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Histamine — Beyond mast cells

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We often talk about histamine, but how much do we really know about it?

Photograph of cubes of Swiss Cheese; from Wikimedia Commons

Swiss cheese can be naturally high in histamine.

Most of us know that it is the release of large amounts of histamine from our mast cells that causes the symptoms so many of us experience. Most of us understand that people who have allergies can experience at least some of the same symptoms, except that in their case the reactions are usually mediated by immunoglobulin E (IgE).

But can histamine be a problem for anyone who does not have mastocytosis, idiopathic anaphylaxis (IA), mast cell activation disorder/syndrome (MCAD/MCAS), interstitial cystitis (IC), allergies, asthma, chronic urticaria, or similar “allergic” diseases? The perhaps-surprising answer to that question is, “Yes!” In this article, we’ll shift our focus away from mast cells and learn more about the fascinating world of histamine.

 
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Introducing histidine

Illustration showing how histamine is created from histidine via decarboxylation, which also releases carbon dioxide; from Wikimedia Commons

Histamine is made from a substance called histidine. Reference [Noszal B, Kraszni M, Racz A. Histamine: Fundamentals of biological chemistry. In: Falus A, Grosman N, Darvas Z, eds. Histamine: Biology and Medical Aspects. Budapest: SpringMed Publishing; 2004:15–28]. Histidine is one of the most common amino acids. What is an amino acid? Amino acids are organic compounds that are the building blocks of proteins. Reference [Guyton AC, Hall JE. Textbook of Medical Physiology. 11th ed. Philadelphia: Elsevier Saunders; 2006]. They are extremely important to our bodies’ normal functioning.

From a nutritional perspective, histidine is considered to be one of the nine essential amino acids. These are amino acids that our body cannot make in quantities that are sufficient for our bodily needs. Reference [Boron WF, Boulpaep EL. Medical Physiology: A Cellular and Molecular Approach. Updated ed. Philadelphia: Elsevier Saunders; 2005]. Therefore, we have to get additional histidine from the foods we eat.

 
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What foods contain histidine?

Illustration of common cuts of beef; from Wikimedia Commons

Beef is naturally high in histidine.

Eggs, cheese, milk, beef, chicken, pork, bacon, venison, veal, cod fish, soy protein, bananas, mustard seed, seaweed, flour made from cottonseeds, sesame seeds or sunflower seeds, and yeast are examples of foods that contain a relatively high amount of histidine. Reference [NutritionData.com. Foods highest in Histidine. Condé Nast Digital. Accessed November 2, 2009.].

Now don’t get the idea that you can solve your histamine problem by decreasing your intake of histidine. Histidine is involved in much more than manufacturing histamine. To give just one example, histidine is essential to the process of stabilizing the oxygen that is bound to iron ions within hemoglobin [respiratory protein within red blood cells that transports oxygen from lungs to the tissues that need it]. Reference [Boron WF, Boulpaep EL. Medical Physiology: A Cellular and Molecular Approach. Updated ed. Philadelphia: Elsevier Saunders; 2005]. In other words, without histidine, your red blood cells would not be able to carry oxygen to the tissues in your body. So, trying to limit your intake of histidine would hurt you — not help you.

 
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How does histidine turn into histamine?

Illustration showing how the enzyme HDC separates histidine into two components: histamine and carbon dioxide; by Candace Van Auken

An enzyme with the tongue-twisting name of histidine decarboxylase (HDC) is responsible for turning histidine into histamine. HDC shears off a molecule of carbon dioxide (CO2) from histidine, and what remains is histamine. Reference [Repka-Ramirez MS, Baraniuk JN. Histamine in Health and Disease. In: Simons FER, ed. Histamine and H1-Antihistamines in Allergic Disease. 2nd ed., Revised & Expanded. New York: Marcel Dekker; 2002. 1–25].

