Key takeaways:
~Mast cells launch histamine when triggered.
~Estrogen receptors on mast cells might make them barely extra simply triggered when estrogen ranges are excessive.
~Histamine from sure meals can add to your general histamine ranges.
~Genetic variants influence how properly you break down histamine and do away with histamine.
~ Endocrine disruptors, resembling BPA and PFOAs, may also bind to estrogen receptors on mast cells, rising degranulation.
Members will see their genotype report under, plus many extra options within the Lifehacks part. Contemplate becoming a member of right this moment.
Estrogen, Histamine Intolerance, and Mast Cell Activation:
Estrogen is a kind of hormones that everybody is aware of about, however most of us don’t actually perceive the way it works. I do know that I didn’t.
Each women and men produce estrogen as a steroid hormone, which is derived from ldl cholesterol.
Ladies produce extra estrogen than males, particularly throughout reproductive years (previous to menopause). In girls, estrogen is created within the ovaries in bigger quantities. Males convert testosterone into estrogen, and estrogen concentrations are literally the very best within the testes.[ref]
Okay, however what precisely does estrogen do?
Estrogen is a hormone that causes actions in cells to happen by binding to estrogen receptors (ERα, ERβ, and GPER1). Estrogen simply by itself isn’t doing a lot — it’s by means of its binding to the receptors that it initiates totally different mobile processes.
Estrogen receptors (ERs) are current in all kinds of tissues within the physique. For instance, ERs are essential in vascular endothelial cells, which line blood vessels. Estrogen receptors are present in cardiomyocytes (coronary heart muscle cells), neurons, airway cells, muscle tissue, the uterus, testes, fats tissue, bone, breast, kidneys, and extra.
Estrogen receptors operate in two methods:[ref]
- ERs trigger genes within the nucleus to be transcribed (activates particular estrogen-responsive genes)
- ERs can set off speedy activation of signaling pathways (quick modifications)
On the whole, estrogens improve development by turning on genes for transcription which are associated to mobile development.
Mobile development is important and good – besides in instances the place it promotes most cancers development.
There are a number of sub-types of estrogen (estrone (E1), 17β-estradiol (E2), estriol (E3), and estetrol (E4). On this article, once I discuss with estrogen, I’ll normally be referring to estradiol (E2), which is the physiologically lively type.[ref]
Let’s subsequent take a look at histamine and mast cells, after which I’ll tie all the things collectively by discussing how estrogen may influence histamine ranges within the physique.
Histamine and Mast Cells
Histamine is a molecule mostly related to inflicting allergy-like signs resembling runny nostril, hives, watery eyes, and even anaphylaxis. These quick allergy signs are because of massive quantities of histamine being launched and binding to mobile receptors.
Mast cells are the supply of the histamine launched in an allergic response. They are often activated by allergens and launch histamine and different inflammatory mediators, with the objective of defending us from pathogens and international substances. Mast cells are part of the innate immune response.
There’s extra to this story than mast cells releasing histamine because of an allergen.
Histamine additionally acts as a signaling molecule all through the physique at regular ranges. It binds to receptors and initiates mobile actions.
For instance, histamine within the abdomen binds to H2 receptors to provoke the discharge of abdomen acid from cells lining the abdomen. It’s triggered as you begin to eat (or on the time you normally eat), and the abdomen acid helps to interrupt down your meals.
There are 4 totally different histamine receptors with distinctive features. Totally different histamine receptors are discovered in several elements of the physique:[ref]
H1 receptors:
Present in clean muscle, endothelial cells (lining the blood vessels), the central nervous system, and mast cells. Activating the H1 receptors causes allergy-type signs resembling itching, swelling, vasodilation, nostril working, and pores and skin reactions. H1 receptors are additionally essential in bronchial asthma reactions.
H2 receptors:
Acid is secreted within the abdomen when histamine prompts the H2 receptors. H2 receptors are additionally discovered within the intestinal tract and the partitions of blood vessels. Mast cells even have H2 receptors, which, when activated, trigger the discharge of extra histamine. Within the coronary heart, H2 receptors are essential in controlling the rhythm.
