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Effects of a low-protein nutritional formula with dietary counseling in older adults with chronic kidney disease stages 3-5: a randomized controlled trial.
Yang, WC, Hsieh, HM, Chen, JP, Liu, LC, Chen, CH
BMC nephrology. 2023;24(1):372
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Chronic kidney disease (CKD) is a prevalent clinical issue often observed in older adults. Nutritional management has become essential for older adults with CKD. Recent nutritional guidelines have suggested that a low-protein diet (LPD) can be prescribed. The aim of this study was to compare the effects of a regular LPD alone or a 6% LPF combined with a regular LPD prescription on nutrition status, physical performance, and clinical parameter changes in older adults with CKD stages 3–5. This study was a single-centre, two-armed, open-label, parallel, randomised controlled clinical trial. Participants were allocated at a 1:1 ratio - (1) the control group, patients received a regular LPD prescription; (2) the intervention group, patients received a regular LPD prescription with 6% LPF. Results showed that an LPD plus a 6% LPF provided no changes in energy and protein intake while increasing fatty acid and specific micronutrient intake during the 3-month follow-up period. Furthermore, blood urea nitrogen (clinical parameter) was significantly reduced in the intervention group over three months. Authors concluded that an LPD prescription with a 6% LPF can delay physical performance deterioration and increase micronutrient intake in three months compared to LPD education alone in older adults with CKD stages 3–5.
Abstract
BACKGROUND Although combining a low-protein diet (LPD) with oral nutritional supplements increases treatment adherence and nutritional status in patients with chronic kidney disease (CKD), the effect of this combination approach in older adults remains unclear. This study examined the impact of a 6% low-protein formula (6% LPF) with diet counseling in older adults with stage 3-5 CKD. METHODS In this three-month randomized controlled study, 66 patients (eGFR < 60 mL/min/1.73 m2, non-dialysis, over 65 years of age) were randomly assigned to an intervention group (LPD plus a 6% LPF) or control group (LPD alone). The 6% LPF comprised 400 kcal, 6 g of protein, eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and various micronutrients. All data were collected at baseline and after three months, including physical performance based on hand grip strength (HGS) and gait speed, nutritional status using Mini Nutritional Assessment-Short Form (MNA-SF) scores, body composition through bioelectrical impedance analysis, and dietary intake from 24-h dietary records. RESULTS This study incorporated 47 participants (median age, 73; median eGFR, 36 ml/min/1.73 m2; intervention group: 24; control group: 23). The intervention group exhibited significant differences in HGS and gait speed, and micronutrient analysis revealed significantly higher monounsaturated fatty acids (MUFA), EPA, DHA, calcium, iron, zinc, copper, thiamine, riboflavin, niacin, B6, B12, and folic acid intake than the control group. MNA-SF scores, macronutrient intake, and body composition did not differ significantly between the two groups. CONCLUSIONS Compared to LPD counseling alone, an LPD prescription with 6% LPF in older adults with CKD stages 3-5 helped relieve physical deterioration and increased micronutrient intake after three months. TRIAL REGISTRATION ClinicalTrials.gov NCT05318014 (retrospectively registered on 08/04/2022).
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Healthy Lifestyle Is Associated with Reduced Mortality in Patients with Non-Alcoholic Fatty Liver Disease.
Yu, C, Gao, J, Ge, X, Wang, X, Ding, Y, Tian, T, Xu, X, Guo, W, Wang, Q, Ge, Z, et al
Nutrients. 2022;14(18)
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Non-alcoholic fatty liver disease (NAFLD) has emerged as the predominant cause of chronic liver disease. Given the association between NAFLD and metabolic syndrome [11,12], lifestyle modification can improve patients’ life quality and prognosis. The aim of this study was to assess the joint association of several modifiable lifestyle factors with overall and cause-specific mortality among NAFLD individuals and depict the mortality risk of varied composite modes of lifestyle. This study is a large, nationally representative, population-based study. It is based on the NHANES III (1988–1994, the National Center for Health Statistics, the Center for Disease Control and Prevention), which used a complex multistage probability design to recruit a representative sample of participants. Results show a protective effect among NAFLD participants following a healthy lifestyle, particularly impacting CVD-related mortality. Notably, among the most common lifestyle factor combinations, the effect of risk reduction on mortality was particularly strong when smoking was avoided. Authors conclude that their findings can be a useful tool to help the general public and patients with NAFLD to understand the importance of maintaining a healthy lifestyle.