This means that the histamine molecule is smaller than the histidine molecule. In fact, histamine is one of the smallest molecules produced by a living cell. And while histamine is involved in almost two dozen different physiological functions, its structure is usually unchanged by these interactions. This last point is important because if physiological processes don’t “use up” histamine, then it will remain active until it is broken down by specific processes. We’ll talk more about this later. Reference [Noszal B, Kraszni M, Racz A. Histamine: Fundamentals of biological chemistry. In: Falus A, Grosman N, Darvas Z, eds. Histamine: Biology and Medical Aspects. Budapest: SpringMed Publishing; 2004:15–28].

Many of us know that both mast cells and basophils are capable of synthesizing histamine. On average a mast cell contains between two and five picograms [abbreviated “pg,” a picogram is one trillionth of a gram] of histamine. However, while mast cells and basophils may be the major sources of histamine, recent research suggests that human blood monocytes and lymphocytes can contain 0.05 pg of histamine, and other cells, such as fibroblasts and ovarian cells can contain histamine in still smaller amounts (less than 0.008 pg per cell). However, only mast cells and basophils seem to be able to store the histamine they create. Reference [Watt AP, Ennis M. Characterization of histamine release by mast cells, basophils, and monocytes. In: Falus A, Grosman N, Darvas Z, eds. Histamine: Biology and Medical Aspects. Budapest: SpringMed Publishing; 2004. 99–111].

 
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Graphic of emergency medical services vehicle

Bacteria can also make histamine!

Bacterial HDC [histidine decarboxylase, an enzyme that creates histamine from the amino acid histidine] can also convert histidine into histamine, and bacterial infection of food can result in elevated levels of histamine, which can in turn cause food poisoning.

This is one reason why leftovers from a previous night's meal can sometimes be problematic for someone who has a mast cell disease. Even if week-old leftovers don't make the rest of the family sick, the person with IA or mastocytosis may end up in the bathroom with diarrhea.

Wounds and infections

Microphotograph of haemophilus parainfluenzae; from Wikimedia Commons

Respiratory bacteria like haemophilus parainfluenzae can produce significant amounts of histamine.

Also, a wound infected with bacteria can generate histamine that then causes local inflammatory reactions.

Graphic of Bandaid - ventilated adhesive strip with sterile gauze pad on it

A number of species of respiratory bacteria can produce histamine, which in turn can exacerbate histamine-driven respiratory symptoms like a runny nose or mucus in the lungs. Reference [Repka-Ramirez MS, Baraniuk JN. Histamine in Health and Disease. In: Simons FER, ed. Histamine and H1-Antihistamines in Allergic Disease. 2nd ed., Revised & Expanded. New York: Marcel Dekker; 2002. 1–25].

So, it’s not just the case that our mast cells can release histamine in response to certain foods or infections, some bacteria can manufacture even more histamine!

 
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What exactly does histamine do?

Cells have different kinds of receptors on their surfaces, each of which functions like a lock that can only be opened by a molecule or compound that has a particular design and particular biochemical qualities. Different receptors on the cell surface respond in different ways if they are "unlocked." So if a substance can connect with a cell's receptors, it can bring about changes in that cell or its functioning.

Histamine exerts its effects on cells through four different kinds of receptors: H1, H2, H3, and H4. Reference [Castells M. Mast cell mediators in allergic inflammation and mastocytosis. Immunol Allergy Clin N Am. 2006; 26:465–85]. Only the first two are currently well understood. H1 and H2 receptors are involved in the changes that cause flushing, itching, increase in vascular permeability (third-spacing), changes in blood pressure, contractions or spasms of intestinal, bronchial and uterine muscles, increases in mucus production, increases in the rate of — and perhaps irregularity of — heartbeat, and increases in gastric acid production. Reference [Hill SJ, Ganellin CR, Timmerman H, Schwartz JC, Shankley NP, Young JM, et al. International Union of Pharmacology. XIII. Classification of histamine receptors. Pharmacol Rev. 1997; 49:253–78]. So, diarrhea, flatulence, vomiting, stomach ache, low blood pressure, increased heart rate, and headache can all be due to high levels of histamine. Reference [Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. 2007; 85:1185–96].