H3 receptors:
The central and peripheral nervous programs comprise H3 receptors, which act as a suggestions loop for histamine ranges within the mind. Activating the H3 receptors impacts serotonin, norepinephrine, and acetylcholine launch.[ref]
H4 receptors:
The H4 receptors are on the coronary heart of the inflammatory response. H4 receptors are discovered within the bone marrow, basophils (a sort of white blood cell), the thymus, small gut, spleen, colon, and mast cells.[ref]
Histamine from meals:
Along with creating histamine within the physique (mast cells, different immune cells, within the mind as a neurotransmitter), we additionally get histamine from sure meals.
Right here’s a partial listing of high-histamine meals:
- Processed meats (deli meat, sausages, beef jerky, pepperoni)
- Most cheeses (besides farmer cheese)
- Fish and seafood that isn’t utterly recent
- Spinach
- Chocolate
- Tomatoes
- Strawberries
- Wine and sake
I discover this histamine meals listing to be essentially the most thorough: Full listing of excessive histamine meals (pdf).
Along with absorbing histamine from meals, your intestine microbes may also produce histamine.[ref]
What’s the underside line right here? Histamine is required on the proper ranges and acts as a signaling molecule in addition to a neurotransmitter. An excessive amount of histamine from meals generally is a drawback when you can’t remove it very properly.
Mast cells, histamine, and estrogen
As talked about above, mast cells launch massive quantities of histamine when triggered to degranulate.
Mast cells are discovered all through the physique. Nevertheless, they’re extra plentiful close to tissue frequently uncovered to pathogens and allergens — pores and skin, respiratory tract, intestinal tract, and blood vessels.
As a major a part of the immune system, mast cells react instantly to international invaders by releasing histamine, serotonin, tryptase, and inflammatory cytokines. It’s a right away response to something perceived as dangerous or international — important for reacting shortly to one thing that shouldn’t be within the physique.
The quick launch of mediators from mast cells, resembling histamine, can quickly induce modifications, resembling to the endothelium lining the blood vessels. The creation and launch of inflammatory cytokines will help orchestrate the exercise of different immune cells, bringing in T-cells and neutrophils to the world.[ref]
When mast cells are triggered too simply or inadvertently, it may possibly result in the numerous totally different signs present in mast cell activation syndrome.
Signs of Mast Cell Activation Syndrome:
Signs of mast cell activation syndrome could be damaged down into the next classes:[ref]
- Pores and skin signs: swelling, flushing, itching, hives, dermatographia (pores and skin response when scratched)
- Gastrointestinal signs: stomach ache, bloating, diarrhea, heartburn, nausea/vomiting
- Cardiovascular signs: chest ache, low blood stress, altered coronary heart rhythm
- Respiratory signs: hoarseness, sore throat, stridor, throat swelling, wheezing
- Neurological signs: headache, mind fog, peripheral neuropathy, tingling
- Muscular and bone signs: bone or muscle ache, osteoporosis, degenerative disc illness
- Nostril and eye signs: congestion, itching, and watery eyes
- Systemic signs: anaphylaxis, fatigue
Individuals with mast cell activation syndrome normally have some, however not all, of the above signs.
How does estrogen work together with mast cells?
Researchers have discovered that prime ranges of estradiol can stimulate mast cells to partially degranulate.
At increased than regular physiological ranges, estradiol (E2) may also trigger mast cell degranulation. The researchers used cell traces and animals to review mast cell degranulation. Primarily, the mast cells had been extra prone to degranulate when uncovered to an allergen in the event that they had been additionally within the presence of estrogen.[ref]
Further analysis additionally factors to mast cell activation when estrogen ranges improve. For instance, mast cell derived leukotrienes (inflammatory mediators) are increased in girls proper earlier than their intervals, when estrogen is highest. Researchers have additionally proven that drugs that block the estrogen receptors, resembling tamoxifen, are linked to a decreased launch of leukotrienes.[ref]
What this provides as much as is that ladies may very well be extra delicate to mast cells degranulating within the presence of a triggering compound — particularly when estrogen ranges fluctuate to increased ranges.
Does fixed increased estrogen ranges, resembling in estrogen dominance, all the time trigger mast cell issues? I don’t assume the analysis exhibits this. When estrogen ranges are persistently increased, estrogen receptor alpha is downregulated.[ref] In different phrases, increased fixed estrogen ought to trigger a decreased manufacturing of the estrogen receptor discovered on mast cells. However fluctuations in estrogen might trigger elevated susceptibility to mast cell degranulation. It could be why perimenopausal girls usually tend to have points associated to mast cells.[ref]
Endocrine-disrupting chemical compounds that mimic estrogen:
Added to the estrogen created within the physique is publicity to environmental estrogen mimics. BPA is one estrogen mimic that could be a element of many sorts of plastic.
