How Vitamin B3 Can Replace for Benzodiazepines

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Nicotine, niacinamide and the benzodiazepine class of drugs all have anxiety-reducing effects via different mechanisms, but all three enhance the activity of GABA in the brain. Although the benzodiazepines have been linked to dementia, niacinamide and nicotine protect the brain from stress.

The benzodiazepine diazepam (Valium) has a central nervous system (CNS) depressive effect, and in experiments, it slows the head turning of animals. In a research study led by Prousky,  niacinamide actually abolished diazepam’s slowing of head turning, but niacinamide did not have any effect on head turning when administered by itself, which underscores its different mode of action and its lower likelihood of causing deficits in reaction time.

In the diabetic brain, niacinamide tends to lower serotonin and increase GABA levels. Niacinamide tends to slow down synaptic firing between brain cells (as a CNS depressant, and as with many benzodiazepine drugs).

In the study published by Prousky, a 34-year-old male patient took 2,500 milligrams of niacinamide daily for anxiety relief. A 41-year-old man took 4.5 grams of niacinamide daily for six months and damaged his liver, but the damage corrected itself within a month after cessation of the vitamin. Dosages over 3 grams of niacinamide have a high likelihood of reversibly damaging the liver, whereas smaller amounts can inflame the liver and trigger other side effects including an allergic reaction. Dr. Raymond Peat, PhD recommends 100 mg of niacinamide taken three times daily after each meal. Niacinamide can dramatically lower blood sugar, which can be uncomfortable or dangerous in some cases, particularly with diabetics.

References

Bold JM, Gardner CR, Walker RJ. Central effects of nicotinamide and inosine which are not mediated through benzodiazepine receptors. Br J Pharmacol. 1985 Mar;84(3):689–96.

“The actions of nicotinamide and inosine were investigated on rat cerebellar Purkinje cells using ionophoretic and extracellular recording techniques. Ionophoretic application of nicotinamide or inosine showed that they were potent inhibitors of Purkinje cell firing. This inhibition differed from that induced by benzodiazepines in that it was not reversed by the GABA antagonists bicuculline methiodide and picrotoxin. RO 15-1788, the specific benzodiazepine antagonist, did not reverse the effects of nicotinamide. Chlordiazepoxide has been shown to increase significantly social interaction between pairs of male rats and this increase can be reversed by RO 15-1788, 20 mg kg-1 i.p. Nicotinamide also caused a small increase in social interaction but this effect was not reversed by the benzodiazepine antagonist. Inosine did not increase social interaction. [3H]-flunitrazepam binding studies showed that nicotinamide and inosine have only low affinities for the benzodiazepine binding site. These results suggest that while nicotinamide may exert some neuronal depressant and anxiolytic activity, its site of action appears not to be associated with the benzodiazepine receptor site. Similarly, inosine exerts a neuronal depressant effect dissimilar from that of benzodiazepines.”

Donchenko GV, Kuchmerovskaia TM, Parkhomets PK, Obrosova IG, Klimenko AP, Efimov AS. [Effect of nicotinamide on the uptake and release of serotonin and GABA by cerebral cortex synaptosomes in rats with diabetes induced by streptozotocin]. Ukr Biokhim Zh. 1995 Feb;67(1):105–11.

“Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels, while the GABA uptake tended to decrease in diabetic rats. With this dose of NAm the partial restoration of serotonin and GABA release was achieved. The modulating effect of in vivo administered NAm acts via NAD which binds specifically with synaptic membranes. It has been shown that brain NAD(P)/NAD(P)H decreased while sorbitol level increased in streptozotocin-diabetic rats as compared to control. The NAm administration to diabetic rats is accompanied by the increase of NAD(P)/NAD(P)H and the reduction of brain sorbitol level. Data obtained confirm the important role of NAm in the pathogenesis of diabetic encephalopathies.”

Niacinamide: MedlinePlus Supplements. https://medlineplus.gov/druginfo/natural/1534.html. Accessed 16 Nov. 2018.

“Niacinamide is LIKELY SAFE for most adults when taken by mouth. Unlike niacin, niacinamide does not cause flushing. However, niacinamide might cause minor adverse effects such as stomach upset, intestinal gas, dizziness, rash, itching, and other problems. When applied on the skin, niacinamide cream might cause mild burning, itching, or redness.

Patterson DJ, Dew EW, Gyorkey F, Graham DY. Niacin hepatitis. South Med J. 1983 Feb;76(2):239–41.

