Participants in meditation conditions have longer telomeres than participants in comparison conditions.

PMID: 

Psychol Health. 2020 Jan 5:1-15. Epub 2020 Jan 5. PMID: 31903785

Abstract Title: 

Meditation and telomere length: a meta-analysis.

Abstract: 

Telomeres are the caps at the end of chromosomes. Short telomeres are a biomarker for worsening health and early death.The present study consolidated research on meditation and telomere length through a meta-analysis of results of studies examining the effect of meditation on telomere length by comparing the telomere length of meditating participants with participants in control conditions.A search of the literature identified 11 studies reporting 12 comparisons of meditating individuals with individuals in control conditions. An overall significant weighted effect size of=.40 indicated that the individuals in meditation conditions had longer telomeres. When an outlier effect size was trimmed from the analysis, the effect size was smaller,=.16. Across studies, a greater number of hours of meditation among participants in meditation conditions was associated with larger effect sizes.These findings provide tentative support for the hypothesis that participants in meditation conditions have longer telomeres than participants in comparison conditions, and that a greater number of hours of meditation is associated with a greater impact on telomere biology. The results of the meta-analysis have potential clinical significance in that they suggest that meditation-based interventions may prevent telomere attrition or increase telomere length.

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Ketogenic diet activates protective γδ T cell responses against influenza virus infection.

PMID: 

Sci Immunol. 2019 Nov 15 ;4(41). PMID: 31732517

Abstract Title: 

Ketogenic diet activates protectiveγδ T cell responses against influenza virus infection.

Abstract: 

Influenza A virus (IAV) infection-associated morbidity and mortality are a key global health care concern, necessitating the identification of new therapies capable of reducing the severity of IAV infections. In this study, we show that the consumption of a low-carbohydrate, high-fat ketogenic diet (KD) protects mice from lethal IAV infection and disease. KD feeding resulted in an expansion ofγδ T cells in the lung that improved barrier functions, thereby enhancing antiviral resistance. Expansion of these protective γδ T cells required metabolic adaptation to a ketogenic diet because neither feeding mice a high-fat, high-carbohydrate diet nor providing chemical ketone body substratethat bypasses hepatic ketogenesis protected against infection. Therefore, KD-mediated immune-metabolic integration represents a viable avenue toward preventing or alleviating influenza disease.

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A ketogenic diet attenuates proliferation and stemness of glioma stem‑like cells by altering metabolism resulting in increased ROS production.

PMID: 

Int J Oncol. 2020 Feb ;56(2):606-617. Epub 2019 Dec 13. PMID: 31894296

Abstract Title: 

A ketogenic diet attenuates proliferation and stemness of glioma stem‑like cells by altering metabolism resulting in increased ROS production.

Abstract: 

Abnormal metabolism serves a critical role in the development and progression of different types of malignancies including glioblastoma (GBM), and may therefore serve as a promising target for treatment of cancer. Preclinical studies have indicated that a ketogenic diet (KD) may exhibit beneficial effects in patients with GBM; however, the underlying mechanisms remain incompletely understood. The aim of the present study was to evaluate the effects of a KD on glioma stem‑like cells (GSCs), by culturing patient‑derived primary GSCs as well as a GSC cell line in glucose‑restricted, β‑hydroxybutyrate‑containing medium (BHB‑Glow) which was used to mimic clinical KD treatment. GSCs cultured in BHB‑Glow medium exhibited reduced proliferation and increasedapoptosis compared with cells grown in the control medium. Furthermore, decreased expression of stem cell markers, diminished self‑renewal in vitro, and reduced tumorigenic capacity in vivo, providing evidence that the stemness of GSCs was compromised. Mechanistically, culturing in BHB‑Glow medium reduced glucose uptake and inhibited glycolysis in GSCs. Furthermore, culturing in the BHB‑Glow medium resulted in morphological and functional disturbances to the mitochondria of GSCs. These metabolic changes may have reduced ATP production, promoted lactic acid accumulation, and thus, increased the production of reactive oxygen species (ROS) in GSCs. The expression levels and activation of mammalian target of rapamycin, hypoxia‑inducible factor 1 and B‑cell lymphoma 2 were decreased, consistent with the reduced proliferation of GSCs in BHB‑Glow medium. ROS scavenging reversed the inhibitory effects of a KD on GSCs. Taken together, the results demonstrate that treatment with KD inhibited proliferation of GSCs, increased apoptosis and attenuated the stemness in GSCs by increasing ROS production.

