According to a 2016 census, eight million adults conform to a vegetarian diet within the United States, and about 50% of these adults follow a vegan diet. The census determined that plant-based diets are quickly growing in popularity particularly in young adults between the ages of 18 to 34 years. Many Americans are aware of the health benefits of a plant-based diet, however, the dietary risks associated with these diets are not well emphasized. Health concerns such as vitamin deficiencies and altered metabolism are heightened in vegetarian populations.

One Particular nutrient that is commonly lacking in the vegetarian diet is vitamin B12. Vitamin B12 is found mainly in animal-derived food sources such as meat, poultry, fish, dairy, and eggs. Although some vegetarians, called lacto-ovo vegetarians, consume dairy and eggs, vegans do not consume any animal products at all. Vitamin B12 deficiency can have devastating consequences on the human body due to its role as a methylation cofactor. Metabolism, DNA replication, and cancer formation all involve methylation processes.

This cross-sectional, differential study aimed to further understand the relationship between vegetarianism, vitamin B12 status, and methylation capacity in healthy adults. A group of 34 healthy adults (18 vegetarians and 16 omnivores) was recruited to analyze serum B12, homocysteine, methylmalonic acid, serum total folate, and transcobalamin II status. It was hypothesized that (1) vegetarians would have a lower vitamin B12 status, and thus, a lower methylation capacity than omnivores and that (2) low vitamin B12 status would be correlated with low methylation capacity.

The data show that vegetarians did not have significantly lower vitamin B12 methylation capacity status than omnivores. Nor was vitamin B12 status correlated with methylation capacity. However, the data revealed that diet quality had a positive influence on folate status. There was also a statistical trend (p=0.08) for homocysteine reduction in participants consuming high-quality diets. The data herein suggest that methylation capacity may be impacted by the quality of diet rather than the type of diet.

Turmeric, scientifically known as Curcuma longa, is a tropical plant that is most often consumed in India.1 The rhizome of the plant is dried and then ground into a fine, vibrant yellow powder. In addition to its function as a spice, turmeric is also used in traditional Ayervedic medicine due to its unique medical properties. These unique properties are attributed to the three major constituents of turmeric: curcumin, α-isocurcumin, and β-isocurcumin.2 Curcumin (Diferuloylmethane; C21H20O6), makes up 5% of turmeric by weight, and is the most prominent active ingredient within the turmeric root. Perhaps the most intriguing characteristic about curcumin is its ability to modulate targets such as, but not limited to, transcription factors, enzymes, apoptosis genes, and growth factors.1 Modern medical research has determined curcumin to be a viable treatment and prevention method for disease such as type II diabetes mellitus, rheumatoid arthritis, liver cirrhosis, and certain cancers. However, research on turmeric’s effects on gastrointestinal health is significantly lacking. This randomized, double-blind, cross-over trial looked to see if supplemental turmeric (500 mg as dried root powder) would significantly raise breath hydrogen emission (BHE) and reduce small bowel transit time (SBTT) in 8 female adults who were suffering from chronic constipation. Although supplemental turmeric did not significantly impact BHE or SBTT, the number of bowel movements greatly increased during turmeric intervention.