The B-vitamins in malnutrition with alcoholism: A model of intervitamin relationships

Abstract

1. The B-vitamin status of fifty-nine patients, mainly from the lower socio-economic classes in Bombay, with a history of chronic malnutrition, and of alcoholism of 1·5–20 years’ duration, was studied before and during treatment, and in relation to their clinical, especially neurological, condition. These patients were divided into two neurological categories: (1) those with peripheral neuropathy (mainly sensory and distal) alone, (2) those with mental changes (mainly confusion and disorientation) also. Both categories frequently showed pellagrous pigmentation and mucocutaneous signs of B-vitamin deficiency.2. Thiamin and erythrocyte transketolase (EC 2.2.1.1) activity, riboflavin, nicotinic acid, pantothenic acid, total and pyridoxal fraction of vitamin B6, folate and total vitamin B12 were estimated in the blood and the cerebrospinal fluid (CSF) of these patients, and also in the blood of sixty-nine control subjects and in the CSF of some of them. The concentrations of all the vitamins, except vitamin B12, were highly significantly lower in the blood of patients of category 1 compared to the controls, and erythrocyte transketolase activity and pyridoxal concentration in patients of category 2 were significantly lower than those of category 1 patients. Blood pantothenic acid and folate concentrations were reduced less consistently.3. Serum vitamin B12 concentration was significantly increased (though within normal range) in the patients compared to the control group, probably because of the moderate hepatic insufficiency (as assessed by liver function tests) in the former.4. The concentrations of thiamin, riboflavin, nicotinic acid and total vitamin B6 were also highly significantly lower in the CSF in patients of category 1 compared with controls. Furthermore, thiamin, nicotinic acid and total vitamin B6 concentrations were significantly lower in patients of category 2 than those of category 1 patients, indicating that CSF levels reflect better the neurological status of these patients.5. There was a moderate increase in the blood concentration of all the vitamins tested, after a relatively poor hospital diet alone. There was a concurrent increase in the blood levels of thiamin, riboflavin, nicotinic acid and pantothenic acid after parenteral treatment with either thiamin or nicotinic acid. The administration of pyridoxine resulted in a significant increase in the blood levels of riboflavin and the pyridoxal fraction of vitamin B6.

A Pilot Metabolomic Study on Myocardial Injury Caused by Chronic Alcohol Consumption—Alcoholic Cardiomyopathy

“…Numerous studies have demonstrated that chronic alcohol consumption leads to B vitamin deficiency [36,37]. Compared with the control group, the myocardial tissue of mice in the ACM group exhibited decreased levels of several B vitamins, including thiamine (vitamin B1), riboflavin (vitamin B2), pantothenic acid (vitamin B5), and nicotinamide (the metabolite of niacin, vitamin B3).…”

The niacin receptor HCAR2 modulates microglial response and limits disease progression in a mouse model of Alzheimer’s disease

“…Increased dietary intake of niacin (nicotinic acid) has been associated with improved cognitive performance ( 5 ) and reduced risk of age-associated cognitive decline and AD ( 6 ). Niacin is obtained principally through diet and is able to cross the blood-brain barrier ( 7 ), as evidenced by its detection in the mouse brain and human cerebrospinal fluid ( 8 , 9 ). Thus, we postulated that the actions of niacin within the brain may be of therapeutic utility for AD.…”

CD38: A NAADP degrading enzyme

“…However, this reaction requires an acidic pH and millimolar concentrations of nicotinic acid. These requirements will hardly be met in vivo [7,8]. CD38 is a multifunctional enzyme which in addition catalyses the hydrolysis of NAD to ADPR, and to a minor extent also to cADPR [9], and the degradation of NAADP [10].…”