Archive for April 2006
Certain bacteria produce the enzyme histidine decarboxylase during growth. This enzyme reacts with free histidine, a naturally occurring chemical that is present in larger quantities in some fish than in others. The result is the formation of histamine. […]
Once the enzyme histidine decarboxylase has been formed, it can continue to produce histamine in the fish even if the bacteria are not active. The enzyme can be active at or near refrigeration temperatures. The enzyme is likely to remain stable while in the frozen state and may be reactivated very rapidly after thawing.
Freezing may inactivate the enzyme-forming bacteria. Both the enzyme and the bacteria can be inactivated by cooking. However, once histamine is formed, it cannot be eliminated by heat or freezing. After cooking, recontamination of the fish with the enzyme-forming bacteria is necessary for additional histamine to form. For these reasons, histamine development is more likely in raw, unfrozen fish. […]
The potential for histamine formation is increased when the flesh of the fish is directly exposed to the enzyme-forming bacteria. This occurs when the fish are processed (e.g. butchering or filleting).
At least some of the histamine-forming bacteria are halotolerant (salt-tolerant) or halophilic (salt-loving). This causes some salted and smoked fish products produced from scombrotoxin-forming species to continue to be suspect for histamine development. Further, a number of the histamine-forming bacteria are facultative anaerobes that can grow in reduced oxygen environments. Scombrotoxin Formation in Fish
For those who are curious: no, candida yeasts do not produce significant quantities of amines. In fact, candida growth appears to be inhibited by putrescine and cadaverine, and serotonin. This is not surprising. We have been using yeasts and moulds to kill bacteria and vice versa for over a centuary now.
One more nail in the coffin for those alternative therapists who eagerly diagnose “a candida overgrowth” without any proof, for those of us who are actually experiencing the symptoms of food intolerance and/or intestinal dysbiosis caused by amine-producing bacteria.
Candida is the cholesterol of alternative medicine: it gets blamed for everything.
Different strains of amine producing bacteria grow under different circumstances:
Dimethylamine, methylamine, propylamine, and pyrrolidine were the major amines formed by Bacteroides fragilis NCDO 2217 during the active phase of growth in batch culture. Production of these metabolites was strongly pH dependent and was optimal under acidic conditions (pH 6.0). Low pH also favored the formation of pyrrolidine, cadaverine, and dimethylamine by Clostridium perfringens C523, but the reverse was the case with putrescine, butylamine, and propylamine, where production was maximal at neutral pH. B. fragilis was grown in continuous culture under either starch or casein limitation. Amine formation was influenced by carbohydrate availability and was greatest when the bacteria were grown at high growth rates (dilution rate, 0.20/h) under starch limitation, where they constituted about 18% of the total fermentation products measured. Amine production was optimal and increased concomitantly with growth rate when C. perfringens was grown in glucose-limited continuous culture. Under conditions of high growth rate and glucose limitation, amines accounted for approximately 27% of the fermentation products measured. When glucose in the feed medium was increased from 5 to 15 g/liter, amine production was repressed, and under these nutritional conditions the growth rate had little effect on the process. Influence of pH, nutrient availability, and growth rate on amine production by Bacteroides fragilis and Clostridium perfringens
Acute laminitis has been associated with the overgrowth of gram-positive bacteria within the equine hindgut, causing the release of factor(s) leading to ischemia-reperfusion of the digits. The products of fermentation which trigger acute laminitis are, as yet, unknown; however, vasoactive amines are possible candidates. The objectives of this study were to use an in vitro model of carbohydrate overload to study the change in populations of cecal streptococci and lactobacilli and to establish whether certain species of these bacteria were capable of producing vasoactive amines from amino acids. Cecal contents from 10 horses were divided into aliquots and incubated anaerobically with either corn starch or inulin (fructan; both at 1 g/100 ml). Samples were taken at 6-h intervals over a 24-h period for enumeration of streptococci, lactobacilli, and gram-negative anaerobes by a dilution method onto standard selective growth media. The effects of the antibiotic virginiamycin (1 mg/100 ml) and calcium hydrogen phosphate (CaHPO4; 0.3 g/100 ml) were also examined. Fermentation of excess carbohydrate was associated with increases in numbers of streptococci and lactobacilli (2- to 3.5-log unit increases; inhibited by virginiamycin) but numbers of gram-negative anaerobes were not significantly affected. A screening agar technique followed by 16S rRNA gene sequence analysis enabled the identification of 26 different bacterial strains capable of producing one or more vasoactive amines. These included members of the species Streptococcus bovis and five different Lactobacillus spp. These data suggest that certain bacteria, whose overgrowth is associated with carbohydrate fermentation, are capable of producing vasoactive amines which may play a role in the pathogenesis of acute laminitis. Identification of Equine Cecal Bacteria Producing Amines in an In Vitro Model of Carbohydrate Overload
Bacteroides fragilis and many species of lactobacillus are normal inhabitants of the gut. They produce amines when they are allowed to feed on poorly digested protein, particularly in the presence of carbohydrate fermentation. Bacteria can even liberate phenols from phenol containing amino acids like tyrosine and phenylalanine. It seems that undigested starch and protein can both play a role in the production of amines. I have yet to find any information that implicates fat, since bacteria don’t really digest fat.
