On December 17, 2018, the North American branch of the International Life Sciences Institute (ILSI North America) convened a workshop “Can We Begin to Define a Healthy Gut Microbiome Through Quantifiable Characteristics?” with >40 invited academic, government, and industry experts in Washington, DC. The workshop objectives were to 1) develop a collective expert assessment of the state of the evidence on the human gut microbiome and associated human health benefits, 2) see if there was sufficient evidence to establish measurable gut microbiome characteristics that could serve as indicators of “health,” 3) identify short- and long-term research needs to fully characterize healthy gut microbiome–host relationships, and 4) publish the findings. Conclusions were as follows: 1) mechanistic links of specific changes in gut microbiome structure with function or markers of human health are not yet established; 2) it is not established if dysbiosis is a cause, consequence, or both of changes in human gut epithelial function and disease; 3) microbiome communities are highly individualized, show a high degree of interindividual variation to perturbation, and tend to be stable over years; 4) the complexity of microbiome-host interactions requires a comprehensive, multidisciplinary research agenda to elucidate relationships between gut microbiome and host health; 5) biomarkers and/or surrogate indicators of host function and pathogenic processes based on the microbiome need to be determined and validated, along with normal ranges, using approaches similar to those used to establish biomarkers and/or surrogate indicators based on host metabolic phenotypes; 6) future studies measuring responses to an exposure or intervention need to combine validated microbiome-related biomarkers and/or surrogate indicators with multiomics characterization of the microbiome; and 7) because static genetic sampling misses important short- and long-term microbiome-related dynamic changes to host health, future studies must be powered to account for inter- and intraindividual variation and should use repeated measures within individuals.

Background: Fiber regulates the rate and site of lipid and carbohydrate digestion and absorption and thus can modify the alimentary responses to a meal. When fiber sources containing viscous polysaccharides are included in a meal, a slower rate of carbohydrate and lipid absorption will modify the alimentary hormone and lipid responses. Objective: We investigated in 11 healthy men the response of insulin, glucose, cholecystokinin, and lipid to 2 test meals containing ␤-glucan. Design: One of the meals was high in fiber (15.7 g) and the other meal was low in fiber (5.0 g). The low-fiber meal contained pasta made with wheat flour. The high-fiber meals contained pasta prepared by replacing 40% of the wheat with 2 types of barley flour: barley naturally high in ␤-glucan and the other a flour enriched in ␤-glucan during processing. Results: Plasma glucose and insulin concentrations increased significantly after all meals but the insulin response was more blunted after the barley-containing meals. The test meals were low in fat (25% of energy) but elicited an increase in plasma triacylglycerol and cholecystokinin. Cholecystokinin remained elevated for a longer time after the barley-containing meals. After the low-fiber meal, plasma cholesterol concentrations did not change significantly; however, 4 h after the barley-containing meals, the cholesterol concentration dropped below the fasting concentration and was significantly lower than that after the lowfiber meal. Conclusions: Carbohydrate was more slowly absorbed from the 2 high-fiber meals. Consumption of the barley-containing meals appeared to stimulate reverse cholesterol transport, which may contribute to the cholesterol-lowering ability of barley.Am J Clin Nutr 1999;69:55-63.

