Using H2 Blockers (H2-receptor antagonists) and to a lesser extent H1 receptors antagonists block stomach acid (aka. gastrin) increase plasma estradiol and prolactin. Drugs like cimetidine and ranitidine (others too) inhibit stomach acid, though ranitidine to a lesser extent nukes the cytochrome (CYP) P450 enzymes. Cimetidine is for short time (I believe 2-4weeks) to treat stomach acid. If you have normal stomach acid cimetidine and the like aren't necessary, as always consult a health professional.
histamine (an allergic response, basically) is also produced in the CNS (central nervous system), but for this discussion we're limiting it to stomach acid. I've looked for alternatives and found a few that have a direct link to possibly increasing prolactin by way of reduced stomach acid:
Olives
MSM
Forskolin
Coleus Forskohlii
Other Clinical Indications
Research has shown
forskolin stimulates thyroid hormone release and increases thyroid hormone production. 15,16
Forskolin has been shown to stimulate digestive secretions, including hydrochloric acid, pepsin, amylase, and pancreatic enzymes, 4,7 suggesting clinical benefits in digestive disorders and malabsorption. Animal research indicates forskolin exerts an antidepressant action via activation of cAMP. 33 In vitro research indicates forskolin has potent immune- stimulating properties. 34,35
http://www.altmedrev.com/publications/11/1/47.pdf
(19-01-2015, 10:45 PM)Lotus Wrote: Olives
In addition to their function as antioxidants, many of the phytonutrients found in olives have well-documented anti-inflammatory properties. Extracts from whole olives have been shown to function as anti-histamines at a cellular level. By blocking special histamine receptors (called H1 receptors), unique components in whole olive extracts help to provide us with anti-inflammatory benefits. In addition to their antihistamine properties, whole olive extracts have also been shown to lower risk of unwanted inflammation by lowering levels of leukotriene B4 (LTB4), a very common pro-inflammatory messaging molecule. Oleuropein—one of the unique phytonutrients found in olives—has been shown to decrease the activity of inducible nitric oxide synthase (iNOS). iNOS is an enzyme whose overactivity has been associated with unwanted inflammation. Taken as a group, these research findings point to olives as a uniquely anti-inflammatory food.
Olives
http://www.whfoods.com/genpage.php?tname=foodspice&dbid=46
Histaminergic regulation of prolactin secretion.
Knigge UP1.
Author information
Department of Surgical Gastroenterology, Hvidovre Hospital.
Abstract
Histamine (HA), which acts as a neurotransmitter in the central nervous system, participates in the neuroendocrine regulation of prolactin (PRL) secretion. HA has a predominant stimulatory effect which is mediated via H2-receptors following central administration and via H1-receptors following systemic infusion of the amine. Inaddition, HA seems to exert a minor inhibitory effect on PRL secretion, an effect unmasked only during blockade of the receptor mediating the stimulatory effect. Following central administration the inhibitory effect is mediated via
H1-receptors, while following systemic administration this effect is mediated via H2-receptors. In accordance with these findings, the H2-receptor antagonist cimetidine (CIM) has an inhibitory (following central administration) or stimulatory (following systemic administration) effect on PRL secretion. However, high doses of CIM possess an additional PRL stimulatory action not related to blockade of H2-receptors. This non-specific action is not exerted by the chemically different H2-receptor antagonist ranitidine. Since HA has no effect directly at the pituitary level, the actions of the amine may occur at different sites within the hypothalamus by an effect on hypothalamic transmitters regulating PRL secretion. Dopaminergic as well as serotoninergic neurons are involved in the mediation of the action of HA, since the dopamine (DA) concentration in the pituitary portal vessels is decreased by central or systemic infusion of HA, and since blockade of DA synthesis and of DA or serotonin (5-HT) receptors inhibit or prevent the PRL stimulatory action of HA infused centrally or systemically. However, other factors regulating PRL secretion (e.g. beta-endorphin, vasoactive intestinal peptide, vasopressin or TRH) may be involved in the mediation of the PRL response to HA. In men the effects of HA on PRL secretion are similar to the effects in male rats.
Systemic infusion of HA stimulates PRL secretion via H1-receptors and inhibits PRL secretion via H2-receptors. The PRL-stimulatory effect of HA is caused by an inhibition of the dopaminergic system, while the PRL-inhibitory effect of HA may involve other transmitters than DA. In contrast to its stimulatory effect in men,
HA had no effect on basal PRL secretion in women, but enhanced the PRL response to TRH. In rats or in humans the PRL stimulatory effect of HA is not caused by the cardiovascular actions of the amine.(ABSTRACT TRUNCATED AT 400 WORDS)
The effect of histamine and H1 and H2 receptors on prolactin and luteinizing hormone release in humans: sex differences and the role of stress.
Pontiroli AE, De Castro e Silva E, Mazzoleni F, Alberetto M, Baio G, Pellicciotta G, De Pasqua A, Stella L, Girardi AM, Pozza G.
