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

Molybdenum, a trace element essential for micro-organisms, plants, and animals, was discovered in 1778 by a Swedish chemist named Karl Scheele. Initially mistaken for lead, molybdenum was named after the Greek work molybdos, meaning lead-like. In the 1930s, it was recognized that ingestion of forage with high amounts of molybdenum by cattle caused a debilitating condition. In the 1950s, the essentiality of molybdenum was established with the discovery of the first molybdenum-containing enzymes. In humans, only 4 enzymes requiring molybdenum have been identified to date: sulfite oxidase, xanthine oxidase, aldehyde oxidase, and mitochondrial amidoxime-reducing component (mARC). Sulfite oxidase, an enzyme found in mitochondria, catalyzes oxidation of sulfite to sulfate, the final step in oxidation of sulfur amino acids (cysteine and methionine). Xanthine oxidase converts hypoxanthine to xanthine, and further converts xanthine to uric acid, preventing hypoxanthine, formed from spontaneous deamination of adenine, from leading to DNA mutations if paired with cytosine in place of thymine. Aldehyde oxidase is abundant in the liver and is an important enzyme in phase 1 drug metabolism. Finally, mARC, discovered less than a decade ago, works in concert with cytochrome b₅ type B and NAD(H) cytochrome b₅ reductase to reduce a variety of N-hydroxylated substrates, although the physiologic significance is still unclear. In the case of each of the molybdenum enzymes, activity is catalyzed via a tricyclic cofactor composed of a pterin, a dithiolene, and a pyran ring, called molybdenum cofactor (MoCo) (1).

Background: Cardiometabolic risk is the risk of cardiovascular disease (CVD), diabetes, or stroke, which are leading causes of mortality and morbidit

Background: Almond processing has been shown to differentially impact metabolizable energy; however, the effect of food form on the gastrointestinal microbiota is under-investigated. Objective: We aimed to assess the interrelationship of almond consumption and processing on the gastrointestinal microbiota. Design: A controlled-feeding, randomized, five-period, crossover study with washouts between diet periods was conducted in healthy adults (n = 18). Treatments included: (1) zero servings/day of almonds (control); (2) 1.5 servings (42 g)/day of whole almonds; (3) 1.5 servings/day of whole, roasted almonds; (4) 1.5 servings/day of roasted, chopped almonds; and (5) 1.5 servings/day of almond butter. Fecal samples were collected at the end of each three-week diet period. Results: Almond consumption increased the relative abundances of Lachnospira, Roseburia, and Dialister (p ≤ 0.05). Comparisons between control and the four almond treatments revealed that chopped almonds increased Lachnospira, Roseburia, and Oscillospira compared to control (p < 0.05), while whole almonds increased Dialister compared to control (p = 0.007). There were no differences between almond butter and control. Conclusions: These results reveal that almond consumption induced changes in the microbial community composition of the human gastrointestinal microbiota. Furthermore, the degree of almond processing (e.g., roasting, chopping, and grinding into butter) differentially impacted the relative abundances of bacterial genera.