“A 41 year old man with a history of taking 4.5 grams of niacin daily for 6 months presented with nausea, anorexia, weakness and abdominal pain followed by jaundice.  He was icteric but had no fever or rash.  Blood tests showed marked elevations in serum aminotransferase levels and hyperbilirubinemia (Table).  Tests for hepatitis B and for autoantibodies were negative.  An initial prothrombin time was 28.5 seconds, but it corrected within 3 days of stopping niacin.  A liver biopsy showed submassive lobular collapse, marked cholestasis, ballooned hepatocytes and mild fibrosis.  Once niacin was stopped, he improved rapidly and serum enzymes fell to normal within a month.  Review of this history revealed that he had developed jaundice while taking niacin in the past, had recovered on stopping, but nevertheless began taking it again.

Prousky J. Niacinamide’s potent role in alleviating anxiety with its benzodiazepine-like properties: A case report. Journal of Orthomoleculular Medicine. 2004 Jun 1;19:104–10.

“It is of no surprise that this patient benefited tremendously from the benzodiazepines. Benzodiazepines bind to a macromolecular complex that is found within the CNS and is referred to as the GABA-benzodiazepine receptor-chloride ion channel complex. 7 When benzodiazepines bind onto or near this macro-molecular complex they potentiate GABAergic synaptic inhibition through membrane hyperpolarization, thus enhancing the conductance of the chloride ion by increasing the frequency of channel-opening events. 7 The net result is the reduction of anxiety and related symptoms via the diminution of neurotransmission (i.e., neuronal firing) among many brain regions such as the spinal cord, hypothalamus, hippocampus, substantia nigra, cerebellar cortex and cerebral cortex. 7 It appears that niacinamide has similar anxiolytic properties to that of the benzodiazepines. This is supported by the fact that the patient did not feel any difference, in terms of response and effectiveness, between the benzodiazepines and niacinamide. He was able to switch with little difficulty from the daily use of a benzodiazepine to niacinamide. Furthermore, during the transition he did not experience common withdrawal symptoms such as insomnia, recurrent anxiety or panic attacks. However, unlike the benzodiazepines, the pharmacologic data pertaining to the anxiolytic properties of niacinamide are not well known since its precise mechanisms of action upon the central nervous system (CNS) have yet to be conclusively determined.

Möhler et al. suggested that niacinamide is pharmacologically similar to benzodiazepines due to its presynaptic inhibition, as demonstrated in the cat lumbo-sacral spinal cord, anticonflict effect, and anticonvulsant, muscle relaxing and hypnotic effects. 8 Based on these results, these investigators suggested that the endogenous ligand for the benzodiazepine receptor in the mammalian brain was niacinamide. Slater and Longman used a rat headturning model as a method of evaluating whether niacinamide and inosine affect the GABA-mimetic actions of diazepam in vivo. 9 Diazepam caused a highly statistically significant slowing of the head-turn, which is to be expected when injected into the globus pallidus. However, when diazepam was combined with niacinamide, the slowing of the head-turn initially produced by diazepam, reversed to its pretreatment time. In other words, niacinamide may have negated or abolished the effects of diazepam. From these results, it was assumed that niacinamide antagonized the effects of diazepam, therefore interacting with the benzodiazepine receptor in vivo. However, niacinamide administered by itself did not result in reduced headturning behaviour, and did not mimic the benzodiazepine properties of diazepam when tested with the head-turning model. The authors concluded that niacinamide probably does have benzodiazepine-like properties at different benzodiazepine receptor sites in the CNS, but its effects are unrelated to the actions of GABA. In rat studies, Kennedy and Leonard assessed the similarity between the action of niacinamide and diazepam on neurotransmitter metabolism. 10 They considered neurotransmitter turnover of serotonin, noradrenaline (norepinephrine), dopamine and GABA. In their three experiments on rats, they found that niacinamide had a qualitatively similar effect to that of diazepam. It was further concluded that niacinamide exerted its effects by influencing the turnover of serotonin, noradrenaline, dopamine and GABA in those areas of the brain thought to be unbalanced in anxiety. Lapin compared the effects of putative endogenous benzodiazepine receptor ligands (i.e. niacinamide, inosine and hypoxanthine) against kynurenine and pentylenetetrazol, agents that have benzo-diazepine receptor affinity and induce seizures in mice. 11 Niacinamide decreased the kynurenine-induced seizures in C57BL/6 adult male mice and prolonged the latency of pentylenetetrazol seizures. Niacinamide could possibly be a competitive antagonist for the benzodiazepine receptor since it prevented the binding of kynurenine to the benzodiazepine receptor.”​

When doses of over 3 grams per day of niacinamide are taken, more serious side effects can happen. These include liver problems or high blood sugar.”

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