Abstract
BACKGROUND AND AIMS It is unclear whether a healthy lifestyle impacts mortality in the presence of non-alcoholic fatty liver disease (NAFLD). The present study aimed to examine the joint association of several modifiable lifestyle factors with mortality risk for NAFLD patients. METHODS We collected lifestyle behavior data form the National Health and Nutrition Examination Survey (NHANES) III from 1988 to 1994 and follow-up data form NHANES III-linked mortality data through 2015. We estimated joint association between four healthy lifestyle factors (non-smoking, non-drinking, regular physical activity, a healthy diet) after NAFLD diagnosis and mortality using Cox proportional hazards regression models. RESULTS During a median of 22.83 years of follow-up, 2932 deaths occurred. The risk of all-cause mortality decreased significantly with the healthy lifestyle scores increasing (p < 0.001). NAFLD patients with a favorable lifestyle (3 or 4 healthy lifestyle factors) reduced 36% of all-cause mortality and 43% of cardiovascular disease (CVD) mortality compared with those with an unfavorable lifestyle (0 or 1 healthy lifestyle factor) (HR, 0.64 [95% CI, 0.50-0.81], 0.57 [95% CI, 0.37-0.88]). Compared with the non-NAFLD group, the number of NAFLD patients required to adhere to a favorable lifestyle to prevent one cardiovascular disease death in 20 years was fewer (77 vs. 125). CONCLUSIONS For the NAFLD patients, adopting a healthy lifestyle could significantly reduce their risk of death.
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Effect of Urolithin A Supplementation on Muscle Endurance and Mitochondrial Health in Older Adults: A Randomized Clinical Trial.
Liu, S, D'Amico, D, Shankland, E, Bhayana, S, Garcia, JM, Aebischer, P, Rinsch, C, Singh, A, Marcinek, DJ
JAMA network open. 2022;5(1):e2144279
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Older adults are the fastest growing age group in the world. As we age, we tend to lose muscle mass and strength which has consequences. Studies have shown that mitochondrial dysfunction plays an important part in age-related diseases. A reduction in the cells ability to dispose of its dysfunctional mitochondria (mitophagy) contributes to poor mitochondrial quality. Urolithin A is a natural food metabolite of the gut microbiome and has been shown to boost mitochondrial health by triggering mitophagy in both preclinical models of aging and in older adults. In this double-blind, placebo-controlled randomized clinical trial, 66 older adults were given either 1000mg of urolithin A or a placebo for 4 months. Muscle fatigue tests and plasma analysis of biomarkers were assessed at baseline, 2 months, and 4 months. Six-minute walk distance and maximal ATP production were assessed using magnetic resonance spectroscopy at baseline and at the end of study at 4 months. This study found that the improvements in the 6-minute walk distance and maximal ATP production in hand muscles were not significant for urolithin A. However, long-term supplementation with urolithin A significantly enhanced skeletal muscle endurance and improved the metabolic markers of mitochondrial function in older adults. This trial suggests that urolithin A may be a promising approach to counteract age-associated muscle decline. Future study is needed to confirm the role of urolithin A supplementation in healthy aging.
Abstract
Importance: Aging is associated with a decline in mitochondrial function and reduced exercise capacity. Urolithin A is a natural gut microbiome-derived food metabolite that has been shown to stimulate mitophagy and improve muscle function in older animals and to induce mitochondrial gene expression in older humans. Objective: To investigate whether oral administration of urolithin A improved the 6-minute walk distance, muscle endurance in hand and leg muscles, and biomarkers associated with mitochondrial and cellular health. Design, Setting, and Participants: This double-blind, placebo-controlled randomized clinical trial in adults aged 65 to 90 years was conducted at a medical center and a cancer research center in Seattle, Washington, from March 1, 2018, to July 30, 2020. Muscle fatigue tests and plasma analysis of biomarkers were assessed at baseline, 2 months, and 4 months. Six-minute walk distance and maximal ATP production were assessed using magnetic resonance spectroscopy at baseline and at the end of study at 4 months. The analysis used an intention-to-treat approach. Interventions: Participants were randomized to receive daily oral supplementation with either 1000 mg urolithin A or placebo for 4 months. Main Outcomes and Measures: The primary end point was change from baseline in the 6-minute walk distance and change from baseline to 4 months in maximal ATP production in the hand skeletal muscle. The secondary end points were change in muscle endurance of 2 skeletal muscles (tibialis anterior [TA] in the leg and first dorsal interosseus [FDI] in the hand). Cellular health biomarkers were investigated via plasma metabolomics. Adverse events were recorded and compared between the 2 groups during the intervention period. Results: A total of 66 participants were randomized to either the urolithin A (n = 33) or the placebo (n = 33) intervention group. These participants had a mean (SD) age of 71.7 (4.94) years, were predominantly women (50 [75.8%]), and were all White individuals. Urolithin A, compared with placebo, significantly improved muscle endurance (ie, increase in the number of muscle contractions until fatigue from baseline) in the FDI and TA at 2 months (urolithin A: FDI, 95.3 [115.5] and TA, 41.4 [65.5]; placebo: FDI, 11.6 [147.4] and TA, 5.7 [127.1]). Plasma levels of several acylcarnitines, ceramides, and C-reactive protein were decreased by urolithin A, compared with placebo, at 4 months (baseline vs 4 mo: urolithin A, 2.14 [2.15] vs 2.07 [1.46]; placebo, 2.17 [2.52] vs 2.65 [1.86]). The mean (SD) increase from baseline in the 6-minute walk distance was 60.8 (67.2) m in the urolithin A group and 42.5 (73.3) m in the placebo group. The mean (SD) change from baseline to 4 months in maximal ATP production in the FDI was 0.07 (0.23) mM/s in the urolithin A group and 0.06 (0.20) mM/s in the placebo group; for the TA, it was -0.03 (0.10) mM/s in the urolithin A group and 0.03 (0.10) mM/s in the placebo group. These results showed no significant improvement with urolithin A supplementation compared with placebo. No statistical differences in adverse events were observed between the 2 groups. Conclusions and Relevance: This randomized clinical trial found that urolithin A supplementation was safe and well tolerated in the assessed population. Although the improvements in the 6-minute walk distance and maximal ATP production in the hand muscle were not significant in the urolithin A group vs the placebo group, long-term urolithin A supplementation was beneficial for muscle endurance and plasma biomarkers, suggesting that urolithin A may counteract age-associated muscle decline; however, future work is needed to confirm this finding. Trial Registration: ClinicalTrials.gov Identifier: NCT03283462.