Fortunately, the effects of a given quantity of histamine are not effective for more than about thirty minutes. Unless more histamine is released, consumed or manufactured, the histamine in the body will be broken down fairly quickly. Reference [Castells M. Mast cell mediators in allergic inflammation and mastocytosis. Immunol Allergy Clin N Am. 2006; 26:465–85].

Only 0.5% to 1.5% of histamine (in other words, approximately one percent) is excreted in urine. The bulk of the histamine is metabolized rapidly. Reference [Myers G, Donlon M, Kaliner M. Measurement of urinary histamine: development of methodology and normal values. J Allergy Clin Immunol. 1981; 67:305-11.].

However, the metabolites [products of metabolism, mostly waste products] from the breakdown of histamine may be found in a person’s urine for up to 24 hours after onset of anaphylaxis. Reference [Ogawa Y, Grant J. Mediators of anaphylaxis. Immunol Allergy Clin N Am. 2007; 27:249–60]. These urinary histamine metabolites include N-methyl histamine [sometimes abbreviated as UMH for urinary N-methyl histamine] and N-methyl imidazole acetic acid [abbreviated as MIAA]. Reference [McPherson RA, Pincus MR. Henry's Clinical Diagnosis and Management by Laboratory Methods. 21st ed. Philadelphia, PA: Saunders Elsevier; 2007].

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Table 1. The physiological effects of histamine

EffectExampleMediated by
Smooth muscle contraction Airway constriction, cramping H1 receptors
Increased vascular permeability Swelling H1 receptors
Mucous gland secretion Runny nose H1 receptors
Gastric acid secretion Gastric acid secretion H2 receptors
Inhibition of basophil histamine release   H2 receptors
Inhibition of lymphokine release   H2 receptors
Vasodilation Reduced blood pressure H1 and H2 receptors
Hypotension Abnormally low blood pressure H1 and H2 receptors
Flush Face and neck turning red H1 and H2 receptors
Headache   H1 and H2 receptors
Tachycardia Rapid heartbeat H1 and H2 receptors

Reference [Metcalfe DD, Sampson HA, Simon RA, eds. Food Allergy: Adverse Reactions to Food and Food Additives, 4th ed. Malden, MA: Blackwell Publishing; 2008, p. 432] for Table 1.

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What is hyperhistaminemia?

Diagram breaking down the term hyperhistaminemia; by Candace Van Auken

In researching this article, I learned a new term, a real “fifty-cent word”: hyperhistaminemia (it can also be spelled hyperhistaminaemia).

What is hyperhistaminemia? Well, it’s the medical term used to describe the effects of having too much histamine floating around inside your body. “Hyper—” is a prefix that means “too much” or “excessive.” We know what “histamine” is, and “-emia” or “-aemia” is a prefix that is used to describe a condition of having too much of something in one’s blood. So, literally, hyperhistaminemia is the condition of having too much histamine in your blood.

 
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How much histamine is too much?

Photograph of tin of mackerels in tomator sauce; from Wikimedia Commons

Canned mackerels in tomato sauce can be naturally high in histamine.

However it gets there, if you end up with too much histamine in your bloodstream at any point in time, you are going to feel its effects.

The table [Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. 2007; 85:1185–96] below shows how various amounts of histamine, expressed in ng/mL [nanograms per milliliter], correlate with histamine's physiological effects on a human body.

Of course, there are other factors besides histamine levels — including other medical conditions, use of other medications or drugs, and presence of other mast cell mediators — that may cause a person’s symptoms to progress in a different manner.

