, 2004). Both studies measured responses of sexually functional women to sexual, anxiety inducing, sexually threatening, and neutral film excerpts, and found maximal increases in VPA to the sexual stimulus and moderate increases to the sexually threatening film. (Participants also reported intermediate levels of sexual arousal to the sexual-threat stimulus.) On both studies, VPA did not increase in response to anxiety-inducing stimuli. These results demonstrate response specificity of vaginal vasocongestion to sexual stimuli.

  From E. Janssen, N. Prause, and J. Geer, “The Sexual Response,” in Handbook of Psychophysiology, eds. J. T. Cacioppo, L. G. Tassinary, and G. G. Berntson, 3rd ed. (New York: Cambridge University Press, 2007).

  5. Dr. Louann Brizendine, The Female Brain, 77-86.

  6. Beverly Whipple and John Delbert Perry, “Pelvic Muscle Strength of Female Ejaculators: Evidence in Support of a New Theory of Orgasm,” Journal of Sex Research 17, no. 1 (1981): 22–39.

  7. Ibid., 22–39. Whipple and Perry also looked at the neural connections in the lower spine to explain their hypothesis. Indeed, one member of the research team had suffered a sprained lower back and then found that her Kegel-type uterine contraction strength measurements were significantly lower than usual: the health and functionality of the spinal cord, in this study, was confirmed to have affected the contracting powers of the vagina.

  8. Ibid., 22–39.

  9. Ibid., 22–39.

  10. Ibid., 22–39.

  11. Janniko R. Georgiadis and others, “Regional Cerebral Blood Flow Changes Associated with Clitorally Induced Orgasm in Healthy Women,” European Journal of Neuroscience 24, no. 11 (2006): 3305–16.

  12. K. Mah and Y. M. Binik, “The Nature of Human Orgasm: A Critical Review of Major Trends,” Clinical Psychology Review 6 (August 21, 2002): 823–56. See also R. King and others, “Are There Different Types of Female Orgasm?” Archives of Sexual Behavior 40, no. 5 (October 2010): 865–75:

  In attempt to identify and validate different types of orgasms which females have during sex with a partner, data collected by Mah and B
inik (2002) on the dimensional phenomenology of female orgasm were subjected to a typological analysis. A total of 503 women provided adjectival descriptions of orgasms experienced either with a partner (n = 276) or while alone (n = 227). Latent-class analysis revealed four orgasm types which varied systematically in terms of pleasure and sensations engendered. Two types, collectively labelled “good-sex orgasms,” received higher pleasure and sensation ratings than solitary-masturbatory ones, whereas two other types, collectively labelled “not-as-good-sex orgasms,” received lower ratings. These two higher-order groupings differed on a number of psychological, physical and relationship factors examined for purposes of validating the typology. Evolutionary thinking regarding the function of female orgasm informed discussion of the findings. Future research directions were outlined, especially the need to examine whether the same individual experiences different types of orgasms with partners with different characteristics, as evolutionary theorizing predicts should be the case.

  13. Kevin Nelson, M.D., The Spiritual Doorway in the Brain: A Neurologist’s Search for the God Experience (New York: Penguin, 2012), 242–43.

  14. R. W. B. Lewis and Nancy Lewis, The Letters of Edith Wharton (New York: Scribner, 1989), 12.

  15. Edith Wharton, The House of Mirth (New York: Barnes and Noble Classics, 2003), 177.

  16. Georgiadis, “Regional Cerebral Blood Flow,” 3305–16.

  17. Ibid., 3305–16

  18. Sally Ryder Brady, A Box of Darkness: The Story of a Marriage (New York: St. Martin’s Press/Griffin), 114.

  19. Mary Roach, Bonk: The Curious Coupling of Science and Sex (New York: W. W. Norton, 2008), 293.

  20. Wen Zhou and Denise Chen, “Encoding Human Sexual Chemosensory Cues in the Orbitofrontal and Fusiform Cortices,” Journal of Neuroscience 28, no. 53 (December 31, 2004): 14416–21.

  21. Ibid., 14416–21.

  22. Virpi Lummaa and Alexandra Alvergne, “Does the Contraceptive Pill Alter Mate Choice in Humans?” Trends in Ecology and Evolution 25, no. 3 (October 6, 2009): 171–79.

