The purpose of the present study was to determine the time course of changes in in vitro lipolysis and in perilipin content (Western blot) in the mesenteric and/or the retroperitoneal fat depots in relation to the development of hepatic steatosis in high-fat diet-fed rats. Female Sprague-Dawley rats were submitted to a high-fat diet (HF diet; 42% as kJ) or a standard diet (SD diet) for 1, 2, 3 or 8 weeks. Fat accretion in the mesenteric and retroperitoneal tissues was higher (P<0·01) in HF diet-fed than in SD diet-fed rats as soon as 1 week after the beginning of the diet. Liver triacylglycerol concentrations were significantly (P<0·01) higher in HF diet-fed than in SD diet-fed rats throughout the experiment, the highest values being reached at week 2 of the diet. Basal and stimulated lipolysis (10−4 to 10−7m-isoproterienol) in the mesenteric and retroperitoneal fat depots was not changed during the first 3 weeks, regardless of the diet. Lipolysis in the mesenteric adipose tissue in the basal and stimulated states was, however, higher (P<0·01) in HF diet-fed than in SD diet-fed rats after 8 weeks of the diets. There were no significant (P>0·05) effects of diet and time on perilipin content of mesenteric tissue. In spite of a rapid fat accretion, the present results do not provide any evidence of a rapid (3 weeks) increase in in vitro lipolysis in intra-abdominal fat depots upon the undertaking of an HF diet at a time where liver lipid infiltration is the most significant.

A diet rich in fruits, vegetables and minimally refined cereals is associated with lower risk for chronic degenerative diseases. Since oxidative stress is common in chronic degenerative disease, it has been assumed that dietary antioxidants may explain this protective effect. Every dietary plant contains numerous types of antioxidants with different properties. Many of these antioxidants cooperate in oxidative stress reduction in plants, and we hypothesize that many different antioxidants may also be needed for the proper protection of animal cells. To test this hypothesis, it is useful to identify dietary plants with high total antioxidant content. Several nuts are among the dietary plants with the highest content of total antioxidants. Of the tree nuts, walnuts, pecans and chestnuts have the highest contents of antioxidants. Walnuts contain more than 20 mmol antioxidants per 100 g, mostly in the walnut pellicles. Peanuts (a legume) also contribute significantly to dietary intake of antioxidants. These data are in accordance with our present extended analysis of an earlier report on nut intake and death attributed to various diseases in the Iowa Women's Health Study. We observed that the hazard ratio for total death rates showed a U-shaped association with nut/peanut butter consumption. Hazard ratio was 0·89 (CI =0·81–0·97) and 0·81 (CI =0·75–0·88) for nut/peanut butter intake once per week and 1–4 times per week, respectively. Death attributed to cardiovascular and coronary heart diseases showed strong and consistent reductions with increasing nut/peanut butter consumption. Further studies are needed to clarify whether antioxidants contribute to this apparent beneficial health effect of nuts.

Adult female Sprague–Dawley rats were fed ad libitum during pregnancy and lactation a control diet (CD; 16·1 kJ/g) or a low-energy diet with wheat gluten as the main protein source (LED; 13·3 kJ/g). Body weight, food intake, resting energy expenditure, respiratory quotient and substrate use by the mammary gland were measured. After the animals had been killed, the parametrial and retroperitoneal fat pads were weighed. The mean food intake (g) of the two groups of rats was similar, resulting in a lower energy intake by the LED rats, significantly different during the last 2 weeks of lactation. The mean body weight of both dams and pups in the LED group was lower, starting at day 9 of lactation. The resting energy expenditure increased gradually during lactation in the control group, whereas this increase was not seen in rats of the LED group in the last week of lactation. Rats that had fasted overnight had a respiratory quotient of 0·7 or less, whereas for rats that had been fed, the mean respiratory quotient was over 1·0. Under both conditions, rats showed ketonuria. The arteriovenous difference in 3-hydroxybutyrate level was higher and those for glucose, lactate and triacylglycerol were lower across the mammary glands of LED rats. The parametrial fat depot weighed less in LED rats. Reducing the increase in resting energy expenditure and using ketone bodies to a greater extent as fuels may represent important mechanisms in the LED dams to cover the energy cost of milk production.

