A high consumption of tomato and lycopene is associated with a lower risk of cancer mortality.

PMID: 

Public Health Nutr. 2020 Feb 27:1-7. Epub 2020 Feb 27. PMID: 32102720

Abstract Title: 

A high consumption of tomato and lycopene is associated with a lower risk of cancer mortality: results from a multi-ethnic cohort.

Abstract: 

OBJECTIVE: We investigated the association between the consumption of tomato and lycopene and cancer mortality among US adults.DESIGN: Prospective.SETTING: The National Health and Nutrition Examination Survey (1999-2010).PARTICIPANTS: Participants with estimated dietary data on tomato and lycopene consumption were included. Outcome data up until 31 December 2011 were also ascertained. Cox proportional hazard regression models were used to relate baseline tomato and lycopene consumption with cancer mortality. We conducted a competing-risk survival analysis to account for deaths from other causes.RESULTS: Adjusted Cox models showed that tomato and lycopene intake were inversely related (hazard ratio (95 % CI)) to cancer mortality: 0·86 (0·81, 0·92) and 0·79 (0·74, 0·82), respectively. In the adjusted competing-risk models, the sub-hazard ratios (95 % CI) were 0·89 (0·83, 0·94) and 0·82 (0·78, 0·86) for cancer mortality for tomato and lycopene intake, respectively. No significant interaction was found for the association between tomato and lycopene consumption and cancer mortality while comparing older (aged>50 years) v. younger adults (Pinteraction>0·173 for all) and obese v. non-obese (Pinteraction>0·352 for all).CONCLUSIONS: Our results demonstrate the potential beneficial effects of a high dietary intake of tomato and lycopene on cancer death. Further prospective studies are needed to explore the association.

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Protective effects of lycopene in cancer, cardiovascular, and neurodegenerative diseases.

PMID: 

Pharmacol Res. 2020 Feb 29:104730. Epub 2020 Feb 29. PMID: 32126272

Abstract Title: 

Protective effects of lycopene in cancer, cardiovascular, and neurodegenerative diseases: An update on epidemiological and mechanistic perspectives.

Abstract: 

Recent mechanistic and epidemiological studies have provided insights into health benefits of dietary lycopene to decrease the risk and complications associated with several chronic diseases such as cardiovascular diseases (CVD), obesity, type 2 diabetes, cancer, and neurodegenerative disorders. These chronic diseases are primarily associated with oxidative stress-induced systemic and low-grade chronic inflammation. Owing to its potent antioxidant properties, lycopene can potentially alleviate enhanced levels of proinflammatory mediators (e.g., proinflammatory cytokines IL-8, -6, and -1, and oxidized phospholipids) and prevent NF-κB activation by modulating oxidative stress. Moreover, lycopene serves as a precursor for various oxidative cleavage products and metabolites including Apo-8'-, apo-10'-, and apo-12'-lycopenals that can interact with multiple transcription factors (e.g., Nrf2, RARs, RXRs, and PPARs) to overexpressantioxidant and cytoprotective Phase II enzymes and other growth-stimulating proteins (e.g., brain-derived neurotrophic factor (BDNF) for enhanced neuroprotection. These events altogether can protect the body from chronic inflammatory disorders. In the present review, the latest mechanistic development from cell and animal models and results of case-control, cohort, and randomized trials are discussed to support the protective part of lycopene in cancer, CVD, and neurodegenerative disorders. This review focuses on cellular and molecular events involved in protective effects of lycopene. Although molecular and cellular mechanisms involved in health-promoting activities of lycopene have been reported, no detailed mechanistic studies have been published. Hence, future studies should be conducted to elucidate the mechanistic role(s) of lycopene-derived oxidation products in modulating cellular signaling.

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Obesity-related microenvironment promotes emergence of virulent influenza virus strains.

PMID: 

mBio. 2020 Mar 3 ;11(2). Epub 2020 Mar 3. PMID: 32127459

Abstract Title: 

Obesity-Related Microenvironment Promotes Emergence of Virulent Influenza Virus Strains.

