The Effects of a Vitamin B Nutritional Deficiency

It has long been understood there is a link between a nutrient deficiency and visually measurable health. In our study, Sprague Dawley rats were fed diets lacking 100% of one B vitamin until a single mortality occurred. Vitamins studied were thiamin, riboflavin, niacin, pyridoxine, pantothenic acid, cobalamin and folate. Body mass, food consumption and images were recorded at weekly intervals. Rats were euthanized and liver, kidney, heart and brain samples for histological analysis were prepared. Liver and brain tissues were chosen as markers because of the high need of that organ for B vitamins and the likelihood of secondary lesion development. Correlation of deficiency symptoms with one missing nutrient was explored.

B vitamins are essential nutrients that support carbohydrate metabolism, enhance immune system function, and promote cell growth. For example, riboflavin (vitamin B2), niacin (vitamin B3), and pantothenic acid (vitamin B5) share a role with thiamine (vitamin B1) as essential coenzymes for energy metabolism.

Phosphorylated forms of thiamine (vitamin B1) catalyze the formation of acetyl-coenzyme A, succinyl-coenzyme A, and amino acid derivatives that play critical roles in cellular energy production  and the pentose phosphate pathway. It is also required for the synthesis of the nucleic acids, DNA and RNA, and the niacin-containing coenzyme NADPH, which is essential for a number of biosynthetic reactions. Thiamin deficiency affects the cardiovascular, nervous, muscular, and gastro- intestinal systems. In mammals, deficiency results in Korsakoff’s syndrome, optic neuropathy, and a disease called beriberi that affects the peripheral nervous (polyneuritis) and/or cardiovascular system. Thiamine deficiency has a potentially fatal outcome if it remains untreated.

Niacin (B3) occur in biological systems as free acids (as nicotinamide) and in the form of coenzymes, nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). As many as 200 enzymes require the niacin coenzymes, NAD and NADP, mainly to accept or donate electrons for redox reactions. NAD functions most often in energy producing reactions involving the degradation (catabolism) of carbohydrates, fats, proteins, and alcohol.

Pantothenic acid (vitamin B5) is a component of coenzyme A (CoA), an essential coenzyme in a variety of reactions that sustain life. CoA is required for chemical reactions that generate energy from food (fat, carbohydrates, and proteins). The synthesis of essential fats, cholesterol, and steroid hormones requires CoA, as does the synthesis of the neurotransmitter, acetylcholine, and the hormone, melatonin. Symptoms of pantothenic acid deficiency include impaired energy production, irritability, fatigue, and apathy.

Pyridoxine (vitamin B6) is a coenzyme in over one- hundred essential metabolic reactions, particularly those associated with metabolism of amino acids. It is essential for normal brain development and function, as it aids in the production of neurotransmitters such as serotonin, dopamine, norepinephrine and gamma-aminobutyric acid. Vitamin B6 deficiency is associated with growth depression, mild microcytic hypochromic anemia, convulsive seizures and calcium oxalate nephrosis.

Folic acid (vitamin B9) coenzymes appear to mediate the transfer of one-carbon units in reactions critical to the metabolism of nucleic acids and amino acids.

Cobalamin (vitamin B12) has the largest and most complex chemical structure of all the vitamins. It is unique among vitamins in that it contains a metal ion, cobalt. Vitamin B12 deficiency can potentially cause severe and irreversible damage to the brain and nervous system.

Vitamin B2 is required for a wide variety of cellular processes. Riboflavin is the central component of the cofactors flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), and is therefore required by all flavoproteins. Flavo-coenzymes participate in redox reactions in numerous metabolic pathways and are critical for the metabolism of carbohydrates, fats, and proteins. FAD is part of the electron transport (respiratory) chain, which is central to energy production.

Our research clearly proves that a deficiency in a single B vitamin can stunt growth and produce significant adverse effects. Depression exhibited in thiamine or pyridoxine depleted rats are consistent with the roles these vitamins play in amino acid metabolism and the formation of key neurotransmitters such as serotonin, melatonin, and dopamine. Reductions in rat growth rates accompanying B vitamin deficiencies are consistent with the importance of B vitamins in cellular energy metabolism. Other adverse events observed in our study include hair loss, weakness, loss of appetite, inflammation, dermatitis, and bloody discharge. Necropsy showed reductions in liver and heart development, and absence of the thymus.

A true state of deficiency arises when methionine, folate, choline and B12 are kept at zero; however, survival is only 4 weeks with inadequate time for development of liver lesions. When a minimal amount of methionine is added, survival is extended and pre-cancerous lesions can occur. Deficient animals had 50% incidence of precancerous lesions and no detectable adrenal glands.

The results of the study were published in journal: The Effects of a Primary Nutritional Deficiency (Vitamin B Study)  Riordan HD, Mikirova NA, Taylor PR, Feldkamp CA, Casciari JJ.  Food and Nutrition Sciences, 2012, 3(9):1238-1244.