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A Freshwater Fish-Based Diet Alleviates Liver Steatosis by Modulating Gut Microbiota and Metabolites: A Clinical Randomized Controlled Trial in Chinese Participants With Nonalcoholic Fatty Liver Disease.
He, K, Guo, LL, Tang, H, Peng, X, Li, J, Feng, S, Bie, C, Chen, W, Li, Y, Wang, M, et al
The American journal of gastroenterology. 2022;117(10):1621-1631
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The diagnosis and treatment of non-alcoholic fatty liver disease (NAFLD) is critical, however, there isn’t an effective treatment readily available. On the other hand, lifestyle modifications, particularly a calorie-restricted diet, habitual physical activity, and weight loss, have been advocated for the treatment of NAFLD. The hypothesis of this study was that a freshwater fish-based diet would induce a greater improvement in hepatic steatosis by regulating gut microbiota and its metabolites compared with an alternating combination of freshwater fish-based and red meat-based diets. This study was a randomised, open-label and controlled clinical trial which enrolled participants who were clinically diagnosed of NAFLD with a presence of hepatic steatosis. Participants (n=34) were randomly assigned to either a freshwater fish-based diet or the combination of a freshwater fish-based diet and a red meat-based diet at a daily alternating frequency in a 1:1 ratio. Results showed that dietary freshwater fish consumption: - alleviates liver steatosis in participants with NAFLD; - ameliorates several metabolic phenotypes in participants with NAFLD; - partially redresses gut microbiota dysbiosis in the improvement of the metabolic phenotypes of participants with NAFLD; - improves NAFLD by inducing metabolites alternation. Authors conclude that even though the freshwater fish-based diet showed various positive results for participants with NAFLD, the alternating freshwater fish and red meat consumption may not exacerbate NAFLD, which may be more appropriate to fit the daily eating habits and food diversity for long-term implementation.
Abstract
INTRODUCTION We aimed to assess the effects of 2 isoenergetic intervention diets (a freshwater fish-based diet [F group] or freshwater fish-based and red meat-based diets alternately [F/M group]) on liver steatosis and their relationship with intestinal flora in patients with nonalcoholic fatty liver disease (NAFLD). METHODS In this open-label, 84-day randomized controlled trial, 34 NAFLD patients with hepatic steatosis ≥10% were randomly assigned to the F group or F/M group in a 1:1 ratio using a computer-generated random number allocation by a researcher not involved in the study. Liver fat content and gut microbiota and its metabolites were measured. RESULTS At the end of intervention, the absolute reduction of hepatic steatosis was significantly greater in the F group than in the F/M group (-4.89% vs -1.83%, P = 0.032). Of the 16 secondary clinical outcomes, the improvement in 7 in the F group was greater compared with the F/M group, including alanine aminotransferase and gamma-glutamyl transferase. Furthermore, dietary freshwater fish and red meat consumption alternately did not exacerbate NAFLD. Moreover, changes in the enrichment of Faecalibacterium, short-chain fatty acids, and unconjugated bile acids and the depletion of Prevotella 9 and conjugated bile acids in the F group were significantly greater compared with the F/M group. DISCUSSION Higher intake of freshwater fish may be beneficial to NAFLD by regulating gut microbiota and its metabolites, whereas intake of a similar total of animal protein and fat from the alternating freshwater fish and red meat may not be harmful for NAFLD in the dietary management of patients with NAFLD.
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Effect of Serum Lipid Profile on the Risk of Breast Cancer: Systematic Review and Meta-Analysis of 1,628,871 Women.