The concentration of triglyceride-rich lipoproteins containing apolipoprotein (apo) B-48 (chylomicrons) and apo B-100 (very low density lipoproteins) was measured in blood plasma of healthy young men after an ordinary meal containing one-third of daily energy and fat. Plasma obtained in the postabsorptive state and at intervals up to 12 hr after the meal was subjected to immunoaffinity chromatography against a monoclonal antibody to apo B-100 that does not bind apo B-48 and a minor fraction of apo B-100 rich in apo E. Measurements of the concentrations of components of the total and unbound triglyceride-rich lipoproteins separated from plasma by ultracentrifugation showed that about 80% of the increase in lipoprotein particle number was in very low density lipoproteins containing apo B-100 and only 20% was in chylomicrons containing apo B-48 that carry dietary fat from the intestine. The maximal increments and the average concentrations of apo B-48 and B-100 during the 12 hr were highly correlated (r2 = 0.80), suggesting that preferential clearance of chylomicron triglycerides by lipoprotein lipase leads to accumulation of hepatogenous very low density lipoproteins during the alimentary period. The composition of the bulk of very low density lipoproteins that were bound to the monoclonal antibody changed little and these particles contained about 90% of the cholesterol and most of the apo E that accumulated in triglyceride-rich lipoproteins. The predominant accumulation of very low density lipoprotein rather than chylomicron particles after ingestion of ordinary meals is relevant to the potential atherogenicity of postprandial lipoproteins.Most individuals spend 12 hr or more daily in an alimentary (postprandial) state during which dynamic remodeling of lipoprotein particles occurs. After the first meal of the day, the typical pattern of meal eating is likely to sustain a lipemic state throughout the day since the peak in triglyceride response is usually 3-4 hr after the meal (1-5). The increase in plasma triglycerides after a meal is derived from exogenous (dietary) and endogenous (hepatic) sources, as indicated by increased levels of apolipoprotein (apo) B-100 and B-48 in triglyceride-rich lipoproteins (TRL) (2-4). In humans, apo B-48 is derived from secretion of chylomicrons from the small intestine, whereas apo B-100 is predominantly associated with TRL made in the liver (6).Apo B-containing lipoproteins have been associated with risk of cardiovascular disease. However, the interrelationships among the various apo B-containing fractions and risk are complex. Remnants generated from chylomicrons as well as very low density lipoproteins (VLDL) are cleared by receptor-mediated processes in the liver (7). Since cholesteryl esters are transferred to TRL during the postprandial period, hepatic remnant uptake, in addition to delivering diet-derived lipids to the liver, is involved in reversecholesterol transport, which is thought to be an antiatherogenic process (8, 9). Alternatively, the TRL generated ...

Epidemiologic and clinical studies have shown that nut consumption is associated with favorable plasma lipid profiles and reduced cardiovascular risk. These effects may result from their high monounsaturated fat (MUFA) content but nuts contain constituents other than fatty acids that might be cardioprotective. We conducted a study to compare the effects of whole-almond vs. almond oil consumption on plasma lipids and LDL oxidation in healthy men and women. Using a randomized crossover trial design, 22 normolipemic men and women replaced half of their habitual fat (approximately 14% of approximately 29% energy) with either whole almonds (WA) or almond oil (AO) for 6-wk periods. Compliance was ascertained by monitoring dietary intake via biweekly 5-d food records, return of empty almond product packages and weekly meetings with a registered dietitian. Fat replacement with either WA and AO resulted in a 54% increase in percentage of energy as MUFA with declines in both saturated fat and cholesterol intake and no significant changes in total energy, total or polyunsaturated fat intake. The effects of WA and AO on plasma lipids did not differ compared with baseline; plasma triglyceride, total and LDL cholesterol significantly decreased, 14, 4 and 6% respectively, whereas HDL cholesterol increased 6%. Neither treatment affected in vitro LDL oxidizability. We conclude that WA and AO do not differ in their beneficial effects on the plasma lipid variables measured and that this suggests that the favorable effect of almonds is mediated by components in the oil fraction of these nuts.

The biological, chemical and physical properties of dietary fibers are associated with physiologic actions in the small and large intestine that have important metabolic implications for health. These properties of fiber include dispersibility in water, bulk, viscosity, adsorption and binding of compounds and fermentability. Dietary fructans share some of the properties of dietary fiber and thus are likely to have similar metabolic effects. Within the small intestine, properties such as dispersibility in water, bulking and viscosity are associated with slowing the digestion and absorption of carbohydrate and lipid and promoting nutrient absorption along a greater length of the small intestine. Both of these actions are related to cholesterol reduction and blunting of alimentary gylcemia. Although fructans are dispersible in water and will provide some bulk because they are nondigestible in the small intestine, they do not appear to be associated with significant increases in viscosity. Thus one would predict that any immediate effects on alimentary glycemia or on cholesterol reduction are likely to be modest compared with more viscous polysaccharides. Fermentability and bulking capacity of nondigestible carbohydrates define an essential role of fiber in maintaining gastrointestinal health. Within the large intestine, carbohydrates that are not digested in the small intestine are available for fermentation by the microflora present. Carbohydrates that are dispersible in the aqueous phase are more readily digested by microbes. A large body of evidence indicates that dietary fructans are digested in the large intestine, resulting in an increase in microbial mass and production of short-chain fatty acids.