Observations regarding the female libido from a male to
Hi ladies,
I'm a 52 y/o male to female transsexual. After going on feminization treatment my sexual orientation flipped from being primarily interested in women to being into men. Not a problem. When in Rome do as the Romans do!
Some observations I've made may be of interest to the group.
1. Testosterone is over-rated. My lab confirmed testosterone is low female normal and my libido is just fine.
2. Our member, Marrena Lindberg author of "The Orgasmic Diet", appears to have nailed it in her observation that omega 3s enhance libido. I can't say whether she is correct about the value of lowering caffeine intake since I'm a coffee addict. I'll have to cut way back to test her idea. Thanks ahead of time, Marrena, if the idea works!
3. Recently published research suggests value in elevating our intake of sulfur containing amino acids. The abstract below from PubMed explains. The gas, hydrogen sulphide, helps the male erection. Since the clitoris responds in a similar fashion it should help women also. This gas is generated from sulfur containing amino acids. In my experimentation N-acetyl-cysteine (NAC) has been particularly effective.
4. Published research shows a high intake of vitamin C enhances female sexuality. 2 grams/day seems to work well for me.
5. Since my hormones are medically supplied I can easily determine my estrogen and progesterone situtation. Estrogen seems to have little to no effect on libido. OTOH progesterone at least in the synthetic mimetic form, Provera, seems to greatly increase libido.
6. There is disagreement in the literature over this but I lean to the side that claims that DHEA enhances female libido. This is probably only the case if your DHEA is low to begin with in which case supplementation should enhance libido.
7. If anyone in this group doesn't know this then they're not female, but for completeness sake I'll mention that stress is a huge libido killer for most women. My earlier comment about vitamin C ties in with this. The literature suggests vitamin C works by lowering anxiety.
8. My libido *greatly* increases when I drop weight. Indeed this has been the single most effective thing I've done. Not to an anorexic weight, mind you. Just to a healthy, low normal BMI. Since it is extremely difficult to maintain a low body weight on the hormones I'm on, I keep cycling my libido up and down depending on my success in controlling my weight. This effect may be entirely psychological. At a low body weight I can dress sharp and feel good about myself. However, the effect is so significant that I can't help but suspect that lowering weight has benefit for physical reasons in addition to the psychological ones. For the anthropologists in the group this might make sense. Consider way back when in situations of low food availability. Need I mention that a few powerful men probably controlled the food supply? It would make sense for women wishing not to starve to death to be more into men, particularly successful ones, at lighter body weights. These situational horny women would be the ones who produced more off spring leading over time for a tendency for women to have higher libidos when thinner. Note, however, that anoroxic thin women don't normally reproduce so the effect would be greatest at low normal BMIs.
9. The literature and my experience indicate that getting a lot of sunlight exposure enhances libido. This does not appear to be due to an elevation in vitamin D.
10. Getting adequate sleep is vital.
J Sex Med. 2007 Sep;4(5):1304-11
Hydrogen sulphide: a novel endogenous gasotransmitter facilitates erectile function.
Srilatha B, Adaikan PG, Li L, Moore PK.
Department of Obstetrics & Gynaecology, National University Hospital, National University of Singapore, Singapore.
Introduction. In a pilot study, we found that the novel gasotransmitter, hydrogen sulfide (H(2)S), had a vasodilatory and proerectile action on the cavernosum. In the present work, we explored the ability of the cavernosum to synthesize H(2)S and its mechanism on the cavernosal pathways. Aim. To evaluate the physiopharmacological responses and mechanism in the erectile function of H(2)S in rabbit cavernosum. Methods. Rabbit corpus cavernosum (CC) smooth muscle tissue (N = 5) was homogenized and incubated with L-cysteine (10 mM) and pyridoxal 5'-phosphate (2 mM) to detect H(2)S formation. In isometric tension studies on rabbits (N = 12), the effect of sodium hydrogen sulfide (NaHS; stable H(2)S donor, 100 microM-3.2 mM) was evaluated on the relaxant and contractile pathways in the cavernous smooth muscle using standard pharmacological tools. Main Outcome Measures. In vitro evidences for cavernosal H(2)S formation and proerectile pharmacological effects. Results. H(2)S was readily synthesized in the rabbit CC (2.1 +/- 0.4 nmol/mg protein). In organ bath studies, NaHS consistently relaxed the rabbit CC in a concentration-dependent manner. MDL 12,330A and 1-H-[1,2,4]-oxadiazolo-[4,3-a]-quinoxalin-1-one inhibited the NaHS relaxation by 22.5% and 14.7%, respectively. All three enzyme inhibitors (aminooxyacetic acid [AOAA], beta-cyanoalanine [beta-CA], and DL-propargylglycine [PAG][1 mM]) markedly increased the noradrenergic contractile neurotransmission of CC strips to field stimulation with minimal reversal by cysteine (1 mM) indicating the possible inherent inhibition of the relaxant H(2)S formation. AOAA, beta-CA, or PAG had no significant effect on nitrergic relaxation of noradrenaline-precontracted CC strips. Conclusion. These pioneering studies provide evidence for the endogenous formation of H(2)S and its proerectile relaxant effect on the cavernosum, with the possibility of involvement of the cyclic adenosine monophosphate pathway.
PMID: 17655658
Nerissa