This one in Korean adults found individuals with a high sodium intake, as assessed by sodium excretion, to be more likely to have NAFLD, as reflected by the fatty liver index, and sarcopenia.
- Individuals with the highest 24-hour urinary sodium excretion showed a 46% higher risk of NAFLD.
- The risk was maintained independent of the presence of sarcopenia and was increased by up to 110% in the participants without sarcopenia.
- The risk of sarcopenia increased by 49% in individuals with the highest 24-hour urinary sodium excretion, but only in the non-NAFLD group.
- Thus, the association between a high sodium intake and NAFLD and sarcopenia was found to be stronger where there was a coexistence of NAFLD and sarcopenia rather than in NAFLD or sarcopenia alone.
- By analyzing the interaction between sodium intake and NAFLD in sarcopenia, the study found that NAFLD might be an effect modifier to sarcopenia in high sodium intake.
High Sodium Intake, as Assessed by Urinary Sodium Excretion, Is Associated with Nonalcoholic Fatty Liver Disease or Sarcopenia (open access)
This one in individuals at clinical high-risk for psychosis suggests that the beneficial impact of omega-3 PUFAs on clinical symptoms in psychosis is mediated, at least in part, through the complement and coagulation pathway proteins.
- The complement system is a network of proteins that play an important role in host defense and inflammation.
- The coagulation system, you guessed it, is the good ol' system that is made up of blood cells and proteins, responsible for creating blood clots to allow for rapid healing and prevention of excessive bleeding.
Here, 4000 IU/day vitamin D supplementation in older adults aged 50–80 years with overweight or obesity and vitamin D deficiency had no effect on gait speed either with or without exercise, but combined with exercise, it was more likely to result in decreased waist circumference.
- Further, Vitamin D supplementation taken alone also reduced stair climb times, an effect not observed in combination with exercise, but had no beneficial effects on any other biochemical, body composition or physical function parameters.
- Finally, vitamin D supplementation increased muscle density during exercise, but only in men and "however, this finding should be interpreted with caution given the low numbers in our subgroups".
Here, physically inactive primary care patients aged between 19 and 80 years living in Spain, were more likely to have a reduced risk of mortality by increasing their physical activity, even in doses below the recommended levels.
- Physical activity levels in this inactive population of primary care patients translated into risk reductions in mortality.
- These benefits followed a clear dose–response relationship, in which mortality started to fall even with only small increases in physical activity.
In this one in mice, branched-chain amino acid (BCAA) ingestion suppressed chronic detraining-induced reductions of skeletal muscle mitochondrial content.
- The BCAA dose was 0.6 mg/g of body weight twice daily for 2 mouse weeks of detraining, which translates roughly into ~50 mg/kg of body weight for 560 human days of detraining.
- BCAA supplementation suppressed the reduction of mitochondrial enzyme activities and protein content in skeletal muscle.
In this one, Lawrence Mandarino and colleagues clearly show that fuel choice during mild exercise is unaffected by insulin resistance, doing away with the notion that insulin resistant muscle may use and sometimes prefer lipid oxidation.
- There is evidence that resting, insulin-resistant skeletal muscle prefers to oxidize carbohydrate. This contrasts with a preference for lipid oxidation in skeletal muscle from active, fit, healthy individuals.
- This preference for carbohydrate in resting muscle has been proposed to be responsible for insulin resistance in skeletal muscle, at least in part.
In this one in mice, branched-chain amino acid (BCAA) ingestion suppressed chronic detraining-induced reductions of skeletal muscle mitochondrial content.
- The BCAA dose was 0.6 mg/g of body weight twice daily for 2 mouse weeks of detraining, which translates roughly into ~50 mg/kg of body weight for 560 human days of detraining.
- BCAA supplementation suppressed the reduction of mitochondrial enzyme activities and protein content in skeletal muscle.