Abstract: 

Obesity is associated with increased disease severity, elevated viral titers in exhaled breath, and significantly prolonged viral shed during influenza A virus infection. Due to the mutable nature of RNA viruses, we questioned whether obesity could also influence influenza virus population diversity. Here, we show that minor variants rapidly emerge in obese mice. The variants exhibit increased viral replication, resulting in enhanced virulence in wild-type mice. The increased diversity of the viral population correlated with decreased type I interferon responses, and treatment of obese mice with recombinant interferon reduced viral diversity, suggesting that the delayed antiviral response exhibited in obesity permits the emergence of a more virulent influenza virus population. This is not unique to obese mice. Obesity-derived normal human bronchial epithelial (NHBE) cells also showed decreased interferon responses and increased viral replication, suggesting that viral diversity also was impacted in this increasing population.Currently, 50% of the adult population worldwide is overweight or obese. In these studies, we demonstrate that obesity not only enhances the severity of influenza infection but also impacts viral diversity. The altered microenvironment associated with obesity supports a more diverse viral quasispecies and affords the emergence of potentially pathogenic variants capable of inducing greater disease severity in lean hosts. This is likely due to the impaired interferon response, which is seen in both obese mice and obesity-derived human bronchial epithelial cells, suggesting that obesity, aside from its impact on influenza virus pathogenesis, permits the stochastic accumulation of potentially pathogenic viral variants, raising concerns about its public health impact as the prevalence of obesity continues to rise.

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The results suggest that combined therapy with crocin and exercise may be protective for motor and memory deficits in Parkinson’s disease patients.

PMID: 

Metab Brain Dis. 2019 04 ;34(2):459-468. Epub 2019 Jan 16. PMID: 30652256

Abstract Title: 

Pretreatment with crocin along with treadmill exercise ameliorates motor and memory deficits in hemiparkinsonian rats by anti-inflammatory and antioxidant mechanisms.

Abstract: 

The motor symptoms of Parkinson's disease (PD) are preceded by non-motorized symptoms including memory deficits. Treatment with dopamine replacement medications, such as L-DOPA only control motor symptoms and does not meet the clinical challenges of the disease, such as dyskinesia, non-motor symptoms, and neuroprotection. The purpose of the current study was to examine the neuroprotective potential of crocin and physical exercise in an animal model of PD. Male Wistar rats ran on a horizontal treadmill and/or pretreated with crocin at a dose of 100 mg/kg. Then, 16 μg of the neurotoxin 6-hydroxydopamine (6-OHDA) was microinjected into left medial forebrain bundle. Crocin treatment and/or exercise continued for 6 more weeks. Spatial and aversive memories, rotational behaviour, inflammatory and oxidative stress parameters were assessed at theend of week 6 post surgery. The results showed that pretreatment with crocin alone and in combination with exercise decreased the total number of rotaions as compared with 6-OHDA-lesioned group. Furthermore, treatment of parkinsonian rats with crocin along with exercise training improved aversive and spatial memories. Biochemical analysis showed that crocin and exercise (alone and in combination) reduced tumor necrosis factor- (TNF) α levels in the striatum. Moreover, treatment with crocin at a dose of 100 mg/kg decreased the lipid peroxidation levels in the hippocampus, while exercise training increased the total thiol concentration. In conclusion, our findings indicated that pretreatment with crocin along with treadmill exercise ameliorated motor and memory deficits induced by 6-OHDA, which is considered to be due to their antioxidant and anti-inflammatory activities. The results suggest that combined therapy with crocin and exercise may be protective for motor and memory deficits in PD patients.

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High doses of anti-inflammatory drugs compromise muscle strength and hypertrophic adaptations to resistance training in young adults.

PMID: 

Acta Physiol (Oxf). 2018 02 ;222(2). Epub 2017 Sep 16. PMID: 28834248

Abstract Title: 

High doses of anti-inflammatory drugs compromise muscle strength and hypertrophic adaptations to resistance training in young adults.

