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Genomics and bioinformatics have the vast potential to identify genes that cause disease by investigating whole-genome databases. Comparison of an individual's geno-type with a genomic database will allow the prescription of drugs to be tailored to an individual's genotype. This same bioinformatic approach, applied to the study of human metabolites, has the potential to identify and validate targets to improve personalized nutritional health and thus serve to define the added value for the next generation of foods and crops. Advances in high-throughput analytic chemistry and computing technologies make the creation of a vast database of metabolites possible for several subsets of metabolites, including lipids and organic acids. In creating integrative databases of metabolites for bioinformatic investigation, the current concept of measuring single biomarkers must be expanded to 3 dimensions to 1) include a highly comprehensive set of metabolite measurements (a profile) by multiparallel analyses, 2) measure the metabolic profile of individuals over time rather than simply in the fasted state, and 3) integrate these metabolic profiles with genomic, expression, and proteomic databases. Application of the knowledge of individual metabolism will revolutionize the ability of nutrition to deliver health benefits through food in the same way that knowledge of genomics will revolutionize individual treatment of dis-ease with pharmaceuticals. Copyright © 2001 American Society for Clinical Nutrition [ABSTRACT FROM AUTHOR]

The goal of this investigation was to determine whether participation in an atherosclerosis treatment program would reduce the oxidative susceptibility of LDL from patients with coronary artery disease. The treatment program included intensive exercise therapy, stress management, and consumption of a diet containing 10% fat. The size and antioxidant and lipid contents of LDL particles from 25 patients were analyzed at baseline and after 3 mo of therapy. The susceptibility of LDL to copper-mediated oxidation was measured by a conjugated diene assay and headspace gas chromatography (HSGC). Atherosclerosis treatment significantly reduced plasma total cholesterol and apolipoprotein B concentrations and the molar ratio of LDL cholesterol ester to apolipoprotein B (P < 0.01). The LDL content of alpha-tocopherol and beta-carotene was increased (27% and 17%, respectively, P < 0.04) and the molar ratio of LDL cholesterol ester the sum of LDL alpha-tocopherol and LDL beta-carotene decreased from 159 at baseline to 122 at 3 mo (P < 0.01). The lag phase of LDL conjugated diene formation increased 24%, whereas the maximum rate of oxidation slowed 29% (P < 0.01). As assessed by HSGC, copper-catalyzed formation of volatile lipid oxidation products was reduced 15% (P < 0.007); the reduction in volatiles was correlated with an increase in the alpha-tocopherol content of LDL (r=-0.48, P < 0.01). The principal determinants of reduced LDL oxidative susceptibility were the particle contents of alpha-tocopherol and beta-carotene. To our knowledge, this is the first report to document a reduction in LDL oxidation in coronary artery disease patients undergoing atherosclerosis-reversal therapy. Copyright (c) 1998 American Society for Clinical Nutrition [ABSTRACT FROM AUTHOR]

Lactation biology, microbial selection, and human diversity are central themes that could guide investment in scientific research, industrial innovation, and regulatory policy oversight to propel yogurt into the central role for health-promoting food products. The ability of yogurt to provide the nourishing properties of milk together with the live microorganisms from fermentation provides a unique combination of food assets. Academic research must now define the various targets on which these biological assets act to improve health and develop the metrics that can quantitatively document their benefits. The food industry must reconcile that yogurt and its microorganisms cannot be expected to provide measurable benefits for all consumers, at all doses, and at all times. A supportive regulatory oversight must demand safety and yet encourage innovations that support a value proposition for yogurt in health. Health valuation in the marketplace will be driven by parallel innovations, including accurate assessment technologies, validated microbial ingredients, and health-aware consumers.

