Evidence supports that a high proportion of calories from protein increases weight loss and prevents weight (re)gain. Proteins are known to induce satiety, increase secretion of gastrointestinal hormones, and increase diet-induced thermogenesis, but less is known about whether various types of proteins exert different metabolic effects. In the Western world, dairy protein, which consists of 80% casein and 20% whey, is a large contributor to our daily protein intake. Casein and whey differ in absorption and digestion rates, with casein being a "slow" protein and whey being a "fast" protein. In addition, they differ in amino acid composition. This review examines whether casein, whey, and other protein sources exert different metabolic effects and targets to clarify the underlying mechanisms. Data indicate that whey is more satiating in the short term, whereas casein is more satiating in the long term. In addition, some studies indicate that whey stimulates the secretion of the incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide more than other proteins. However, for the satiety (cholecystokinin and peptide YY) and hunger-stimulating (ghrelin) hormones, no clear evidence exists that 1 protein source has a greater stimulating effect compared with others. Likewise, no clear evidence exists that 1 protein source results in higher diet-induced thermogenesis and promotes more beneficial changes in body weight and composition compared with other protein sources. However, data indicate that amino acid composition, rate of absorption, and protein/food texture may be important factors for protein-stimulated metabolic effects.

The aim of this systematic review and meta-analysis was to summarize the evidence from observational studies assessing the association between intake of trans fatty acids (TFA) and the risk of coronary heart disease (CHD), with a specific emphasis on distinguishing between TFA of industrial and ruminant origin. By searching five bibliographic databases, analyses from six published and two unpublished prospective cohort studies, assessing the association of intake of TFA with fatal and/or non-fatal CHD, were identified. Four and three studies reported separate associations for intake of ruminant or industrial-TFA, respectively. The pooled relative risk estimates for comparison of extreme quintiles of total-TFA intake (corresponding to intake increments ranging from 2.8 to B10 g/day) were 1.22 (95% confidence interval: 1.08-1.38; P ¼ 0.002) for CHD events and 1.24 (1.07-1.43; P ¼ 0.003) for fatal CHD. Ruminant-TFA intake (increments ranging from 0.5 to 1.9 g/day) was not significantly associated with risk of CHD (risk ratio (RR) ¼ 0.92 (0.76-1.11); P ¼ 0.36), and neither was industrial-TFA intake, although there was a trend towards a positive association (RR ¼ 1.21 (0.97-1.50); P ¼ 0.09). In conclusion, our analysis suggests that industrial-TFA may be positively related to CHD, whereas ruminant-TFA is not, but the limited number of available studies prohibits any firm conclusions concerning whether the source of TFA is important. The null association of ruminant-TFA with CHD risk may be due to lower intake levels.

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Background: Evidence suggests that dietary calcium intake may be inversely related to body weight. One explanatory mechanism is that dietary calcium increases fecal fat excretion, due to either calcium soap formation and/or binding of bile acids (BAs) in the intestine. Objective: To examine the effect of calcium from low-fat dairy products on fecal fat excretion. Design: A randomized crossover study with 11 subjects, comparing two 7-d diets: one high in calcium from low-fat dairy products (high-Ca; 2300 mg Ca per d) and one low in calcium (low-Ca; 700 mg Ca per d). Measurements: All feces were collected during the last 5 days of each diet period and analyzed for fat, energy and calcium content and fatty acid (FA) and BA composition. Results: Dairy calcium significantly increased the total fecal fat excretion from 5.4 ± 0.5 g d À1 on the low-Ca diet to 11.5 ± 1.4 g d À1 on the high-Ca diet (Po0.001). The fecal energy excretion increased almost correspondingly. Saturated, monounsaturated and polyunsaturated FAs were all excreted in larger amounts on the high-Ca diet (Po0.001 for all), with the effect of calcium being greater for monounsaturated than for saturated FAs. The fecal excretion of BAs was unaffected of calcium intakes. Conclusions: Increasing the intake of calcium from low-fat dairy products by 1600 mg d À1 for 7 days doubled total fecal fat excretion, but did not affect the excretion of BAs. The results may partially explain why a high-calcium diet can produce weight loss. Keywords: dietary calcium; dairy products; fecal fat excretion; fecal bile acids; fecal fatty acid composition IntroductionAn inverse association between calcium intake and body weight in humans was reported for the first time in the mid1980s, based on data from the first National Health and Nutrition Examination Survey.1 More than a decade later, an increased fat loss of almost 5 kg, due to an augmented calcium intake from dairy products, was observed in an antihypertension trial. 2 Since then, increasing evidence that dairy calcium reduces body weight has emerged from both observational and intervention studies. 3-7 However, not all investigations have confirmed these findings. 8-14The mechanism responsible for the effect of increased calcium intake on energy balance is not clear, but a number of different mechanisms have been suggested. One possible explanation, proposed by Zemel et al., 2 is that serum calcium plays a regulatory role in lipid metabolism by influencing intracellular calcium levels through hormonal regulation. According to this hypothesis, an increase in dietary calcium would result in increased lipolysis and decreased lipogenesis, thereby stimulating body fat loss. An alternative, or additional, possibility is that calcium interferes with fat absorption in the intestine by forming insoluble calcium soaps with fatty acids (FAs) or by forming precipitates with phosphate and bile acids (BAs), resulting in decreases in the digestible energy of the diet. 15-18A decrease in fat absorption, inferred from increases in feca...

A systematic review was conducted to assess the evidence linking beer consumption to abdominal and general obesity. Following a systematic search strategy, 35 eligible observational studies and 12 experimental studies were identified. Regarding abdominal obesity, most observational data pointed towards a positive association or no association between beer intake and waist circumference or waist-to-hip ratio in men, whereas results for women were inconsistent. Data from a subset of studies indicated that beer intake > 500 mL/day may be positively associated with abdominal obesity. Regarding general obesity, most observational studies pointed towards an inverse association or no association between beer intake and body weight in women and a positive association or no association in men. Data from six experimental studies in men, in which alcoholic beer was compared with low-alcoholic beer, suggested that consumption of alcoholic beer (for 21-126 days) results in weight gain (0.73 kg; P < 0.0001), but data from four studies comparing intake of alcoholic beer with intake of no alcohol did not support this finding. Generally, experimental studies had low-quality data. In conclusion, the available data provide inadequate scientific evidence to assess whether beer intake at moderate levels (<500 mL/day) is associated with general or abdominal obesity. Higher intake, however, may be positively associated with abdominal obesity.