1:Pharmacol Ther. 1995 Jun;66(3):413-63. Links
Molecular pharmacological aspects of histamine receptors.
Leurs R, Smit MJ, Timmerman H.

2:Chrousos. Stress, chronic inflammation, and emotional and physical wellbeing: concurrent effects and chronic sequellae
JACI 2000;106S275-91

J Immunol. 1998 Sep 1;161(5):2586-93. Links
Histamine potently suppresses human IL-12 and stimulates IL-10 production via H2 receptors.Elenkov IJ, Webster E, Papanicolaou DA, Fleisher TA, Chrousos GP, Wilder RL.
Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892, USA. ElenkovI@cc1.nichd.nih.gov

IL-12 and IL-10, respectively, stimulate Th1 and Th2 immune responses. The development of some allergic reactions, infections, and tumors are associated with excessive histamine production and a shift toward Th2 responses. Here we address the possibility that this association is causally linked, at least in part, to modulation of IL-12 and IL-10 production by histamine. We report that histamine dose-dependently inhibited the secretion of human IL-12 (p70) and increased the production of IL-10 in LPS-stimulated whole blood cultures. These effects of histamine were antagonized by cimetidine, an H2 receptor antagonist, but not by selective H1 and H3 receptor blockers, and were mimicked by an H2 receptor agonist. The effects of histamine on IL-12 and IL-10 secretion were independent of endogenous secretion of IL-10 or exogenous addition of IL-12, while Ro 20-1724, a phosphodiesterase inhibitor, potentiated the effects of histamine on IL-12 and IL-10 production, implicating cAMP in its actions. Similar modulatory effects of histamine on IL-12 and IL-10 production, which were reversed by the H2 antagonist cimetidine, were observed in PBMC and isolated monocytes stimulated by Staphylococcus aureus Cowan strain 1 and LPS, respectively. Thus, histamine, via stimulation of H2 receptors on peripheral monocytes and subsequent elevation of cAMP, suppresses IL-12 and stimulates IL-10 secretion, changes that may result in a shift of Th1/Th2 balance toward Th2-dominance. This may represent a novel mechanism by which excessive secretion of histamine potentiates Th2-mediated allergic reactions and contributes to the development of certain infections and tumors normally eliminated by Th1-dependent immune mechanisms


1: Int J Immunopharmacol. 2000 Oct;22(10):755-63. Links
The anti-allergic drug histaglobin inhibits NF-kappaB nuclear translocation and down-regulates proinflammatory cytokines.Ayoub M, Mittenbühler K, Sütterlin BW, Bessler WG.
Institut für Molekulare Medizin und Zellforschung, AG Tumorimmunologie/Vakzine, Medizinische Fakultät der Universität Freiburg, D-79104, Freiburg, Germany.

The transcription factor NF-kappaB is the central regulator for the expression of various genes involved in inflammation, infection and immune response including the genes for IL-1beta, TNF-alpha, IL-6 and leukocyte adhesion molecules. Here, we show that the anti-allergic drug histaglobin down-regulates the release of IL-1beta, TNF-alpha, IL-6 and IL-10 in human peripheral blood mononuclear cell cultures. This down-regulatory effect becomes even more pronounced when the cultures are simultaneously activated with the T-lymphocyte mitogen phytohemagglutinin (PHA) or with the B-lymphocyte and macrophage activator lipopeptide (P(3)CSK(4)). We also demonstrate that histaglobin inhibits the nuclear translocation of NF-kappaB in response to TNF-alpha or lipopolysaccharide (LPS) in bone marrow-derived macrophages of Balb/c mice. The inhibitory effect of histaglobin on NF-kappaB activation and cytokine release might be responsible for its anti-allergic effect as demonstrated in clinical studies


5.K.Ito. "Clinical evaluation of histaglobin for bronchial asthma-a double-blind study using human gammaglobulin as control".1979;56:3085-69





there are many many more references but basically what im suggesting is that Histamine and its congengers can be used in a therapeutic setting. I came to this conclusion from reading a book based on this therapy, and also general study of the histamine receptors along with anti-inflammatory cytokines and current asthma treatments.

Atopy and its treatment generally consists of H1 receptor antagonist which neutralize the histamine released via de granulation of mast cells, basophils,LC's etc.. which cause allergy, asthma......atopy. However, there are other histmine receptors which seem to stimulate anti-inflammatory or healthy immune polarization towards histamine control. H2 receptor agonists induce histamine supressor factor or IL-10 which has potent anti-allergy effects. Not only do H2 receptor agonists stimulate Treg cells and suppressor factors which reduce inflammation and releive allergy but this activation seems to have long term effects via H2 control of diseased H1 receptors which are hyperexcitable thus releasing histamine in both late and early stage allergy.

Activation of H2 also raise intracellular levels of cAMP which is patently low in atopy patients and are the recent focus of allergology with PDE agonists, which hope to improve on theophylline. However, stopping the breakdown of already low levels of cAMP may be futile, while increases via H2 agonism are ideal.

Histamine as a physiological autocoid is the most potent stimulator of H2/H3 receptors known and in either singular form or as a histoglobulin demonstrates its clinical effectiveness as a treatment for atopy.

H3 receptor agonists (histamine congengers) also quells the release on histamine from basophils and is involved in this process. Low activation of H2/H3 receptors in turn leads to low levels of tsup cells and factors, leading to lower levels of cAMP, increased pro-inflammatory chemistry and excessive H1 stimulation and histamine hyperreleasability from mast cells etc..


so if Histamine as a drug is shown to reduce atopy, and as a congenger (histoglobulin) with little side effects (autocoid) why and how could one go about using this treatment. Histamine is routinely used in gastric testing, thus is pretty easy to acquire. it should help fatigue, allergies, migraines etc.


thus is this a pluasible treatment, and how would one go about doing something like this?

Dumb question probably, but wouldn't just taking histamine be unselective for the receptors you outline?

It's sold pretty widely by bulk supplement cos.

low dose histamine seems to be a more potent stimulator of H2/H3 with little effect on H1/H4 in low doses.

if that was the case then you wouldnt seem an increase in il-10 and decrease in il-12 which is associated with H2 activation.

however, it is still a good question as i dont really know why injected histamine is selective for these receptors, more then likely its greater affinity.