Estrogen-mimicking compounds, resembling BPA, can bind to estrogen receptor alpha and trigger mast cell degeneration. PFOA and PFOS additionally bind to estrogen receptor alpha.[ref]
Analysis in cell traces and in animals exhibits that environmental estrogens add to the impact of estrogen within the physique, inflicting the activation of mast cells.[ref][ref]
Right here’s a superb instance of how this may very well be affecting individuals right this moment…
A 2019 research (in feminine mice) confirmed that BPA publicity at regular, human ranges had an impact on mast cells within the coronary heart — when uncovered to a virus. The research used mice housed in plastic cages and ingesting from plastic water bottles and tracked their response to myocarditis (coronary heart irritation) from a virus. The researchers in contrast this to a management group of mice with no BPA publicity (glass cage, glass water bottles). The group uncovered to BPA of their water and cages had elevated myocarditis and pericarditis (25% vs. 10%) when injected with a virus in comparison with the management group with out BPA publicity.[ref]
The BPA uncovered group had higher numbers of mast cells within the coronary heart and extra degranulation, worsening irritation and cardiac fibrosis. Moreover, the BPA uncovered group had increased ranges of a number of inflammatory cytokines within the coronary heart.
What does this need to do with mast cells and estrogen? The researchers discovered that the BPA (once more, at regular human publicity ranges) elevated the variety of mast cells within the coronary heart and that the mast cells had been extra prone to degranulate. From the research: “BPA publicity in ingesting water elevated mast cell degranulation within the coronary heart general”.[ref]
Associated article: Spike protein, mast cells, histamine, and coronary heart rhythm
Histamine as a mast cell degranulation set off:
Along with being triggered by pathogens (micro organism, parasites, viruses) and allergens, excessive ranges of histamine may also trigger mast cells to degranulate — giving off much more histamine. This feed ahead loop will increase mast cell degranulation in a tissue, resembling when your physique fights off micro organism in a minimize in your pores and skin.
Mast cells have each H1 and H4 histamine receptors on their cell floor. The histamine launch from mast cells can set off close by mast cells to launch extra histamine. It additionally helps to recruit different immune system cell varieties to the tissue.[ref]
Recap up to now:
~Mast cells which are triggered launch histamine.
~Histamine may also come from meals or your intestine microbiome.
~Estrogen receptors are discovered on mast cells. Elevated estrogen might enable mast cells to be extra simply triggered.
~Estrogen-mimicking chemical compounds can bind to estrogen receptors, together with on mast cells.
~Histamine may also trigger mast cells to degranulate.
Let’s transfer on to how estrogen interacts with histamine, whether or not from mast cells or different sources.
Estrogen and histamine within the mind
Within the Nineteen Seventies, researchers confirmed that histamine acts as a neurotransmitter within the mind. Histaminergic neurons have histamine receptors that reply to histamine signaling.[ref]
All 4 sorts of histamine receptors, H1R, H2R, H3R, and H4R, are discovered within the mind. Performing as a neurotransmitter, histamine regulates reminiscence, cognition, feelings, urge for food, and sleep. When histamine binds to H1R or H2R receptors, it results in excitation within the mind, however H3 receptors act to inhibit histaminergic neurons.[ref]
An animal research elucidated that histaminergic neurons had been discovered within the hypothalamus. The research confirmed that estrogen stimulation affected the extent of H1 receptors within the hypothalamus, which is concerned in sexual arousal.[ref]
Histamine within the hypothalamus can lower urge for food by way of sure receptors. Estrogen will increase histamine within the mind and thus barely reduces urge for food. Menopause – a decreasing of estrogen ranges – triggers weight acquire, and a few researchers assume that diminished histamine within the mind may very well be at play right here.[ref]
Migraines and Mast Cells:
Mast cells are additionally discovered within the mind. The dura is the thick layer of connective tissue surrounding the mind and spinal twine. The dural layer has nerves that relay ache in addition to mast cells.
This connection of nociceptors (ache sensors) and mast cells is believed to play a task in complications and migraines.
Animal research present that mast cell degranulation within the dura causes ache just like migraines. The researchers additionally discovered that estradiol will increase the variety of mast cells within the dura matter.