Abstract
The present experiments were performed to investigate the possible role of histamine and its receptors, H1 and H2, in the control of PRL and LH release in normal adult humans of both sexes. Histamine infusion (200 microgram, iv, in 15 min) induced PRL and LH release in men; in women, histamine inhibited LH release without affecting PRL release. Two H1 antagonists, dexchlorpheniramine (10 mg, iv) and promethazine (50 mg, im), reduced PRL release in both sexes, stimulated LH release in men, and inhibited LH release in women. Cimetidine, an H2 antagonist (400 mg, iv), elicited PRL release in both sexes, more consistently in females than in males, and was without effect on LH release in either sex. These data suggest that in humans, the effect of histamine on PRL release is linked to H1 and H2 receptors, which respectively stimulate and inhibit PRL release independently of sex. The effect of histamine on LH release appears to depend on sex and to be mediated only by H1 receptors. To rule out the possibility that the effects of histamine are merely due to a nonspecific stress reaction, we have evaluated PRL and LH release in otherwise normal men and women undergoing surgery for gallstones. Surgery was accompanied by PRL release in both sexes, more evident in women, and by LH release only in men.
These results indicate that the effect of histamine on PRL and LH release in humans is linked to sex and H1 and H2 receptors and is not due to stress; further studies are required to clarify the possible mechanism and site of action of histamine in modifying PRL and LH release in humans.
Prolactin-lowering releasing drugs. Mechanisms of action and therapeutic applications.
Müller EE, Locatelli V, Cella S, Peñalva A, Novelli A, Cocchi D.
Abstract
Drugs whose systemic and/or central administration induce suppression or stimulation of prolactin secretion are reviewed. The most commonly used prolactin-lowering drugs include: (a) direct-acting dopamine receptor agonists (e.g. dopamine, apomorphine and the ergot derivatives); (b) indirect-acting dopamine agonists (e.g. amphetamine, nomifensine, methylphenidate, amineptine); © drugs which impair serotoninergic neurotransmission (e.g. the neurotoxin 5,7-dihydroxytryptamine and the serotonin receptor antagonists methysergide and metergoline); (d) gamma-aminobutyric acid [GABA]-mimetic drugs (e.g. GABA, muscimol, ethanolamine-O-sulphate, sodium valproate); (e) histamine H2-receptor agonists; and (f) cholinergic (muscarinic and nicotinic) receptor agonists.
Major prolactin-stimulating agents comprise: (a) dopamine receptor antagonists (e.g. classic and atypical antipsychotic drugs); (b) drugs differently capable of impairing central nervous system dopamine function (e.g. blockers of dopamine neurotransmission such as alpha-methyl-p-tyrosine and 3-iodo-L-tyrosine, false precursors such as alpha-methyldopa, and inhibitors of L-aromatic amino acid decarboxylase such as carbidopa and benserazide); © drugs enhancing serotoninergic neurotransmission (e.g. the serotoninergic precursors tryptophan and 5-hydroxytryptophan, direct-acting serotonin agonists such as quipazine and MK 212, and indirect-acting serotonin agonists such as fenfluramine); (d) blockers of serotonin reuptake (e.g. fluoxetine, fluvoxamine and clovoxamine); (e) H1-receptor agonists; and (f) H2-receptor antagonists (e.g. cimetidine). Some of the above classes of drugs (e.g. the indirect-acting dopamine agonists, dopamine receptor antagonists, GABA-mimetic drugs, dopamine receptor blocking drugs, and H2-antagonists) may be useful for selecting among hyperprolactinaemic patients those with a prolactin-secreting tumour in an early stage of the disease. Direct-acting dopamine receptor agonists, notably the ergot derivatives; are potent antigalactopoietic agents, can revert impaired gonadal function to normal in both female and male patients with hyperprolactinaemia, and may have antiproliferative effects on pituitary prolactin-secreting tumours.
All prolactin-stimulating agents, but especially the dopamine receptor antagonists, are liable to induce alterations in gonadal function in subjects of either sex. In addition to their usage for diagnostic or therapeutic purposes, the above drugs appear to be invaluable tools for enabling a better understanding of the neurotransmitter control of prolactin secretion.
http://www.ncbi.nlm.nih.gov/pubmed/6133737
Ann Intern Med. 1977 Oct;87(4):398-403.
Pathophysiology of spironolactone-induced gynecomastia.
Rose LI, Underwood RH, Newmark SR, Kisch ES, Williams GH.
Abstract
Peripheral blood levels of testosterone, estradiol, luteinizing hormone, and follicle-stimulating hormone and the metabolic clearance rates of testosterone and estradiol, as well as the peripheral conversion of testosterone into estradiol, were measured in 16 patients with hypertension. Six of these patients were treated with spironolactone and developed gynecomastia. The other 10 patients served as control subjects. The blood testosterone level in the spironolactone-treated group (2.7 +/- 0.5 ng/ml) was significantly less (P less than 0.02) than in the control group (4.4 +/- 0.4 ng/ml). On the other hand, blood estradiol levels in the spironolactone group (30 +/- 4 pg/ml) were significantly greater (P less than 0.01) than in the control group (13 +/- 2 pg/ml). These changes were primarily due to significant increases in the metabolic clearance rate of testosterone (P less than 0.02) and in the rate of peripheral conversion of testosterone into estradiol (P less than 0.001) in the spironolactone-treated group.
