The Low Histamine Chef

Perhaps skip the lunch time protein and just nuke a sweet potato with lots of coconut oil and oil at work?

I understand that you have GI issues - have you considered really following a low histamine diet and see what happens? I have not had a major GI issue since doing so.

I feel that so many people are on all these different diets but are missing the root - histamine. Histamine is released by the act of digestion, by just thinking of food, so for those of us with histamine issues, the act of digestion itself is going to cause a reaction no matter the food. 

I was convinced I had salicylate intolerance and fructose malabrorption - but once I really stuck to a high nutrient low histamine diet - everything resolved. People focus to much on the emilination and not enough on nutrition. To me it has truly been the key to my "recovery". 

 

Hi Mike,

Have just arrived in Kenya, will be online again later, in the meantime, you could do either re the sweet potato.

So sorry to hear about the scarring. I'm actually working on an all liquid cleanse/diet that will be out in the coming months. Maybe I could email you some of the recipes to try? It's going to be very high nutrient and very low histamine, with some antihistamine foods/fresh herbs and new compounds I'm exploring here in Kenya (heard of Baobab tree?).

I'll leave you with some studies on Crohn's. Histamine, as you may already know, plays a starring role in this condition. I personally use holy basil leaf (fresh) on most of my food. As an H2 blocker, I find it helps with any inflammation in my gut.

http://www.ncbi.nlm.nih.gov/pubmed/12492192
J Gastroenterol. 2002 Dec;97(12):3071-7.
Urinary excretion of N-methylhistamine as a marker of disease activity in inflammatory bowel disease.
Winterkamp S, Weidenhiller M, Otte P, Stolper J, Schwab D, Hahn EG, Raithel M.
Source
Department of Medicine I, University of Erlangen-Nuremberg, Erlangen, Germany.
Abstract
OBJECTIVE:
Mast cells are thought to participate in the pathogenesis of inflammatory bowel disease (IBD). In this study, urinary excretion of N-methylhistamine (UMH), a stable metabolite of the mast cell mediator histamine, was evaluated as an indicator of disease activity in patients with IBD.
METHODS:
Urinary excretion of UMH (microg/mmol creatinine x m2 body surface area) was measured by radioimmunoassay in 55 controls, 56 patients with Crohn's disease, and in 36 patients with ulcerative colitis. Excretion rates were correlated with clinical, serological, and endoscopic disease activity, disease extent, and location.
RESULTS:
Urinary excretion of UMH was found to be significantly elevated in IBD. Patients with active Crohn's disease (7.1 +/- 4.2, p = 0.002 vs controls) and active ulcerative colitis (8.1 +/- 4.8, p = 0.02 vs controls) had higher rates of UMH excretion than patients in remission (6.3 +/- 3.8 and 5.2 +/- 2.3, respectively) or controls (4.6 +/- 1.9). In Crohn's disease and ulcerative colitis, a significant correlation of UMH excretion with clinical disease activity was obtained (Crohn's Disease Activity Index r2 = 0.58, Clinical Activity Index r2 = 0.57, p < 0.0001). Serologically, orosomucoid showed the best positive correlation with disease activity (Crohn's Disease Activity Index r2 0.80, Clinical Activity Index r2 = 0.86, p < 0.0001), but UMH excretion was found to reflect disease activity more accurately than C-reactive protein (Crohn's Disease Activity Index r2 = 0.46, Clinical Activity Index r2 = 0.42, p < 0.0001). No association between UMH excretion and disease type or localization could be found in Crohn's disease. However, UMH excretion correlated strongly with endoscopic severity of inflammation in Crohn's disease (Crohn's Disease Endoscopic Index of Severity r2 = 0.70, p < 0.0001) or disease extent in ulcerative colitis.
CONCLUSIONS:
Urinary excretion of the histamine metabolite UMH is enhanced in IBD. It appears to represent an integrative parameter to monitor clinical and endoscopic disease activity in IBD, which appears to be influenced most likely by mediators released from histamine-containing cells, such as intestinal mast cell subtypes.

MAINTS AND NOVAK http://ajcn.nutrition.org/content/85/5/1185.full
http://www.ncbi.nlm.nih.gov/pubmed/7549499

Kurume Med J. 1993;40(3):93-9.
Mast cells and histamine release in Crohn's disease.
Araki Y, Kakegawa T, Stadil F.
Source
Department of Surgery, Kurume University School of Medicine, Japan.
Abstract
To study the role of intestinal mast cells in Crohn's disease, a sensitive glass-fiber histamine assay was conducted in conjunction with mechanical dispersion of surgical specimens of 80 macroscopically actively inflamed colons, 40 non-inflamed colons, 40 actively inflamed ileums, and 16 non-inflamed ileums from patients with Crohn's disease and 96 control subjects. A strong correlation was found between the number of mast cells and the total histamine content in the controls (r = 0.682) (p < 0.05). The number of mast cells was decreased in Crohn's disease as compared with the controls (p < 0.01). Intestinal mast cells release histamine in a dose-dependent manner after challenges with anti-IgE (1.875-240.0 U/ml). A significant difference was noted in the release by anti-IgE between actively inflamed and non-inflamed colons of patients with Crohn's disease or control subjects (p < 0.01). Mast cells in actively inflamed tissue with Crohn's disease were shown to have different roles in the pathogenesis of inflammation.

http://www.ncbi.nlm.nih.gov/pubmed/8139217

Int Arch Allergy Immunol. 1995 Oct;108(2):127-33.
Mucosal histamine content and histamine secretion in Crohn's disease, ulcerative colitis and allergic enteropathy.
Raithel M, Matek M, Baenkler HW, Jorde W, Hahn EG.
Source
1. Department of Medicine, University Erlangen-Nuremberg, Germany.
Abstract
Histamine exhibits various biological effects in inflammatory and immunological reactions. To further define its potential role in allergic enteropathy and inflammatory bowel disease, both gut mucosal histamine levels and histamine release from endoscopic biopsy samples were measured. Tissue histamine content resulted from addition of the released amount of histamine and the remaining part of tissue histamine. The results demonstrate highly elevated mucosal histamine levels of the large intestine in allergic enteropathy. In inflammatory bowel disease histamine content and secretion were found to be significantly increased particularly in affected mucosa of Crohn's disease and ulcerative colitis than in unaffected tissue or in healthy controls. These findings give strong evidence that mast cell mediators like histamine play a role in the pathogenesis of these diseases. Mucosal histamine is thus concluded to contribute to the immuno-inflammatory reactions of the intestine found in these disease states and to reflect the degree of colonic inflammation in Crohn's disease and ulcerative colitis.
PMID: 7549499 [PubMed - indexed for MEDLINE]

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