The authors of the research concluded that the explanation girls get migraines, particularly hormone-related migraines, is probably going as a result of mixture of elevated mast cells within the dura mixed with publicity to a mast cell degranulation set off. The degranulation then will increase histamine, serotonin, and proteases – creating an inflammatory response within the dura layer and triggering the ache receptors across the mind.[ref]
Histamine and Vasodilation
One function of histamine launched from mast cells is to trigger blood vessels to dilate (vasodilation). It permits extra blood circulation into the world of mast cell activation, which is essential when combating a pathogen or international substance in, for instance, a wound in your pores and skin.
A research on cardio train discovered that histamine is launched regionally within the skeletal muscle tissue and acts on H1 and H2 receptors to trigger vasodilation. The post-exercise histamine comes from each mast cell degranulation and from the endogenous formation of histamine by histidine decarboxylase.[ref]
Whereas performing by means of totally different mechanisms, each estrogen and histamine are vasodilators.
Researchers assume estrogen protects premenopausal girls from vascular illness and atherosclerosis by inhibiting irritation and performing as a vasodilator in blood vessels.[ref]
Endothelial nitric oxide additionally causes blood vessel dilation. Estrogen interacts with estrogen receptors within the coronary heart and endothelium to extend endothelial nitric oxide. Animal research present that estrogen in feminine animals promotes systemic anaphylaxis by way of elevated vasodilation with eNOS, which mixes with the elevated vascular permeability from histamine to accentuate the anaphylactic response.[ref][ref]
Bronchial asthma, estrogen, and histamine
Estrogen receptors work together with histamine within the clean muscle tissue of the airway in individuals with bronchial asthma. Curiously, in youngsters, boys have twice the chance of bronchial asthma in comparison with women. However in adults, girls of reproductive age usually tend to have bronchial asthma in comparison with males. Some theorize that the upper estrogen ranges in girls contribute to the elevated bronchial asthma threat.
So — what does estrogen need to do with bronchial asthma?
Bronchial asthma is brought on by an over-reaction within the clean muscle tissue of the airway. Intracellular calcium [Ca2+ ] ranges regulate bronchoconstriction (constricted lungs, wheezing) or bronchodilation (relaxed lungs).
A current analysis research discovered that estrogens scale back calcium response to medicine that trigger bronchoconstriction by way of an estrogen receptor (ERα). The researchers discovered elevated estrogen receptors within the airway clean muscle cells in individuals with bronchial asthma. In airway cells, publicity to a drug that binds to estrogen receptors elevated the response to histamine.[ref]
What does all this imply? Estrogen receptors and estrogen might (barely) improve the response to histamine, inflicting an over-activation of the muscle tissue surrounding the lungs. It may very well be interpreted to imply that prime histamine ranges plus excessive estrogen ranges improve the chance of bronchial asthma – or simply that may’t breathe proper, barely panicky feeling.
Moreover, estrogen-mimicking compounds can improve the interplay with estrogen receptors, histamine, and bronchial asthma. In a research of over 500 teenagers, women with increased PFOS ranges had been extra prone to have issues with bronchial asthma.[ref]
Estrogen, histamine, anaphylaxis:
In mice, “Anaphylactic responses had been extra pronounced in feminine than male mice. The improved severity of anaphylaxis in feminine mice was eradicated after pretreatment with an estrogen receptor antagonist or ovariectomy however restored after administration of estradiol in ovariectomized mice, demonstrating that the sex-specific variations are as a result of feminine steroid estradiol. Estrogen didn’t have an effect on mast cell responsiveness or anaphylaxis onset. As an alternative, it elevated tissue expression of endothelial nitric oxide synthase (eNOS). Blockage of NOS exercise with the inhibitor L-NG-nitroarginine methyl ester or genetic eNOS deficiency abolished the sex-related variations.
Conclusion: Our research defines a contribution of estrogen by means of its regulation of eNOS expression and nitric oxide manufacturing to vascular hyperpermeability and intensified anaphylactic responses in feminine mice, offering extra mechanistic insights into threat components and attainable implications for scientific administration within the additional exploration of human anaphylaxis.”[ref]
Endometriosis and Mast Cells
Endometriosis happens when endometrium-like tissue grows exterior of the uterus. It’s estrogen-dependent.