Abstract: 

AIMS: This study tested the hypothesis that high doses of anti-inflammatory drugs would attenuate the adaptive response to resistance training compared with low doses.METHODS: Healthy men and women (aged 18-35 years) were randomly assigned to daily consumption of ibuprofen (IBU; 1200 mg; n = 15) or acetylsalicylic acid (ASA; 75 mg; n = 16) for 8 weeks. During this period, subjects completed supervised knee-extensor resistance training where one leg was subjected to training with maximal volitional effort in each repetition using a flywheel ergometer (FW), while the other leg performed conventional (work-matched across groups) weight-stack training (WS). Before and after training, muscle volume (MRI) and strength were assessed, and muscle biopsies were analysed for gene and protein expression of muscle growth regulators.RESULTS: The increase in m. quadriceps volume was similar between FW and WS, yet was (averaged across legs) greater in ASA (7.5%) compared with IBU (3.7%, group difference 34 cm; P = 0.029). In the WS leg, muscle strength improved similarly (11-20%) across groups. In the FW leg, increases (10-23%) in muscle strength were evident in both groups yet they were generally greater (interaction effects P 

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Rejuvenating the brain with chronic exercise through adult neurogenesis.

PMID: 

Front Neurosci. 2019 ;13:1000. Epub 2019 Sep 18. PMID: 31619959

Abstract Title: 

Rejuvenating the Brain With Chronic Exercise Through Adult Neurogenesis.

Abstract: 

The aging brain presents a general decline in plasticity that also affects hippocampal neurogenesis. Besides the well-known reduction in the rate of neuronal generation, development of new neurons is largely delayed in the aging brain. We have recently shown that this slow development is accelerated when middle-aged mice perform voluntary exercise in a running wheel. It is unclear whether the effects of exercise on neurogenic plasticity are persistent in time in a manner that might influence neuronal cohorts generated over an extended time span. To clarify these issues, we examined the effects of exercise length in 3-week-old neurons and found that their development is accelerated only when running occurs for long (3-4 weeks) but not short periods (1 week). Furthermore, chronic running acted with similar efficiency on neurons that were born at the onset, within, or at the end of the exercise period, lasting until 3 months. Interestingly, no effects were observed on neurons born 1 month after exercise had ended. Our results indicate that multiple neuronal cohorts born throughout the exercise span integrate very rapidly in the aging brain, such that the effects of running will accumulate and expand network assembly promoted by neurogenesis. These networks are likely to be more complex than those assembled in a sedentary mouse due to the faster and more efficient integration of new neurons.

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Moderate-intensity exercise training ameliorates the diabetes-suppressed spermatogenesis and improves sperm parameters.

PMID: 

Andrologia. 2019 Dec ;51(11):e13457. Epub 2019 Oct 23. PMID: 31642094

Abstract Title: 

Moderate-intensity exercise training ameliorates the diabetes-suppressed spermatogenesis and improves sperm parameters: Insole and simultaneous with insulin.

Abstract: 

The current study was conducted to investigate the ameliorative effect of moderate-intensity exercise training insole and simultaneous with insulin on diabetes (DM)-induced pathogenesis at the testicular tissue and sperm level. For this purpose, 36 mature male Wistar rats were divided into six groups, including sedentary control (Con), exercise training (EX), sedentary experimental DM-induced (SDM), exercise training + DM-induced (DM + EX), insulin-treated sedentary DM-induced (DM + INS) and exercise training and insulin-treated DM-induced (DM + INS + EX) groups. Following DM induction, the 6-week exercise training intervention (30 min of moderate-intensity running on a treadmill, once daily [5 days/week]) was considered in EX groups. The tubular differentiation (TDI) and spermiogenesis (SPI) indices, testicular total antioxidant capacity (TAC), superoxide dismutase (SOD) and glutathione peroxidase (GPX) contents, serum testosterone and insulin levels, the apoptosis ratio and sperm parameterswere assessed. The exercise in sole (EX) and simultaneous forms with INS (DM + INS + EX group) ameliorated the DM-suppressed spermatogenesis and spermiogenesis indices, up-regulated the serum testosterone and insulin levels, enhanced testicular SOD content, inhibited the apoptosis and improved almost all sperm parameters. In conclusion, exercise training, when simultaneously considered with insulin, fairly boosts the insulin-induced impacts, including the up-regulated testicular endocrine and antioxidant status, spermatogenesis and sperm quality.