A voluminous body of epidemiological research concerning the potential role of antioxidant nutrients in the prevention of cancers has accumulated over the past few decades. However, results of large recent intervention trials do not support a preventive effect against cancer for supplementation with antioxidant nutrients. Seemingly contradictory results between observational studies and randomised trials can be explained by the fact that doses used in clinical trials were much higher than the highest levels attained by the usual dietary intake which, in observational studies, were found to be associated with the lowest risk of cancer. Recently, the Supplementation en Vitamines et Mine´raux Antioxydants (SU.VI.MAX) study, a randomised, double-blind, placebo-controlled primary prevention trial, tested the efficacy of supplementation with a combination of antioxidant vitamins and minerals, at nutritional doses, in reducing the cancer incidence in a general population not selected for risk factors. After 7·5 years, low-dose antioxidant supplementation lowered the total cancer incidence in men only. This may be explained by a lower baseline status of certain antioxidants in men compared to women. Finally, the effect of antioxidant supplementation on the incidence of cancer could depend on baseline antioxidant status (which differs from gender and/or nutritional status) and the health status of subjects (healthy v. cancer high-risk subjects). Antioxidant supplementation may have a beneficial effect upon cancer incidence only in healthy subjects who are not exposed to cancer risk and who have a particularly low baseline status. High doses of antioxidant supplementation may be deleterious in subjects in whom the initial phase of cancer development has already started, and they could be ineffective in well-nourished subjects with adequate antioxidant status.

Large-bowel fermentation of resistant starch produces SCFA that are believed to be important in maintaining visceral function. High-amylose maize starch (HAMS) and acylated starches are sources of resistant starch and are an effective means of increasing colonic SCFA. Cooking increases digestibility of starches but its effects on the capacity of these starches to raise large-bowel SCFA are unknown. We have examined the effects of cooking of HAMS and butyrylated HAMS (HAMSB) on amylolysis in vitro and their capacity to raise caeco-colonic SCFA in rats. The starches were boiled in excess water and microwaved, followed by drying at 100°C. Cooking increased in vitro glucose release for both starches but significantly less from HAMSB. Rat growth rates were unaffected when fed cooked resistant starch. Digesta pH was increased in the caecum and proximal colon of rats fed cooked HAMS. Distal colonic pH was highest in rats fed cooked HAMSB. Factorial analyses (2×2) of caecal SCFA pools showed significant differences between HAMS and HAMSB, and that cooking significantly lowered caecal butyrate pools. Portal venous butyrate concentrations were higher in both HAMSB groups than those fed HAMS. The data suggest that HAMSB is less susceptible to in vitro amylolysis than HAMS following cooking and delivers more butyrate to rat caecum than HAMS. This attribute may be useful in food applications for specific delivery of SCFA to the colon. Preparation of carbohydrates to simulate human food in animal experiments may be important to assess nutritional and physiological effects accurately.

It is known that various dietary plant proteins are capable of influencing the lipid metabolism of human subjects and animals when compared with casein. Less, however, is known about the effects of fish protein on the cholesterol and triacylglycerol metabolism. Therefore, two experiments were conducted in which rats were fed diets containing 200 g of either fish protein, prepared from Alaska pollack fillets, or casein, which served as control, per kilogram, over 20 and 22 d, respectively. As parameters of lipid metabolism, the concentrations of cholesterol and triacylglycerols in the plasma and liver, the faecal excretion of bile acids and the hepatic expression of genes encoding proteins involved in lipid homeostasis were determined. In both experiments, rats fed fish protein had higher concentrations of cholesteryl esters in the liver, a lower concentration of cholesterol in the HDL fraction (ρ>1·063 kg/l) and lower plasma triacylglycerol concentrations than rats fed casein (P<0.05). The gene expression analysis performed in experiment 2 showed that rats fed fish protein had higher relative mRNA concentrations of sterol regulatory element-binding protein (SREBP)-2, 3-hydroxy-3-methylglutaryl coenzyme A reductase, LDL receptor, apo AI, scavenger receptor B1 and lecithin-cholesterol-acyltransferase in their liver than did rats fed casein (P<0·05). The faecal excretion of bile acids and the mRNA concentrations of cholesterol 7α-hydroxylase, SREBP-1c and corresponding target genes were not altered. These findings show that fish protein had multiple effects on plasma and liver lipids that were at least in part caused by an altered expression of the hepatic genes involved in lipid homeostasis.