Mast cells are present in increased than regular numbers in endometriosis tissue. Estrogen, particularly when within the presence of IgE (allergen provoked), enhances mast cell activation and is believed to play a task within the growth of endometriosis.[ref]
NLRP3 is a receptor that senses hazard alerts or international particles after which calls up a powerful inflammatory response — it prompts the inflammasome. Current analysis brings collectively estrogen, NLRP3 inflammasome signaling, and mast cells in endometriosis. Researchers found that estrogen can improve the expression of NLRP3 by way of estrogen receptor alpha in mast cells. Estrogen elevated the transcription of inflammation-related genes.[ref]
Does estrogen lower diamine oxidase?
Diamine oxidase (DAO) is the enzyme that’s produced in intestinal cells to interrupt down histamine from meals and from intestine micro organism.
I learn in a number of articles on-line that histamine decreases diamine oxidase. One article linked to a reference from a rat research in 1986.
Aside from just a few animal research from a long time in the past, I’m not discovering any analysis that exhibits that estrogen impacts diamine oxidase ranges. A research revealed in 2000 confirmed that estradiol didn’t have an effect on DAO ranges in rat kidney cells.[ref]
Estrogen and Histamine Genotype Report
The genetic variants included right here influence histamine breakdown and in addition estrogen receptors. Please be aware that there is no such thing as a direct analysis exhibiting a relationship right here between estrogen receptor genes and histamine-related genes. As an alternative, that is provided so that you can decide if genetic variants are including to your histamine-related points.
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Membership permits you to see your knowledge proper in every article and in addition offers you entry to the members’ solely data within the Lifehacks sections.
Genes associated to the breakdown of histamine:
DAO (diamine oxidase) is the enzyme produced by the intestines, breaking down histamine from meals and micro organism. The AOC1 gene codes for the manufacturing of the DAO enzyme. Genetic variants in AOC1 can improve or lower the manufacturing of the enzyme.[ref]
Word that uncommon mutations influencing DAO manufacturing aren’t included in most genetic knowledge information, so the knowledge under might not provide the full image.[ref][ref]
AOC1 gene: encodes diamine oxidase (DAO)
Examine your genetic knowledge for rs10156191 (23andMe v4; AncestryDNA):
- C/C: typical
- C/T: diminished manufacturing of DAO, elevated threat of migraines because of histamine[ref]
- T/T: diminished manufacturing of DAO[ref][ref][ref], elevated threat of migraines because of histamine[ref]
Members: Your genotype for rs10156191 is —.
Examine your genetic knowledge for rs2052129 (23andMe v5; AncestryDNA):
- G/G: typical (most typical genotype)
- G/T: diminished manufacturing of DAO, elevated threat of migraines because of histamine[ref]
- T/T: diminished manufacturing of DAO[ref], elevated threat of migraines because of histamine[ref]
Members: Your genotype for rs2052129 is —.
Examine your genetic knowledge for rs1049742 (23andMe v4 solely):
- C/C: typical
- C/T: diminished manufacturing of DAO
- T/T: diminished manufacturing of DAO[ref]
Members: Your genotype for rs1049742 is —.
Examine your genetic knowledge for rs1049793 H645D (23andMe v4; AncestryDNA (older)):
- C/C: typical, excessive
- C/G: diminished manufacturing of DAO (35% discount)
- G/G: diminished manufacturing of DAO (50% discount)[ref]
Members: Your genotype for rs1049793 is —.
Examine your genetic knowledge for rs2071514 (23andMe v5; AncestryDNA):
- A/A: probably increased DAO[ref]
- A/G: probably increased DAO
- G/G: typical
Members: Your genotype for rs2071514 is —.
HNMT genetic variants:
Histamine n-methyltransferase (HMNT) is the enzyme that regulates histamine within the physique by way of changing it from histamine into N-methylhistamine, which might then be eradicated from the physique. HNMT is liable for eliminating 80% of histamine within the physique.[ref]
Examine your genetic knowledge for rs1050891 (23andMe v4, v5):
- G/G: typical; decrease threat of hyperactivity in ADHD because of meals components[ref]
- A/G: diminished breakdown of histamine in comparison with G/G
- A/A: diminished breakdown of histamine in comparison with G/G[ref]
Members: Your genotype for rs1050891 is —.