Background: The consumption of monounsaturated trans fatty acids (TFAs) increases the risk of cardiovascular disease (CVD). Putative differences between the effects of TFAs from industrially produced and natural sources on CVD risk markers were not previously investigated in healthy subjects., Objective: We aimed to compare the effects of TFAs from industrially produced and natural sources on HDL and LDL cholesterol, lipoprotein particle size and distribution, apolipoproteins, and other lipids in healthy subjects., Design: In a randomized, double-blind, controlled, crossover design, 46 healthy subjects (22 men and 24 women) consumed food items containing TFAs (11-12 g/d, representing approximately 5% of daily energy) from the 2 sources., Results: Forty subjects (19 men and 21 women) completed the study. Compared with TFAs from industrially produced sources, TFAs from natural sources significantly (P = 0.012) increased HDL cholesterol in women but not in men. Significant (P = 0.001) increases in LDL-cholesterol concentrations were observed in women, but not in men, after the consumption of TFAs from natural sources. Apolipoprotein (apo)B and apoA1 concentrations confirmed the changes observed in LDL and HDL cholesterol. Analysis of lipoprotein subclass showed that only large HDL and LDL concentrations were modified by TFAs from natural sources but not by those from industrially produced sources., Conclusions: This study shows that TFAs from industrially produced and from natural sources have different effects on CVD risk factors in women. The HDL cholesterol-lowering property of TFAs seems to be specific to industrial sources. However, it is difficult in the present study to draw a conclusion about the effect of TFAs from either source on absolute CVD risk in these normolipidemic subjects. The mechanism underlying the observed sex- and isomer-specific effects warrants further investigation.

Like other life sciences, nutrition science can benefit enormously from the techniques of bioinformatics. In this article, the steps necessary to enable bioinformatic approaches in nutrition research are outlined, from the short-range goal of immediately making data available in ad hoc author-defined formats to the longer range goals of full standardization of nutrition experiments and migration of all experimental data into databases. Several examples of what will be possible for nutrition researchers in this new paradigm are described. Ultimately, nutrition data can be continually recycled to reinvestigate existing hypotheses and to generate new hypotheses that would not have been conceivable at the time of the original experiments. The standardization of experimental designs and the conversion of nutrition data into a machine-readable format will bring about a renaissance in nutrition research, accelerating the ability of investigators to discover the implications of nonessential nutrients and food components, and enable the study of complex metabolic interactions in human health and disease.

Nonalcoholic fatty liver disease (NAFLD) is a significant health problem and affects 70 million adults in the United States (30% of the adult population), and an estimated 20% of these individuals have the most severe form of NAFLD-nonalcoholic steatohepatitis (NASH). The mechanisms underlying disease development and progression are awaiting clarification. Insulin resistance and obesity-related inflammation, among other possible genetic, dietary, and lifestyle factors, are thought to play a key role. A program targeting gradual weight reduction and physical exercise continues to be the gold standard of treatment for all forms of NAFLD. Even though weight loss and dietary and lifestyle changes are recommended as primary treatment for fatty liver, little to no scientific evidence is available on diet and NAFLD. This article reviews the implications of current dietary approaches, including national guidelines and popular weight-loss diets, with a focus on determining the optimal diet to prescribe for NAFLD and NASH patients. The effects of macronutrient content (carbohydrate, fat, and protein ratios) and specific food components, such as soluble fiber, n-3 fatty acids, and fructose, are discussed. The premises, effects, barriers, and issues related to current dietary guidelines and specific diets are discussed, and the question, "Will it work for the pathogenesis of NAFLD and NASH? ", is addressed.

Public health recommendations for the US population in 1977 were to reduce fat intake to as low as 30% of calories to lower the incidence of coronary artery disease. These recommendations resulted in a compositional shift in food materials throughout the agricultural industry, and the fractional content of fats was replaced principally with carbohydrates. Subsequently, high-carbohydrate diets were recognized as contributing to the lipoprotein pattern that characterizes atherogenic dyslipidemia and hypertriacylglycerolemia. The rising incidences of metabolic syndrome and obesity are becoming common themes in the literature. Current recommendations are to keep saturated fatty acid, trans fatty acid, and cholesterol intakes as low as possible while consuming a nutritionally adequate diet. In the face of such recommendations, the agricultural industry is shifting food composition toward lower proportions of all saturated fatty acids. To date, no lower safe limit of specific saturated fatty acid intakes has been identified. This review summarizes research findings and observations on the disparate functions of saturated fatty acids and seeks to bring a more quantitative balance to the debate on dietary saturated fat. Whether a finite quantity of specific dietary saturated fatty acids actually benefits health is not yet known. Because agricultural practices to reduce saturated fat will require a prolonged and concerted effort, and because the world is moving toward more individualized dietary recommendations, should the steps to decrease saturated fatty acids to as low as agriculturally possible not wait until evidence clearly indicates which amounts and types of saturated fatty acids are optimal?