This study investigated the effects of fish oil (FO) diet on plasma intercellular adhesion molecule 1 (ICAM-1) levels and leucocyte integrin expression in polymicrobial sepsis. Mice were randomly assigned to a control group and an FO group. The control group was fed a medium-fat diet containing soyabean oil, whereas in the FO group, 70 % of the soyabean oil was replaced by FO for 3 weeks. After that, sepsis was induced by caecal ligation and puncture (CLP) in the experimental groups and mice were killed at 0, 6, 12 and 24 h, respectively, after CLP. Results showed that compared with the control group, plasma ICAM-1 levels were higher in the FO group 6 h after CLP. Intra-lymphocyte interferon-γ expression in the FO group was lower, whereas IL-4 expression was higher than in the control group 12 and 24 h after CLP. The expression of leucocyte integrin was significantly higher in the FO group 12 and 24 h after CLP. The FO group had higher IL-6 levels at 12 h in the lungs, at 6 and 12 h in the kidneys, and at 6, 12 and 24 h in the intestines after CLP. The survival rate did not differ between the two groups after CLP. The present findings suggest that pretreatment with an FO diet enhances adhesion molecule and inflammatory cytokine expressions during sepsis, which might aggravate the inflammatory reaction and increase neutrophil infiltration into tissues. In addition, FO diet promotes the Th2-type response and suppresses cellular immune response in polymicrobial sepsis.

We have recently reported that xanthine oxidase is involved in the generation of free radicals in exhaustive exercise. Allopurinol, an inhibitor of xanthine oxidase, prevents it. The aim of the present work was to elucidate the role of exercise-derived reactive oxygen species in the cell signalling pathways involved in the adaptation to exercise in man. We have found that exercise causes an increase in the activity of plasma xanthine oxidase and an activation of NF-κB in peripheral blood lymphocytes after marathon running. This activation is dependent on free radical formation in exercise: treatment with allopurinol completely prevents it. In animal models, we previously showed that NF-κB activation induced by exhaustive physical exercise leads to an increase in the expression of superoxide dismutase, an enzyme involved in antioxidant defence. We report evidence in man that reactive oxygen species act as signals in exercise as decreasing their formation prevents activation of important signalling pathways which can cause useful adaptations in cells.

Six subjects exercised for 120;min on a cycle ergometer (65 (se 3) % V˙O2max) when ingesting a placebo or glucose, fructose or galactose (100g in 1000 ml water) labelled with 13C. The oxidation of energy substrates including exogenous hexoses was compared using indirect respiratory calorimetry and 13CO2 production at the mouth. Total carbohydrate progressively decreased and total fat oxidation increased over the 120min exercise period in the four experimental situations. During the 120min of exercise, the amount of fructose oxidized (38·8 (se 2·6) g; 9·0 (se 0·6)% energy yield) was not significantly (approximately 4%) lower than that of exogenous glucose (40·5 (se 3·4) g; 9·2 (se 0·8)% energy yield), while that of galactose (23·7 (se 3·5) g; 5·5 (se 0·9) % energy yield) was only 59% and 61% that of glucose and fructose, respectively. When compared with the placebo, the ingestion and oxidation of the three hexoses did not significantly modify fat oxidation or total carbohydrate oxidation, but it significantly reduced (9–13%) endogenous carbohydrate oxidation. The present data indicate that fructose and exogenous glucose ingested during exercise could be oxidized at a similar rate, but that the oxidation rate of galactose was only approximately 60% that of the exogenous glucose and fructose, presumably because of a preferential incorporation of galactose into liver glycogen (Leloir pathway). The reduction in endogenous carbohydrate oxidation was, however, similar with the three hexoses.

Glycaemic index (GI) values for fourteen commonly eaten carbohydrate-rich foods processed by various methods were determined using ten healthy subjects. The foods studied were round leaf yellow yam (Dioscorea cayenensis), negro and lucea yams (Dioscorea rotundata), white and sweet yams (Dioscorea alata), sweet potato (Solanum tuberosum), Irish potato (Ipomoea batatas), coco yam (Xanthosoma spp.), dasheen (Colocasia esculenta), pumpkin (Cucurbita moschata), breadfruit (Artocarpus altilis), green banana (Musa sapientum), and green and ripe plantain (Musa paradisiaca). The foods were processed by boiling, frying, baking and roasting where applicable. Pure glucose was used as the standard with a GI value of 100. The results revealed marked differences in GI among the different foods studied ranging from 35 (se 3) to 94 (se 8). The area under the glucose response curve and GI value of some of the roasted and baked foods were significantly higher than foods boiled or fried (P<0·05). The results indicate that foods processed by roasting or baking may result in higher GI. Conversely, boiling of foods may contribute to a lower GI diet.