  23. George Preti and others, cited in “Pheromones in Male Perspiration Reduce Women’s Tension, Alter Hormone Response that Regulates Menstrual Cycle,” Penn News, March 14, 2003. www.upenn.edu/pennnews/news/pheromones-male-perspiration-reduce-womens-tension-alter-hormone-response-regulates-menstrual-c.

  24. Ibid.

  25. Bob Beale, “What Women Need: Sweaty Male Armpits,” ABC Science Online, June 26, 2003. www.abc.net.au/science/articles/2003/06/26/888984.htm.

  26. Dr. Daniel G. Amen, The Brain in Love: Twelve Lessons to Enhance Your Love Life (New York: Three Rivers Press, 2009), 50–72.

  27. Dr. Daniel Goleman, Social Intelligence: The Revolutionary New Science of Human Relationships (New York: Bantam Books, 2006), 63–64.

  28. See Naomi Wolf, Misconceptions: Truth, Lies and the Unexpected on the Journey to Motherhood (New York: Doubleday, 2000).

  29. Ibid.

  30. Brizendine, Female Brain, 77.

  31. Louann Brizendine, M.D., The Male Brain (New York: Three Rivers Press, 2010).

  32. Daniel Goleman, Emotional Intelligence: Why It Can Matter More Than IQ (New York: Bantam, 1995), 129–47.

  33. John M. Gottman, The Seven Principles for Making Marriage Work (New York: Three Rivers Press, 1988), 38, 39.

  34. Kathleen Light, cited in Roger Dobson and Maurice Chittenden, “Women Need that Healthy Touch,” Sunday Times (London), January 16, 2005, www.thetimes.co_uk/tto/public/sitesearch.do?querystring=women+need+that+healthy+touch8p-tto&pf-all&bl-on.

  35. Naomi Wolf, Facebook Community Page, informal online survey, September–October 2011.

  36. See Milan Zaviacic, The Human Female Prostate: From Vestigial Skene’s Paraurethral Glands and Ducts to Woman’s Functional Prostate (Bratislava: Slovak Academic Press, 1999).

  37. Heli Alzate, “Vaginal Eroticism: A Replication Study,” Archives of Sexual Behavior 6 (December 14, 1985): 529–37.

  38. Stuart Brody and Petr Weiss, “Simultaneous Penile-Vaginal Orgasm Is Associated with Satisfaction (Sexual, Life, Partnership, and Mental Health),” Journal of Sexual Medicine 8, no. 3 (2011): 734–41.

  Previous multivariate research found that satisfaction was associated positively with frequency of specifically penile-vaginal intercourse (PVI; as opposed to other sexual activities) as well as with vaginal orgasm. The contribution to satisfaction of simultaneous orgasm produced by PVI merited direct examination in a large representative sample.

  39. G. L. Gravina and others, “Measurement of the Thickness of the Urethrovaginal Space in Women with or without Vaginal Orgasm,” Journal of Sexual Medicine 5, no. 3 (March 2008): 610–18.

  40. See Deborah Coady and Nancy Fish, Healing Painful Sex: A Woman’s Guide to Confronting, Diagnosing, and Treating Sexual Pain (New York: Seal Press, 2011).

  41. Zwi Hoch, “Vaginal Erotic Sensitivity by Sexological Examination,” Acta Obstetricia et Gynecologica Scandinavica 65, no. 7 (1986): 767–73.

  We studied vaginal erotic sensitivity by vaginal sexological examinations as part of the evaluation and treatment process of couples complaining of female coital anorgasmia but readily orgasmic at female self- or partner-performed external genital stimulation. The existence on the anterior vaginal wall of an anatomically clearly definable erotically triggering entity, termed “The G Spot”, was refuted by our findings.

