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Almond Consumption for 8 Weeks Altered Host and Microbial Metabolism in Comparison to a Control Snack in Young Adults.
Dhillon, J, Newman, JW, Fiehn, O, Ortiz, RM
Journal of the American Nutrition Association. 2023;42(3):242-254
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The consumption of almonds can improve cardiometabolic (CM) health. This study explored the effects of consuming a snack of almonds vs. crackers for 8 weeks on changes in cardiometabolic, microbiome and metabolomics markers in young adults. 73 (41 women and 32 men) young adults took part in this 8-week randomized controlled, parallel-arm intervention study. Blood samples were taken at the beginning, at 4 weeks and then at 8 weeks. The results looked at alternations in many serum metabolites involved in metabolic pathways. They therefore provide a deeper understanding of host carbohydrate, lipid and tocopherol metabolism. The findings also show the interconnections between circulating metabolites and microbial metabolism. This provides further evidence for the impacts of dietary changes on host metabolism and associated changes in gut microbe metabolism.
Abstract
Almond consumption can improve cardiometabolic (CM) health. However, the mechanisms underlying those benefits are not well characterized. This study explored the effects of consuming a snack of almonds vs. crackers for 8 weeks on changes in metabolomic profiles in young adults (clinicaltrials.gov ID: NCT03084003). Participants (n = 73, age: 18-19 years, BMI: 18-41 kg/m2) were randomly assigned to consume either almonds (2 oz/d, n = 38) or an isocaloric control snack of graham crackers (325 kcal/d, n = 35) daily for 8 weeks. Blood samples were collected at baseline prior to and at 4 and 8 weeks after the intervention. Metabolite abundances in the serum were quantified by hydrophilic interaction chromatography quadrupole (Q) time-of-flight (TOF) mass spectrometry (MS/MS), gas chromatography (GC) TOF MS, CSH-ESI (electrospray) QTOF MS/MS, and targeted analyses for free PUFAs, total fatty acids, oxylipins and endocannabinoids. Linear mixed model analyses with baseline-adjustment were conducted, and those results were used for enrichment and network analyses. Microbial community pathway predictions from 16S rRNA sequencing of fecal samples was done using PICRUST2. Almond consumption enriched unsaturated triglycerides, unsaturated phosphatidylcholines, saturated and unsaturated lysophosphatidylcholines, tricarboxylic acids, and tocopherol clusters (p < 0.05). Targeted analyses reveal lower levels of omega-3 total fatty acids (TFAs) overall in the almond group compared to the cracker group (p < 0.05). Microbial amino acid biosynthesis, and amino sugar and nucleotide sugar metabolism pathways were also differentially enriched at the end of the intervention (p < 0.05). The study demonstrates the differential effects of almonds on host tocopherol, lipid, and TCA cycle metabolism with potential changes in microbial metabolism, which may interact with host metabolism to facilitate the CM benefits.
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Chocolate milk for recovery from exercise: a systematic review and meta-analysis of controlled clinical trials.
Amiri, M, Ghiasvand, R, Kaviani, M, Forbes, SC, Salehi-Abargouei, A
European journal of clinical nutrition. 2019;73(6):835-849
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Post-exercise nutrition is highly important for recovery and performance. It has been proposed that beverages containing protein, carbohydrates and electrolytes may attenuate exercise-induced fatigue and dehydration. Chocolate milk contains all of these nutrients and has recently drawn attention as a plausible post-exercise recovery drink. Therefore the aim of this study was to assess the efficacy of chocolate milk on post-exercise recovery markers. This review included 12 studies and a sub-analysis found significant improvements in time to exhaustion and lowered post-exercise blood-lactate. There were no significant differences between the other markers considered in the analysis. Based on these results, the authors deem chocolate milk to provide equivalent outcomes to placebo or other recovery drinks. As the available research is limited, the authors recommended high quality controlled trials with larger sample sizes be done to gain more clarity on best-practice for post-exercise recovery.
Abstract
BACKGROUND/OBJECTIVES Chocolate milk (CM) contains carbohydrates, proteins, and fat, as well as water and electrolytes, which may be ideal for post-exercise recovery. We systematically reviewed the evidence regarding the efficacy of CM compared to either water or other "sport drinks" on post-exercise recovery markers. SUBJECTS/METHODS PubMed, Scopus, and Google scholar were explored up to April 2017 for controlled trials investigating the effect of CM on markers of recovery in trained athletes. RESULTS Twelve studies were included in the systematic review (2, 9, and 1 with high, fair and low quality, respectively) and 11 had extractable data on at least one performance/recovery marker [7 on ratings of perceived exertion (RPE), 6 on time to exhaustion (TTE) and heart rate (HR), 4 on serum lactate, and serum creatine kinase (CK)]. The meta-analyses revealed that CM consumption had no effect on TTE, RPE, HR, serum lactate, and CK (P > 0.05) compared to placebo or other sport drinks. Subgroup analysis revealed that TTE significantly increases after consumption of CM compared to placebo [mean difference (MD) = 0.78 min, 95% confidence interval (CI): 0.27, 1.29, P = 0.003] and carbohydrate, protein, and fat-containing beverages (MD = 6.13 min, 95% CI: 0.11, 12.15, P = 0.046). Furthermore, a significant attenuation on serum lactate was observed when CM was compared with placebo (MD = -1.2 mmol/L, 95% CI: -2.06,-0.34, P = 0.006). CONCLUSION CM provides either similar or superior results when compared to placebo or other recovery drinks. Overall, the evidence is limited and high-quality clinical trials with more well-controlled methodology and larger sample sizes are warranted.
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The Effect of Mitochondrial Supplements on Mitochondrial Activity in Children with Autism Spectrum Disorder.