Strength training is usually associated with a reduction in fat mass and with muscle hypertrophy. The aim of the present study was to examine whether the serum free leptin index (FLI), measured by the molar excess of soluble leptin receptor (sOB-R) over leptin, is increased by 6 weeks of strength training. Eighteen male, physical education students were randomly assigned to two groups: a strength-training (n 12) and a control group (n 6). Body composition (lean body mass and body fat) determined by dual-energy X-ray absorptiometry (DXA), muscle performance and leptin, sOB-R, total testosterone and free testosterone concentrations were determined before and after training. Fat mass was reduced by 1 kg with strength training (P < 0·05). Lean body mass of trained extremities was increased by 3 % (P < 0·05), while the concentration of free testosterone in serum was reduced by 17 % (P < 0·05) after training. However, despite the reduction in fat mass and free testosterone, serum leptin concentration was not significantly affected by strength training, even after accounting for the differences in body fat. By contrast, for a given fat mass, the sOB-R was increased by 13 % (P < 0·05) at the end of the strength-training programme, although the molar excess of sOB-R over leptin remained unchanged. Therefore, the quantity of free leptin available to bind to the target tissues was not significantly affected by the short strength-training programme, which elicited a 7 % reduction in fat mass.

The epidemiological evidence for the cardio-protective effect of nut consumption is presented and reviewed. Four large prospective epidemiological studies of primary prevention of coronary heart disease are reviewed and discussed (Adventist Health Study, Iowa Women's Health Study, Nurses' Health Study and the Physicians' Health Study). Other studies of nuts and coronary heart disease risk are addressed. The combined evidence for a cardio-protective effect from nut consumption is summarized and presented graphically. The risk of coronary heart disease is 37 % lower for those consuming nuts more than four times per week compared to those who never or seldom consume nuts, with an average reduction of 8·3 % for each weekly serving of nuts. The evidence for a causal relationship between nut consumption and reduced risk of coronary heart disease is outlined using Hill's criteria for causality and is found to support a causal cardio-protective relationship.

The present experiment was designed to estimate the quantitative contribution of rumen protozoa to the total N, conjugated linoleic acid (CLA) and vaccenic acid (VA; trans-11–18:1) flow to the duodenum of steers fed two silage diets: control silage (CS) and silage high in water-soluble carbohydrates (HS). Protozoal duodenal flows were estimated using a real-time PCR assay to quantify the genes encoding protozoal 18S ribosomal RNA. Denaturing gradient gel electrophoresis was used to confirm that the rumen protozoa populations were similar to the protozoal population flowing to the duodenum. Estimated duodenal flow of protozoal N was 14·2 and 18·2 g/d (P>0·05) for animals fed the CS and HS diets respectively. Protozoal flow thus represented between 12 and 15 % of the total N duodenal flow. In terms of fatty acid flow, protozoa accounted for between 30 and 43 % of the CLA and 40 % of the VA reaching the duodenum. The contribution of protozoa to 16:0 and 18:0 flows to the duodenum was less than 20 and 10 %, respectively. These results show that the fatty acids within protozoa make up a significant proportion of the CLA and VA reaching the duodenum of ruminants.