Nouri, M, Mohsenpour, MA, Katsiki, N, Ghobadi, S, Jafari, A, Faghih, S, Banach, M, Mazidi, M
Journal of clinical medicine. 2022;11(15)
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Elevated fats in the blood have been associated with an increased risk for breast cancer. However, exact relationships between which fats is still unclear. This systematic review and meta-analysis of 26 studies with 36,590 women aimed to investigate the relationship between fat in the blood and breast cancer risk. The results showed that high levels of high-density lipoprotein (HDL) in the blood decreased a woman’s risk of developing breast cancer, however other fats in the blood such as triglycerides, cholesterol and low-density lipoprotein had no relationship with breast cancer risk. It was concluded that low levels of HDL in the blood are related to an increased risk for breast cancer. This study could be used by healthcare professionals to understand that it is important to recommend exercise, which is a way of increasing HDL’s, in women who are at risk of breast cancer development.
Abstract
Dyslipidemia has been linked to breast cancer incidence. The aim of the present meta-analysis was to further investigate the relationship between the serum lipid profile and breast cancer risk. Databases such as PubMed, EMBASE, and Web of Sciences were searched up to the end of January 2021 using certain MeSH and non-MeSH keywords and combinations to extract related published articles. Twenty-six prospective studies involving 1,628,871 women, of whom 36,590 were diagnosed with breast cancer during the follow-up period met the inclusion criteria. A negative and significant association was found between the HDL-C level and the risk of breast cancer (relative risk (RR): 0.85, 95% CI: 0.72-0.99, I2: 67.6%, p = 0.04). In contrast, TG (RR: 1.02, 95% CI: 0.91-1.13, I2: 54.2%, p = 0.79), total cholesterol (TC) (RR: 0.98, 95% CI: 0.90-1.06, I2: 67.2%, p = 0.57), apolipoprotein A (ApoA) (RR: 0.96, 95% CI: 0.70-1.30, I2: 83.5%, p = 0.78) and LDL-C (RR: 0.93, 95% CI: 0.79-1.09, I2: 0%, p = 0.386) were not associated with breast cancer development. In studies adjusting for hormone use and physical activity, breast cancer risk was positively correlated with TC (RR: 1.05, 95% CI: 1.01-1.10). Similarly, TG was significantly related to breast cancer development after adjustment for baseline lipids (RR: 0.92, 95% CI: 0.85-0.99) and race (any races mentioned in each study) (RR: 1.80, 95% CI: 1.22-2.65). In the present meta-analysis, HDL-C was inversely related to breast cancer risk. Overall, data on the links between lipids and breast cancer are conflicting. However, there is increasing evidence that low HDL-C is related to an increased risk for this type of malignancy.
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An updated systematic review and meta-analysis on adherence to mediterranean diet and risk of cancer.
Morze, J, Danielewicz, A, Przybyłowicz, K, Zeng, H, Hoffmann, G, Schwingshackl, L
European journal of nutrition. 2021;60(3):1561-1586
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The development of cancer is associated with a number of risk factors, including smoking, obesity, sedentary lifestyles, alcohol consumption, infections, pollution, and dietary imbalances. Based on previous research, optimal consumption of fruits, vegetables, and whole grains, along with reduced consumption of red and processed meat, reduces cancer risk. According to this systematic review and meta-analysis, adherence to the Mediterranean diet is associated with lower cancer mortality and site-specific cancer development. A Mediterranean diet includes fruits, vegetables, nuts, legumes, fish, whole grains, extra virgin olive oil, and low amounts of red meat, processed meat, egg, and dairy, along with moderate amounts of red wine. According to this systematic review and meta-analysis, adherence to the Mediterranean diet reduces the risk of cancer mortality and the risk of developing cancers specific to the site, such as colorectal cancer, bladder cancer, gastric cancer, and lung cancer. Among the components of the Mediterranean diet, fruits, vegetables, and whole grains have been shown to reduce cancer risk. Bioactive substances found in Mediterranean diet components require additional robust studies to evaluate their benefits. A healthcare professional can use the results of this study to make clinical decisions and recommend therapeutic interventions to cancer patients.
Abstract
PURPOSE The aim of current systematic review was to update the body of evidence on associations between adherence to the Mediterranean diet (MedDiet) and risk of cancer mortality, site-specific cancer in the general population; all-cause, and cancer mortality as well as cancer reoccurrence among cancer survivors. METHODS A literature search for randomized controlled trials (RCTs), case-control and cohort studies published up to April 2020 was performed using PubMed and Scopus. Study-specific risk estimates for the highest versus lowest adherence to the MedDiet category were pooled using random-effects meta-analyses. Certainty of evidence from cohort studies and RCTs was evaluated using the NutriGrade scoring system. RESULTS The updated search revealed 44 studies not identified in the previous review. Altogether, 117 studies including 3,202,496 participants were enclosed for meta-analysis. The highest adherence to MedDiet was inversely associated with cancer mortality (RRcohort: 0.87, 95% CI 0.82, 0.92; N = 18 studies), all-cause mortality among cancer survivors (RRcohort: 0.75, 95% CI 0.66, 0.86; N = 8), breast (RRobservational: 0.94, 95% CI 0.90, 0.97; N = 23), colorectal (RRobservational: 0.83, 95% CI 0.76, 0.90; N = 17), head and neck (RRobservational: 0.56, 95% CI 0.44, 0.72; N = 9), respiratory (RRcohort: 0.84, 95% CI 0.76, 0.94; N = 5), gastric (RRobservational: 0.70, 95% CI 0.61, 0.80; N = 7), bladder (RRobservational: 0.87, 95% CI 0.76, 0.98; N = 4), and liver cancer (RRobservational: 0.64, 95% CI 0.54, 0.75; N = 4). Adhering to MedDiet did not modify risk of blood, esophageal, pancreatic and prostate cancer risk. CONCLUSION In conclusion, our results suggest that highest adherence to the MedDiet was related to lower risk of cancer mortality in the general population, and all-cause mortality among cancer survivors as well as colorectal, head and neck, respiratory, gastric, liver and bladder cancer risks. Moderate certainty of evidence from cohort studies suggest an inverse association for cancer mortality and colorectal cancer, but most of the comparisons were rated as low or very low certainty of evidence.
