Background: The energy content of foods is primarily determined by the Atwater factors, which may not be accurate for certain food groups. Nuts are a food group for which substantial evidence suggests that the Atwater factors may be poorly predictive.Objective: A study was conducted to determine the energy value of almonds in the human diet and to compare the measured energy value with the value calculated from the Atwater factors.Design: Eighteen healthy adults consumed a controlled diet or an almond-containing diet for 18 d. Three treatments were administered to subjects in a crossover design, and diets contained 1 of 3 almond doses: 0, 42, or 84 g/d. During the final 9 d of the treatment period, volunteers collected all urine and feces, and samples of diets, feces, and urine were analyzed for macronutrient and energy contents. The metabolizable energy content of the almonds was determined.Results: The energy content of almonds in the human diet was found to be 4.6 ± 0.8 kcal/g, which is equivalent to 129 kcal/28-g serving. This is significantly less than the energy density of 6.0–6.1 kcal/g as determined by the Atwater factors, which is equivalent to an energy content of 168–170 kcal/serving. The Atwater factors, when applied to almonds, resulted in a 32% overestimation of their measured energy content.Conclusion: This study provides evidence for the inaccuracies of the Atwater factors for certain applications and provides a rigorous method for determining empirically the energy value of individual foods within the context of a mixed diet. This trial was registered at clinicaltrials.gov as NCT01007188.

BackgroundEpidemiologic data suggest that diets rich in nuts have beneficial health effects, including reducing total and cause-specific mortality from cancer and heart disease. Although there is accumulating preclinical evidence that walnuts beneficially affect the gastrointestinal microbiota and gut and metabolic health, these relations have not been investigated in humans.ObjectiveWe aimed to assess the impact of walnut consumption on the human gastrointestinal microbiota and metabolic markers of health.MethodsA controlled-feeding, randomized crossover study was undertaken in healthy men and women [n = 18; mean age = 53.1 y; body mass index (kg/m2): 28.8]. Study participants received isocaloric diets containing 0 or 42 g walnuts/d for two 3-wk periods, with a 1-wk washout between diet periods. Fecal and blood samples were collected at baseline and at the end of each period to assess secondary outcomes of the study, including effects of walnut consumption on fecal microbiota and bile acids and metabolic markers of health.ResultsCompared with after the control period, walnut consumption resulted in a 49–160% higher relative abundance of Faecalibacterium, Clostridium, Dialister, and Roseburia and 16–38% lower relative abundances of Ruminococcus, Dorea, Oscillospira, and Bifidobacterium (P < 0.05). Fecal secondary bile acids, deoxycholic acid and lithocholic acid, were 25% and 45% lower, respectively, after the walnut treatment compared with the control treatment (P < 0.05). Serum LDL cholesterol and the noncholesterol sterol campesterol concentrations were 7% and 6% lower, respectively, after walnut consumption compared with after the control treatment (P < 0.01).ConclusionWalnut consumption affected the composition and function of the human gastrointestinal microbiota, increasing the relative abundances of Firmicutes species in butyrate-producing Clostridium clusters XIVa and IV, including Faecalibacterium and Roseburia, and reducing microbially derived, proinflammatory secondary bile acids and LDL cholesterol. These results suggest that the gastrointestinal microbiota may contribute to the underlying mechanisms of the beneficial health effects of walnut consumption. This trial was registered at www.clinicaltrials.gov as NCT01832909.

The bioavailability of acylated vs nonacylated anthocyanins and the effect of cooking and dose on the comparative bioavailability were investigated in a clinical feeding study using purple carrots as the anthocyanin source. Treatments were purple carrots as follows: 250 g raw (463 micromol of anthocyanins: 400 micromol acylated, 63 micromol nonacylated), 250 g cooked (357 micromol of anthocyanins: 308.5 micromol acylated, 48.5 micromol nonacylated), and 500 g cooked (714 micromol of anthocyanins: 617 micromol acylated, 97 micromol nonacylated). Four of the five carrot anthocyanins were found intact in plasma by 30 min after carrot consumption and peaked between 1.5 and 2.5 h. Acylation of anthocyanins resulted in an 11-14-fold decrease in anthocyanin recovery in urine and an 8-10-fold decrease in anthocyanin recovery in plasma. Cooking increased the recovery of nonacylated anthocyanins but not acylated anthocyanins. Large dose size significantly reduced recovery of both acylated and nonacylated anthocyanins, suggesting saturation of absorption mechanisms.