You are looking in the wrong direction. Look at some of the idiosyncratic aspects of atopic pathology in relation to human IL-4 receptor α chain*1. Mutancy in the Arg551 allele is probably the single best marker. So, what do we draw from this? Well, the Arg/Glut switchover is strongly implicated in association between arg kinase as a both regulator and transporter in the high affinity IgE binding context. Looking from here to splicing factor arginine/serine-rich 8, we can see the connectivity between enzymatic NO formation and atopy. NO synthases have been quite clearly identified with "regulatory processes in the lung, including inflammation, host defense and bronchomotor control" (Grasemann et al., 2005). We also know that oral l-Arg can re-regulate this dysfunction/impairment. So, increasing Arg bioavailability while reducing serum arginase activity should have wide applicability across the spectrum of atopy-associated conditions, including CF, FMS, CFS, etc..

Support from the GERD perspective:

Am J Physiol. 1998 Jun;274(6 Pt 1):G984-91. Links
Effects of long-term oral L-arginine on esophageal motility and gallbladder dynamics in healthy humans.Luiking YC, Weusten BL, Portincasa P, Van Der Meer R, Smout AJ, Akkermans LM.
Department of Surgery, University Hospital Utrecht, Utrecht, The Netherlands.

Inhibitory nitrergic neurons are known to play a role in the regulation of motility patterns of the distal esophagus, the lower esophageal sphincter (LES), and the gallbladder. Our study aim was to investigate the effects of "long-term" (i.e., prolonged) oral intake of L-arginine (L-Arg), the endogenous source for nitric oxide (NO) synthesis, on postprandial LES pressure (LESP), esophageal motility, gastroesophageal reflux, and gallbladder motility. L-Arg (30 g/day) or glycine (placebo; 13 g/day; isosmolar) was given orally to 10 healthy male volunteers for 8 days, according to a randomized, crossover design. Twenty-four-hour urinary nitrite/nitrate excretion was measured to indicate NO synthesis. Basal early postprandial LESP was lower after L-Arg ingestion (2.2 kPa) than after glycine ingestion (2.7 kPa) (P < 0.05). L-Arg abolished the physiological late postprandial rise in LESP. Transient LES relaxations were longer lasting after L-Arg ingestion (P < 0.02). Esophageal motility and reflux were not affected (not significant). Fasting and residual gallbladder volumes were greater after L-Arg ingestion (P < 0.05). Urinary nitrite/nitrate excretion was higher after L-Arg intake (P < 0.05). In conclusion, long-term oral L-Arg suppresses late postprandial LESP increase, prolongs transient LES relaxations, and increases fasting and residual gallbladder volumes. These effects may be mediated by increased NO synthesis.

IBS:

Neurogastroenterol Motil. 2006 Feb;18(2):115-22. Links
Possible role of nitric oxide in visceral hypersensitivity in patients with irritable bowel syndrome.Kuiken SD, Klooker TK, Tytgat GN, Lei A, Boeckxstaens GE.
Department of Gastroenterology and Hepatology, Academic Medical Centre, Amsterdam, The Netherlands.

BACKGROUND: Visceral hypersensitivity is a consistent finding in a considerable proportion of patients with irritable bowel syndrome (IBS), and may provide a physiological basis for the development of IBS symptoms. In this study, we aimed to confirm the hypothesis that nitric oxide (NO) is involved in maintaining visceral hypersensitivity in IBS. Ten healthy volunteers (HV) and 12 IBS patients with documented hypersensitivity to rectal distension underwent a rectal barostat study. The effect of placebo and the specific NO synthase inhibitor NG -monomethyl-L-arginine (L-NMMA) on resting volume, rectal sensitivity to distension and rectal compliance was evaluated in a double-blind, randomized, cross-over fashion. NG -monomethyl-L-arginine did not alter resting volumes in HV or IBS patients. In HV, l-NMMA did not alter rectal sensory thresholds compared to placebo (45 +/- 3 and 46 +/- 3 mmHg, respectively). In contrast, L-NMMA significantly increased the threshold for discomfort/pain in IBS patients (placebo: 18 +/- 2, l-NMMA: 21 +/- 3 mmHg, P < 0.05). Rectal compliance was not affected by L-NMMA. Although NO does not seem to play a major role in normal rectal sensation or tone, we provide evidence that NO may be involved in the pathophysiology of visceral hypersensitivity in IBS.

CF:

Respir Res. 2006 Jun 9;7:87. Links
Decreased systemic bioavailability of L-arginine in patients with cystic fibrosis.Grasemann H, Schwiertz R, Grasemann C, Vester U, Racké K, Ratjen F.
Children's Hospital, University of Duisburg-Essen, Essen, Germany. hartmut.grasemann@sickkids.ca

BACKGROUND: L-arginine is the common substrate for nitric oxide synthases and arginases. Increased arginase levels in the blood of patients with cystic fibrosis may result in L-arginine deficiency and thereby contribute to low airway nitric oxide formation and impaired pulmonary function. METHODS: Plasma amino acid and arginase levels were studied in ten patients with cystic fibrosis before and after 14 days of antibiotic treatment for pulmonary exacerbation. Patients were compared to ten healthy non-smoking controls. RESULTS: Systemic arginase levels measured by ELISA were significantly increased in cystic fibrosis with exacerbation compared to controls (17.3 +/- 12.0 vs. 4.3 +/- 3.4 ng/ml, p < 0.02). Arginase levels normalized with antibiotic treatment. Plasma L-arginine was significantly reduced before (p < 0.05) but not after treatment. In contrast, L-ornithine, proline, and glutamic acid, all downstream products of arginase activity, were normal before, but significantly increased after antibiotic therapy. Bioavailability of L-arginine was significantly reduced in cystic fibrosis before and after exacerbation (p < 0.05, respectively). CONCLUSION: These observations provide further evidence for a disturbed balance between the L-arginine metabolic pathways in cystic fibrosis.

Atopic dermatitis:

Hautarzt. 2004 Jan;55(1):58-64. Links

[Topically applied arginine hydrochloride. Effect on urea content of stratum corneum and skin hydration in atopic eczema and skin aging][Article in German]


Nenoff P, Donaubauer K, Arndt T, Haustein UF.
Laboratorium für medizinische Mikrobiologie, Mölbis. info@mykologie-experten.de

BACKGROUND AND OBJECTIVE: Currently, there are no data on how the topical application of amino acids influences the complex moisture retaining system of the skin in vivo. PATIENTS/METHODS: An open study was performed to investigate the effects of topical application of arginine hydrochloride on epidermal stratum corneum urea content, transepidermal water loss, skin hydration, and clinical status of patients with atopic dermatitis and dry elderly skin. RESULTS: Treatment of patients with atopic dermatitis with 2.5% arginine hydrochloride ointment over 4 weeks showed a significant increase in urea in the stratum corneum as well as a continuous increase in skin moisture. CONCLUSIONS: The urea deficit in the stratum corneum in atopic dermatitis and elderly skin was corrected not by applying the moisturizer urea itself but instead by using arginine - its precursor in the Krebs-Henseleit urea cycle. This topical treatment also improved the clinical symptoms of dry skin.