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Effects of Endurance Training Intensity on Pulmonary Diffusing Capacity at Rest and after Maximal Aerobic Exercise in Young Athletes.
Dridi, R, Dridi, N, Govindasamy, K, Gmada, N, Aouadi, R, Guénard, H, Laher, I, Saeidi, A, Suzuki, K, Hackney, AC, et al
International journal of environmental research and public health. 2021;18(23)
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Intermittent exercise, where small bouts of exercise are performed over a short period of time and endurance exercise, has been shown to be particularly effective at improving different aspects of lung function. This randomised control trial aimed to determine the effects of intense endurance training compared too moderate endurance training on lung function. The results showed that lung function was improved following intense endurance training but not moderate endurance training. It was concluded that training intensity may be the most important factor when increasing lung function in athletes. This study could be used by professionals to recommend intense endurance training to improve exercise capacity in athletes.
Abstract
This study compared the effects of varying aerobic training programs on pulmonary diffusing capacity (TLCO), pulmonary diffusing capacity for nitric oxide (TLNO), lung capillary blood volume (Vc) and alveolar-capillary membrane diffusing capacity (DM) of gases at rest and just after maximal exercise in young athletes. Sixteen healthy young runners (16-18 years) were randomly assigned to an intense endurance training program (IET, n = 8) or to a moderate endurance training program (MET, n = 8). The training volume was similar in IET and MET but with different work intensities, and each lasted for 8 weeks. Participants performed a maximal graded cycle bicycle ergometer test to measure maximal oxygen consumption (VO2max) and maximal aerobic power (MAP) before and after the training programs. Moreover, TLCO, TLNO and Vc were measured during a single breath maneuver. After eight weeks of training, all pulmonary parameters with the exception of alveolar volume (VA) and inspiratory volume (VI) (0.104 < p < 0889; 0.001 < ES < 0.091), measured at rest and at the end of maximal exercise, showed significant group × time interactions (p < 0.05, 0.2 < ES < 4.0). Post hoc analyses revealed significant pre-to-post decreases for maximal heart rates (p < 0.0001, ES = 3.1) and improvements for VO2max (p = 0.006, ES = 2.22) in the IET group. Moreover, post hoc analyses revealed significant pre-to-post improvements in the IET for DM, TLNO, TLCO and Vc (0.001 < p < 0.0022; 2.68 < ES < 6.45). In addition, there were increases in Vc at rest, VO2max, TLNO and DM in the IET but not in the MET participants after eight weeks of training with varying exercise intensities. Our findings suggest that the intensity of training may represent the most important factor in increasing pulmonary vascular function in young athletes.
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Effect of dietary nitrate on human muscle power: a systematic review and individual participant data meta-analysis.
Coggan, AR, Baranauskas, MN, Hinrichs, RJ, Liu, Z, Carter, SJ
Journal of the International Society of Sports Nutrition. 2021;18(1):66
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Previous reviews have concluded that dietary nitrate (NO3−) improves maximal neuromuscular power in humans, but these were based on a limited number of studies. This is the first systematic review and meta-analysis evaluating the effects of dietary NO3− supplementation on muscular power in humans. The study also aims to quantify the size of this beneficial effect. 19 studies with a total of 268 participants were included. Most of these used concentrated beetroot juice as the source of NO3− given as an acute dose (short term high level). A positive effect of dietary NO3− on muscle power was observed in all 19 studies. Analyses were done on sub groups - age, sex and the amount of muscle mass engaged in the activity. Dietary NO3− intake significantly increases maximal muscle power in humans. The magnitude of this effect has practical and clinical importance; not just for athletes but also for patient groups. This effect is independent of subject age, sex, or the amount of muscle mass engaged in the activity but may be greater with acute vs. repeated dosing. Further research is needed to determine factors such as the optimal supplementation regimen and target population.
Expert Review
Conflicts of interest:
None
Take Home Message:
- This meta-analysis lends quantitative support to previous narrative reviews that nitrate supplementation can enhance maximal power output.