These are some statistics from Sue Dengate’s “Fed Up with Asthma”:
In the Children’s Hospital study:
70% of asthmatic children reacted to metabisulphite
20% reacted to salicylates in food
In RPAH studies:
50% of people with food related eczema reacted to salicylates
70% of people with food related irritable bowel (as opposed to non-food factors like stress), headache, or ADHD symptoms reacted to salicylates
Nicotine is an alkaloid found in the tobacco plant, and in the following foods:
- Eggplant (aubergine)
- Capsicum peppers
Nicotine is also used as a pesticide in organic farming, so residues may remain on any vegetables that are not thoroughly washed. (I find it quite disturbing and upsetting that both sulfites and nicotine are allowed in organic farming). Nicotine is extremely toxic. The LD50 of nicotine is around 40-60mg.
Sixty milligrams of nicotine (about the amount in three or four cigarettes if all of the nicotine were absorbed) will kill an adult, but consuming only one cigarette’s worth of nicotine is enough to make a toddler severely ill!
What happens to people after ingesting nicotine? Nicotine poisoning causes vomiting and nausea, headaches, difficulty breathing, stomach pains and seizures. Each of these symptoms can be traced back to excessive stimulation of cholinergic neurons. People poisoned by organophosphate insecticides experience the exact same symptoms. With organophosphates, acetylcholine builds up at synapses and overstimulates the neurons. Because nicotine is so similar to acetylcholine, and binds to cholinergic receptors, nicotine in excess produces the same overstimulation and toxicity. The more nicotine binding to the nicotinic cholinergic receptors, the more acetylcholine is subsequently released and free to activate other subsets of cholinergic receptors. How stuff works
Though many epilepsy charities protest (pathetically) that smoking “does not cause seizures”, the clinical evidence indicates that nicotine can and does cause some kinds of seizures. In fact, nicotine is used to induce seizures in rat models of epilepsy.
Here’s the connection between fibromyalgia and homocysteine.
Studies regarding the correlation between coronary artery disease incidence and abnormally high blood levels of the amino acid homocysteine have been appearing with increasing regularity. Relatively overlooked among the research articles is a recently published Swedish study, the results of which demonstrate consistently high homocysteine levels and low concentrations of vitamin B12 in the cerebrospinal fluid (CSF) of patients meeting established clinical criteria for Chronic Fatigue Syndrome and Fibromyalgia. […]
SAM is an important cofactor in the metabolism of central nervous system monoamine neurotransmitters, including dopamine, norepinephrine and serotonin. It has also been used successfully to treat both Fibromyalgia and depression. Unfortunately, SAM was not measured in the Swedish study.
Another explanation for high cerebrospinal fluid homocysteine levels was considered by the Swedish authors. Nitric oxide, which is an inhibitor of the enzyme that converts homocysteine to methionine, is produced as a result of inflammatory reactions. Most of the patients in the study, in addition to their neurological condition, had accompanying symptoms of viral or bacterial infections. Theoretically, the inflammation caused by these infections increased nitric oxide levels, which in turn increased homocysteine levels. Immune Support
Interesting. This may explain why I have had some positive results with my 1000mcg methyl-B12 tablets. I wonder if we should reduce nitric oxide levels? And if so, how?
The Wiki entries on nitric oxide and asymmetric dimethylarginine offer a lot of insight.
