The rumen is the site of significant interactions between Cu, S and Mo. It also shows reactions between Cu, S and Fe. The interaction between Mo and S results in the formation of thiomolybdates, which in the absence of adequate quantities of rumen Cu are absorbed into the animal and bind to Cu in biological compounds. This is the cause of thiomolybdate toxicity, often misleadingly called Cu deficiency. The effects of thiomolybdates being absorbed into the animal are considered, especially how thiomolybdates bind to Cu-containing compounds such as enzymes, decreasing their activity without removing the active Cu component. The sources of Cu, Mo, Fe and S are examined, including the impacts of water and soil on the animal's intake. Within the present review we have been able to provide evidence that: all classes of thiomolybdates are formed in the rumen; in the absence of available Cu all thiomolybdates can be absorbed into the animal rapidly though the rumen wall or via the small intestine; thiomolybdates bind to Cu in biological compounds and are able to cause problems; effects of thiomolybdate are reversible in vivo and in vitro on cessation of thiomolybdate challenge; the tetra-thiomolybdate form is the most potent Cu binder with decreased potency with decreasing S in the compound. Fe will exacerbate a thiomolybdate problem but will not directly cause it.

Szymanski MC, Gillum TL, Gould LM, Morin DS, Kuennen MR. Short-term dietary curcumin supplementation reduces gastrointestinal barrier damage and physiological strain responses during exertional heat stress. J Appl Physiol 124: 330-340, 2018. First published September 21, 2017; doi: 10.1152/japplphysiol.00515.2017 .-This work investigated the effect of 3 days of 500 mg/day dietary curcumin supplementation on gastrointestinal barrier damage and systems-physiology responses to exertional heat stress in non-heat-acclimated humans. Eight participants ran (65% V̇o) for 60 min in a Darwin chamber (37°C/25% relative humidity) two times (Curcumin/Placebo). Intestinal fatty acid-binding protein (I-FABP) and associated proinflammatory [monocyte chemoattractant protein-1, tumor necrosis factor-α (TNF-α), interleukin-6] and anti-inflammatory [interleukin-1 receptor antagonist (IL-1RA), interleukin-10 (IL-10)] cytokines were assayed from plasma collected before (Pre), after (Post) and 1 (1-Post) and 4 (4-Post) h after exercise. Core temperature and HR were measured throughout exercise; the physiological strain index (PSI) was calculated from these variables. Condition differences were determined with 2-way (condition × time) repeated-measures ANOVAs. The interaction of condition × time was significant ( P = 0.05) for I-FABP and IL-1RA. Post hoc analysis indicated I-FABP increased more from Pre to Post (87%) and 1-Post (33%) in Placebo than in Curcumin (58 and 18%, respectively). IL-1RA increased more from Pre to 1-Post in Placebo (153%) than in Curcumin (77%). TNF-α increased ( P = 0.01) from Pre to Post (19%) and 1-Post (24%) in Placebo but not in Curcumin ( P > 0.05). IL-10 increased ( P < 0.01) from Pre to Post (61%) and 1-Post (42%) in Placebo not in Curcumin ( P > 0.05). The PSI, which indicates exertional heatstroke risk, was also lower ( P < 0.01) in Curcumin than Placebo from 40 to 60 min of exercise. These data suggest 3 days curcumin supplementation may improve gastrointestinal function, associated cytokines, and systems-level physiology responses during exertional heat stress. This could help reduce exertional heatstroke risk in non-heat-acclimated individuals. NEW & NOTEWORTHY Exercise-heat stress increases gastrointestinal barrier damage and risk of exertional heatstroke. Over the past decade at least eight different dietary supplements have been tested for potential improvements in gastrointestinal barrier function and systems-level physiology responses during exercise-heat stress. None have been shown to protect against both insults simultaneously. In this report 3 days of 500 mg/day dietary curcumin supplementation are shown to improve gastrointestinal barrier function, associated cytokine responses, and systems-level physiology parameters. Further research is warranted.