- These findings are highly relevant to team and strength sport athletes, who may not otherwise be supplementing with nitrates.
- These findings are also highly relevant for older populations, where risk of falls and fractures are high and can lead to significant adverse effects on health and quality of life.
Evidence Category:
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A: Meta-analyses, position-stands, randomized-controlled trials (RCTs)
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B: Systematic reviews including RCTs of limited number
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C: Non-randomized trials, observational studies, narrative reviews
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D: Case-reports, evidence-based clinical findings
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E: Opinion piece, other
Summary Review:
- In 2007, researchers uncovered the ingestion of dietary nitrates reduced the oxygen cost of submaximal exercise, and since, over 100 studies have examined the effects of nitrates on endurance performance.
- With regards to the impact of nitrates on maximal force output, only trivial results had been previously found.
- This review study found that while nitrates do not impact force development, they do demonstrate primary effect on the speed of muscle contraction (i.e. muscular power is the product of force x speed).
- The reviews primary finding was that nitrate intake can significantly enhance muscular power, regardless of subject age or sex.
Clinical practice applications:
- These new findings highlight the ability of dietary nitrates to improve neuromuscular power production is highly relevant for team sport athletes, due to the explosive nature of these sports with constant accelerations and decelerations during training and competition.
- In the general population, falls and fractures amongst older adults significantly reduces quality of life and costs the healthcare system hundreds of millions of pounds to treat.
- Improved contractile properties of muscle, most notably speed of contraction, may offer protection to older adults as well as the benefit of additional nitric oxide (NO) to support vascular health as well.
- The typical intake of dietary nitrates in the general population is about 31-185mg/day in Europe and 40-100mg/day in North America. Most studies use doses between 300-600mg of dietary nitrates. Increasing dietary or supplemental intake is key to achieving the neuromuscular effect.
Considerations for future research:
- The results of the present meta-analysis clearly demonstrate that dietary nitrates increases muscle power in humans, but the mechanism responsible for this effect is still unclear.
- There are notable differences between rodent and human metabolism of dietary nitrates, therefore the biochemical mechanism by which nitrate intake improves human muscle power requires additional study.
Abstract
BACKGROUND Previous narrative reviews have concluded that dietary nitrate (NO3-) improves maximal neuromuscular power in humans. This conclusion, however, was based on a limited number of studies, and no attempt has been made to quantify the exact magnitude of this beneficial effect. Such information would help ensure adequate statistical power in future studies and could help place the effects of dietary NO3- on various aspects of exercise performance (i.e., endurance vs. strength vs. power) in better context. We therefore undertook a systematic review and individual participant data meta-analysis to quantify the effects of NO3- supplementation on human muscle power. METHODS The literature was searched using a strategy developed by a health sciences librarian. Data sources included Medline Ovid, Embase, SPORTDiscus, Scopus, Clinicaltrials.gov , and Google Scholar. Studies were included if they used a randomized, double-blind, placebo-controlled, crossover experimental design to measure the effects of dietary NO3- on maximal power during exercise in the non-fatigued state and the within-subject correlation could be determined from data in the published manuscript or obtained from the authors. RESULTS Nineteen studies of a total of 268 participants (218 men, 50 women) met the criteria for inclusion. The overall effect size (ES; Hedge's g) calculated using a fixed effects model was 0.42 (95% confidence interval (CI) 0.29, 0.56; p = 6.310 × 10- 11). There was limited heterogeneity between studies (i.e., I2 = 22.79%, H2 = 1.30, p = 0.3460). The ES estimated using a random effects model was therefore similar (i.e., 0.45, 95% CI 0.30, 0.61; p = 1.064 × 10- 9). Sub-group analyses revealed no significant differences due to subject age, sex, or test modality (i.e., small vs. large muscle mass exercise). However, the ES in studies using an acute dose (i.e., 0.54, 95% CI 0.37, 0.71; p = 6.774 × 10- 12) was greater (p = 0.0211) than in studies using a multiple dose regimen (i.e., 0.22, 95% CI 0.01, 0.43; p = 0.003630). CONCLUSIONS Acute or chronic dietary NO3- intake significantly increases maximal muscle power in humans. The magnitude of this effect-on average, ~ 5%-is likely to be of considerable practical and clinical importance.
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NAD+-Precursor Supplementation With L-Tryptophan, Nicotinic Acid, and Nicotinamide Does Not Affect Mitochondrial Function or Skeletal Muscle Function in Physically Compromised Older Adults.
