While current intakes of phylloquinone (vitamin K1) in many populations are believed to be sufficient to maintain normal blood coagulation, these may be insufficient to cover the requirements for optimal bone metabolism. Therefore, the objective of the present study was to investigate the effect of increasing phylloquinone intakes above the usual dietary intake for 6 weeks on biochemical markers of vitamin K status and bone turnover in postmenopausal women. Thirty-one postmenopausal women completed this 3 × 6-week randomised cross-over study, in which volunteers were supplemented with 0 (placebo), 200, and 500 μg phylloquinone/d. In addition, the volunteers were given 10 μg vitamin D3/d throughout the study period. With increasing phylloquinone intake, the concentration of serum γ-carboxylated and under-γ-carboxylated osteocalcin was significantly increased and decreased, respectively, in a dose-dependent manner (P < 0·001). Mean serum phylloquinone concentration was significantly (P < 0·001) higher with daily supplementation with 500 μg phylloquinone/d compared with that during either of the placebo or 200 μg phylloquinone/d supplementation periods, which did not differ (P = 0·15). Serum total osteocalcin was significantly (P < 0·001) increased in response to daily supplementation with 500 (but not 200) μg phylloquinone compared with placebo. Serum bone-specific alkaline phosphatase as well as the urinary markers of bone resorption (N-telopeptide cross-links of collagen, pyridinoline and deoxypyridinoline) and urinary γ-carboxyglutamate were unaffected by phylloquinone supplementation. In conclusion, while daily supplementation with 200 and 500 μg phylloquinone/d for 6 weeks increased vitamin K status in postmenopausal women, it had no effect on bone turnover.

Policosanols (PC) exist as very-long-chain alcohols derived from sugarcane currently used in many countries as a cholesterol-lowering therapy. PC purity and relative percentage composition have been suggested as primary reasons why the original Cuban PC (OPC) supplements possess lipid-lowering efficacy. The purpose of the present study was, first, to compare the relative percentage purity and PC composition of both OPC and alternative sources of PC (APC). A second objective was to feed Syrian hamsters a diet containing 0·275 mg PC/g of either the OPC or an APC product (APC1) and compare subsequent tissue, plasma and faecal PC levels. Five animals from the APC1 dietary group received a diet containing ten times the original amount of PC. Results indicate that the APC formulations have a composition that is highly consistent with the OPC supplement, with octacosanol being present within the cited 60–70 % range. PC were undetectable in the small intestine, liver, adipose or plasma in animals fed either source. Hamsters fed OPC excreted octacosanol (C28) more rapidly (P < 0·05) than hamsters receiving APC1. If the cholesterol-lowering efficacy of PC mixtures is dependent on their purity and composition, then sugarcane-derived APC products should possess similar therapeutic properties as the OPC supplement.

n-3 PUFA have shown potential anti-obesity and insulin-sensitising properties. However, the mechanisms involved are not clearly established. The aim of the present study was to assess the effects of EPA administration, one of the n-3 PUFA, on body-weight gain and adiposity in rats fed on a standard or a high-fat (cafeteria) diet. The actions on white adipose tissue lipolysis, apoptosis and on several genes related to obesity and insulin resistance were also studied. Control and cafeteria-induced overweight male Wistar rats were assigned into two subgroups, one of them daily received EPA ethyl ester (1 g/kg) for 5 weeks by oral administration. The high-fat diet induced a very significant increase in both body weight and fat mass. Rats fed with the cafeteria diet and orally treated with EPA showed a marginally lower body-weight gain (P = 0·09), a decrease in food intake (P < 0·01) and an increase in leptin production (P < 0·05). EPA administration reduced retroperitoneal adipose tissue weight (P < 0·05) which could be secondary to the inhibition of the adipogenic transcription factor PPARγ gene expression (P < 0·001), and also to the increase in apoptosis (P < 0·05) found in rats fed with a control diet. TNFα gene expression was significantly increased (P < 0·05) by the cafeteria diet, while EPA treatment was able to prevent (P < 0·01) the rise in this inflammatory cytokine. Adiposity-corrected adiponectin plasma levels were increased by EPA. These actions on both TNFα and adiponectin could explain the beneficial effects of EPA on insulin resistance induced by the cafeteria diet.

The objective of the present study was to determine the effects of a long-term moderate-fat diet (30 % energy from fat) v. a low-fat one (20 % energy from fat) on metabolic risks. The study was a randomised, prospective 14-month trial on overweight and obese patients (eighty-nine overweight and obese men and women). The intervention was a moderate-fat diet (30 % energy) or a low-fat diet (20 % energy). The main outcome measurements were change in body weight, waist circumference, LDL-cholesterol, HDL-cholesterol, total cholesterol, TAG, and systolic and diastolic blood pressure. Forty-five subjects on the moderate-fat diet and forty-four subjects on the low-fat one were studied. Characteristics of all randomised participants were similar in both groups. After 7 months, the moderate- and low-fat diets had similar effects on cardiovascular risks. The moderate-fat diet was more successful after 14 months in reducing weight ( − 5·0 (sd 2·5) kg in the moderate-fat group v. − 1·2 (sd 1·1) kg in the low-fat one; P < 0·0001), waist circumference ( − 5·5 (sd 2·4) cm in the moderate-fat group v. − 2·3 (sd 1·3) cm in the low-fat one; P < 0·0001), and other cardiovascular risk factors as well (LDL, TAG, total cholesterol and systolic blood pressure). In conclusion, a moderate-fat energy-restricted diet in the long term might have more beneficial effects on weight maintenance and cardiovascular risk factors compared with a low-fat diet. Better dietary adherence with the moderate-fat diet may be the reason for its successful effects.

The aim of this study was to determine after 52 weeks whether advice to follow a lower carbohydrate diet, either high in monounsaturated fat or low fat, high in protein had differential effects in a free-living community setting. Following weight loss on either a high monounsaturated fat, standard protein (HMF; 50 % fat, 20 % protein (67 g/d), 30 % carbohydrate) or a high protein, moderate fat (HP) (40 % protein (136 g/d), 30 % fat, 30 % carbohydrate) energy-restricted diet (6000 kJ/d) subjects were asked to maintain the same dietary pattern without intensive dietary counselling for the following 36 weeks. Overall weight loss was 6·2 (sd 7·3) kg (P < 0·01 for time with no diet effect, 7·6 (sd 8·1) kg, HMF v. 4·8 (sd 6·6) kg, HP). In a multivariate regression model predictors of weight loss at the end of the study were sex, age and reported percentage energy from protein (R2 0·22, P < 0·05 for the whole model). Fasting plasma insulin decreased (P < 0·01, with no difference between diets), 13·9 (sd 4·6) to 10·2 (sd 5·2) mIU/l, but fasting plasma glucose was not reduced. Neither total cholesterol nor LDL-cholesterol were different but HDL was higher, 1·19 (sd 0·26) v. 1·04 (sd 0·29) (P < 0·001 for time, no diet effect), while TAG was lower, 1·87 (sd 1·23) v. 2·22 (sd 1·15) mmol/l (P < 0·05 for time, no diet effect). C-reactive protein decreased (3·97 (sd 2·84) to 2·43 (sd 2·29) mg/l, P < 0·01). Food records showed that compliance to the prescribed dietary patterns was poor. After 1 year there remained a clinically significant weight loss and improvement in cardiovascular risk factors with no adverse effects of a high monounsaturated fat diet.