Immunosuppression:

J Invest Dermatol. 2003 Sep;121(3):587-93. Links
Nitric oxide appears to be a mediator of solar-simulated ultraviolet radiation-induced immunosuppression in humans.Kuchel JM, Barnetson RS, Halliday GM.
Department of Medicine (Dermatology), The Melanoma and Skin Cancer Research Institute, Royal Prince Alfred Hospital at The University of Sydney, Sydney, NSW 2006, Australia.

Topical application of NG-methyl-L-arginine and 2,2'-dipyridyl were used to examine the respective roles of nitric oxide and reactive oxygen species in solar-simulated ultraviolet radiation-induced immunosuppression in humans in vivo. Immunosuppression was studied using a nickel contact hypersensitivity recall model. Ultraviolet radiation dose-responses were generated to determine the extent to which NG-methyl-L-arginine and 2,2'-dipyridyl affected the immune response. NG-methyl-L-arginine but not 2,2'-dipyridyl protected the immune system from ultraviolet radiation-induced suppression. Both NG-methyl-L-arginine and 2,2'-dipyridyl inhibited nitrite production. Nitrite is a degradation product of peroxynitrite, a cytotoxic mediator resulting from reactions between nitric oxide and reactive oxygen species. This suggests that nitric oxide, not its downstream product peroxynitrite, was likely to be responsible for solar-simulated ultraviolet radiation-induced immunosuppression. In contrast, both nitric oxide and reactive oxygen species were mediators of solar-simulated ultraviolet radiation-induced apoptosis and loss of dendritic S-100+ cells (probably Langerhans cells) from the epidermis. It is likely that different mechanisms are involved in these ultraviolet-induced endpoints and that events in addition to Langerhans cell depletion are important for local immune suppression to recall antigens in humans. Understanding the mechanisms of cutaneous ultraviolet-induced oxidative stress will assist in the future design of novel products that protect skin from photoaging and skin cancer.


More on bronchomotor control:

Rev Med Chir Soc Med Nat Iasi. 2007 Apr-Jun;111(2):454-8.Links
[New insight into nitric oxide involvement in regulation of airways smooth muscle tone][Article in Romanian]


Dumitriu IL, Petrescu BC, Gurzu MB, Gurzu B, Slătineanu SM.
Facultatea de Medicină, Departmentul de Fiziologie, Universitatea de Medicină i Farmacie "Gr.T. Popa" Iaşi.

All three isoforms of NO synthases (NOS) were localised in the lung and are involved in regulation of airways and pulmonary vessels smooth muscle tone and inflammatory response. The participation of nitric oxide in the regulation of airways smooth muscle has not been understood yet. MATERIAL AND METHOD: We studied age-related variation of NO secretion on three lots of bronchi rats: young (4-6 weeks), adults (2-3 months), old (12-14 months). The implied of NO synthesis on airways smooth muscle tone was indirectly investigated by blocking NOS with N(omega)-nitro-L-arginine methyl ester (L-NAME). RESULTS: Pre-treatment of isolated bronchi rings with 0.1 mM L-NAME amplified both tonic contractions induced by cumulative doses of acetylcholine (0.1 nM - 1mM) and various doses of angiotensin II (10 nM - 10 eM). L-NAME actions were lower on old than young rats: at least two times for ACh and three times for Ang II. These results suggest that NO actions decrease with age. Decrease of NO activity on airways was described in pathological states like asthma. CONCLUSIONS: Decrease of NO activity would generate increase of airway smooth muscle tone and would explain partially aging changes on airway reactivity.

Anaphylaxis:

Anesth Analg. 2008 Feb;106(2):392-403. Links
Anaphylaxis during cardiac surgery: implications for clinicians.Levy JH, Adkinson NF Jr.
Emory Hospital, 1364 Clifton Rd., Atlanta, GA 30322, USA.

During surgery, patients are exposed to multiple foreign substances including anesthetic drugs, antibiotics, blood products, heparin, polypeptides (aprotinin, latex, and protamine), and intravascular volume expanders, which have the potential to produce life-threatening allergic reactions termed "anaphylaxis." The hallmark of perioperative anaphylaxis is acute cardiovascular and pulmonary dysfunction. Patients undergoing cardiac surgery have extensive monitoring that permits rapid recognition and treatment when anaphylaxis occurs. Initial, smaller doses of drugs, often called test doses, administered before the therapeutic dose may produce anaphylaxis, and so clinicians need to be prepared to treat reactions if they occur. Institution of cardiopulmonary bypass for hemodynamically unstable patients can be a life-saving maneuver, and should be considered in patients with refractory cardiovascular dysfunction. Arginine vasopressin should also be considered for patients with vasodilatory shock. In this review, we focus on recent concepts in understanding the incidence and management approaches for patients at risk for anaphylaxis in the operating room setting, with an emphasis on cardiac surgical patients.

Pain links:

Life Sci. 2007 Dec 14;81(25-26):1694-702. Links
Role of nitric oxide/cyclic GMP/K(+) channel pathways in the antinociceptive effect caused by 2,3-bis(mesitylseleno)propenol.Jesse CR, Savegnago L, Nogueira CW.
Laboratório de Síntese, Reatividade e Avaliação Farmacológica e Toxicológica de Organocalcogênios, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, CEP 97105-900, RS, Brazil.

The present study examined the antinociceptive effects induced by 2,3-bis(mesitylseleno)propenol, a bis-selenide alkene derivate, given orally, in chemical models of pain in rats and mice. Selenide administered orally (p.o.) into the rats caused antinociception against the first and second phases of the formalin test, with mean ID(50) values of 28.17 and 39.68 mg/kg, respectively. The antinociceptive effect caused by selenide (50 mg/kg, p.o.) on the formalin test was reversed by pretreatment with N(G)-L-nitro-arginine methyl ester (L-NAME, a nitric oxide (NO) synthase inhibitor), methylene blue (a non-specific NO/guanylyl cyclase inhibitor) and glibenclamide (an ATP-sensitive K(+) channel inhibitor), but not by atropine (a muscarinic antagonist). Given orally selenide in mice produced an inhibition of glutamate-, histamine- and compound 48/80-induced nociception with mean ID(50) values of 27.58, 36.18 and 44.53 mg/kg, respectively. Moreover, oral treatment with selenide in mice decreased licking -- induced by serotonin (mean ID(50) value of >50 mg/kg). The data show that selenide exerts pronounced systemic antinociception in chemical (formalin, glutamate, histamine, compound 48/80 and serotonin-induced pain) models of nociception. Taken together, these results suggest that the antinociceptive effect of selenide on the formalin test involves the participation of nitric oxide/cyclic GMP/K(+) channel pathways in rats.

