Vitamin B₁₂ is essential for DNA synthesis and for cellular energy production. This review aims to outline the metabolism of vitamin B₁₂, and to evaluate the causes and consequences of sub-clinical vitamin B₁₂ deficiency. Vitamin B₁₂ deficiency is common, mainly due to limited dietary intake of animal foods or malabsorption of the vitamin. Vegetarians are at risk of vitamin B₁₂ deficiency as are other groups with low intakes of animal foods or those with restrictive dietary patterns. Malabsorption of vitamin B₁₂ is most commonly seen in the elderly, secondary to gastric achlorhydria. The symptoms of sub-clinical deficiency are subtle and often not recognized. The long-term consequences of sub-clinical deficiency are not fully known but may include adverse effects on pregnancy outcomes, vascular, cognitive, bone and eye health.

In atherosclerosis and diabetes mellitus, the concomitant presence of low-grade systemic inflammation and mild zinc deficiency highlights a role for zinc nutrition in the management of chronic disease. This review aims to evaluate the literature that reports on the interactions of zinc and cytokines. In humans, inflammatory cytokines have been shown both to up- and down-regulate the expression of specific cellular zinc transporters in response to an increased demand for zinc in inflammatory conditions. The acute phase response includes a rapid decline in the plasma zinc concentration as a result of the redistribution of zinc into cellular compartments. Zinc deficiency influences the generation of cytokines, including IL-1β, IL-2, IL-6, and TNF-α, and in response to zinc supplementation plasma cytokines exhibit a dose-dependent response. The mechanism of action may reflect the ability of zinc to either induce or inhibit the activation of NF-κB. Confounders in understanding the zinc-cytokine relationship on the basis of in vitro experimentation include methodological issues such as the cell type and the means of activating cells in culture. Impaired zinc homeostasis and chronic inflammation feature prominently in a number of cardiometabolic diseases. Given the high prevalence of zinc deficiency and chronic disease globally, the interplay of zinc and inflammation warrants further examination.

Despite the popularity of low-glycemic index (GI) and high-protein diets, to our knowledge no randomized, controlled trials have systematically compared their relative effects on weight loss and cardiovascular risk. A total of 129 overweight or obese young adults (body mass index, > or =25 [calculated as weight in kilograms divided by the square of height in meters]) were assigned to 1 of 4 reduced-fat, high-fiber diets for 12 weeks. Diets 1 and 2 were high carbohydrate (55% of total energy intake), with high and low GIs, respectively; diets 3 and 4 were high protein (25% of total energy intake), with high and low GIs, respectively. The glycemic load was highest in diet 1 and lowest in diet 4. Changes in weight, body composition, and blood chemistry profile were studied. While all groups lost a similar mean +/- SE percentage of weight (diet 1, -4.2% +/- 0.6%; diet 2, -5.5% +/- 0.5%; diet 3, -6.2% +/- 0.4%; and diet 4, -4.8% +/- 0.7%; P = .09), the proportion of subjects in each group who lost 5% or more of body weight varied significantly by diet (diet 1, 31%; diet 2, 56%; diet 3, 66%; and diet 4, 33%; P = .01). Women on diets 2 and 3 lost approximately 80% more fat mass (-4.5 +/- 0.5 [mean +/- SE] kg and -4.6 +/- 0.5 kg) than those on diet 1 (-2.5 +/- 0.5 kg; P = .007). Mean +/- SE low-density-lipoprotein cholesterol levels declined significantly in the diet 2 group (-6.6 +/- 3.9 mg/dL [-0.17 +/- 0.10 mmol/L]) but increased in the diet 3 group (+10.0 +/- 3.9 mg/dL [+0.26 +/- 0.10 mmol/L]; P = .02). Goals for energy distribution were not achieved exactly: both carbohydrate groups ate less fat, and the diet 2 group ate more fiber. Both high-protein and low-GI regimens increase body fat loss, but cardiovascular risk reduction is optimized by a high-carbohydrate, low-GI diet.

Background: Phenolic compounds act as food antioxidants. One of the postulated mechanisms of action is chelation of prooxidant metals, such as iron. Although the antioxidative effect is desirable, this mechanism may impair the utilization of dietary iron. Objective: We sought to determine the effect of phenolic-rich extracts obtained from green tea or rosemary on nonheme-iron absorption. Design: Young women aged 19–39 y consumed test meals on 4 separate occasions. The meals were identical except for the absence (meal A) or presence (meal B) of a phenolic-rich extract from green tea (study 1; n = 10) or rosemary (study 2; n = 14). The extracts (0.1 mmol) were added to the meat component of the test meals. The meals were extrinsically labeled with either ⁵⁵Fe or ⁵⁹Fe and were consumed on 4 consecutive days in the order ABBA or BAAB. Iron absorption was determined by measuring whole-body retention of ⁵⁹Fe and the ratio of ⁵⁵Fe to ⁵⁹Fe activity in blood samples. Results: The presence of the phenolic-rich extracts resulted in decreased nonheme-iron absorption. Mean (±SD) iron absorption decreased from 12.1 ± 4.5% to 8.9 ± 5.2% (P < 0.01) in the presence of green tea extract and from 7.5 ± 4.0% to 6.4 ± 4.7% (P < 0.05) in the presence of rosemary extract. Conclusion: Phenolic-rich extracts used as antioxidants in foods reduce the utilization of dietary iron.