 

Table 2. Histamine effects according to plasma histamine concentration

Histamine levelClinical effects
0.3–1 Normal reference value for histamine
1–2 Increase in gastric [stomach] acid secretion
Increase in heart rate
3–5 Tachycardia [rapid heartbeat, over 90 bpm]
Headache
Flushing
Urticaria [hives]
Pruritus [itchiness]
6–8 Hypotension [decrease in arterial blood pressure]
7–12 Bronchospasm [narrowing of airway due to smooth muscle contraction]
~100 Cardiac arrest [heart stops]

Table reference [Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. 2007; 85:1185–96].

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How is histamine broken down?

We need to wade through a little brook of biochemistry in order to reach the answer to the above question. Bear with me, it's only a wee rivulet, hardly big enough to hold two little acronyms....

Diagram showing the two ways that histamine can be broken down: Via HNMT and DAO; by Candace Van Auken

There are two main ways that histamine can be inactivated:

1.By direct oxidation — a reaction catalyzed by DAO [DiAmine Oxidase]. Reference [Schwelberger HG. Diamine oxidase (DAO) enzyme and gene. In: Falus A, Grosman N, Darvas Z, eds. Histamine: Biology and Medical Aspects. Budapest: SpringMed Publishing, Ltd.; 2004; 43–52].
2.By adding a methyl group to the histamine’s imidazole ring — a reaction catalyzed by HNMT [Histamine N-MethyTransferase]. Reference [Schwelberger HG. Histamine N-methyltransferase (HNMT) enzyme and gene. In: Falus A, Grosman N, Darvas Z, eds. Histamine: Biology and Medical Aspects. Budapest: SpringMed Publishing, Ltd.; 2004; 53–9].


Even if you haven’t a clue what oxidation or methylation are (and don’t worry, most people don’t), the key point is: There are two ways to deactivate histamine — One using DAO and another using HNMT. Hold onto that thought!

One theory is that since HNMT is an enzyme found inside cells, it breaks down histamine only within cells, whereas DAO “might be responsible for scavenging extracellular [outside of cells] histamine after mediator release.” Reference [Maintz L, Benfadal S, et al. Evidence for a reduced histamine degradation capacity in a subgroup of patients with atopic eczema. J Allergy Clin Immunol. 2006; 117:1106–12].

 
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Histamine intolerance

It turns out that the breakdown of histamine may be of interest even to people who do not have a mast cell-related disease. Why? Diminished histamine degradation due to reduced DAO activity is currently under investigation as a possible cause of non-IgE-mediated food intolerance.

“IgE-mediated food intolerance” is what we usually call allergies to food or other substances we ingest. But some people have the same symptoms without showing evidence of food allergies on skin or RAST [radioallergosorbent tests].

Diagram showing four potential histamine problems: too much absorbed from food, eating too much histamine-containing food, having too little DAO, or ingesting substances that block DAO; by Candace Van Auken

In other words, it is possible that some people have “too much histamine” not because they have too many mast cells or because their mast cells are degranulating abnormally, but because the process by which the person’s body breaks down and gets rid of histamine could be deficient. This is sometimes called “histamine intolerance” and is abbreviated as HIT. Reference [Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. 2007; 85:1185–96].

Why is the DAO activity reduced? This could be due to either genetic problems or an acquired condition, such as some gastrointestinal diseases. Reference [Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. 2007; 85:1185–96].

Interestingly, a commonly reported symptom is that “Histamine-intolerant women often suffer from headache that is dependent on their menstrual cycle and from dysmenorrhea [painful or difficult menstrual periods]. Besides the contractile action of histamine, these symptoms may be explained by the interplay of histamine and hormones.” Reference [Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. 2007; 85:1185–96]. That’s one symptom that many women with mast cell-related disorders are familiar with!

It is also interesting to note that while histamine can interact with estrogen, estrogen can return the favor, namely, “A significant increase in weal and flare size in response to histamine has been observed to correspond to ovulation and peak estrogen concentrations.” Reference [Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. 2007; 85:1185–96].

