No abstract

In the United States, intake of n-3 fatty acids is approximately 1.6 g/d ( approximately 0.7% of energy), of which 1.4 g is alpha-linolenic acid (ALA; 18:3) and 0.1-0.2 g is eicosapentaenoic acid (EPA; 20:5) and docosahexaenoic acid (DHA; 22:6). The primary sources of ALA are vegetable oils, principally soybean and canola. The predominant sources of EPA and DHA are fish and fish oils. Intake data indicate that the ratio of n-6 to n-3 fatty acids is approximately 9.8:1. Food disappearance data between 1985 and 1994 indicate that the ratio of n-6 to n-3 fatty acids has decreased from 12.4:1 to 10.6:1. This reflects a change in the profile of vegetable oils consumed and, in particular, an approximate 5.5-fold increase in canola oil use. The ratio of n-6 to n-3 fatty acids is still much higher than that recommended (ie, 2.3:1). Lower ratios increase endogenous conversion of ALA to EPA and DHA. Attaining the proposed recommended combined EPA and DHA intake of 0.65 g/d will require an approximately 4-fold increase in fish consumption in the United States. Alternative strategies, such as food enrichment and the use of biotechnology to manipulate the EPA and DHA as well as ALA contents of the food supply, will become increasingly important in increasing n-3 fatty acid intake in the US population.

Alpha-linolenic acid (ALA) reduces cardiovascular disease (CVD) risk, possibly by favorably changing vascular inflammation and endothelial dysfunction. Inflammatory markers and lipids and lipoproteins were assessed in hypercholesterolemic subjects (n = 23) fed 2 diets low in saturated fat and cholesterol, and high in PUFA varying in ALA (ALA Diet) and linoleic acid (LA Diet) compared with an average American diet (AAD). The ALA Diet provided 17% energy from PUFA (10.5% LA; 6.5% ALA); the LA Diet provided 16.4% energy from PUFA (12.6% LA; 3.6% ALA); and the AAD provided 8.7% energy from PUFA (7.7% LA; 0.8% ALA). The ALA Diet decreased C-reactive protein (CRP, P < 0.01), whereas the LA Diet tended to decrease CRP (P = 0.08). Although the 2 high-PUFA diets similarly decreased intercellular cell adhesion molecule-1 vs. AAD (-19.1% by the ALA Diet, P < 0.01; -11.0% by the LA Diet, P < 0.01), the ALA Diet decreased vascular cell adhesion molecule-1 (VCAM-1, -15.6% vs. -3.1%, P < 0.01) and E-selectin (-14.6% vs. -8.1%, P < 0.01) more than the LA Diet. Changes in CRP and VCAM-1 were inversely associated with changes in serum eicosapentaenoic acid (EPA) (r = -0.496, P = 0.016; r = -0.418, P = 0.047), or EPA plus docosapentaenoic acid (r = -0.409, P = 0.053; r = -0.357, P = 0.091) after subjects consumed the ALA Diet. The 2 high-PUFA diets decreased serum total cholesterol, LDL cholesterol and triglycerides similarly (P < 0.05); the ALA Diet decreased HDL cholesterol and apolipoprotein AI compared with the AAD (P < 0.05). ALA appears to decrease CVD risk by inhibiting vascular inflammation and endothelial activation beyond its lipid-lowering effects.

