Sodium benzoate

Sodium benzoate:

• Increases memory and is a cognitive enhancer, by increasing Long Term Potentiation (LTP) and synaptic plasticity (R).  The mechanism is via NMDA activation (R).
• Increases growth factors in the brain such as BDNF and Neurotrophin-3 via CREBactivation (R).
• Treatment for Schizophrenia (R), Alzheimer’s (R), Bipolar (R), Depression (R), ALS (R), Parkinson’s (R), Anxiety (R) Dementia (R) via NMDA activation.
• Decreases cholesterol just as much as some statins (R).  The pathway that increases cholesterol synthesis is inherently inflammatory, which is why statins are considered powerful anti-inflammatory drugs. The cholesterolitself isn’t inflammatory; rather, enzymes in the pathway are (R).

Sodium Benzoate Decreases Inflammation and Cholesterol

I recently bought this lemon juice from my corner grocery.  Looking at the ingredients, I noticed sodium benzoate and sodium sulfite.  I commonly see potassium sorbate in a lot of foods, too.  I generally try to stay away from food additives because they can have an effect on gut flora, theoretically at least. Normally I try to get better quality foods from the health food store but I figured some sodium benzoate once in a while won’t kill me.

Recently,  I became interested in researching therapeutic options for autoimmune conditions because of its growing prevalence and our increased understanding that more and more diseases are of autoimmune origin.  See a list of autoimmune diseases, which seems incomplete based on my research.

Anyway, I came across a few interesting studies that demonstrated how sodium benzoate can dampen inflammation (R) and help autoimmune diseases (R).

Sodium benzoate (NaB) actually is a derivative (or metabolite) of cinnamon.  While not as promising, studies also show that potassium sorbate (sorbic acid) and sodium sulfite can suppress Th1-type immune responses, which has an anti-inflammatory effect.

Interestingly, sodium benzoate decreases cholesterol, too, in the same manner, that statins do – by inhibiting an enzyme called HMG-CoA reductase.   It’s in this manner that it has an anti-inflammatory effect.

It counteracts autoimmune diseases by decreasing inflammation (R).  It acts via inhibiting T cell proliferation, the Mevalonate pathway, iNOS, NF-kb, TNF-α, IL-1β, Th-1, adhesion molecules and by increasing Tregs (R).

It inhibits iNOS via NF-kb inhibition.  Inhibiting iNOS reduces nitric oxide (NO), which has a host of downstream (or domino) effects.

For example, NO increases CD11b, a protein on cells that binds to ICAM-1 and complement C3bi, which are other proteins that cause inflammation.  In various neuroinflammatory diseases, the increased CD11b expression corresponds to the severity of microglial activation (R).

NO also increases MHCII and other “co-stimulatory molecules”, which are other proteins on cells that stimulate inflammation (R).  In addition, it increases a protein called “GFAP.”  In various neuroinflammatory diseases, the increased GFAP expression corresponds to the severity of astroglial activation (R). So by NaB inhibiting NO in astroglia (a type of brain cell), it decreases these proteins.

NaB also markedly inhibits the expression of other receptor proteins on cells called “integrins” (VLA-4 and LFA-1: α4, β1, αL, and β2), which are located on T cells.  These receptors make it easier for T cells to activate and attack our own tissue, so by inhibiting them we decrease our risk of autoimmunity (R).

Last, NaB inhibits “adhesion molecules” such as E-selectin and P-selectin, ICAM-1 and VCAM-1, which allows the immune cells to attach and roll along the brain barrier and get into the brain.  NaB inhibits these adhesion molecules (R).

Sodium Benzoate and D-amino acid oxidase

Sodium benzoate is also a potent inhibitor of an enzyme called D-amino acid oxidase (DAAO).

Less of this enzyme is a good thing  because DAAO breaks down d-serine, resulting in less d-serine and therefore less activation NMDA receptors (d-serine activates NMDA) (R).

Less activation of NMDA receptors has been found to be a contributory factor in multiple chronic, cognitive-based disorders.

While researching this article, I was surprised to find 2 double-blind placebo-controlled clinical trials of sodium benzoate with positive results for schizophrenia and Alzheimer’s.  In schizophrenia,  D-amino acid oxidase has been connected to the brain D-serine metabolism and to the regulation of the glutamatergic neurotransmission.

In a postmortem study, the activity of DAAO was found to be two-fold higher in schizophrenia (R).  By inhibiting this enzyme (DAAO) benzoate is working via a completely different mechanism than its anti-inflammatory and cholesterol lowering role.

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