Are histamines beneficial?
L-Histidine is an amino acid from which Histamine is derived. L-Histidine is an amino acid that the human body cannot manufacture, hence, it must be obtained from your diet, which is generally deficient, or from supplements which you can purchase. A discussion of Histamine and it’s role in the sexuality of humans follows with references annotated.
A hormone/chemical transmitter (biogenic monoamine, similar to serotonin, epinephrine, norepinephrine ) involved in local immune responses, regulating stomach acid production and in allergic reactions as a mediator of Immediate Hypersensitivity . When released from mast cells, histamine causes vasodilation (relaxation or dilation of the blood vessel walls) !
The influence of the endocrine, neurotransmitter, and central nervous systems influences the male and female sexual functions for sexual desire, arousal, and orgasm or ejaculation stages of sexual responding. Endocrine factors include the following: androgens, estrogens, progesterone, prolactin, oxytocin, cortisol, and pheromones. Neurotransmitters and neuropeptides include nitric oxide (see L-Argingine), serotonin, dopamine (see Uprima), epinephrine, norepinephrine, opioids, acetylcholine, histamine, and gamma-amino-butyric acid (Gaba)1.
Recent advances in the neurobiology of sexual behavior have helped to refine our understanding of the neuroanatomical, neuroendocrine and neurochemical systems that modulate responses to sexual stimulation. Both appetitive and consummatory sexual behaviors have been studied in several laboratory species and in humans using traditional and novel behavioral paradigms. New knowledge has emerged concerning the role of hypothalamic (dopamine & Uprima), limbic and brainstem structures, neuropeptides, brain monoamines and nitric oxide (see L-Argingine) in the control of partner preference, sexual desire, erection, copulation, ejaculation, orgasm and sexual satiety (satisfaction).2
The human sexual response is a complicated biopsychosocial phenomenon in which internal and external stimuli are modulated by the central and peripheral nervous system, resulting in a cascade of biochemical, hormonal and circulatory changes that lead to cognitive and physical sexual arousal. Current knowledge of the relationships between central processes, mediated by neuropeptides and neurotransmitters, and the hypothalamo-pituitary-gonadal axis indicates that they are all involved. Hormonal aspects of sexual arousability and sexual excitement are mainly related to androgens (that is, the male hormones). The possible influences of hormonal therapies such as hormonal contraception and perimenopausal hormone suplementation are involved. The main conclusion is that clinicians should be aware of possible sexual problems resulting from changes in circulating sex hormone binding globulin and free testosterone in men and women due to endogenous (generated in the body) or exogenous (introduced into the body from external sources such as supplements) hormonal changes.3
Physicians or gynecologists, specifically in their general practice or in the setting of a menopause clinic, are more and more frequently confronted with sexual complaints of menopausal women. Among these, decline in sexual desire is probably the most usually reported. The first study to evaluate a potential relationship between sexual functioning and menopause was conducted by Hallstrom in 1977. Thereafter, a review of the literature was able to show that there is nearly a consensus regarding the role of estrogens in that condition. They effectively relieve vaginal atrophy (shriveling up) and resulting dyspareunia (painful intercourse). There is less agreement, however, regarding a direct effect of estrogens on more complex sexual behavior and motivation. When analyzing potential influence of sex hormones, estrogens may exert a positive effect on the quality of the sexual relationship whereas androgens can definitely increase sexual “motivation” including sexual desire. In spite of the potentially important part played by androgens as promoters of libido and in the maintenance of sexual functioning in men and women, the exact role of the hormonal treatment in reliving sexual complaints still remains controversial. In some women where decline of sexual desire can be reasonably attributed to menopause, androgens in non-masculinizing adequate dosages, can be effectively included in the postmenopausal hormone replacement regimen. However, etiology of diminished sexual motivation and desire is far from univocal particularly in the human being where psychological, social and cultural influences are endowed with a prominent importance. It is accordingly quite conspicuous that our sexual life is not reduced to hormonal fluctuations only.4 From the preceding in may be possible to conclude that it takes more than testosterone to make sexual things right, hence, our inclusion of the active amino Acids L-Argingine and L-Histidine to our portfolio of available products.
Dopamine and serotonin are the neurotransmitters most directly involved in sexual activity. Dopamine plays a stimulatory role while serotonin has an inhibitory effect (That’s why antidepressant Selective Serotonin Reuptake Inhibitors such as Prozac, Paxil, etc. can cause impotence). The two monoaminergic systems modulate the secretion of many hormones such as testosterone and endorphins (chemical compounds that occur naturally in the brain and have pain relieving properties similar to those of the opiates. They are thought to be concerned with controlling the activity of the endocrine glands) and are involved in sexual functional capacity. Furthermore, hormones influence synthesis and storage of brain neurotransmitters. Impotence can often be associated to clinical depression and altered neurotransmitter function. Moreover, stress represents an unbalance between various neurotransmitter systems and can induce impotence especially when disorders of the endorphinic system are present. Replacement therapy is based upon the understanding of these basic concepts. Impotence due to an underlying depressive illness must be treated with dopaminergic antidepressant drugs; while in stressful conditions a good response to the naloxone test is the preliminary criterion to subsequent naltrexone treatment. When a hormonal deficiency has been proved, the hormone replacement therapy is of course highly effective (gonadotropins in hypogonadotropic syndromes, testosterone in aging, etc.). Finally, idiopathic (denoting a disease or condition the cause of which is not known or that arises spontaneously) impotence could be treated by a Dopamine agonist (Editors Note:Such as Uprima) and/or serotonin antagonist (reduces serotonin) drugs either alone or better yet in association with psychotherapy.5
The corpora cavernosa (CC) muscles of the human penis and their structural arrangements are essential for the physiology of erection. Contraction of this muscle causes detumescence (the reverse of erection), and relaxation, tumescence (swelling or erection). The motor excitatory neurotransmission is adrenergic, acting through the alpha adrenoceptors. Continuous adrenergic transmitter noradrenaline (Norepinephrine) release is necessary for the maintenance of non-erectile (contractile) state of the penis. (Editors note: Contrarily, excessively high levels of noradrenaline (Norepinephrine) could cause a permanent non-erect state, i.e. impotence) The inhibitory neurotransmitter that relaxes CC muscle to produce erection is nitrergic i.e., the chemical messenger being nitric oxide (See L-Argingine). The latter can also be released from cavernous endothelium. Presence of NO increases intracellular cGMP through activation of the enzyme guanylate cyclase. This causes relaxation of CC muscle. Phosphodiesterase type 5 (PDE5) is responsible for the degradation of cGMP and regulation of CC muscle tone. Specific PDE inhibitors such as sildenafil & Cialis enhance the intracellular cGMP to improve erection. Increase in intracellular cAMP can also bring about pharmacological (drug induced) erection in man (e.g. PGE1, papaverine and histamine). Inhibition of excessive adrenergic tone with appropriate alpha-adrenergic blocking agents (e.g. phentolamine) can also contribute to the onset of pharmacological erection.6