Studies reporting blood levels of the omega-3 polyunsaturated fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), were systematically identified in order to create a global map identifying countries and regions with different blood levels. Included studies were those of healthy adults, published in 1980 or later. A total of 298 studies met all inclusion criteria. Studies reported fatty acids in various blood fractions including plasma total lipids (33%), plasma phospholipid (32%), erythrocytes (32%) and whole blood (3.0%). Fatty acid data from each blood fraction were converted to relative weight percentages (wt.%) and then assigned to one of four discrete ranges (high, moderate, low, very low) corresponding to wt.% EPA+DHA in erythrocyte equivalents. Regions with high EPA+DHA blood levels (>8%) included the Sea of Japan, Scandinavia, and areas with indigenous populations or populations not fully adapted to Westernized food habits. Very low blood levels (≤4%) were observed in North America, Central and South America, Europe, the Middle East, Southeast Asia, and Africa. The present review reveals considerable variability in blood levels of EPA+DHA and the very low to low range of blood EPA+DHA for most of the world may increase global risk for chronic disease.

A systematic review was used to identify randomized controlled trials (RCTs) and observational epidemiologic studies (OBSs) that examined protein intake consistent with either the US RDA (0.8 g/kg or 10–15% of energy) or a higher protein intake (≥20% but <35% of energy or ≥10% higher than a comparison intake) and reported measures of kidney function. Studies (n = 26) of healthy, free-living adults (>18 y old) with or without metabolic disease risk factors were included. Studies of subjects with overt disease, such as chronic kidney, end-stage renal disease, cancer, or organ transplant, were excluded. The most commonly reported variable was glomerular filtration rate (GFR), with 13 RCTs comparing GFRs obtained with normal and higher protein intakes. Most (n = 8), but not all (n = 5), RCTs reported significantly higher GFRs in response to increased protein intake, and all rates were consistent with normal kidney function in healthy adults. The evidence from the current review is limited and inconsistent with regard to the role of protein intake and the risk of kidney stones. Increased protein intake had little or no effect on blood markers of kidney function. Evidence reported here suggests that protein intake above the US RDA has no adverse effect on blood pressure. All included studies were of moderate to high risk of bias and, with the exception of 2 included cohorts, were limited in duration (i.e. <6 mo). Data in the current review are insufficient to determine if increased protein intake from a particular source, i.e., plant or animal, influences kidney health outcomes. These data further indicate that, at least in the short term, higher protein intake within the range of recommended intakes for protein is consistent with normal kidney function in healthy individuals.

Dietary exposure to potentially high‐risk compounds such as heterocyclic aromatic amines (HAAs) or the polycyclic aromatic hydrocarbon, benzo[a]pyrene (BaP), formed in meat during cooking, or from exposure to hemeiron naturally occurring in meat, have all been proposed as possible mechanisms responsible for the reported weak association between red and processed meat consumption and increased cancer risk in observational studies. In this study, a systematic review of the mechanistic literature was used to examine the available evidence‐base to determine if sufficient evidence exists to link heme iron, BaP, or HAAs from red and processed meat to increased cancer risk. Inclusion criteria required that study designs accommodate exposure from a whole food or in the context of a well‐described diet and that outcomes adequately represent normal physiology of the tissue of interest. Results regarding dietary Ba Prevealed, of 51 studies published since 2000, only 4 met the full criteria for inclusion. The primary reasons for study exclusion were a failure to evaluate effects of BaP administered orally or as part of a diet and a failure to adequately represent non‐cancerous tissue physiology. Regarding dietary HAAs, of 294studies published since 2000, 29 publications met the full criteria for inclusion. Only 3 of the included studies utilized an animal model to investigate HAA intake from foods or as part of a well‐described diet and only one type of HAA was evaluated in the included animal studies. In the human studies there was near‐exclusive use of a single, non‐comprehensive database, rather than actual and/or direct analytical measurement of dietary HAAs. And regarding dietary heme iron, of 210 search results since 2000, only 13publications met the full criteria for inclusion. The type of heme iron supplemented in animal diets, as surrogates for naturally occurring heme iron, were found to independently affect the outcomes in some studies. The use of hemeiron surrogates has not been systematically validated against naturally occurring heme iron. For all compounds, the exclusive use of carcinogen‐treated animals was questioned as well as the use of in vitro cytotoxicity assays as surrogates for normal colon physiology. In each case, evidence was found to be weak and inadequate in both humans and animals concerning the mechanistic relationship between the dietary exposures of BaP, HAAs, or heme iron and human cancer.Support or Funding InformationSupport from the Beef Checkoff