Nutritional interventions are not commonly a standard of care in rehabilitation interventions. A nutritional approach has the potential to be a low-cost, high-volume strategy that complements the existing standard of care. In this commentary, our aim is to provide an evidence-based, practical guide for athletes with injuries treated surgically or conservatively, along with healing and rehabilitation considerations. Injuries are a normal and expected part of exercise participation. Regardless of severity, an injury typically results in the athlete's short- or long-term removal from participation. Nutritional interventions may augment the recovery process and support optimal healing; therefore, incorporating nutritional strategies is important at each stage of the healing process. Preoperative nutrition and nutritional demands during rehabilitation are key factors to consider. The physiological response to wounds, immobilization, and traumatic brain injuries may be improved by optimizing macronutrient composition, caloric consumption, and nutrient timing and using select dietary supplements. Previous research supports practical nutrition recommendations to reduce surgical complications, minimize deficits after immobilization, and maximize the chance of safe return to play. These recommendations include identifying the individual's caloric requirements to ensure that energy needs are being met. A higher protein intake, with special attention to evenly distributed consumption throughout the day, will help to minimize loss of muscle and strength during immobilization. Dietary-supplement strategies may be useful when navigating the challenges of appropriate caloric intake and timing and a reduced appetite. The rehabilitation process also requires a strong nutritional plan to enhance recovery from injury. Athletic trainers, physical therapists, and other health care professionals should provide basic nutritional recommendations during rehabilitation, discuss the timing of meals with respect to therapy, and refer the patient to a registered dietitian if warranted. Because nutrition plays an essential role in injury recovery and rehabilitation, nutritional interventions should become a component of standard-of-care practice after injury. In this article, we address best practices for implementing nutritional strategies among patients with athletic injuries.

Objectives: To evaluate body composition, fat distribution, and metabolism at rest and during exercise in premenopausal, perimenopausal, and postmenopausal women.Methods: This cross-sectional study in 72 women ages 35 to 60 years evaluated body composition via a fourcompartment model, fat distribution using dual-energy x-ray absorptiometry-derived android to gynoid ratio, metabolic measures via indirect calorimetry, and lifestyle factors using surveys. One-way analyses of variance and one-way analyses of covariance covaried for age and hormone levels (estrogen and progesterone) were used to compare groups.Results: Body fat percent was significantly lower in premenopausal than perimenopausal women (mean difference AE standard error: À10.29 AE 2.73%, P¼0.026) despite similarities in fat mass and fat-free mass between groups (P!0.217). Android to gynoid ratio was significantly lower in premenopausal than perimenopausal women (MD AE SE: À0.16 AE 0.05 a.u., P ¼ 0.031). Resting energy expenditure was similar between groups (P ¼ 0.999). Fat oxidation during moderate intensity cycle ergometer exercise was significantly greater in premenopausal than postmenopausal women (MDAESE: 0.09 AE 0.03 g/min, P ¼ 0.045). The change in respiratory exchange ratio between rest and moderate intensity exercise was significantly lower in premenopausal women than peri-(MDAESE: À0.05 AE 0.03 a.u., P ¼ 0.035) and postmenopausal women (MDAESE: À0.06 AE 0.03 a.u., P ¼ 0.040). Premenopausal women reported significantly fewer menopause symptoms than peri-(MDAESE: À6.58 AE 1.52 symptoms, P ¼ 0.002) and postmenopausal participants (MDAESE: À4.63 AE 1.52 symptoms, P ¼ 0.044), while similarities between groups were observed for lifestyle factors including diet and physical activity (P > 0.999).Conclusions: Perimenopause may be the most opportune window for lifestyle intervention, as this group experienced the onset of unfavorable body composition and metabolic characteristics.

Previous studies have shown a variety of immunological abnormalities in Type 1 (insulin-dependent) diabetes, including disturbances in peripheral lymphocytes and anti-lymphocyte antibodies. We measured subsets of T and natural killer cells with monoclonal antibodies in patients with diabetes, and also assayed for anti-lymphocyte antibodies using dual colour immunofluorescence and flow cytometry. We found a significant decrease in numbers of Leu 3a (helper/inducer) cells in Type 1 diabetic patients of recent onset and intermediate levels in patients with longer duration of the disease. Leu 4 (pan T cell) levels were reduced in Type 1 diabetic patients of more than 4 months duration. Leu 7 (natural killer cells) were increased in Type 2 (non-insulin-dependent) diabetic patients. Individual Type 1 diabetic patients of recent onset showed low levels of Leu 7 and 11 a (natural killer cell) levels with normal 3a levels. Autoantibodies against Leu 3a + cells were present in higher titres in the Type 1 diabetic patients of recent onset than in control subjects. We conclude: (1) Leu 3a cells may be decreased in Type 1 diabetic patients of recent onset and return to normal with time; (2) low numbers of Leu 7 and 11a cells with normal numbers of Leu 3a may be seen in some Type 1 diabetic patients of recent onset, which may help explain previous reports of decreased suppressor cells; (3) Leu 7 levels may be increased in Type 2 diabetes; (4) autoantibodies against Leu 3a + peripheral lymphocytes may be seen in Type 1 diabetic patients of recent onset. These appear to be a marker of autoimmune phenomena rather than immunological mediators.