Curr Med Chem. 2007;14(18):1945-55. Links
The involvement of the nitric oxide in the effects and expression of opioid receptors during peripheral inflammation.Pol O.
Laboratori de Neurofarmacologia Molecular, Institut de Recerca, Hospital de la Sta Creu i Sant Pau & Institut de Neurociències, Universitat Autònoma de Barcelona, Barcelona, Spain. opol@santpau.es

Peripheral inflammation enhances the antinociceptive effects of opioid receptor agonists through the activation of peripheral opioid receptors whose expression also increases during inflammatory pain. Similarly, intestinal inflammation also increases the antitransit and antiexudative effects of opioids as well as the expression of neuronal and extra-neuronal opioid receptors located in the gut. Nitric oxide has been described either as pro- or antiinflammatory and could produce both pro- and antinociceptive effects. In addition, numerous studies have shown that the L-arginine-nitric oxide-cGMP system participates in the antinociceptive and in the intestinal effects produced by opioids during peripheral inflammation by enhancing their effects. Thus, substances capable of inhibiting cyclic guanosine-3',5'-monophosphate (cGMP) degradation or nitric oxide donors increase the analgesic effects of opioid receptor agonists during peripheral inflammation. At the same time, the administration of nitric oxide synthase (NOS) or guanylate cyclase inhibitors decreases those effects. In accordance with these results, different clinical trials have also demonstrated that the co-administration of nitric oxide donors with opioids is highly beneficial in the treatment of pain in patients. In the gut, nitric oxide has a further pro- and antiinflammatory action. It is also involved in the enhanced antitransit and antiexudative effects produced by opioids and in the up-regulation of the mu-opioid receptor gene transcription observed in the inflamed intestine. To sum up, a better knowledge of the involvement of the L-arginine-nitric oxide-cGMP pathway in the opioid mechanisms of action and a better understanding of the pathways that regulate the expression of opioid receptors during peripheral inflammation are essential to developing improved analgesic/antiinflammatory therapies.

Acta Anaesthesiol Taiwan. 2007 Jun;45(2):65-72.Links
Effect of intrathecal NG-nitro-L-arginine methyl ester administration on Fos expression in the spinal dorsal horn in rats following sciatic nerve ligation.Li P, Xue FS, Li CW, Liu KP, Liu Y, Xu YC, Yang QY.
Department of Anesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences, Beijing, China.

BACKGROUND: In the available literature, the pro- or antinociceptive role of nitric oxide (NO) is warmly disputed. As a marker of neuronal activation of the central nervous system, Fos expression has been widely used to assess the change in central neuronal activity evoked by peripheral input. In this study, we examined the effect of intrathecal L-NAME, a non-selective nitric oxide synthase (NOS) inhibitor, on nociceptive behavior and spinal Fos expression in rats following chronic constriction injury (CCI) of sciatic nerve, a model of neuropathic pain similar to that observed in clinical setting. METHODS: Eighty adult male SD rats showing no neurological deficiency a week after intrathecal catheterization were used in this study. L-NAME 250 microg of 10 microl (an equivalent or 0.9% saline) was injected intrathecally 15 min prior to CCI or sham operation. In addition to examination of thermal hyperalgesia by paw withdrawal latency (PWL), measurement of Fos protein staining neurons in the lumbar spinal cord using an immunohistochemistry technique were made at 1, 3, 7 and 14 days after operation. RESULTS: As compared with untreated animals, both CCI and sham operations evoked an early and long-term Fos expression, whereas a significant decrease in PWL was demonstrated only in rats receiving CCI. On days 3, 7 and 14 after CCI, the number of FLI neurons in the spinal dorsal horn ipsilateral to the injury decreased by 54%, 57% and 43%, respectively, in CCI-L-NAME group when compared with CCI-saline group, corresponding to the significant attenuation of thermal hyperalgesia. However, intrathecal L-NAME preadministration had no effect on the spinal Fos expression evoked by sham operation. CONCLUSIONS: Spinal Fos expression could be induced by different mechanisms, and it should not regarded as a reliable marker of pain sensation disorders. NO plays an important role in the development of nociception and spinal Fos expression through central sensitization mediated by peripheral nerve injury.

J Pharmacol Exp Ther. 1998 Aug;286(2):767-71. Links
Oral administration of L-arginine potentiates allergen-induced airway inflammation and expression of interleukin-5 in mice.Takano H, Lim HB, Miyabara Y, Ichinose T, Yoshikawa T, Sagai M.
Research Team for Health Effects of Air Pollutants, National Institute for Environmental Studies, Tsukuba, Ibaraki, Japan.

The role of nitric oxide in the airway hyperresponsiveness and inflammation of bronchial asthma has not yet been established. However, L-arginine, the substrate for nitric oxide synthases, reportedly alleviates airway hyperresponsiveness caused by parainfluenza virus and reduces granulocytic inflammation induced by ischemia-reperfusion. We investigated the effects of L-arginine on a murine model of allergic asthma that included airway hyperresponsiveness, eosinophilic inflammation and expression of interleukin (IL)-5 in the lung. The mice received drinking water with or without L-arginine for 9 weeks. Histologic evaluation and cellular profiles in bronchoalveolar lavage fluid showed that p.o. administration of L-arginine (72 micromol/kg/day) significantly enhanced eosinophilic airway inflammation and goblet cell proliferation that were associated with intratracheal instillation of ovalbumin. L-Arginine also increased protein levels of IL-5 and IL-2 in supernatants from the lung exposed to ovalbumin. The number of eosinophils in bronchoalveolar lavage fluid correlated significantly with the expression of IL-5. L-Arginine did not reverse ovalbumin-associated airway hyperresponsiveness to inhaled ACh. These results suggest that p.o. administration of L-arginine aggravates allergen-induced eosinophilic airway inflammation via expression of IL-5, and in this model it does not show therapeutic efficacy against airway hyperresponsiveness associated with allergen exposure. Oral administration of L-arginine, the precursor of nitric oxide, may not be an effective intervention in allergic asthma.