Connell, NJ, Grevendonk, L, Fealy, CE, Moonen-Kornips, E, Bruls, YMH, Schrauwen-Hinderling, VB, de Vogel, J, Hageman, R, Geurts, J, Zapata-Perez, R, et al
The Journal of nutrition. 2021;151(10):2917-2931
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Ageing is associated with the progressive loss of muscle, which can result in impaired movement, an increased risk for falls and disrupted energy production. During ageing there is a decrease in one of the substrates involved in producing energy known as NAD+. Studies in animals have shown that supplementing with a precursor of NAD+ promotes longevity and energy production. In humans supplementation with a precursor of NAD+ has been shown to improve heart health and be of benefit to individuals with obesity. This randomised control trial aimed to determine the effect of supplementing the NAD+ precursors, tryptophan, nicotinic acid, and nicotinamide on muscle function in 14 older adults with impaired physical function. The results showed that supplementation had no effect on NAD+ and had no effect on muscular energy production nor exercise performance following a cycling test. It was concluded that supplementation with an NAD+ precursor does not improve muscle function. This study could be used by healthcare professionals to understand that a combination supplement of tryptophan, nicotinic acid, and nicotinamide may not benefit the physical function of older adults.
Abstract
BACKGROUND Boosting NAD+ via supplementation with niacin equivalents has been proposed as a potential modality capable of promoting healthy aging and negating age-dependent declines of skeletal muscle mass and function. OBJECTIVES We investigated the efficacy of NAD+-precursor supplementation (tryptophan, nicotinic acid, and nicotinamide) on skeletal muscle mitochondrial function in physically compromised older adults. METHODS A randomized, double-blind, controlled trial was conducted in 14 (female/male: 4/10) community-dwelling, older adults with impaired physical function [age, 72.9 ± 4.0 years; BMI, 25.2 ± 2.3 kg/m2]. Participants were supplemented with 207.5 mg niacin equivalents/day [intervention (INT)] and a control product (CON) that did not contain niacin equivalents, each for 32 days. The primary outcomes tested were mitochondrial oxidative capacity and exercise efficiency, analyzed by means of paired Student's t-tests. Secondary outcomes, such as NAD+ concentrations, were analyzed accordingly. RESULTS Following supplementation, skeletal muscle NAD+ concentrations [7.5 ± 1.9 compared with 7.9 ± 1.6 AU, respectively] in INT compared with CON conditions were not significantly different compared to the control condition, whereas skeletal muscle methyl-nicotinamide levels were significantly higher under NAD+-precursor supplementation [INT, 0.098 ± 0.063 compared with CON, 0.025 ± 0.014; P = 0.001], suggesting an increased NAD+ metabolism. Conversely, neither ADP-stimulated [INT, 82.1 ± 19.0 compared with CON, 84.0 ± 19.2; P = 0.716] nor maximally uncoupled mitochondrial respiration [INT, 103.4 ± 30.7 compared with CON, 108.7 ± 33.4; P = 0.495] improved under NAD+-precursor supplementation, nor did net exercise efficiency during the submaximal cycling test [INT, 20.2 ± 2.77 compared with CON, 20.8 ± 2.88; P = 0.342]. CONCLUSIONS Our findings are consistent with previous findings on NAD+ efficacy in humans, and we show in community-dwelling, older adults with impaired physical function that NAD+-precursor supplementation through L-tryptophan, nicotinic acid, and nicotinamide does not improve mitochondrial or skeletal muscle function. This study was registered at clinicaltrials.gov as NCT03310034.
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10.
Effect of sleep duration on dietary intake, desire to eat, measures of food intake and metabolic hormones: A systematic review of clinical trials.
Soltanieh, S, Solgi, S, Ansari, M, Santos, HO, Abbasi, B
Clinical nutrition ESPEN. 2021;45:55-65
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Plain language summary
Adequate sleep is crucial to health. Yet, sleep disturbances have become very common in modern societies. A lack of sleep is linked to increased risk for several chronic diseases such as diabetes, high blood pressure, metabolic syndrome and cardiovascular disease. Furthermore, appetite-regulating hormones can be disrupted by sleep shortages, which is thought to drive chronic overeating, leading to weight gain, obesity and its associated health consequences. This review examined the relationship between sleep duration and food consumption and energy intake, whilst also monitoring changes in body weight and appetite-regulating hormones. The review encompassed 50 randomized controlled trials (RCTs) with 3387 participants, including 1079 children and adolescents and 2308 adults. The findings suggested that sleep shortages contribute to significant increases in calorie intake, fat intake, increased body weight, appetite, hunger, more frequent eating and bigger portion sizes. In this review lack of sleep did not change protein and carbohydrate intake. Nor did lack of sleep make people exert more or less energy overall, however, a variance amongst ethnic groups was observed here. There was not enough evidence for changes in metabolic rate, so the review assumed no significant effect. When viewed collectively, the appetite-regulating hormones of leptin and ghrelin, the stress hormone cortisol and the sugar-regulating hormone insulin were not significantly influenced by sleep duration. However, there seemed to be a wide variance of outcomes when looking at individual studies' results. In conclusion, the authors reiterated the importance of sleep for health maintenance, advocating for a minimum of 7 hours of sleep per day for adults and that, despite busy modern lifestyles, sleep optimisation strategies should be prioritised. Less than 6 hours of sleep per day increases the risk of health consequences, like weight gain and metabolic disorders and sleep management should be considered part of their treatment protocols.