If someone has an impaired ability to get rid of histamine, then, for example, eating a histamine-rich diet could cause the same kinds of symptoms that people with mastocytosis experience.

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Blocking DAO

Photograph of a bottle of soy sauce; from Wikimedia Commons

Soy sauce can be naturally high in histamine.

It’s also possible for a person to take drugs that block the effects of DAO, in which case the histamine is not broken down. Table 2 (on the next tab) lists a number of drugs that either cause histamine release or inhibit DAO. Here are a few more substances that may interfere with the action of DAO:

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Table 2. Drugs that cause histamine release or inhibit DAO

Substance classAgent interfering with histamine metabolism
Contrast media
Muscle relaxantsPancuronium, alcuronium, D-tubocurarine
NarcoticsThiopental
AnalgeticsMorphine, pethidine, nonsteroidal anti-inflammatory drugs (NSAIDs), acetylsalicylic acid (aspirin), metamizole
Local anestheticsPrilocaine
AntihypotonicsDobutamine
Antihypertensive drugsVerapamil, alprenolol, dihydralazine
AntiarrhythmicsPropafenone
DiureticsAmiloride
Drugs influencing gut motilityMetoclopramide
AntibioticsCefuroxime, cefotiam, isoniazid, pentamidin, clavulanic acid, chloroquine
MucolyticsAcetylcysteine, ambroxol
BroncholyticsAminophylline
H2-receptor antagonistsCimetidine
CytostaticsCyclophosphamide
AntidepressantsAmitriptyline

Table reference [Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. 2007; 85:1185–96].

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Absorbing too much histamine from food

Photograph of spinach leaves; from Wikimedia Commons

Spinach can be naturally high in histamine.

A third possible histamine-related problem would occur if the bodily process that prevents a person from absorbing too much histamine from the foods he or she eats were faulty or impaired by medications that the person is taking (sometimes called “enteral histaminosis”). Reference [Schwelberger HG. Diamine oxidase (DAO) enzyme and gene. In: Falus A, Grosman N, Darvas Z, eds. Histamine: Biology and Medical Aspects. Budapest: SpringMed Publishing, Ltd.; 2004; 43–52].

For example, another biogenic amine, such as putrescine, may displace histamine from its connection to intestinal muscosa, and this, in turn, may increase the amount of free histamine available for absorption into the circulatory system. Reference [Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. 2007; 85:1185–96].

A diet too rich in histamine

And the fourth possibility is that a “normal” person (one who has no mast cell-related or histamine-related disorder) can simply eat too many foods that are high in histamine, which can then overwhelm his or her natural ability to process histamine.

An example of this is called histamine fish poisoning, pseudoallergic fish poisoning, scombroid fish poisoning, histamine overdose, or mahi-mahi flush. It most often results from fish that have not been kept at a sufficiently cold temperature or that are beginning to spoil. The bacteria that naturally live on the fish, Escherichia coli or the Proteus and Klebsiella species, carry HDC [histidine decarboxylase], which can then convert histidine to histamine in large quantities if the fish isn’t stored at temperatures low enough to inhibit the activity of the bacteria. Reference [Noltkamper D. Toxicity, marine - Histamine in fish. In: Zempsky WT, Windle ML, et al., eds. eMedicine. WebMD; 2006].

There is also an aspect of scombroid fish poisoning that probably relates to enhanced absorption of histamine (the third histamine-related problem mentioned above). It seems that a substance like saurine (histamine hydrochloride) may function in that way. Reference [Noltkamper D. Toxicity, marine - Histamine in fish. In: Zempsky WT, Windle ML, et al., eds. eMedicine. WebMD; 2006].

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What foods are high in histamine?

All foods undergoing fermentation contain histamine, as do foods containing certain bacteria or yeast. Reference. 18 Also, “matured” (that is, older) food has higher levels of histamine. Reference. 9 Also, some vegetables and fruits are just naturally high in histamine.