Effects of L-arginine and phosphodiesterase-5 inhibitor, sildenafil, on inflammation and airway responsiveness of sensitized BP2 mice.Al Qadi-Nassar B, Bichon-Laurent F, Portet K, Tramini P, Arnoux B, Michel A.
UMR Qualisud - Laboratoire de Pharmacologie, Faculté de Pharmacie, Montpellier, France.

Nitric oxide (NO) levels are elevated in the exhaled breath of asthmatic patients and NO is considered as a biomarker of airway inflammation. However, the functions of NO in the airways are not completely understood. L-arginine, as the substrate of NO synthases, is the precursor of NO which stimulates guanylate cyclase and leads to the formation of cyclic GMP (cGMP). Sildenafil, a phosphodiestérase-5 (PDE-5) inhibitor, prevents the degradation of cGMP. In this study the effects of L-arginine and sildenafil treatment, alone or in combination, were evaluated in ovalbumin-sensitized BP2 mice. These effects concerning the airway responsiveness to inhaled methacholine (MCh) were evaluated by whole-body plethysmography (WBP), the inflammatory response evaluated by bronchoalveolar lavage fluid (BALF) analyses and lung tissue biopsies (eosinophilic inflammation associated with lung remodelling), and NO metabolite measurements (by Griess reaction) in BALF. Ovalbumin sensitization induced: (a) an inflammatory reaction with eosinophil and neutrophil influx in BALF and lung; and ( an increased bronchial responsiveness to MCh. L-arginine treatment [50 mg/kg intraperitoneally (i.p.), for 7 days] increased the relative amount of eosinophils and neutrophils in BALF, had a tendency to increase the airway responsiveness to inhaled MCh and increased the NO metabolite level in BAL. Sildenafil treatment (20 mg/kg i.p. for 7 days) did not affect the airway responsiveness to MCh and had a lower effect compared with L-arginine on inflammatory reactions. The combination of the two treatments resulted in a dramatic enhancement of the airway responsiveness to inhaled MCh. The relative amount of eosinophils was increased and lung histology showed obvious worsened tissular lesions such as epithelial shedding and hypertrophy, hyperplasia of smooth muscle cells, and fibrosis. These findings are consistent with the notion that NO production plays a role in the development of airway inflammation and hyperresponsiveness of sensitized mice and highlighted the potential risk of the L-arginine dietary complement or PDE5 treatment in asthmatic patients.

Both of these studies underscore the hypothesis that NO biosynthesis is implicated in atopy, and in no way refutes my suggestion that "increasing Arg bioavailability while reducing serum arginase activity should have wide applicability across the spectrum of atopy-associated conditions."

Wait a minute, shouldn't you have to provide evidence that my theory is incorrect, we haven't elucidated whether histamine or NO is primary or epiphenominal to atopy.


histamine is a known component, if it is a result of the arginine malformity i would be convinced.However, it seems that histamine has anti allergenic properties and is used in intractable vascular headaches , another co-mordid pathology implicated in atopic conditions.

I at no point said that your 'theory' is incorrect, young jedi. It is pretty clear that you have misidentified the primary pathway, however.

...FIGHT!

I dont hit women

That's not what Julia's restraining order says.

Why do you hate histamine?

Why do YOU hate Julia? Is it because of her discovery of cold heat?

she is working on soft hard right now. Similar to your transient ED.

So does this mean that topical arginine might treat atopic eczema?

That's what the one of the studies posted above suggests.

Do we have a method to increase the bioavailability of L-arg?

Back to the histamine question - If histamine down regulates IL-5 which helps decrease allergic reactions then why is benedryl the traditional cure for these ailments?

EDIT: what a great topic btw. Histamine is extremely intereting to me. On several different levels in different aspects. I first became attune to it when discussing refractory periods and sexual duration/delaying orgasm or increasing it's frequency. Applying it to smooth muscle is a new angle that interests me, and now we see it present in immunology. Cool stuff.

Arginase inhibition would increase arginine bioavailability. Oral L-arginine supplementation could correct this and the corresponding NO deficit. This of course dovetails with general endothelial dysfunction, implicating vasomotor tone.

Antihistamines are used to treat symptoms. What you are looking at here is, in part, the possibility of a histamine innoculation of sorts.

would correcting the expression of NO or enhancing it correlate with increased arginine uptake? While research histamine and it's link to penile sensativity I ran across a study KLee found on icariin increasing nNOS expression.

If nothing else maybe it makes NO more susceptable to arginine which isn't the same as increasing bioavailability but it results in the same thing.

So antihistamines are releaving symptoms, not actual allergies... wouldn't we want to only innoculate a certain histamine receptor? What type of synergism do the H receptors have with one another?

1) would correcting the expression of NO or enhancing it correlate with increased arginine uptake?
If nothing else maybe it makes NO more susceptable to arginine which isn't the same as increasing bioavailability but it results in the same thing.

This is what the CF studies are suggesting.

2) So antihistamines are releaving symptoms, not actual allergies... wouldn't we want to only innoculate a certain histamine receptor? What type of synergism do the H receptors have with one another?

The question of receptor specificity was discussed earlier in the thread between Necrosis and Graatch. Necrosis also posted a very good overview of histamine receptor pharmacology as well.

Did any of you try this solutions (oral arginine, oral histidine)??

More evidence for Histamine therapy. The effects of immunotherapy(the gold standard in allergology) works via il-10 up regulation and increases in treg production. This is the same exact mechanism as histamine therapy, and histamine therapy has no chances of anaphlyaxsis and requires far shorter durations of treatment.y


Int Immunopharmacol. 2006 Aug;6(8):1370-3. Epub 2006 Apr 19. Links
Sublingual immunotherapy induces spirometric improvement associated with IL-10 production: preliminary reports.Ciprandi G, Cirillo I, Fenoglio D, Marseglia G, Tosca MA.
Azienda Ospedaleria Universitaria San Martino, Largo R. Benzi 10, 16132 Genoa, Italy. gio.cip@libero.it

