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Alcohol

Many of the deleterious effects of excess alcohol consumption are related more to its metabolism than the alcohol per se. Alcohol is initially oxidised to acetaldehyde and then to acetate, reactions requiring NAD as a co-factor. Acetaldehyde is a potent toxin and its accumulation impairs mitochondrial function - reducing energy levels; as well as contributing to liver damage - hepatitis, and sclerosis. When acetaldehyde spills over into the blood stream it then has wide spread systemic effects particularly in the brain where it combines with neurotransmitters to produce morphine-like substances (THIAs).

The detoxification of excess alcohol increases the conversion of oxidised NAD+ to reduced NADH. This alteration in the NAD+ / NADH ratio, the redox potential within cells, has numerous metabolic consequences. Excess NADH increases the conversion of pyruvate to lactate, reducing glucose synthesis and causing hypoglycaemia (low blood sugar). It also increases the synthesis of fatty acids resulting in fat accumulation both in the liver and blood stream predisposing to liver failure and cardiovascular disease.

Most cellular energy is produced during the process of oxidative phosphorylation in mitochondria. This complex process involves the transfer of electrons from NADH to power ATP production. Increasing NADH levels will, therefore, increase the production of reactive oxygen species (ROS) and the consequent level of oxidative stress. As we will see this phenomenon is a common feature in many of the potential therapeutic outlets for NAD supplementation (see Section ?).

NAD+ therapy should redress the imbalance in the NAD+ / NADH ratio, increase the catabolism of acetaldehyde and reduce oxidative stress, thereby greatly improving the health and on-going prognosis for the alcohol-dependent.

A major concern for clients undergoing withdrawal from alcohol is both the discomfort experienced and the risk of seizures. Clients undergoing NAD-assisted withdrawal have reported an approximately 80 % reduction in symptoms compared with 'cold turkey.' Both the risk of seizures and the general hyperexcitability in withdrawal is explained by the up-regulated effects of the excitatory neurotransmitter glutamate, a mechanism known to be inhibited by NAD+.

Practitioners hope to work within National Institute for Health and Care Excellence (NICE) guidelines to withdraw patients from tranquillisers at a pace suited to each individual. They believe tailor-made protocols could help some withdraw in weeks rather than months and years.

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