Table 3. Foods high in histamine

Kind of foodExamples
Fermented foodsCheeses (Gouda, Emmenthal, Harzer, Roquefort, Tilsiter,Swiss, Camembert, Cheddar, Parmesan)
Processed meats (sausage, salami, ham)
Soy sauce and other soy products
Sauerkraut
Alcoholic beverages (Champagne, red wine, beer, white wine)
Vinegar, red wine vinegar
Sour cream
Yogurt
Yeast extract
Frozen/smoked or salted/canned fishAnchovies
Mackerel
Herring
Sardine
Tuna
Microbial activity in foodsUngutted fish
Leftover meat
Some fruits and vegetablesSpinach
Eggplant
Tomato
Tomato ketchup
Berries (especially strawberry)
Jams/preserves
Avocados

Table references: Maintz & Novak [Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. 2007; 85:1185–96], Bodemer [Bodemer AA. Urticaria. In: Rakel D, ed. Integrative Medicine, 2nd ed. Philadelphia, PA: Saunders Elsevier; 2007], Joneja [Joneja JMV. Digestion, Diet, and Disease: Irritable Bowel Syndrome and Gastrointestinal Function. Piscataway, NJ: Rutgers Univ. Pr.; 2004].

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Foods that may release histamine

Photograph of pile of chocolate; from Wikimedia Commons

Chocolate may encourage the release of histamine.

Table 3 does not include foods that seem to encourage the release of histamine, and so I have included those foods in Table 4 (below).

Table 4. Foods with suggested histamine-releasing capacities

SourceFood
Plant-derivedCitrus fruit
Papaya
Strawberries
Pineapple
Some nuts
Peanuts
Tomatoes
Spinach
Chocolate
Banana
Eggs
Milk
Animal-derivedFish
Crustaceans, shellfish
Pork
Egg white
OtherAdditives (for example, sulfiting agents)
Alcohol
Liquorice
Spices

Table references: Maintz & Novak [Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. 2007; 85:1185–96], Bodemer [Bodemer AA. Urticaria. In: Rakel D, ed. Integrative Medicine, 2nd ed. Philadelphia, PA: Saunders Elsevier; 2007].

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Atopic eczema and histamine intolerance

Photograph of a person's eczema-covered forearms; from Wikimedia Commons

The undersides of this woman's forearms are covered with eczema.

A study published in 2006 looked at people who had atopic [allergic] eczema (AE) but who tested negative for food allergies. The rationale for this investigation was the clinical observation that “in a subgroup of patients with AE, allergy testing proves negative, although these patients report a coherence of food intake and worsening of AE and describe symptoms that are very similar to histamine intolerance (HIT).” Reference [Maintz L, Benfadal S, et al. Evidence for a reduced histamine degradation capacity in a subgroup of patients with atopic eczema. J Allergy Clin Immunol. 2006; 117:1106–12].

The study found that people with AE who also demonstrated histamine intolerance had either total remission or significant improvement in their symptoms after two weeks on a histamine-free diet.

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Could some cases of MCAS/MCAD actually be histamine intolerance?

Now this is a very interesting question, but it is not one that I have seen addressed directly in the literature. I would think that if someone who experienced what appeared to be mast cell activation symptoms were able to completely control their problems by limiting their intake of histamine-containing foods with or without the use of H1– and H2– blocking antihistamines (without taking leukotriene inhibitors, NSAIDs, and/or mast cell stabilizers), then it is possible that his or her problems could be the result of histamine intolerance rather than mast cell activation.

Why? Well, mast cell stabilizers (like Gastrocrom or ketotifen), leukotriene inhibitors (like Singulair, Accolate or Zyflo), and/or nonsteroidal anti-inflammatory drugs (NSAIDs) would probably not do much for someone suffering from histamine intolerance unaccompanied by mast cell activation. However, diagnosis by treatment outcome is not considered to be a scientifically rigorous approach (because various other factors could affect the effectiveness of a particular treatment).