  42. Cambridge Women’s Pornography Collective, Porn for Women (San Francisco: Chronicle Books, 2007).

  43. Lumaa and Alvergne,“Does Contraceptive Pill Alter Mate Choice?”

  44. Dr. Jim Pfaus, interview, Montreal, Quebec, January 29–30, 2012.

  45. The impact of antidepressants on sexual function is not an insignificant warning, as Anita Clayton, M.D., and Angel L. Montejo, M.D., reported in “Major Depressive Disorder, Antidepressants, and Sexual Dysfunction,” Journal of Clinical Psychiatry 67, Suppl. 6 (2006): S33–S37:

  Sexual dysfunction is a common problem with a number of causes, including psychosocial factors, general medical illness, psychiatric disorders, and psychotropic and nonpsychiatric medications. It . . . has been strongly associated with antidepressant medications. Selective serotonin reuptake inhibitors (SSRIs) in particular have demonstrated a higher incidence of sexual dysfunction than other antidepressants that work through different mechanisms of action. Further supporting the relationship between sexual dysfunction and antidepressant mechanism of action, data from a number of studies indicate that bupropion, nefazodone, and mirtazapine alleviate symptoms of sexual dysfunction and are as effective as SSRIs at controlling depressive symptoms. Although a number of strategies besides drug substitution have been utilized to help manage antidepressant-induced sexual dysfunction, many patients remain suboptimally treated; as many as 42% of patients were found to passively wait for spontaneous remission. . . .

  Sexual dysfunction is a frequent problem that occurs in both healthy patients and patients with depression. According to the National Health and Social Life Survey, sexual dysfunction is more prevalent in women (43%) than men (31%); furthermore, sexual dysfunction is more prevalent in both sexes with poor emotional health than in healthy controls. Sexual dysfunction is a side effect that is particularly attributed to the use of antidepressant medication and represents a substantial problem, especially with regard to long-term treatment compliance. Approximately 36% of patients find antidepressant-induced sexual dysfunction to be an unacceptable side effect of treatment, constituting possible grounds for treatment discontinuation. Data suggest that the mechanism of action behind antidepressants is a key contributor to sexual dysfunction. A better understanding of these data and of the physiology and etiology of sexual dysfunction will lead to more effective management strategies, which may result in better therapeutic compliance.

  Dr. Helen Fisher also believes that SSRIs are part of the picture of women experiencing blunted desire. In a 2004 presentation she gave at an American Psychiatric Association Forum with J. Anderson Thomson Jr., “Sex, Se
xuality And Serotonin: Do Sexual Side Effects of Most Antidepressants Jeopardize Romantic Love and Marriage?,” she noted that in 2002, millions of prescriptions for antidepressants were written in the United States, most for SSRI-enhancing medication. As many as 73 percent of patients on these medications, she reported, can suffer from one or more of a range of sexual side effects:

  It’s well established that these drugs can cause sexual dysfunction, diminished sexual desire, delayed sexual arousal and muted or absent orgasm. . . .

  The bottom line is that serotonin-enhancing antidepressants that negatively affect [the] sex drive can quite logically also negatively affect the brain circuits for romantic love. . . .

  From a Darwinian perspective, orgasm also is a primary mechanism by which women unconsciously assess a mating partner. For a long time, anthropologists have thought that this is a bad design; women just don’t have an orgasm every time. More recently, we came to realize that. We call it the ‘fickle female orgasm’ and we regard it now as a very serious adaptive mechanism that enables women to distinguish between those partners who are willing to spend time and energy on them—those we call Mr. Right— and those who are impatient or lack empathy and who might not be a good husband and father—Mr. Wrong. When women take serotonin-enhancing antidepressants that inhibit the orgasmic response, among some of these women you’re jeopardizing the ability to assess the commitment level of a partner. Women also use orgasm to assess existing partnerships; women tend to orgasm more regularly with a long-term partner. With the onset of anorgasmia, this can destabilize a match.

  46. Cindy M. Meston and David M. Buss, Why Women Have Sex (New York: Times Books, 2009), 252.

  47. Dr. Jim Pfaus, interview, Montreal, Quebec, January 29–30, 2012.

  48. Kurt Hahlweg and Notker Klann, “The Effectiveness of Marital Counseling in Germany: A Contribution to Health Services Research,” Journal of Family Psychology 11, no. 4 (December 1997): 410–21.

  49. Beverly Whipple, Barry Komisaruk, and Julie Askew, “Neuro-Bio-Experiential Evidence of the Orgasm,” paper presented at the annual meeting of the International Society for the Study of Women’s Sexual Health, Scottsdale, AZ, February 10–13, 2011, Desert Heat: International Society for the Study of Women’s Sexual Health, 2011 Annual Meeting Program Book, 153–84.