Delhey, LM, Nur Kilinc, E, Yin, L, Slattery, JC, Tippett, ML, Rose, S, Bennuri, SC, Kahler, SG, Damle, S, Legido, A, et al
Journal of clinical medicine. 2017;6(2)
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Primary mitochondrial disease and secondary mitochondria disorders have received increasing recognition in the medical world. In fact, mitochondrial dysfunction plays a significant role in many common illnesses such as diabetes, obesity, cancer and heart disease, as well as neurologic and psychiatric conditions. Yet less is known about the optimal treatment for mitochondrial disorders. Given the scarcity of clinical research, current treatment is mostly based on expert opinions, preclinical trials and animal models. Autism spectrum disorder (ASD) is a neurological and developmental condition that manifests in divergent behaviours affecting learning, communication and social engagement. Recent research suggests that there may be a link between mitochondrial abnormalities and ASD. About half of children with ASD display measurable biomarkers indicative of mitochondrial dysfunction, and the prevalence of primary mitochondrial disorders is much higher in children with ASD compared to those without ASD presentation. Several mitochondrial co-factors are supplemented in the management of mitochondria disease and also have shown promising effects on ASD symptoms. Hence this observational study sought to explore the impact of such substances on mitochondrial function in children with ASD. The project involved 127 children with ASD, some subjects were on specific mitochondrial supplements and some also had a diagnosed mitochondrial disease. The activity of mitochondrial metabolism was assessed at several stages, via a salivary mouth swab. Results from this study suggested that several common mitochondrial supplements such as fatty acids, antioxidants, B12 and folate influence mitochondrial function. However, some of these influences were more pronounced or in some cases limited to the subgroup that also had prevailing mitochondrial disease. The findings affirm that these interventions improve mitochondrial function and maybe be most effective in ASD cases with underlying metabolic disorders.
Abstract
Treatment for mitochondrial dysfunction is typically guided by expert opinion with a paucity of empirical evidence of the effect of treatment on mitochondrial activity. We examined citrate synthase and Complex I and IV activities using a validated buccal swab method in 127 children with autism spectrum disorder with and without mitochondrial disease, a portion of which were on common mitochondrial supplements. Mixed-model linear regression determined whether specific supplements altered the absolute mitochondrial activity as well as the relationship between the activities of mitochondrial components. Complex I activity was increased by fatty acid and folate supplementation, but folate only effected those with mitochondrial disease. Citrate synthase activity was increased by antioxidant supplementation but only for the mitochondrial disease subgroup. The relationship between Complex I and IV was modulated by folate while the relationship between Complex I and Citrate Synthase was modulated by both folate and B12. This study provides empirical support for common mitochondrial treatments and demonstrates that the relationship between activities of mitochondrial components might be a marker to follow in addition to absolute activities. Measurements of mitochondrial activity that can be practically repeated over time may be very useful to monitor the biochemical effects of treatments.
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Metabolism of phytanic acid and 3-methyl-adipic acid excretion in patients with adult Refsum disease.
Wierzbicki, AS, Mayne, PD, Lloyd, MD, Burston, D, Mei, G, Sidey, MC, Feher, MD, Gibberd, FB
Journal of lipid research. 2003;44(8):1481-8
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Phytanic acid (PA) is a branched-chain fatty acid, found in many animal products, that, unlike most fatty acids, cannot be metabolised by beta-oxidation. Instead, it undergoes alpha-oxidation in the peroxisome. Adult Refsum Disease is a genetic neurological disease, in which alpha-oxidation is impaired, resulting in the accumulation of PA in nerves and fat tissues. Other pathways for the metabolism of PA are not fully understood, such as omega-oxidation, which results in the production of 3-methyl-organic acids (3-MAA). This study assessed the contribution of the omega-oxidation pathway to the metabolism of PA by measuring 3-MAA excretion in patients with ARD. Eleven patients with ARD were put on a low-PA diet for 12 weeks. Blood, urine and tissue samples were taken at the start and end of the 12-week period to assess levels of PA and its metabolites. The low-PA diet led to an average 21% fall in blood PA levels over 12 weeks. The capacity of the omega-oxidation pathway was 6.9mg PA/day. The authors concluded that the omega-oxidation pathway can metabolise PA ingested by patients with ARD. Therefore, omega-oxidation is a potential target for therapeutic intervention to reduce PA levels in ARD patients.
Abstract
Adult Refsum disease (ARD) is associated with defective alpha-oxidation of phytanic acid (PA). omega-Oxidation of PA to 3-methyl-adipic acid (3-MAA) occurs although its clinical significance is unclear. In a 40 day study of a new ARD patient, where the plasma half-life of PA was 22.4 days, omega-oxidation accounted for 30% initially and later all PA excretion. Plasma and adipose tissue PA and 3-MAA excretion were measured in a cross-sectional study of 11 patients. The capacity of the omega-oxidation pathway was 6.9 (2.8-19.4) mg [20.4 (8.3-57.4) micromol] PA/day. 3-MAA excretion correlated with plasma PA levels (r = 0.61; P = 0.03) but not adipose tissue PA content. omega-Oxidation during a 56 h fast was studied in five patients. 3-MAA excretion increased by 208 +/- 58% in parallel with the 158 (125-603)% rise in plasma PA. Plasma PA doubled every 29 h, while 3-MAA excretion followed second-order kinetics. Acute sequelae of ARD were noted in three patients (60%) after fasting. The omega-oxidation pathway can metabolise PA ingested by patients with ARD, but this activity is dependent on plasma PA concentration. omega-Oxidation forms a functional reserve capacity that enables patients with ARD undergoing acute stress to cope with limited increases in plasma PA levels.