When pregnant adolescent sheep are overnourished to promote maternal growth during pregnancy, growth of the placenta is impaired and results in the premature delivery of low birth weight lambs relative to control-fed adolescents of equivalent age. These effects have been achieved by feeding two levels of the same complete diet. The present study evaluated the role of protein in pregnancy outcome in our adolescent sheep paradigm. Adolescent ewes were implanted with single embryos on day 4 post-oestrus. Thereafter ewes were offered ad libitum an isoenergetic diet (11·4 MJ metabolisable energy/kg DM) containing either 12 % (basic, B) or 17 % (extra, E) crude protein. At day 75 of gestation, half the pregnant ewes on each protein level were switched to yield four groups, BB, EE, BE and EB protein. A further optimally nourished control group received a moderate quantity of a ration (14 % crude protein) designed to provide 100 % of the estimated energy and protein requirement of the adolescent sheep according to stage of pregnancy. Pregnancy outcome was determined at term. Feed intakes were independent of protein level in the four groups of ewes fed ad libitum and were higher (P < 0·001) than in the control group throughout. Maternal plasma urea concentrations reflected the current crude protein content of the diet offered and were elevated in the 17 % compared with 12 % protein groups (P < 0·001). Within groups fed ad libitum, maternal plasma insulin, glucose, NEFA and homocysteine concentrations were largely independent of protein level. Gestation length, placental weight, lamb birth weight and initial colostrum yield were reduced (P < 0·05) in all groups fed ad libitum relative to the optimally nourished control group. Similarly, total colostrum IgG, butterfat, lactose and crude protein content at parturition were attenuated in the ad libitum compared with the control groups. However, within ad libitum groups pregnancy outcome parameters were largely unaffected by level or timing of exposure to high protein intakes. The data imply that it is high-energy intakes that are the primary cause of impaired placental development and adverse pregnancy outcome in rapidly growing adolescent sheep.

The objective of the present study is to demonstrate the effect of nucleotide intake and intensive nutritional support on the concentration of insulin-like growth factor I (IGF-I) and other hormonal biomarkers in severely malnourished children. Twenty-six severely malnourished children <48 months of age received formula without lactose via enteral feeding for 2 weeks and ad libitum for an additional 2 weeks. Anthropometrical measurements were performed and serum concentrations of IGF-I, insulin-like growth factor binding protein-3 (IGFBP-3), leptin, soluble leptin receptor (sOB-R), as well as the estimated molar excess of sOB-R over leptin were obtained. Two groups were formed. One group received formula with nucleotides (NT+; n 13) and the other without nucleotides (NT−; n 13). A control group was included (n 13). Parametric and non-parametric tests as well as ANOVA models were used. Nutritional recovery, nucleotides intake, type of malnutrition, age and the interaction between gender and malnutrition influenced the concentration of IGF-I (P<0·001). Nutritional recovery, nucleotides intake, gender and type of malnutrition had an effect on IGFBP-3 (P<0·001). Nutritional recovery had a significant effect on serum leptin (P=0·001). Age and nutritional recovery had an effect on sOB-R (P<0·001); all variables included affected the molar excess of sOB-R over leptin (P<0·001). In conclusion, nucleotide intake and nutritional recovery had a notable effect on IGF-I, IGFBP-3 and other hormonal biomarkers. This outcome could stimulate the catch-up growth of severely malnourished infants and toddlers during the nutritional recovery period.

During endurance exercise, oxygen consumption by the skeletal muscle can increase 100–200 times. We previously found that during an ultramarathon race (50 km, forest trail through hilly terrain) compared with a day of rest, vitamin E disappeared faster (as measured using 2H-labelled α-tocopherol) and lipid peroxidation increased. Therefore, we hypothesized that prior supplementation with antioxidants (vitamins E and C) would decrease oxidative stress during distance running and, therefore, decrease lipid peroxidation and inflammation, decreaseDNA damage, decrease muscle damage and/or improve recovery. To test these hypotheses, we carried out a randomized, double-blind study in runners (n 11 females, 11 males) who were participants in an annual ultramarathon race. We found that supplementation with both vitamins E and C only prevented increases in lipid peroxidation, but had no apparent effect on DNA damage, inflammation or muscle damage. These results suggest that the mechanism of oxidative damage is operating independently of the inflammatory and muscle damage responses.

Epidemiological data suggest that those who consume a diet rich in quercetin-containing foods may have a reduced risk of CVD. Furthermore, in vitro and ex vivo studies have observed the inhibition of collagen-induced platelet activation by quercetin. The aim of the present study was to investigate the possible inhibitory effects of quercetin ingestion from a dietary source on collagen-stimulated platelet aggregation and signalling. A double-blind randomised cross-over pilot study was undertaken. Subjects ingested a soup containing either a high or a low amount of quercetin. Plasma quercetin concentrations and platelet aggregation and signalling were assessed after soup ingestion. The high-quercetin soup contained 69mg total quercetin compared with the low-quercetin soup containing 5mg total quercetin. Plasma quercetin concentrations were significantly higher after high-quercetin soup ingestion than after low-quercetin soup ingestion and peaked at 2·59 (sem 0·42) μmo/. Collagen-stimulated (0·5μ/l) platelet aggregation was inhibited after ingestion of the high-quercetin soup in a time-dependent manner. Collagen-stimulated tyrosine phosphorylation of a key component of the collagen-signalling pathway via glycoprotein VI, Syk, was significantly inhibited by ingestion of the high-quercetin soup. The inhibition of Syk tyrosine phosphorylation was correlated with the area under the curve for the high-quercetin plasma profile. In conclusion, the ingestion of quercetin from a dietary source of onion soup could inhibit some aspects of collagen-stimulated platelet aggregation and signalling ex vivo. This further substantiates the epidemiological data suggesting that those who preferentially consume high amounts of quercetin-containing foods have a reduced risk of thrombosis and potential CVD risk.

