Based on animal studies, epidemiologic studies and intervention trials, maternal folic acid is known to be protective for neural tube defects (NTD), primarily spina bifida and anencephalus. To reduce the risk of NTD, the U.S. Food and Drug Administration mandated that all enriched cereal grain products be fortified with folic acid as of January 1998. Recent data demonstrate that this public health action is associated with increased folate blood levels among U.S. women of childbearing age and that the national rate of spina bifida has decreased by 20%. Rates of anencephaly appear not to have declined. Epidemiologic data on use of folate and folate antagonists have also implicated folic acid in prevention of other birth defects such as facial clefts and cardiac and limb defects. Dietary folic acid is likely to be inadequate for maximal protection against NTD. Because about half of pregnancies in the U.S. are unplanned, according to the March of Dimes, birth defect prevention includes a recommended daily dose of 400 μg synthetic folic acid for women of childbearing age. Uniform compliance is estimated to decrease the incidence of NTD by up to 70%. This could reduce the overall incidence from 2 to 0.6 per 1000 pregnancies and prevent disease in ∼2000 babies per year in the U.S. Four thousand micrograms of folic acid per day is recommended for women with previous pregnancies affected by NTD.

There is substantial evidence to support an important role for zinc in immune processes. Adequate zinc status is essential for T-cell division, maturation and differentiation; lymphocyte response to mitogens; programmed cell death of lymphoid and myeloid origins; gene transcription; and biomembrane function. Lymphocytes are one of the types of cells activated by zinc. Zinc is the structural component of a wide variety of proteins, neuropeptides, hormone receptors and polynucleotides. Among the best known zinc-dependent hormones/enzymes are Cu, Zn superoxide dismutase, an enzyme component of the antioxidant defense system, and thymulin, which is essential for the formation of T-lymphocytes. In animals and humans, zinc deficiency results in rapid and marked atrophy of the thymus, impaired cell-mediated cutaneous sensitivity and lymphopenia. Primary and secondary antibody responses are reduced in zinc deficiency, particularly for those antigens that require T-cell help, such as those in heterologous red blood cells. In addition, antibody response and the generation of splenic cytotoxic T cells after immunization are reduced. Zinc also inhibits the production of tumor necrosis factor, which is implicated in the pathophysiology of cachexia and wasting in acquired immune deficiency syndrome.

Adequate folate and iron intake during pregnancy is critical for maternal and fetal health. No previous studies to our knowledge have reported dietary supplement use and folate status among pregnant women sampled in NHANES, a nationally representative, cross-sectional survey. We analyzed data on 1296 pregnant women who participated in NHANES from 1999 to 2006 to characterize overall supplement use, iron and folic acid use, and RBC folate status. The majority of pregnant women (77%) reported use of a supplement in the previous 30 d, most frequently a multivitamin/-mineral containing folic acid (mean 817 μg/d) and iron (48 mg/d). Approximately 55–60% of women in their first trimester reported taking a folic acid- or iron-containing supplement compared with 76–78% in their second trimester and 89% in their third trimester. RBC folate was lowest in the first trimester and differed by supplement use across all trimesters. Median RBC folate was 1628 nmol/L among users and 1041 nmol/L among nonusers. Among all pregnant women, median RBC folate increased with trimester (1256 nmol/L in the first, 1527 nmol/L in the second, and 1773 nmol/L in the third). Given the role of folic acid in the prevention of neural tube defects, it is notable that supplement use and median RBC folate was lowest in the first trimester of pregnancy, with 55% of women taking a supplement containing folic acid. Future research is needed to determine the reasons for low compliance with supplement recommendations, particularly folic acid, in early pregnancy.

Infection caused by HIV and malnutrition have a complex interaction and often coexist geographically. Malnutrition has synergistic immune effects and HIV affects nutritional status. HIV care and treatment programs are compelled to confront this dual burden to optimize HIV outcomes. In this article, we review the published literature concerning intervention studies in adults and children and the effect of food prices on HIV treatment programs. While the evidence base is relatively incomplete for specific macronutrient interventions in the context of HIV treatment, it is clear that a new standard of care is needed, guided by experience, rationale, and existing data, in which malnourished patients may easily access nutritional therapies within HIV treatment. From this clinical foundation, we may both treat patients and evaluate novel therapies. Some HIV care and treatment programs provide food-based supplements; however, rising food costs and economic instability may jeopardize the success of these programs. HIV treatment programs may struggle to meet the needs of patients with potential increased rates of malnutrition and food insecurity in the setting of high food prices.

Osteoporosis is a serious public health concern. Understanding the extent to which a bone density assessment affects change in dietary intake in postmenopausal women is needed. This study investigated whether results of bone density screening tests resulted in reported initiation or change in either dietary and/or supplemental calcium intake. Between 1997 and 2000, dual-energy X-ray absorptiometry (DXA) screening was conducted on 1468 postmenopausal women as part of an ancillary study of the Women's Health Initiative Observational Study in Buffalo, New York. One year after bone density testing, a questionnaire was sent to determine change in lifestyle behaviors and dietary intake. Participants included in this analysis were 923 Caucasian women who had not had a prior bone density screening test, reported no prior diagnosis of osteoporosis and were not taking medication (other than hormone therapy) for osteoporosis. Of these, according to WHO T-score criteria, 36% had osteoporosis, 48% had osteopenia, and 17% had normal bone density. Factors associated (P < 0.05) with increase in calcium intake in crude analyses included: BMI, follow-up consultation with a health care provider, and osteopenia or osteoporosis compared with normal T-score level. In multivariate adjusted analyses, both osteopenia [OR = 2.37, 95% CI (1.45–3.89); P = 0.001] and osteoporosis [OR = 3.86, 95% CI (2.30–6.46); P = <0.001] found on DXA were strong independent predictors of women's decision to start or increase calcium intake. This study provided evidence that the results of osteoporosis DXA screening influence postmenopausal women's decisions to increase calcium intake.

There is evidence for the role of genetic and environmental factors in feline and canine diabetes. Type 2 diabetes is the most common form of diabetes in cats. Evidence for genetic factors in feline diabetes includes the overrepresentation of Burmese cats with diabetes. Environmental risk factors in domestic or Burmese cats include advancing age, obesity, male gender, neutering, drug treatment, physical inactivity, and indoor confinement. High-carbohydrate diets increase blood glucose and insulin levels and may predispose cats to obesity and diabetes. Low-carbohydrate, high-protein diets may help prevent diabetes in cats at risk such as obese cats or lean cats with underlying low insulin sensitivity. Evidence exists for a genetic basis and altered immune response in the pathogenesis of canine diabetes. Seasonal effects on the incidence of diagnosis indicate that there are environmental influences on disease progression. At least 50% of diabetic dogs have type 1 diabetes based on present evidence of immune destruction of β-cells. Epidemiological factors closely match those of the latent autoimmune diabetes of adults form of human type 1 diabetes. Extensive pancreatic damage, likely from chronic pancreatitis, causes ∼28% of canine diabetes cases. Environmental factors such as feeding of high-fat diets are potentially associated with pancreatitis and likely play a role in the development of pancreatitis in diabetic dogs. There are no published data showing that overt type 2 diabetes occurs in dogs or that obesity is a risk factor for canine diabetes. Diabetes diagnosed in a bitch during either pregnancy or diestrus is comparable to human gestational diabetes.