Thus, spironolactone does alter the peripheral metabolism of testosterone resulting in changes in the ratio of testosterone to estradiol, which could contribute to the production of gynecomastia.
PMID: 907238
Safety issues relating to long-term treatment with histamine H2-receptor antagonists.
Sabesin SM1.
Author information
Abstract
H2-receptor antagonist therapy is associated with a low incidence of adverse reactions. Adverse events reported in clinical trials of ranitidine in daily doses of up to 1200 mg include headache, tiredness and mild gastrointestinal disturbances, but the incidence is similar to or less than that for placebo. High doses of cimetidine (> 5 g/day) can cause reversible impotence or gynaecomastia. While ranitidine exhibits no clinically significant drug-drug interactions, cimetidine interacts with many drugs metabolized by cytochrome P450. In contrast to ranitidine and cimetidine, where safety data are available for up to 10 years of continuous therapy, experience with famotidine and nizatidine is limited.
The safety of long-term H2-receptor antagonist therapy needs to be considered in relation to the potential consequences of prolonged acid suppression, including the risk of proliferation of gastric flora and the risk of developing enterochromaffin-like cell hyperplasia, which could in turn, theoretically, lead to gastric malignancy. Such problems have not been observed in patients during long-term therapy at low or full doses of H2-receptor antagonists. Standard doses of currently available H2-receptor antagonists permit acid secretion in response to food and other stimuli, and this daily acid tide prevents persistent bacterial colonization.
Comparative pharmacodynamics and pharmacokinetics of cimetidine and ranitidine.
Richards DA.
Abstract
Ranitidine and cimetidine are competitive antagonists of histamine at H2-receptor sites in the gastric mucosa. Both drugs reduce output of basal and stimulated gastric acid and pepsin secretion in normal healthy subjects and duodenal ulcer patients. Pharmacodynamic and pharmacokinetic differences exist between the drugs, some of which are of clinical significance.
Ranitidine is a 6-8 times more potent inhibitor of gastric secretions and also causes a greater reduction in intragastric acidity of nocturnal secretions after usual therapeutic doses. Absorption from the gastrointestinal tract of both drugs is good, with peak plasma concentration occurring approximately 90 minutes after oral administration.
Systemic bioavailability is approximately 70% with cimetidine and 50% with ranitidine. Both drugs demonstrate biexponential elimination curves from the plasma after intravenous administration and a bimodal curve after oral administration which is probably the result of enterohepatic recirculation. The elimination half-lives of cimetidine and ranitidine are 1.7-2.1 hours and 2.1-3.1 hours, respectively, with apparent volumes of distribution approximating 50L and 75L, respectively. Both drugs are eliminated, largely unchanged, via the kidneys.
Major differences between these agents are found in cimetidine's biological activity at sites other than the gastric H2-receptors. These include: antiandrogenic effects with the appearance of feminizing characteristics in men, especially with large doses, like those used to treat Zollinger-Ellison syndrome; interference with the hepatic P-450 mixed-function oxidase enzyme system, which results in drug interactions with warfarin, phenytoin, theophylline and other drugs; and central nervous system effects characterized by confusion, particularly in elderly patients and those with renal failure. Such side effects have not been directly related to ranitidine treatment and substitution of ranitidine for cimetidine has reportedly provided effective alternative treatment in patients intolerant to cimetidine.
Cimetidine blocks testosterone synthesis
https://www.researchgate.net/publication..._synthesis
The Effects of Cimetidine on the Oxidative Metabolism of Estradiol
https://www.researchgate.net/publication..._Estradiol
More info to follow:
a most recent test was back to +2200 pg/mL. My thoughts are (in part) that a couple of things are driving the increase....certainly the pre-fasting (10-12 hours by the time I take the blood draw ) test requirement has a part, though other things I normally do (lemons to water.....other fresh fruit too), coffee (yup lol) and certain other foods all play a part I think. Also, I have a thyroid issue (hashimotos).....a disadvantage. My blood sugar, cholesterol are within normal limits....sodium is slightly elevated which is being addressed. My T however is tanked at 9 g/dL, but that was up slightly (from previous test).....I used reishi instead of spiro for 3 weeks......it worked great tbh. 
thanks for a good laugh and compliment, (too).
I still have to extrapolate (big word, haha) the info for human consumption. For instance, co-administration of estradiol and prolactin does indeed look doable. In other words, raising PRL (prolactin) inhibits LH (lutenizing hormone) which turns testosterone production off (or reduces it significantly) while co-administration of E2 (estradiol), or phytoestrogens if strong enough (like authentic PM).