BACKGROUND: Sublingual immunotherapy (SLIT) has been demonstrated to be able of inducing immunologic changes as evidenced by IL-10 production. Forced expiratory flow between 25% and 75% of the vital capacity (FEF(25-75)) may be considered a good marker of early bronchial involvement in patients with pure allergic rhinitis. OBJECTIVE: The aim of this study was to evaluate the possible association of IL-10 production with FEF(25-75) values in patients with perennial allergic rhinitis (PAR) successfully treated with SLIT. METHODS: 19 patients with PAR were studied: 9 successfully assumed SLIT for 3 years, 10 were considered as control. In vitro IL-10 production was evaluated after SLIT. Spirometry and bronchodilation test were performed in all subjects at baseline and after 3 years. RESULTS: After 3 years, FEF(25-75) values significantly (p=0.0131) increased in SLIT group (80.5+/-6.7), whereas they significantly (p=0.0021) decreased in non-treated patients (60.8+/-2.62). In addition, SLIT-induced increase of FEF(25-75) values is significantly associated with IL-10 production (p=0.0025). CONCLUSIONS: This study provides the first evidence that SLIT is capable of improving early bronchial involvement in patients with pure allergic rhinitis and this functional effect may be associated with immunological changes, such as the induction of IL-10 production


Clin Exp Allergy. 2006 Mar;36(3):261-72. Links
Sublingual immunotherapy with Dermatophagoides monomeric allergoid down-regulates allergen-specific immunoglobulin E and increases both interferon-gamma- and interleukin-10-production.Cosmi L, Santarlasci V, Angeli R, Liotta F, Maggi L, Frosali F, Rossi O, Falagiani P, Riva G, Romagnani S, Annunziato F, Maggi E.
Center of Research, Transfer, High Education 'DENOthe', University of Florence, Firenze, Italy.

BACKGROUND: The clinical efficacy and safety of sublingual immunotherapy (SLIT) for aeroallergens has been demonstrated in several trials, whereas the immunological changes induced by this treatment, which may account for the clinical improvement, are still unclear. OBJECTIVE: To investigate the effects of a successful SLIT on the in vitro allergen-driven T cell response and cytokine secretion as well as on the serum levels of chemokines and of IgE, IgG1 and IgG4 antibodies (Abs). MATERIALS AND METHODS: Twenty-five Dermatophagoides pteronyssinus (Dp)-sensitive patients with perennial rhinitic and/or rhinitic and asthmatic symptoms were randomized into two groups (13 untreated (UT) and 12 SLIT-treated) for a 1 year and half study. The proliferative response of peripheral blood mononuclear cell (PBMC) to purified Der p1 allergen, their cytokines (IFN-gamma, IL-4, IL-10 and TGF-beta) production and serum levels of chemokines associated with T helper type 1 (Th1) (CXCL10) or T helper type 2 (Th2) (CCL22) responses and of Dp-specific IgE, IgG1 and IgG4 Abs were evaluated before and after 6 months of treatment. RESULTS: SLIT induced a significant reduction of symptom medication scores after 6, 12 and 18 months of treatment in comparison with UT patients. SLIT-treated patients showed a significant decrease in serum levels of DP-specific IgE Abs, whereas total IgE, and specific IgG1 and IgG4 Abs remained unchanged. The proliferative response of allergen-specific T cells to Der p1 in vitro after 6 months of treatment was reduced, while no effect was observed on T cell proliferation to recall antigen (streptokinase). Moreover, Der p1-driven IFN-gamma and IL-10 were significantly increased in culture supernatants of PBMC from 6 month-treated patients in comparison with those detected at the beginning of therapy. CONCLUSIONS: These data suggest that the allergen-driven enhancement of IL-10- and IFN-gamma-producing T cells precedes and associates with SLIT-induced down-regulation of specific IgE, thus providing a rationale to explain the clinical benefit of SLIT in allergic patients.

Int Immunopharmacol. 2003 Apr;3(4):523-39. Links
Modulation of the Th1/Th2 bias by an immunoglobulin histamine complex in the ovalbumin allergy mouse model.Ayoub M, Lallouette P, Sütterlin BW, Bessler WG, Huber M, Mittenbühler K.
Institut für Molekulare Medizin und Zellforschung, AG Tumorimmunologie/Vakzine, Universitätsklinikum Freiburg, Stefan-Meier-Str 8, D-79104 Freiburg, Germany.

Vaccination with the antiallergic drug Histaglobin is used to treat a broad range of human allergic diseases including bronchial asthma, allergic rhinitis, and atopic dermatitis. In order to further elucidate its functional activity, Histaglobin was investigated in an in vivo mouse allergy model. Mice were sensitized with ovalbumin either prior to or after Histaglobin treatment, and its antiallergic potential was evaluated. Ovalbumin-sensitized mice exhibited increased serum levels of IL-4, tumor necrosis factor alpha (TNF-alpha), and an increase of total and ovalbumin-specific IgE; total and ovalbumin-specific IgG levels were also elevated. Subsequent administration (therapeutic treatment) of Histaglobin resulted in a decrease of total and specific serum IgE levels; total and specific IgG1 serum levels were reduced by more than 50% and 45%, respectively; the mice displayed a down-regulation of IL-4 and TNF-alpha serum levels and showed increased levels of IFN-gamma and IgG2a. Mice pretreated with Histaglobin, prior to ovalbumin sensitization (prophylactic treatment), were found to be widely unresponsive to ovalbumin. They exhibited higher serum levels of IFN-gamma and IgG2a (total and specific) compared to saline-treated control mice. The inhibitory effects were still observed 1 month post-immunization.Our data, indicating a Histaglobin-induced modulation of the Th1/Th2 balance in favour of Th1, correspond with the well-known antiallergic activity of Histaglobin observed in patients



Further evidence of the efficacy of histamine in patients with eosinophilia. Atopic patients usually have some level of eosinophilia which is the accumulation of a PMN cell called a eosinophil. eosinophils contain histaminase and are found in very low levels in the blood, with basophils being slightly lower in concentration. They are found times of parasictic infection and allergies, which highlights the current understanding of helminth infections and atopy, which is inversely correlated. Less parasites equals more allergies it seems along with both TH1 and TH2 disease. This is another mechanism in which this therapy exceeds.

J Allergy Clin Immunol. 1997 Dec;100(6 Pt 1):809-16. Links
A complex of histamine/mouse gamma-globulin preferentially inhibits allergen-induced peritoneal accumulation of eosinophils, but not neutrophils, in mice.Yoshii H, Fukata-Yamazaki Y, Yamamoto K, Yago H, Yanagihara Y, Okudaira H.
Department of Allergology, Institute of Bio-Active Science, Nippon Zoki Pharmaceutical Company, Hyogo, Japan.