Examine your genetic knowledge for rs11558538 C314T (23andMe outcomes for i3000469, v4; AncestryDNA):
- T/T: diminished HNMT exercise[ref][ref] increased histamine ranges, elevated relative threat of bronchial asthma[ref]
- C/T: diminished breakdown of histamine in comparison with C/C
- C/C: typical[ref]
Members: Your genotype for rs11558538 is — -or- your 23andMe genotype for i3000469 is —.
Examine your genetic knowledge for rs2071048 -464(23andMe v4; AncestryDNA):
- T/T: elevated threat of bronchial asthma (and better histamine), widespread variant[ref]
- C/T: typical bronchial asthma threat
- C/C: typical bronchial asthma threat
Members: Your genotype for rs2071048 is —.
Methylation Cycle:
The methylation cycle performs a task in breaking down monoamine neurotransmitters, together with histamine. It’s also essential in creating the methyl teams wanted for the HMNT enzyme to work. So your methylation cycle genes may also assist steadiness histamine intolerance.
The MTHFR gene codes for an enzyme that could be a key participant within the folate cycle. It’s one supply of methyl teams for the methylation cycle. Decreased enzyme exercise of MTHFR – mixed with a food plan missing in folate or choline – might trigger a diminished breakdown of histamine.
Examine your genetic knowledge for rs1801133 (23andMe v4, v5; AncestryDNA):
- G/G: typical
- A/G: one copy of MTHFR C677T allele (heterozygous) decreased enzyme operate by 40%
- A/A: two copies of MTHFR C677T (homozygous) decreased enzyme operate by 70 – 80%
Members: Your genotype for rs1801133 is —.
Estrogen Receptor Genes:
The estrogen receptors are liable for sending the sign from circulating hormones to provoke the interpretation of different proteins.
ESR1 gene: encodes Estrogen Receptor alpha
ESR1 mediates estrogen exercise within the mind and has been studied as a threat for illnesses resembling breast most cancers, osteoporosis, and endometriosis, in addition to extreme PMS. ESR1 has additionally been studied in relation to cognitive impairment and Alzheimer’s Illness.[ref]
Examine your genetic knowledge for rs9340799 (23andMe v4, v5; AncestryDNA):
- G/G: increased threat for extreme PMS[ref][ref] elevated relative threat of endometriosis, doubtless increased estrogen receptors[ref]
- A/G: elevated threat of endometriosis
- A/A: typical
Members: Your genotype for rs9340799 is —.
GPER1 gene: G-protein estrogen receptor
This part outlines concepts on lowering or balancing estrogen ranges, histamine-reducing dietary supplements, and avoiding mast cell triggers.
Balancing estrogen ranges:
The remainder of this text explains the options for estrogen associated histamine issues. It’s for Genetic Lifehacks members solely. Contemplate becoming a member of right this moment to see the remainder of this text.
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Associated Articles and Subjects:
Mind Fog: Genetics and Options
There are a number of causes of the cognitive points often called ‘mind fog’. Genetics might assist you determine your root trigger and customized options.
Mast cell activation syndrome
Take a deep dive into how mast cells work and what goes unsuitable in mast cell activation syndrome (MCAS).
Estrogen: How it’s made and the way we do away with it
Estrogen-from how a lot is made to how it’s damaged down – relies on genetics and life-style components and impacts each women and men.
Migraines: Genes, Root Causes, and Customized Options
Your genes play a task in your susceptibility to migraines. Discover out what’s going on when you’ve gotten a migraine and options that suit your genes.
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Ayuso, Pedro, et al. “Genetic Variability of Human Diamine Oxidase: Incidence of Three Nonsynonymous Polymorphisms and Research of Their Impact on Serum Enzyme Exercise.” Pharmacogenetics and Genomics, vol. 17, no. 9, Sept. 2007, pp. 687–93. PubMed, https://doi.org/10.1097/FPC.0b013e328012b8e4.
“Finest 15 Vitamin B-6 Meals: Advantages and Recipes.” Healthline, 26 Might 2017, https://www.healthline.com/well being/vitamin-b6-foods.
Boes, Tanner, and Dan Levy. “Affect of Intercourse, Estrous Cycle and Estrogen on Intracranial Dural Mast Cells.” Cephalalgia : An Worldwide Journal of Headache, vol. 32, no. 12, Sept. 2012, pp. 924–31. PubMed Central, https://doi.org/10.1177/0333102412454947.