Expert Review
Conflicts of interest:
None
Take Home Message:
- Reduced sleep duration may serve as a mediator for weight gain in part due to increased appetite, increased fat intake and disruptions to energy balance.
- Enhancing sleep quality may serve to support weight loss protocols.
Evidence Category:
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A: Meta-analyses, position-stands, randomized-controlled trials (RCTs)
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B: Systematic reviews including RCTs of limited number
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C: Non-randomized trials, observational studies, narrative reviews
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D: Case-reports, evidence-based clinical findings
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E: Opinion piece, other
Summary Review:
Introduction
Short sleep duration and disruptions to circadian rhythm have been associated with being overweight and obese. It has been suggested that sleep restriction may interfere with appetite regulating hormones leading to increased appetite and disrupted energy balance.
This study aimed to systematically review studies exploring the relationship between sleep duration and food consumption, energy intake, anthropometric characteristics and appetite-regulating hormones.
Methods
This systematic review included 50 randomised controlled trials including 3,387 participants.
Results
Energy intake
- 13 out of 30 the included studies found that short sleep conditions led to higher energy intake.
- 1 study identified that sleep restriction resulted in a 15.3% and 9.2% increase in energy intake in both women and men.
- 3 studies noted that prolonging sleep duration led to a reduction in energy intake.
- 1 study reported a reduction in energy intake after sleep restriction (P=0.031).
Fat consumption
- 9 studies out of 22 identified a significant association between short sleep and increased fat consumption.
- 7 studies did not identify a difference between groups.
- 3 studies noted a decrease in fat consumption following prolonged sleep (P<0.001, P<0.05, P=0.04).
Hunger and appetite
- 11 studies out of 17 observed that sleep restriction resulted in increased hunger ratings.
- 3 studies found an increase in appetite following sleep restriction (P<0.01) with 3 finding no difference..
- 1 study reported a decrease in appetite following sleep restriction.
- 2 studies noted that portion sizes increased as a result of sleep restriction (P<0.01).
- 1 study reported an increase in eating occasions following restricted sleep compared to habitual sleep (6.08 vs 4.96).
Body weight
- 6 studies out of 14 found no effect of sleep loss on body weight.
- 4 studies identified that sleep restriction led to weight gain (P<0.001, P<0.05, P=0.14, P=0.031).
- 2 studies reported weight loss following increased sleep duration (P<0.001).
Ghrelin and leptin
- Leptin and ghrelin levels were generally not found to be influenced by sleep duration, with the exception of a few studies.
Clinical practice applications:
Reduced sleep duration may promote weight gain by:
- Increasing energy intake.
- Increasing fat consumption.
- Increasing hunger and appetite.
- Increasing portion sizes and eating occasions.
Prolonging sleep duration may support weight loss by:
- Reducing energy intake.
- Reducing fat intake.
Considerations for future research:
- Mixed results on the influence of sleep restriction on appetite regulating hormones, leptin and ghrelin.
- Some studies noted the negative impact of sleep restriction on leptin and ghrelin concentrations, collectively shortened sleep duration did not appear to influence these hormones.
- Further sleep restriction studies exploring additional appetite regulating hormones and neuropeptides and the reward system may provide a more definitive understanding of the underlying mechanism for reduced sleep duration to disrupt the appetite and energy balance and promote weight gain.
Abstract
BACKGROUND AND AIMS Sleep, as well as diet and physical activity, plays a significant role in growth, maturation, health, and regulation of energy homeostasis. Recently, there is increasing evidence indicating a possible causal association between sleep duration and energy balance. We aimed to examine the relationship between sleep duration and food consumption, energy intake, anthropometric characteristics, and appetite-regulating hormones by randomized controlled trials (RCTs). METHODS Electronic literature searches were conducted on Medline, Web of Science, and Google Scholar until July 2020. The search was conducted with the following words: "Sleep Duration", "Circadian Rhythm", "Sleep Disorders" in combination with "Obesity", "Overweight", "Abdominal Obesity", "Physical Activity", "Energy Intake", "Body Mass Index", "Lipid Metabolism", "Caloric Restriction", Leptin, "Weight Gain", and "Appetite Regulation" using human studies.methods RESULTS After screening 708 abstracts, 50 RCTs (7 on children or adolescents and 43 on adults) were identified and met the inclusion criteria. In general, the findings suggested that sleep restriction may leads to a significant increment in energy intake, fat intake, body weight, appetite, hunger, eating occasions, and portion size, while protein and carbohydrate consumption, total energy expenditure, and respiratory quotient remained unaffected as a result of sleep restriction. Serum leptin, ghrelin, and cortisol concentrations were not influenced by sleep duration as well. CONCLUSION Insufficient sleep can be considered as a contributing factor for energy imbalance, weight gain, and metabolic disorders and it is suggested that to tackle disordered eating it may be necessary to pay more attention to sleep duration.