"Nicotinamide, a form of the B vitamin niacin, is known to exert similar effects on the brain as benzodiazapenes.13 Nicotinamide stimulates the GABA-benzodiazapene receptor complex, an inhibitory neuron grouping. By activating these neurons, a calming effect is the end result.14 Other investigations designed to test the efficacy of nicotinamide and brain function revealed that GABA nerve receptors were under less control (meaning that because they are inhibitory in nature, when they are not activated the brain is more excitable-which in theory may lead to more anxiety) when nicotinamide was found at suboptimal levels in the subject, and reintroduction of nicotinamide led to a calming effect on the GABA receptors.
Approaches to Anxiety (Oct. 2004)
No time right now but will look into possible pathways related to this. Is the amide group necessary even? For this to be important it would seem necessae=ry that the oxidation product itself by psychoactive (not reliant on metabolism - slow).
+++++++++++
A little later ...
Niacin itself passes the blood-brain barrier easily (while the amide much less so) and is also psychoactive in a way that fits (calming; a MAOI, via histamine release).
"The most promising theoretical base at this point in time appears to lie in the metabolism of 5-OHtryptamine, or the monoamine oxidase reaction, The cerebral catecholamines have already been implicated in previous work with schizophrenics. An adrenochrome or serotonin-chrome has been postulated. Although some of the phenomena observed in our study could be related to a dna mechanism, the observed effects were much more global and occurred too quickly in many cases to be confined only to this theoretical base. The breakdown of 5-OH-tryptamine into serotonin, dopamine, noradrenalin, and nicotinic acid explains all of the presently observed phenomena far better. These psychoactive substances have now been shown to be responsible for sensory perception, sleep, appetite, mood, and alertness among other important and vital functions. Levels of these biogenic amines are regulated both at the site of production and through controlled degradation to inactive metabolites through the monoamine oxidase reaction. It should again be emphasized that nicotinic acid is a normal byproduct of this important body reaction.
In theory we find the 5-OH-tryptamine mechanism most compatible with observed and reported phenomena regarding nicotinic acid in alcoholics. Nicotinic acid is a simple molecule capable of passing the blood-brain barrier. This fact alone could explain the failure of nicotinamide to significantly benefit alcoholics. The saturation of the CNS nicotinic acid mechanism could inhibit 5-OHtryptamine metabolism reducing levels of serotonin, dopamine, and noradrenalin. Nicotinic acid is a proved histamine stimulant. High levels of histamine tend to inhibit the monoamine oxidase reaction causing reaccumulation of the biogenic amines. Nicotinic acid could well be a biochemical governor regulating in a very significant way the metabolic levels of the cerebral catecholamines."
http://www.orthomed.org/resources/papers/alsmith2.htm
Obviously read between the lines, so to speak, given that the paper is primarily about alcoholics.
The thing is - I have niacin in my cupboard in something like 50mg tablets (with histamine flush in ~10 minutes), so how does niacin achieve its effect in smoke (if it does) at tiny doses? A similar but more potent variant? Or it's simply the combined effect with the other alkaloids (synergy) ? (likely)
Approaches to Anxiety (Oct. 2004)
No time right now but will look into possible pathways related to this. Is the amide group necessary even? For this to be important it would seem necessae=ry that the oxidation product itself by psychoactive (not reliant on metabolism - slow).
+++++++++++
A little later ...
Niacin itself passes the blood-brain barrier easily (while the amide much less so) and is also psychoactive in a way that fits (calming; a MAOI, via histamine release).
"The most promising theoretical base at this point in time appears to lie in the metabolism of 5-OHtryptamine, or the monoamine oxidase reaction, The cerebral catecholamines have already been implicated in previous work with schizophrenics. An adrenochrome or serotonin-chrome has been postulated. Although some of the phenomena observed in our study could be related to a dna mechanism, the observed effects were much more global and occurred too quickly in many cases to be confined only to this theoretical base. The breakdown of 5-OH-tryptamine into serotonin, dopamine, noradrenalin, and nicotinic acid explains all of the presently observed phenomena far better. These psychoactive substances have now been shown to be responsible for sensory perception, sleep, appetite, mood, and alertness among other important and vital functions. Levels of these biogenic amines are regulated both at the site of production and through controlled degradation to inactive metabolites through the monoamine oxidase reaction. It should again be emphasized that nicotinic acid is a normal byproduct of this important body reaction.
In theory we find the 5-OH-tryptamine mechanism most compatible with observed and reported phenomena regarding nicotinic acid in alcoholics. Nicotinic acid is a simple molecule capable of passing the blood-brain barrier. This fact alone could explain the failure of nicotinamide to significantly benefit alcoholics. The saturation of the CNS nicotinic acid mechanism could inhibit 5-OHtryptamine metabolism reducing levels of serotonin, dopamine, and noradrenalin. Nicotinic acid is a proved histamine stimulant. High levels of histamine tend to inhibit the monoamine oxidase reaction causing reaccumulation of the biogenic amines. Nicotinic acid could well be a biochemical governor regulating in a very significant way the metabolic levels of the cerebral catecholamines."
http://www.orthomed.org/resources/papers/alsmith2.htm
Obviously read between the lines, so to speak, given that the paper is primarily about alcoholics.
The thing is - I have niacin in my cupboard in something like 50mg tablets (with histamine flush in ~10 minutes), so how does niacin achieve its effect in smoke (if it does) at tiny doses? A similar but more potent variant? Or it's simply the combined effect with the other alkaloids (synergy) ? (likely)