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Running and swimming prevent the deregulation of the BDNF/TrkB neurotrophic signalling at the neuromuscular junction in amyotrophic lateral sclerosis.

PMID: 

Cell Mol Life Sci. 2019 Oct 23. Epub 2019 Oct 23. PMID: 31646358

Abstract Title: 

Running and swimming prevent the deregulation of the BDNF/TrkB neurotrophic signalling at the neuromuscular junction in mice with amyotrophic lateral sclerosis.

Abstract: 

Nerve-induced muscle contraction regulates the BDNF/TrkB neurotrophic signalling to retrogradely modulate neurotransmission and protect the neuromuscular junctions and motoneurons. In muscles with amyotrophic lateral sclerosis, this pathway is strongly misbalanced and neuromuscular junctions are destabilized, which may directly cause the motoneuron degeneration and muscular atrophy observed in this disease. Here, we sought to demonstrate (1) that physical exercise, whose recommendation has been controversial in amyotrophic lateral sclerosis, would be a good option for its therapy, because it normalizes and improves the altered neurotrophin pathway and (2) a plausible molecular mechanism underlying its positive effect. SOD1-G93A mice were trained following either running or swimming-based protocols since the beginning of the symptomatic phase (day 70 of age) until day 115. Next, the full BDNF pathway, including receptors, downstream kinases and proteins related with neurotransmission, was characterized and motoneuron survival was analysed. The results establish that amyotrophic lateral sclerosis-induced damaging molecular changes in the BDNF/TrkB pathway are reduced, prevented or even overcompensated by precisely defined exercise protocols that modulate TrkB isoforms and neurotransmission regulatory proteins and reduce motoneuron death. Altogether, the maintenance of the BDNF/TrkB signalling and the downstream pathway, particularly after the swimming protocol, adds new molecular evidence of the benefits of physical exercise to reduce the impact of amyotrophic lateral sclerosis. These results are encouraging since they reveal an improvement even starting the therapy after the onset of the disease.

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A systematic review and meta-analysis running to lower resting blood pressure.

PMID: 

Sports Med. 2020 Mar ;50(3):531-541. PMID: 31677122

Abstract Title: 

Running to Lower Resting Blood Pressure: A Systematic Review and Meta-analysis.

Abstract: 

BACKGROUND: According to previous epidemiological studies, there are pros and cons for the relationship between running regularly and changes in resting blood pressure (RBP), and the changes may depend on the form of exercise.OBJECTIVE: The aims of the current systematic review were to summarize the effects of running regularly on RBP and to investigate the most efficacious form of running in reducing RBP for this purpose.METHODS: The inclusion criteria were: randomized controlled trials, involving healthy adults or adults with hypertension, the exercise group only performed regular running and the control group did not exercise, and the study reported the mean resting systolic blood pressure (RSBP) and/or diastolic blood pressure (RDBP). The mean difference (MD) in RBP in each trial was defined as follows: (mean value at post-intervention in the exercise group - mean value at baseline in the exercise group) - (mean value at post-intervention in the control group - mean value at baseline in the control group) and was calculated. The weighted MD (WMD) was defined as the synthesis of all MD. A linear meta-regression analysis, exercise intensity[the percentage of maximum heart rate] (%) and total exercise time throughout the intervention (hours) were selected as explanatory variables and the MD in RBP served as the objective variable.RESULTS: Twenty-two trials (736 subjects) were analyzed. When trials were limited to those involving healthy subjects, the WMD in RBP decreased significantly [RSBP: - 4.2 mmHg (95% confidence intervals (95% CI) - 5.9 to - 2.4); RDBP: - 2.7 mmHg (95% CI - 4.2 to - 1.1)] and did not contain significant heterogeneity (RSBP: P = 0.67, I = 0.0%; DBP: P = 0.38, I = 7.2%). When trials were limited to those involving subjects with hypertension, the WMD in RBP decreased significantly [RSBP: - 5.6 mmHg (95% CI - 9.1 to - 2.1); RDBP: - 5.2 mmHg (95% CI - 9.0 to - 1.4)] but contained significant heterogeneity (RSBP: P = 0.01, I = 62.2%; DBP: P 

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