In the body, nitric oxide serves several roles, mainly involving small blood vessels. Nitric oxide is synthesized from L-arginine and oxygen by various nitric oxide synthase (NOS) enzymes. The endothelium (inner lining) of blood vessels uses nitric oxide to signal the surrounding smooth muscle to relax, thus dilating the artery and increasing blood flow. This phenomenon is thought to be central to endothelial health. A large percentage of humans are deficient in their manufacture of nitric oxide, placing them at increased risk of cardiovascular disease. This underlies the action of nitroglycerin, amyl nitrate and other nitrate derivatives in the treatment of heart disease: The compounds are converted to nitric oxide (by a process that is not completely understood), which in turn dilates the coronary artery (blood vessels around the heart), thereby increasing its blood supply. A chemical known as asymmetric dimethylarginine can interfere with the production of nitric oxide and is considered a marker of cardiovascular disease.
Macrophages, cells of the immune system, produce nitric oxide in order to kill invading bacteria. Under certain conditions, this can backfire: Fulminant infection (sepsis) causes excess production of nitric oxide by macrophages, leading to vasodilatation (widening of blood vessels), probably one of the main causes of hypotension (low blood pressure) in sepsis.
Nitric oxide also serves as a neurotransmitter between nerve cells. Unlike most other neurotransmitters that only transmit information from a presynaptic to a postsynaptic neuron, the small nitric oxide molecule can diffuse all over and can thereby act on several nearby neurons, even on those not connected by a synapse. It is conjectured that this process may be involved in memory through the maintenance of long-term potentiation. Nitric oxide is an important non-adrenergic, non-cholinergic (NANC) neurotransmitter in various parts of the gastrointestinal tract. It causes relaxation of the gastrointestinal smooth muscle. In the stomach it increases the capacity of the fundus to store food/fluids. Nitric Oxide
Asymmetric dimethylarginine (ADMA) is a naturally occurring chemical found in blood plasma. It is a metabolic by-product of continual protein modification processes in the cytoplasm of all human cells. It is closely related to L-arginine, a conditionally-essential amino acid. ADMA interferes with L-arginine in the production of nitric oxide, a key chemical to endothelial and hence cardiovascular health. […]
Asymmetric dimethylarginine is created in protein methylation, a common mechanism of post-translational protein modification. This reaction is catalyzed by an enzyme set called S-adenosylmethionine protein N-methyltransferases (protein methylases I and II). The methyl groups transferred to create ADMA are derived from the methyl group donor S-adenosylmethionine, an intermediate in the metabolism of homocysteine. (Homocysteine is an important blood chemical, because it is also a marker of cardiovascular disease). After synthesis, ADMA migrates into the extracellular space and thence into blood plasma. [..]
ADMA concentrations are substantially elevated by native or oxidized LDL cholesterol. Thus a spiralling effect occurs with high endothelial LDL levels causing greater ADMA values, which in turn inhibit NO production needed to promote vasodilation. The elimination of ADMA occurs through urine excretion and metabolism by the enzyme dimethylarginine dimethylaminohydrolase (DDAH). The role of homocysteine as a risk factor for cardiovascular disease is suggested to be mediated by homocysteine down-regulating production of DDAH in the body. Asymmetric Dimethylarginine
The “cardiovascular” effect of NO is basically vasodilation. Asymmetric dimethylarginine is being painted as a bad guy for reducing vasodilation in people with heart disease, however, too little is as bad as too much.
I wonder if too much nitric oxide is a problem, particularly as an inhibitor of the enzyme that converts homocysteine to methionine, as per my last post. The fact that ADMA is produced in the presence of SAM (derived from methionine) when methylation is increased, is part of an interesting feedback loop that could be out of sorts.
If levels of nitric oxide are a problem, I wonder if this would explain why nitrate and nitrite additives cause reactions in the food chemical intolerant, by further supplying fuel to the NO fire? Or are nitrates interfering with the production of NO and the opposite is true? This is of course pure speculation. Nitric oxide may just be a symptom of something else. It would also contradict the asthma issue, for which nitric oxide is extremely important in relaxing the bronchi.
Unfortunately for those of us relying on potatoes, one of the highest sources of natural nitrates and nitrites (even higher than the average additive-containing slice of bacon) is potatoes grown in artificially fertilised soil.
Folks with food chemical intolerance tend to have too much vasoconstriction: histamine, serotonin, dopamine, and tyramine all have vasoactive effects and lead to some of the unpleasant effects we experience, from skin flushing and inflammation, to varicose veins and headaches. Tyramine is a vasoconstrictor. Histamine is supposed to have mediatory effects. Perhaps nitric oxide levels are high for the same reason? And this then inhibits methylation?
Serotonin has a perverse effect, it can produce both vasoconstriction and vasodilation, depending on the receptors present. Serotonin migraines seem to be produced firstly by constriction, then the pain occurs on dilation.