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Association between COVID-19 and Male Fertility: Systematic Review and Meta-Analysis of Observational Studies.
Wang, S, Zhang, A, Pan, Y, Liu, L, Niu, S, Zhang, F, Liu, X
The world journal of men's health. 2023;41(2):311-329
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Several studies have been published documenting possible relationships between Covid-19 and male infertility, but it remains unclear whether Covid-19 affects sperm quality and sex hormones. This meta-analysis and systematic review of observational studies aimed to determine any relationship between Covid-19 infection and male fertility. The results showed that Covid-19 decreased sperm count, sperm concentration, motility, but had no effect on semen volume, immotility, normal morphology or nonprogressive sperm motility. Infection also affected some hormone levels and that effects on hormones were dependent on age of infection onset. Covid-19 infection with or without fever also differentially affected outcomes with those with fever having reduced sperm concentration and progressive sperm motility, which was not seen in those who did not experience fever. Disease severity also affected outcomes with those with moderate Covid-19 having reduced sperm motility, which was not seen in individuals who had mild disease. It was concluded that Covid-19 infection reduced sperm quality and disrupted sex hormones. This study could be used by healthcare professionals to understand that Covid-19 infection may affect the fertility of men.
Abstract
PURPOSE Whether COVID-19 reduces male fertility remains requires further investigation. This meta-analysis and systematic review evaluated the impact of COVID-19 on male fertility. MATERIALS AND METHODS The literature in PubMed, Embase, MEDLINE, Web of Science, and Cochrane Library up to January 01, 2022 was systematically searched, and a meta-analysis was conducted to investigate the effect of COVID-19 on male fertility. Totally 17 studies with a total of 1,627 patients and 1,535 control subjects were included in our meta-analysis. RESULTS Regarding sperm quality, COVID-19 decreased the total sperm count (p=0.012), sperm concentration (p=0.001), total motility (p=0.001), progressive sperm motility (p=0.048), and viability (p=0.031). Subgroup analyses showed that different control group populations did not change the results. It was found that during the illness stage of COVID-19, semen volume decreased, and during the recovery stage of COVID-19, sperm concentration and total motility decreased <90 days. We found that sperm concentration and total motility decreased during recovery for ≥90 days. Fever because of COVID-19 significantly reduced sperm concentration and progressive sperm motility, and COVID-19 without fever ≥90 days, the sperm total motility and progressive sperm motility decreased. Regarding disease severity, the moderate type of COVID-19 significantly reduced sperm total motility, but not the mild type. Regarding sex hormones, COVID-19 increased prolactin and estradiol. Subgroup analyses showed that during the illness stage, COVID-19 decreased testosterone (T) levels and increased luteinizing hormone levels. A potential publication bias may have existed in our meta-analysis. CONCLUSIONS COVID-19 in men significantly reduced sperm quality and caused sex hormone disruption. COVID-19 had long-term effects on sperm quality, especially on sperm concentration and total motility. It is critical to conduct larger multicenter studies to determine the consequences of COVID-19 on male fertility.
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The effects of Berberis vulgaris consumption on plasma levels of IGF-1, IGFBPs, PPAR-γ and the expression of angiogenic genes in women with benign breast disease: a randomized controlled clinical trial.
Pirouzpanah, S, Asemani, S, Shayanfar, A, Baradaran, B, Montazeri, V
BMC complementary and alternative medicine. 2019;19(1):324
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Individuals diagnosed with benign breast disease (BBD) are at an increased risk of developing breast cancer. A hormone known as insulin-like growth factor-1 (IGF-1) has been reported to correlate with the development of BBD into breast cancer. Berberis vulgaris (BV) is a herbal plant, which may have anti-cancer properties. Previous studies have reported alterations in proteins involved in tumour growth upon regular consumption, but none have looked at IGF-1 in individuals with BBD. This randomised double-blind trial aimed to study the effects of BV on IGF-1 and other proteins involved in tumour growth in 85 women recently diagnosed with BBD over an 8-week period. The results showed that compliance to BV treatment was high. IGF-1 significantly decreased within both groups. When compared to each other, there was a 16% drop in IGF-1 in the BV group compared to the placebo group. Several proteins and growth factors were also altered by BV treatment in favour of reducing breast cancer risk. The authors concluded that BV juice may reduce the risk of BBD turning into breast cancer. Clinicians could use this study to recommend regular consumption of BV to individuals with BBD as part of a wellness regime to reduce their risk of developing breast cancer.
