Several preventive strategies to reduce dyslipidemia have been suggested, of which dietary modification features as an important one. Dyslipidemia is a major risk factor for coronary heart disease and strategies to manage dyslipidemia have been shown to reduce the incidence of cardiovascular disease (CVD). Although there are proven pharmacological therapies to help manage this condition, nutritional interventions are a safer option to help prevent and manage dyslipidemia. Addition of almonds in the daily diet has been proposed to beneficially impact the lipid profile. This review critically examines the available evidence assessing the effect of almonds on dyslipidemia in the South Asian (particularly Indian) context. An extensive review comprised of epidemiological studies, clinical trials, meta-analyses, and systematic reviews was conducted from published literature from across the world. Studies examining the effect of almonds on different aspects of dyslipidemia viz. high low-density lipoprotein-cholesterol (LDL-C), low high-density lipoprotein-cholesterol (HDL-C), triglyceridaemia, and high total cholesterol levels have been included. In several studies, almonds have been shown to reduce LDL-C—which is a known risk factor for CHD—and the effect of almonds has been well documented in systematic reviews and meta-analysis of clinical trials. Addition of almonds in the diet has been shown to not only to reduce LDL-C levels, but also to maintain HDL-C levels. This review provides information about the use of this simple nutritional strategy which may help manage known major risk factors for heart disease, such as high LDL-C and low HDL-C levels especially in the context of South Asians.

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Objective: To study the effect of infection on iron status in children suffering from acute, mild or severe respiratory infections and to determine the nature of anemia in infection using serum transferrin receptor (sTfR) levels. Design: Forty-three children aged between 3 and 5 y with no evidence of infection and receiving iron supplements in the preceding 100 days served as controls. Twenty-one children with mild upper respiratory infection and 94 children hospitalized for acute pneumonia constituted the experimental group. Hemoglobin (Hb), sTfR and serum ferritin were estimated in all the children at the time of diagnosis and again on the 15th and 30th days after the infection in those who were available for followup. Results: Mean (95% CI) sTfR was 6.08 (5.1 -7.1) mg=l in healthy non-anemic children. Upper respiratory infection had no impact on Hb or sTfR but it significantly elevated serum ferritin levels. Eighty-three percent of the children with pneumonia had Hb less than 110 g=l at the time of diagnosis and had elevated mean sTfR, 18.0 (15.7 -20.3) mg=l. There was a decline in mean sTfR by the 15th day of infection to 14.3 (11.3 -17.4) mg=l with further rise to 22.9 (13.0 -31.9) mg=l by 30 days. Serum ferritin was significantly elevated at the time of diagnosis (85.9; 71.1 -100.8 mg=l) as well as at 15 days (89.1; 68 -110.1 mg=l) with a decline by 30 days. Conclusions: Severe lower respiratory infection exaggerates iron-deficient erythropoiesis by blocking release of iron from the storage pools. sTfR may not be a sensitive and specific tool of assessing true iron status of children exposed to severe infections.

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