A complex of histamine/human gamma-globulin (HhG) has been widely used in Japan for more than 25 years as a nonspecific hyposensitization drug in the treatment of allergic diseases. It has been reported that HhG decreases the number of eosinophils in the nasal secretions and peripheral blood of patients with allergy. In this study we used a mouse system to explore the possibility that HhG may actively inhibit the accumulation of eosinophils at inflammation sites. A complex of 0.15 microg of histamine dihydrochloride/12 mg of mouse gamma-globulin (HmG) was incubated for 2 hours in saline solution in the normal fashion for HhG. HmG at 50 to 150 mg/kg/day inhibited the peritoneal accumulation of eosinophils induced by ragweed pollen in BALB/c mice in a dose-dependent fashion when the HmG was administered subcutaneously six times during a 20-day sensitization period. The inhibitory effect of HmG on this eosinophil accumulation was significant at 24 and 48 hours after challenge, but HmG had no effect on neutrophil accumulation. Complexes of serotonin/mouse gamma-globulin (mgammaG), glutamine/mgammaG, and histamine dihydrochloride (His)/mouse albumin had no inhibitory effect when administered in the same way. The optimum combination ratio was between 0.15 microg of His/12 mg of mgammaG and 0.015 microg of His/12 mg of mgammaG for this eosinophil inhibition. Moreover, a 1- to 2-hour incubation period of His and mgammaG was needed to induce a plateau inhibition of the eosinophil accumulation. These results in mice suggest that HhG may actively inhibit allergen-induced eosinophil accumulation, which may be therapeutically useful in the treatment of allergic disease.



I am trying to establish that histamine is perhaps the best most effective treatment choice for allergy and atopy patients and all of its co-morbid features (migraines, CNS disturbances etc). It's mechanism of action is accepted in immunology and is the best possible scenario. That is, restoration of the immune response (modulation) and long term effects equating somewhat of a cure for atopy.

ill post more as im going to look into other syndromes with histamine inclusion.

Agents Actions. 1992 Mar;35(3-4):185-91.Links
Modulation of IgE-mediated histamine release from human leukocytes by a new class of histamine H2-agonists.Kleine-Tebbe J, Buschauer A, Friese A, Schunack W, Kunkel G.
Clin. Immunology and Asthma OPD, Free University Berlin, Germany.

A new class of phenyl (pyridylalcyl) guanidines, acting as potent histamine H2-agonists, inhibits IgE-mediated human basophil histamine release in a nanomolar range. IC30-level of three substitutes of this group (arpromidine, BUA-75, and FRA-19) were found to be 0.02, 0.015 and 0.008 microM. The inhibition appeared with a fast onset (plateau after 10 min. preincubation) and claimed its maximum (60 +/- 2.9%, 63 +/- 1.8%, and 61 +/- 3.1%, n = 7) with 10 microM of the compounds. H2-mediated inhibition was totally blocked by 10 microM famotidine, a potent histamine H2-antagonist. The amount of anti-IgE or antigen for the initiation of the immunological release influenced the strength of inhibition of H2-agonist FRA-19 (p less than 0.05). Combined preincubation of FRA-19 with zardaverine, a cAMP-specific phosphodiesterase III/IV inhibitor, produced a synergistical inhibitory effect of leukocyte histamine release, which might explained by their different sites of action on intracellular cAMP levels. The capability of histamine to inhibit its own release is mediated by H2-receptors exclusively. New, potent H2-receptor stimulating compounds with positive inotropic effects possess additional potent anti-allergic properties


I cant get the full texts nor abstract of this paper but they are outlined in ALLERGY. if anyone can get them PM me please, thank you.

Nature. 1973 Aug 3;244(5414):287-8.Links
Inhibition of histamine release by histamine controlled by H2 receptor.Lichtenstein LM, Gillespie E.


This paper provides possible evidece that atopy is a disease of H2 receptors (namely type four hypersensitivity), and that H1 pharmacology is bascially pointless, as its action is histamine release, and its antagonists provide relief that is shortlived.

Science. 1977 Feb 18;195(4279):683-5. Links
Selective display of histamine receptors on lymphocytes.Roszkowski W, Plaut M, Lichtenstein LM.
Histamine, acting on histamine type 2 receptors, increases intracellular cyclic adenosine monophosphate (AMP) and thus modulates the immunologic functions of lymphocytes. Lymphocyte cyclic AMP levels were used to follow the development of histamine receptors. The B lymphocytes have no functional histamine receptors. As T lymphocytes "mature" in immunologic function--from thymocytes to cortisone-resistant thymocytes to splenic T lymphocytes--their response to histamine increases. The response of these subpopulations of lymphocytes to isoproterenol is the inverse of the histamine response. It is suggested that the changing display of histamine receptors plays an important part in the control of immunologic responses.


ILL post more later as im zonked right now.


LIOR, i havent used either therapy yet. Im not sure hom histidine would work, and im thinking of trying Ras arginine therapy as i have mild allergis and asthma. I would honestly like to inject histamine, but i cant find a good source. I would be willing to be the guinea pig

ignore Histamine's effect on teh PVN/CNS at your peril, or you saying that the receptor state is the same everywhere in the body?

PS

oral histidine is very effective in raising Histamine blood levels.

the bulk of the lit shows no ill effects.


Im not sure if your talking about histamine release from PMN's or exogenous histamine. Please expand on your thought.

sorry, I need more clarification of your post.

the bulk of what?

expand on on which of the items I talked about?

The research on histamine and histaglobin therapy.(refer to the studies above)


expand on the negatives of histamine therapy with regards to the CNS, PVN.

What does "hsitamine therapy" mean? I thought it meant increasing blood levels of histamine?

While I don't think this is the aim of Necrosis's research, there is obviously a plethora of adverse side effects associated with increased histamine levels, not least of which are myocardial. Granted, we don't fully understand histamine-mediated cytokine production, but recent studies certainly warrant further research and exploration. An interesting example of this is current work in concomitant IL-2 and histamine dihydrochloride therapy in several types of cancer (TPT1 mediated?).