Abstract
BACKGROUND The present study was designed to investigate the effects of Berberis vulgaris (BV) juice consumption on plasma levels of insulin-like growth factor (IGF-1), IGF-binding proteins (IGFBPs), and the expression of PPAR-γ, VEGF and HIF in women with benign breast disease. METHODS This parallel design randomized, double-blind controlled clinical trial was conducted on 85 eligible patients diagnosed with benign breast disease. They were assigned randomly into either BV juice group (n = 44, BV juice: 480 ml/day) or placebo group (n = 41, BV placebo juice: 480 ml/day) for 8 weeks intervention. Participants, caregivers and those who assessed laboratory analyses were blinded to the assignments. Plasma levels of biomarkers were measured at baseline and after 8 weeks by ELISA. Quantitative real-time PCR was used to measure the fold change in the expression of each interested gene. RESULTS The compliance of participants was 95.2% and 40 available subjects analyzed in each group at last. Relative treatment (RT) effects for BV juice caused 16% fall in IGF-1 concentration and 37% reduction in the ratio of IGF-1/1GFBP1. Absolute treatment effect expressed 111 ng/ml increased mean differences of IGFBP-3 between BV group and placebo. Plasma level of PPAR-γ increased in both groups but it was not significant. Fold changes in the expressions of PPAR-γ, VEGF and HIF showed down-regulation in the intervention group compared to placebos (P < 0.05). CONCLUSIONS The BV juice intervention over 8 weeks was accompanied by acceptable efficacy and decreased plasma IGF-1, and IGF-1/IGFBP-1 ratio partly could be assigned to enhanced IGFBP-1 level in women with BBD. The intervention caused reductions in the expression levels of PPAR, VEGF, and HIF which are remarkable genomic changes to potentially prevent breast tumorigenesis. TRIAL REGISTRATION IRCT2012110511335N2. Registered 10 July 2013 (retrospectively registered).
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How Does the Brain Implement Adaptive Decision Making to Eat?
Compan, V, Walsh, BT, Kaye, W, Geliebter, A
The Journal of neuroscience : the official journal of the Society for Neuroscience. 2015;35(41):13868-78
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While food intake is critical for survival, adaptive decision-making can be altered through various mechanisms and eventually lead to disordered eating patterns. Feeding behaviour is dependent on homeostatic rules, motivational drives, biological predispositions and external stressors. This complex web elucidates how humans can decide to satisfy or abstain from hunger cues, and the underlying mechanisms of this behaviour have been increasingly explored. This review summarises the overall neural circuitry in restrictive food choice and binge eating. Serotonergic systems play a key role in eating disorders because they are involved in responses to stress, emotions and feeding behaviour. The decision to overeat or abstain from eating is a reward, and this goal-directed and persistent behaviour mirror some aspects of drug dependence. This review found that voluntary processes in the nervous system could be modified to predominate over homeostatic control of hunger. Eating disorders may emerge when serotonin neurons reach their limit of adaptive capacities, potentially to the extent of compromised survival. This study provides a basis for developing more effective interventions for this population.
Abstract
Adaptive decision making to eat is crucial for survival, but in anorexia nervosa, the brain persistently supports reduced food intake despite a growing need for energy. How the brain persists in reducing food intake, sometimes even to the point of death and despite the evolution of multiple mechanisms to ensure survival by governing adaptive eating behaviors, remains mysterious. Neural substrates belong to the reward-habit system, which could differ among the eating disorders. The present review provides an overview of neural circuitry of restrictive food choice, binge eating, and the contribution of specific serotonin receptors. One possibility is that restrictive food intake critically engages goal-directed (decision making) systems and "habit," supporting the view that persistent caloric restriction mimics some aspects of addiction to drugs of abuse. SIGNIFICANCE STATEMENT An improved understanding of the neural basis of eating disorders is a timely challenge because these disorders can be deadly. Up to 70 million of people in the world suffer from eating disorders. Anorexia nervosa affects 1-4% of women in United States and is the first cause of death among adolescents in Europe. Studies relying on animal models suggest that decision making to eat (or not) can prevail over actual energy requirements due to emotional disturbances resulting in abnormal habitual behavior, mimicking dependence. These recent studies provide a foundation for developing more specific and effective interventions for these disorders.
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Simultaneous comparison of helium and nitrogen expiratory "closing volumes".
Travis, DM, Green, M, Don, H
Journal of applied physiology. 1973;34(3):304-8
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Restricted sleep has been linked to obesity but the underlying mechanisms are not clear. This study aimed to assess whether restricted sleep (4.5hrs for 4 consecutive nights) alters the appetite-regulating hormones ghrelin, leptin and pancreatic polypeptide in the following 24hrs in 19 healthy, lean men (BMI 19-24.9). This randomised crossover study assessed whether those hormonal changes predicted the food intake during ad libitum feeding. The study found that Ghrelin levels were increased after sleep restriction but did not alter leptin or pancreatic polypeptide profiles. Sleep restriction was associated with an increase in calorie consumption from snacks, primarily from carbohydrates. They concluded that restricted sleep significantly increases ghrelin levels. Elevated ghrelin is associated with an increased calorie consumption which may lead to the development of obesity.