Also, it is not impossible to imagine that some people could have problems with both mast cell activation and histamine intolerance.

The possible confusion between mast cell activation and histamine intolerance points up the pressing need for the development of clinical tests to distinguish between different potential causes of hyperhistaminemia.

Using currently available tests, a person with histamine intolerance would probably not demonstrate increases in tryptase, carboxypeptidase-a, prostaglandins, or leukotrienes, whereas a person with MCAD [mast cell activation disorder] might show increases in one or more of those substances.

To summarize, hyperhistaminemia could potentially result from the following causes (and this is probably not a complete list:

  • Mastocytosis
  • Idiopathic anaphylaxis
  • Mast cell activation disorder/syndrome
  • Basophil activation
  • Basophil leukemia
  • IgE-mediated oral allergies
  • Drugs that cause or promote histamine release
  • Histamine intolerance (reduced levels of DAO)
  • Drugs that block the action of DAO [DiAmine Oxidase]
  • Drugs or conditions that increase GI absorption of histamine from food
  • MAO [MonoAmine oxidase] inhibitors’ interference in histamine breakdown
  • Infection with histamine-generating bacteria
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Should people with mastocytosis or IA avoid histamine-rich foods?

A recent review of studies done between 1966 and 2004 did not turn up any “double-blind placebo-controlled food challenge (DBPCFC) studies with biogenic amines and/or histamine-releasing foods in mastocytosis.” Reference [Vlieg-Boerstra BJ, van der Heide S, Oude Elberink JNG, Kluin-Nelemans JC, Dubois AEJ. Mastocytosis and adverse reactions to biogenic amines and histamine-releasing foods: what is the evidence? Netherlands J Med. 2005; 63:244–9]. This literature review concludes: “Despite the widespread belief that biogenic amines and histamine-releasing foods may cause allergy-like, non-IgE-mediated symptoms in certain patients, the role of diets restricted in biogenic amines and histamine-releasing foods in the treatment of mastosytosis [sic] remains hypothetical but worthy of further investigation. There is some evidence for adverse reactions to alcohol in mastocytosis.” Reference [Vlieg-Boerstra BJ, van der Heide S, Oude Elberink JNG, Kluin-Nelemans JC, Dubois AEJ. Mastocytosis and adverse reactions to biogenic amines and histamine-releasing foods: what is the evidence? Netherlands J Med. 2005; 63:244–9].

This does not mean that restricting the consumption of histamine-rich foods or alcohol will not ameliorate the symptoms of mastocytosis — it just means that as yet there is no solid research study that demonstrates the effectiveness of dietary restrictions.

I was not able to find anything in the literature on idiopathic anaphylaxis that suggested diet modification as a treatment strategy.

Still, given that even a “normal” person can have serious symptoms from ingesting food that is overloaded with histamines, common sense would suggestion that people with mastocytosis, IA or MCAD would do well to avoid histamine-rich foods or DAO-inhibiting drugs as a general rule.

As I learn more about the complexity of the systems involved in producing, releasing and destroying histamine, I appreciate more why our diseases manifest themselves so differently from one person to the next. Differences in our diets, our physiology, and the nature of concomitant conditions could help explain why some of us, for example, can drink alcoholic beverages or eat particular foods while others cannot.

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An earlier version of this article appeared in the Winter 2008 issue of The Mastocytosis Chronicles, the quarterly newsletter of the Mastocytosis Society (TMS).


Page last updated: July 9, 2011

 
All information contained in this site is one layperson's interpretation of medical journal articles, textbooks, seminars, presentations, and other materials. Nothing that is stated here should carry more weight than the informed and considered opinions of your own highly trained and qualified medical caregivers. The author of this site is not a doctor and has absolutely no authority to prescribe or diagnose.

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