Bruno, Katelyn Ann, et al. “BPA Alters Estrogen Receptor Expression within the Coronary heart After Viral An infection Activating Cardiac Mast Cells and T Cells Resulting in Perimyocarditis and Fibrosis.” Frontiers in Endocrinology, vol. 10, Sept. 2019, p. 598. PubMed Central, https://doi.org/10.3389/fendo.2019.00598.
Cao, X. L., et al. “Concentrations of Bisphenol A within the Composite Meals Samples from the 2008 Canadian Whole Food regimen Research in Quebec Metropolis and Dietary Consumption Estimates.” Meals Components & Contaminants. Half A, Chemistry, Evaluation, Management, Publicity & Danger Evaluation, vol. 28, no. 6, June 2011, pp. 791–98. PubMed Central, https://doi.org/10.1080/19440049.2010.513015.
Cooke, Paul S., et al. “Estrogens in Male Physiology.” Physiological Evaluations, vol. 97, no. 3, July 2017, pp. 995–1043. journals.physiology.org (Atypon), https://doi.org/10.1152/physrev.00018.2016.
Dalessandri, Kathie M., et al. “Pilot Research: Impact of three,3’-Diindolylmethane Dietary supplements on Urinary Hormone Metabolites in Postmenopausal Ladies with a Historical past of Early-Stage Breast Most cancers.” Diet and Most cancers, vol. 50, no. 2, 2004, pp. 161–67. PubMed, https://doi.org/10.1207/s15327914nc5002_5.
ELDAFIRA, Eldafira, et al. “Polymorphisms of Estrogen Receptor-α and Estrogen Receptor-β Genes and Its Expression in Endometriosis.” Turkish Journal of Pharmaceutical Sciences, vol. 18, no. 1, Feb. 2021, pp. 91–95. PubMed Central, https://doi.org/10.4274/tjps.galenos.2019.94914.
García-Martín, Elena, et al. “Histamine Pharmacogenomics.” Pharmacogenomics, vol. 10, no. 5, Might 2009, pp. 867–83. PubMed, https://doi.org/10.2217/pgs.09.26.
Gotoh, Koro, et al. “Hypothalamic Neuronal Histamine Signaling within the Estrogen Deficiency-Induced Weight problems.” Journal of Neurochemistry, vol. 110, no. 6, Sept. 2009, pp. 1796–805. PubMed, https://doi.org/10.1111/j.1471-4159.2009.06272.x.
Guo, Xinyue, et al. “NLRP3 Inflammasome Activation of Mast Cells by Estrogen by way of the Nuclear-Initiated Signaling Pathway Contributes to the Growth of Endometriosis.” Frontiers in Immunology, vol. 12, Sept. 2021, p. 749979. PubMed Central, https://doi.org/10.3389/fimmu.2021.749979.
Hon, Yuen Yi, et al. “Endogenous Histamine and Cortisol Ranges in Topics with Totally different Histamine N-Methyltransferase C314T Genotypes.” Molecular Prognosis & Remedy, vol. 10, no. 2, 2006, pp. 109–14. PubMed Central, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4178529/.
—. “Endogenous Histamine and Cortisol Ranges in Topics with Totally different Histamine N-Methyltransferase C314T Genotypes : A Pilot Research.” Molecular Prognosis & Remedy, vol. 10, no. 2, 2006, pp. 109–14. PubMed, https://doi.org/10.1007/BF03256450.
Hox, Valerie, et al. “Estrogen Will increase the Severity of Anaphylaxis in Feminine Mice by means of Enhanced Endothelial Nitric Oxide Synthase Expression and Nitric Oxide Manufacturing.” The Journal of Allergy and Scientific Immunology, vol. 135, no. 3, Mar. 2015, pp. 729-736.e5. PubMed, https://doi.org/10.1016/j.jaci.2014.11.003.
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Jones, Bridgette L., et al. “Genetic Variation within the Histamine Manufacturing, Response, and Degradation Pathway Is Related to Histamine Pharmacodynamic Response in Youngsters with Bronchial asthma.” Frontiers in Pharmacology, vol. 7, 2016. www.ncbi.nlm.nih.gov, https://doi.org/10.3389/fphar.2016.00524.
Jotova, I., et al. “Results of Testosterone and 17, Beta-Estradiol on the Polyamine Metabolism in Cultivated Regular Rat Kidney Epithelial Cells.” Amino Acids, vol. 18, no. 4, 2000, pp. 353–61. PubMed, https://doi.org/10.1007/pl00010322.
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