Research suggests that children with autism spectrum disorder (ASD) often exhibit lower levels of glutathione. Although interventions targeting increased glutathione show promise in improving ASD behaviors, findings have been inconsistent. This study explored the efficacy of a 90-day intervention using a cysteine-rich whey protein isolate (CRWP), known to boost glutathione, in preschoolers (ages 3 to 5) with confirmed ASD. In a randomized, double-blind, placebo-controlled trial involving 46 enrolled children, CRWP was administered daily in varying doses based on weight. The assessment encompassed glutathione levels and behavioral changes using multiple scales. Results showed that while some behavioral improvements were similar between groups, children receiving CRWP demonstrated significant enhancements in the Vineland Adaptive Behavior Scale, notably in adaptive behavior, socialization, maladaptive behavior, and internalizing behavior, compared to the placebo group. Moreover, the CRWP group exhibited notable increases in glutathione levels. Analysis indicated that older age and higher initial glutathione levels were associated with positive behavioral responses to CRWP. The study suggests that CRWP intervention in children with ASD holds promise in enhancing both glutathione levels and specific ASD-related behaviors, warranting further investigation to confirm these findings. <!----> <!----> <!----> <!---->

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating, multi-system disease characterized by profound fatigue, post-exertional malaise (PEM), and a constellation of immune, neurological, and autonomic symptoms. Despite its global prevalence, the pathophysiology of ME/CFS remains elusive, and there are no FDA-approved treatments targeting the underlying mechanisms. Symptom-based pharmacologic management is often complicated by hypersensitivity reactions and mitochondrial toxicity. Non-pharmacologic interventions, such as energy conservation, autonomic regulation, and nutritional strategies, are frequently employed to mitigate symptom burden. Emerging research points to mitochondrial dysfunction as a core contributor to ME/CFS pathology, marked by impaired ATP production, oxidative stress, and bioenergetic failure. Mitochondrial-derived peptides (MDPs), particularly MOTS-c, offer a novel therapeutic avenue by enhancing mitochondrial biogenesis, reducing oxidative damage, and modulating inflammatory responses through AMPK and NRF2 activation. Preclinical evidence suggests that MOTS-c improves glucose metabolism, increases mitochondrial density, and enhances fatigue resistance. However, safety and efficacy data in humans are lacking. Future investigations are needed to evaluate MOTS-c's potential as a disease-modifying therapy in ME/CFS.