Resveratrol has been widely investigated for its potential health properties, although little is known about its metabolism in vivo Here we investigated the distribution of metabolic products of [3H]trans-resveratrol, following gastric administration. At 2h, plasma concentrations reached 1·7% of the administered dose, whilst liver and kidney concentrations achieved 1·0 and 0·6%, respectively. Concentrations detected at 18h were lower, being only 0·5% in plasma and a total of 0·35% in tissues. Furthermore, whilst kidney and liver concentrations fell to 10 and 25%, respectively, of concentrations at 2h, the brain retained 43% of that measured at 2h. Resveratrol-glucuronide was identified as the major metabolite, reaching 7μm in plasma at 2h. However, at 18h the main form identified in liver, heart, lung and brain was native resveratrol aglycone, indicating that it is the main form retained in the tissues. No phenolic degradation products were detected in urine or tissues, indicating that, unlike flavonoids, resveratrol does not appear to serve as a substrate for colonic microflora. The present study provides additional information about the nature of resveratrol metabolites and which forms might be responsible for its in vivo biological effects.

The present study evaluated the effects of moderate intakes of myristic acid (MA), at 1·2% and 1·8% of total energy (TE), associated with a 0·9% TE intake of α-linolenic acid (ALA) on lipid and fatty acid profiles and red blood cell membrane fluidity. Twenty-nine monks without dyslipidaemia were enrolled in a 1-year nutritional study in which two experimental diets were tested for 3 months each: diet 1, MA 1·2% and ALA 0·9%; diet 2, MA 1·8% and ALA 0·9%. A control diet (MA 1·2%, ALA 0·4%) was given 3 months before diets 1 and 2. Thus, two different levels of MA (1·2%, 1·8%) and ALA (0·4%, 0·9%) were tested. Intakes of other fatty acids were at recommended levels. Samples were obtained on completion of all three diets. For fluidity analysis, the red blood cells were labelled with 16-doxylstearate and the probe incorporated the membrane where relaxation-correlation time was calculated. Diet 1 was associated with a decrease in total cholesterol, in LDL-cholesterol, in triacylglycerols and in the ratio of total to HDL-cholesterol; ALA and EPA levels were increased in both phospholipids and cholesterol esters. Diet 2 was associated with a decrease in triacylglycerols and in the ratios of total to HDL-cholesterol and of triacylglycerols to HDL-cholesterol, and with an increase in HDL-cholesterol; EPA levels were decreased in phospholipids and cholesterol esters. Red blood cell membrane fluidity was increased in both diets (P<0·0001), but the higher increase was obtained with diet 1, mainly in the oldest subjects. Intakes of myristic acid (1·2%TE) and ALA (0·9%TE), both mainly in the sn-2 position, were associated with favourable lipid and n−3 long-chain fatty acid profiles. These beneficial effects coexisted with particularly high membrane fluidity, especially among the oldest subjects.

Tree nuts have a fatty acid profile that favourably affects blood lipids and lipoproteins. They are low in saturated fat and high in unsaturated fatty acids and are rich sources of other nutrients. An extensive database consistently shows total and LDL cholesterol-lowering effects of diets low in saturated fat and cholesterol and high in unsaturated fat provided by a variety of tree nuts. Collectively, a summary of studies conducted to date shows that tree nuts reduce LDL cholesterol by 3–19 % compared with Western and lower-fat diets. Nuts also contain many nutrients and bioactive compounds that appear to contribute to the favourable effects on lipids and lipoproteins – these include plant sterols, dietary fibre and antioxidants. Because of their unique nutrient profile, nuts can be part of a diet that features multiple heart-healthy foods resulting in a cholesterol lowering response that surpasses that of cholesterol-lowering diets typically used to reduce CVD risk.