A fake journal:

Altern Med Rev. 1999 Dec;4(6):424-8. Links
Transdermal histamine in multiple sclerosis: part one -- clinical experience.Gillson G, Wright JV, DeLack E, Ballasiotes G.
Histamine has a long history of therapeutic use in many diseases, including multiple sclerosis (MS). Recently, transdermal histamine has been successfully employed for the amelioration of symptoms of both relapsing-remitting and progressive multiple sclerosis. This paper summarizes preliminary experiences with transdermal histamine for MS at the Tahoma Clinic: 67 percent of 55 patients using histamine transdermal cream had improvements in one or more areas, including extremity strength, balance, bladder control, fatigue, activities of daily living, and cognitive functioning, sustained for periods of up to three months. One-third of patients had improvements in three or more areas of functioning. Five possible mechanisms of action are postulated: augmentation of subnormal cerebral tissue levels of histamine; improved electrical function of demyelinated fibers; increased cerebral blood flow; suppression of autoimmune responses; and stimulation of remyelination. These will be discussed in detail in Part 2 of this article.

A real journal:

Neurochem Int. 2006 Jul;49(2):170-82. Epub 2006 Jun 12. Links
Pharmacological strategies for the regulation of inducible nitric oxide synthase: neurodegenerative versus neuroprotective mechanisms.Pannu R, Singh I.
Centre for Developmental Neurological Disorders, Charles P. Darby Children's Research Institute, Department of Pediatrics, Medical University of South Carolina, Charleston, SC 29425, United States.

Inducible nitric oxide synthase (iNOS) is one of three NOS isoforms generating nitric oxide (NO) by the conversion of l-arginine to l-citrulline. iNOS has been found to be a major contributor to initiation/exacerbation of the central nervous system (CNS) inflammatory/degenerative conditions through the production of excessive NO which generates reactive nitrogen species (RNSs). Activation of iNOS and NO generation has come to be accepted as a marker and therapeutic target in neuroinflammatory conditions such as those observed in ischemia, multiple sclerosis (MS), spinal cord injury (SCI), Alzheimer's disease (AD), and inherited peroxisomal (e.g. X-linked adrenoleukodystrophy; X-ALD) and lysosomal disorders (e.g. Krabbe's disease). However, with the emergence of reports on the neuroprotective facets of NO, the prior dogma about NO being solely detrimental has had to be modified. While RNSs such as peroxynitrite (ONOO(-)) have been linked to lipid peroxidation, neuronal/oligodendrocyte loss, and demyelination in neurodegenerative diseases, limited NO generation by GSNO has been found to promote vasodilation and attenuate vascular injury under the same ischemic conditions. NO generated from GSNO acts as second messenger molecular which through S-nitrosylation has been shown to control important cellular processes by regulation of expression/activity of certain proteins such as NF-kappaB. It is now believed that the environment and the context in which NO is produced largely determines the actions (good or bad) of this molecule. These multi-faceted aspects of NO make therapeutic interference with iNOS activity even more complicated since complete ablation of iNOS activity has been found to be rather more detrimental than protective in most neurodegenerative conditions. Investigators in search of iNOS modulating pharmacological agents have realized the need of a delicate balance so as to allow the production of physiologically relevant amounts of NO (such as those required for host defence/neutotransmission/vasodilation, etc.) but at the same time block the generation of RNSs through repressing excessive NO levels (such as those causing neuronal/tissue damage and demyelination, etc.). The past years have seen a noteworthy increase in novel agents that might prove useful in achieving the aim of harnessing the good and blocking the undesirable actions of NO. It is the aim of this review to provide basic insights into the NOS family of enzymes with special emphasis of the role of iNOS in the CNS, in the first part. In the second part of the review, we will strive to provide an exhaustive compilation of the prevalent strategies being tested for the therapeutic modulation of iNOS and NO production.

no


blood levels should decrease via H2/H3 suppression on degranulation. Overall you are decreasing release of endogenous histamine via exogenous histamine and then after withdrawl of exogenous the endogenous histamine regulation is maintained, and allergy is decreased.

injecting histaglobin(histamine) reduces allergies very effectively, and placebo controlled studies show that IG produces no effects when compared to HG, implicating histamine as the active component.


atopic people have too much histamine being produced, and inappropriate release via inactive H2 receptors with dominant H1 receptors (hence H1 antihistamines)



so basically there will be a decrease in plasma levels of histamine, because of proper regulation.


here is the drug.

http://home.intekom.com/pharm/mirren/histglob.html


simple protocol to be followed, and the results usually last long term, with booster shots being advisable.

Originally posted by Sanction:

Could a high intake of histamine-rich foods also decrease endogenous production?

1: Arch Intern Med. 1983 Nov;143(11):2099-102.
Histaminuria from histamine-rich foods. Feldman JM.
Using a highly specific and sensitive assay, the histamine content of foodstuffs and the effect of ingesting these foodstuffs on urinary histamine excretion were measured. Certain vegetables (spinach, eggplant), cheeses (Parmesan, blue, Roquefort), and red wines (Chianti and Burgundy) had a high content of histamine. Although only 0.21% of the ingested histamine was excreted unchanged in the urine, the histamine content of some of the foods was so high (Parmesan cheese, 185 micrograms/g; spinach, 60 micrograms/g; baked eggplant, 26 micrograms/g) that they caused histaminuria. Patients collecting urine for analysis for 24-hour histamine excretion for diagnosis of systemic mastocytosis or carcinoid syndrome should avoid intake of these foods and beverages on the day of the urine collection.


QUOTE
1: Food Chem Toxicol. 1989 May;27(5):283-7. Links
The histamine content of oriental foods.Chin KW, Garriga MM, Metcalfe DD.
Mast Cell Physiology Section, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.

Several of the symptoms of scombroid poisoning (i.e. histamine toxicity) resemble those observed in people suffering from Chinese restaurant syndrome. Therefore, the histamine content of representative Chinese cuisine, which included 31 common dishes, 12 condiments and 12 basic ingredients from several sources, was measured using a sensitive and specific radioenzymatic assay. A further enzymatic procedure involving diamine oxidase was used to verify that the substance measured was histamine. A total of 184 assays were performed on 57 samples in the study. High levels of histamine were found in the cheeses, which were used as positive controls (863.6 micrograms histamine/g blue cheese and 107.4 micrograms histamine/g Parmesan cheese), and in some common condiments, including tamari (2392.2 micrograms histamine/g sample) and one brand of soy sauce (220.4 micrograms histamine/g sample). The histamine content of four condiments and three common dishes was over 10 micrograms histamine/g sample, while four condiments and 16 common dishes contained less than 1 microgram histamine/g sample. Calculations involving representative amounts of food that can be consumed at a typical oriental meal suggest that, in some cases, histamine intake may approach toxic levels. The results are discussed with regard to the possible role of histamine in reactions associated with restaurant meals.

PMID: 2744659 [PubMed - indexed for MEDLINE]