Background: Polyphenolic phytochemicals inhibit vascular and inflammatory processes that contribute to disease. These effects are hypothesized to result from polyphenol-mediated alterations in cellular eicosanoid synthesis., Objective: The objective was to determine and compare the ability of cocoa procyanidins to alter eicosanoid synthesis in human subjects and cultured human aortic endothelial cells., Design: After an overnight fast, 10 healthy subjects (4 men and 6 women) consumed 37 g low-procyanidin (0.09 mg/g) and high-procyanidin (4.0 mg/g) chocolate; the treatments were separated by 1 wk. The investigation had a randomized, blinded, crossover design. Plasma samples were collected before treatment and 2 and 6 h after treatment. Eicosanoids were quantitated by enzyme immunoassay. Endothelial cells were treated in vitro with procyanidins to determine whether the effects of procyanidin in vivo were associated with procyanidin-induced alterations in endothelial cell eicosanoid synthesis., Results: Relative to the effects of the low-procyanidin chocolate, high-procyanidin chocolate induced increases in plasma prostacyclin (32%; P<0.05) and decreases in plasma leukotrienes (29%; P<0.04). After the in vitro procyanidin treatments, aortic endothelial cells synthesized twice as much 6-keto-prostaglandin F(1alpha) (P<0.01) and 16% less leukotriene (P<0.05) as did control cells. The in vitro and in vivo effects of procyanidins on plasma leukotriene-prostacyclin ratios in culture medium were also comparable: decreases of 58% and 52%, respectively., Conclusion: Data from this short-term investigation support the concept that certain food-derived flavonoids can favorably alter eicosanoid synthesis in humans, providing a plausible hypothesis for a mechanism by which they can decrease platelet activation in humans.

Background: Red wine consumption may decrease the risk of coronary heart disease through the actions of its constituent flavonoids. (+)-Catechin is an abundant flavonoid in red wine., Objective: The objective was to determine changes in plasma (+)-catechin concentrations after ingestion of a single, moderate serving of dealcoholized red wine reconstituted with either water (DRW) or water and alcohol (ARW)., Design: Nine subjects (5 men, 4 women) ingested, in random order, 120 mL DRW on one day and 120 mL ARW on another day. Both the DRW and ARW contained 35 mg (121 micromol) free (+)-catechin. Blood samples were collected at 0, 0.5, 1, 2, 3, 4, and 8 h. Plasma was analyzed by gas chromatography-mass spectrometry for (+)-catechin after enzymatic release of sulfate and glucuronide conjugates., Results: Calcium ions were needed to effectively hydrolyze (+)-catechin conjugates in plasma containing EDTA. Neither the ARW or DRW nor sex affected the area under the curve at 8 h, the maximum concentration (c(max)), or the time it took for plasma total (+)-catechin to reach maximum concentration (t(max)). Pooled mean (+/-SEM) values for the ARW and DRW were as follows: area under the curve, 306.1 +/- 29.5 nmol*h/L; c(max), 76.7 +/- 7.5 nmol/L; and t(max), 1.44 +/- 0.13 h. The half-life of (+)-catechin in plasma was significantly less (P = 0.038) after ingestion of the ARW (3.17 h) than after ingestion of the DRW (4.08 h)., Conclusions: Increases in plasma total (+)-catechin concentrations were not significantly different after single moderate servings of either the ARW or DRW. Alcohol in the ARW hastened the elimination of (+)-catechin from the plasma compartment. (+)-Catechin elimination may represent excretion or conversion to methylated derivatives.