Histamine & Motivation
Histaminergic neurons are found in the hypothalamus. The roles of these neurons are primarily appetite behaviour, food anticipatory responses, & sleep/wake cycles. Studies investigating the role or histaminergic neurons, however, have found that dysfunction of Histaminergic neurons can lead to decreased motivation.
Reduced motivation or apathy is commonly seen in a variety of conditions including some forms of depression, dementia, Schizophrenia, Huntington’s and Alzheimer’s disease.
Reduction of histamine 1 (H1) receptor binding in the frontal lobe has been reported in depressed and schizophrenic patients. Lower than normal histamine levels may cause poor motivation related to food choices or reducing drug addiction. When a person lacks motivation, drinks too much alcohol and is unable to control their appetite and food consumption, histamine dysfunction maybe the trigger.
A higher histamine level was observed in those with compulsive and obsessive behaviours. This may demonstrate higher histamine levels can induce a state of greater motivation.
It is believed that histamine is unable to cross the blood brain barrier… Recent studies show histamine is produced in the hypothalamus and gets stored in the so-called histaminergic neurons where it is released upon stimulation.
Histamine receptors in the brain
The brain has receptors for histamine, and mental disorders result when there is abnormality of these receptors. In general histamine has four kinds of receptors, designated as H1R, H2R, H3R, and H4R. Only the first three are present in the brain.
- H1R excites the neurons in the brain and is responsible for the sleep-wake cycle. This explains why insomnia is one of the most common symptoms of histamine intolerance and how antihistamines that act on them produce sedative effect.
- H2R, like H1R, is also excitatory but its role is mainly on perception, memory, learning, reward, pleasure, and pain. This explains why antihistamines that act on H2 receptors affect our perception of pain. Addiction and compulsive disorders work on these receptors & addictive substances like alcohol and illicit drugs have been found to interfere with histamine activity in H2R. Appetite, drinking and eating behaviours are affected by histamine. Compulsive behaviour such as anorexia and bulimia are related to the histamine’s effect on the reward systems of the brain.
- H3R, on the other hand, inhibits neurons from releasing histamine. These receptors are also responsible for regulating the release of other neurotransmitters from the brain. This may provide a promising solution to address the effects of histamine in the brain.
Histamine, Epinephrine & Anxiety
Histamine may trigger the release of epinephrine, the major player in the body’s fight-or-flight response, and it may be this mechanism that causes mood issues to occur when histamine is high. Epinephrine, like histamine, cannot cross the blood-brain barrier but it can trigger anxiety symptoms such as rapid heartbeat, sweating, shaking, shortness of breath & nausea.
Histamine and Oestrogen
Another interesting explanation is that histamine causes oestrogen levels to rise, and this hormone can cross the blood-brain barrier. Oestrogen has powerful effects on mood. Increasing levels of histamine create a vicious cycle wherein one induces the release of the other and vice versa. In this case, once oestrogen crosses the blood-brain barrier and reaches the brain, it stimulates the production of histamine. Histamine in turn, increases oestrogen levels. This makes it more difficult for progesterone to rise, making us even more stressed.
Histamine is more than just an allergy response messenger; it is an important neurotransmitter that has somewhat been forgotten. Like all neurotransmitters it is about getting the balance right. Too much of a good thing is not a good thing, yet neither is too little…
References:
https://mthfrsupport.com.au/2016/09/histamine-and-mental-health/
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Torrealba F, Riveros M, Contreras, Valdes J. Histamine and Motivation. Frontiers in Systems Neuroscience. 2012;6(51):1-11