Background: Low-fat diets increase plasma triacylglycerol and decrease HDL-cholesterol concentrations, thereby potentially adversely affecting cardiovascular disease (CVD) risk. High-monounsaturated fatty acid (MUFA), cholesterol-lowering diets do not raise triacylglycerol or lower HDL cholesterol, but little is known about how peanut products, a rich source of MUFAs, affect CVD risk.Objective: The present study compared the CVD risk profile of an Average American diet (AAD) with those of 4 cholesterol-lowering diets: an American Heart Association/National Cholesterol Education ProgramStep II diet and 3 high-MUFA diets [olive oil (OO), peanut oil (PO), and peanuts and peanut butter (PPB)]. Design: A randomized, double-blind, 5-period crossover study design (n = 22) was used to examine the effects of the diets on serum lipids and lipoproteins: AAD [34% fat; 16% saturated fatty acids (SFAs), 11% MUFAs], Step II (25% fat; 7% SFAs, 12% MUFAs), OO (34% fat; 7% SFAs, 21% MUFAs), PO (34% fat; 7% SFAs, 17% MUFAs), and PPB (36% fat; 8% SFAs, 18% MUFAs). Results:The high-MUFA diets lowered total cholesterol by 10% and LDL cholesterol by 14%. This response was comparable with that observed for the Step II diet. Triacylglycerol concentrations were 13% lower in subjects consuming the high-MUFA diets and were 11% higher with the Step II diet than with the AAD. The high-MUFA diets did not lower HDL cholesterol whereas the Step II diet lowered it by 4% compared with the AAD. The OO, PO, and PPB diets decreased CVD risk by an estimated 25%, 16%, and 21%, respectively, whereas the Step II diet lowered CVD risk by 12%. Conclusion: A high-MUFA, cholesterol-lowering diet may be preferable to a low-fat diet because of more favorable effects on the CVD risk profile.Am J Clin Nutr 1999;70:1009-15. KEY WORDSPlasma triacylglycerol, HDL cholesterol, LDL cholesterol, monounsaturated fatty acids, dietary fat, peanuts, peanut products, Step II diet, cardiovascular disease, humans INTRODUCTIONDiet is the cornerstone of the prevention and treatment of cardiovascular disease (CVD). Currently, National Cholesterol Education Program/American Heart Association Step I or Step II diets are typically recommended for lowering blood cholesterol concentrations. The primary objective of these diets is to lower saturated fat (8-10% and < 7% of energy, respectively), cholesterol (300 or 200 mg/d), and total fat (< 30% of energy). Typically, a Step I diet lowers total cholesterol and LDL cholesterol by Ϸ5-7% (1-3). A Step II diet can lower total cholesterol and LDL cholesterol an additional 3-7% (1, 2). In these diets, saturated fat energy is replaced by carbohydrate, resulting in a low-fat, high-carbohydrate diet. Although these diets have beneficial effects on total cholesterol and LDL cholesterol, they increase plasma triacylglycerol concentrations and decrease HDL-cholesterol concentrations, thereby potentially adversely affecting CVD risk. This has caused some to question whether a Step I or Step II diet is the ideal diet for maximally reducing...

Step I and Step II dietary interventions have multiple beneficial effects on important cardiovascular disease risk factors.

Impressive progress has been made during the past 15 years in our understanding of the biology of somatotropin (ST) in domestic animals. In part, this progress was sparked by advances in biotechnology that made feasible the production of large quantities of recombinant bovine ST (bST) and porcine ST (pST). The availability of recombinant bST and pST resulted in an exponential increase in investigations that explored their role in growth and lactation biology, as well as evaluated their potential for commercial use. Collectively, these studies established that administration of bST to lactating dairy cows increased milk yield, and treatment of growing pigs with pST markedly stimulated muscle growth and reduced fat deposition. In addition to these "efficacy" studies, a substantial number of investigations examined the mechanisms by which ST affects lactation and growth of domestic animals. This review summarizes the diverse physiological effects ST has on growth and lactation and discusses the underlying mechanisms that mediate these effects in domestic animals.

No abstract

Increased intakes of dietary ALA elicit antiinflammatory effects by inhibiting IL-6, IL-1beta, and TNF-alpha production in cultured PBMCs. Changes in PBMC ALA and eicosapentaenoic acid (derived from dietary ALA) are associated with beneficial changes in TNF-alpha release. Thus, the cardioprotective effects of ALA are mediated in part by a reduction in the production of inflammatory cytokines.