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A ketogenic diet combined with melatonin overcomes cisplatin and vincristine drug resistance in breast carcinoma syngraft.

PMID: 

Nutrition. 2019 Nov 27 ;72:110659. Epub 2019 Nov 27. PMID: 31986320

Abstract Title: 

A ketogenic diet combined with melatonin overcomes cisplatin and vincristine drug resistance in breast carcinoma syngraft.

Abstract: 

OBJECTIVES: Chemotherapy is one of the major treatments of cancer. However, the emergence of resistance to chemotherapeutic agents is still a major obstacle in the successful management of resistant tumors. Therefore, development of new mechanisms to overcome drug resistance is essential and may be further developed into effective therapies that can flip the switch from drug resistance to susceptibility. The aim of this study was to evaluate a combination consisting of a ketogenic diet and melatonin to determine whether it would inhibit cisplatin- and vincristine-resistant breast cancer.METHODS: In the in vitro part of the study, drug-resistant cell lines were treated with melatonin and real-time polymerase chain reaction was used to measure levels of gene expression involved in apoptosis and resistance. On the protein level, the activity of caspase-3 and the level of vascular endothelin growth factor protein were determined. In the in vivo part, tumor-bearing mice received one of the following treatments: ketogenic diet, melatonin, combination of melatonin and ketogenic diet, vehicle, or chemotherapy.RESULTS: Successful inhibition of resistant cell lines was achieved by melatonin. This inhibition was mediated by induction of apoptosis, inhibition of angiogenesis, and downregulation of resistance genes. A synergistic anticancer effect was observed between melatonin and the ketogenic diet against resistant breast tumors inoculated in mice with a cure rate of 70%.CONCLUSIONS: The combination of melatonin and a ketogenic diet represents a promising option to overcome drug resistance in cancer chemotherapy. However, further testing on the protein level using flow cytometry is important to better understand the mechanisms of action.

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A review of the ketogenic diet for the treatment and prevention of dementia.

PMID: 

J Geriatr Psychiatry Neurol. 2020 Jan 30:891988720901785. Epub 2020 Jan 30. PMID: 31996078

Abstract Title: 

Ketogenic Diet for the Treatment and Prevention of Dementia: A Review.

Abstract: 

Dementia (major neurocognitive disorder) is an increasingly common syndrome with a significant burden on patients, caregivers, the health-care system, and the society. The prevalence of dementia will certainly continue to grow as the US population ages. Current treatments for dementia, though, are limited. One proposed nonpharmacologic approach for the delay or prevention of dementia is the use of a ketogenic diet. The ketogenic diet was originally employed to treat refractory epilepsy and has shown promise in many neurologic diseases. It has also gained recent popularity for its weight loss effects. Several preclinical studies have confirmed a benefit of ketosis on cognition and systemic inflammation. Given the renewed emphasis on neuroinflammation as a pathogenic contributor to cognitive decline, and the decreased systemic inflammation observed with the ketogenic diet, it is plausible that this diet may delay, ameliorate, or prevent progression of cognitive decline. Several small human studies have shown benefit on cognition in dementia with a ketogenic diet intervention. Future, large controlled studies are needed to confirm this benefit; however, the ketogenic diet has shown promise in regard to delay or mitigation of symptoms of cognitive decline.

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The association between traffic-related air pollution and skin aging has been well-established.

PMID: 

Curr Environ Health Rep. 2020 Jan 11. Epub 2020 Jan 11. PMID: 31927691

Abstract Title: 

Air Pollution and Skin Aging.

Abstract: 

PURPOSE OF THE REVIEW: The evidence on the role of air pollution on skin aging has increased in recent years. The accumulating evidence is based on both, epidemiological and mechanistic studies. The purpose of this review is to evaluate the recent evidence on the impacts of air pollution on skin aging as well as identify knowledge gaps for future research.RECENT FINDINGS: Traffic-related air pollution exposure (particulate matter (PM), soot and nitrogen dioxide (NO)) has been associated with premature skin aging in several independent cohorts. In real life, human skin is additionally exposed to UV radiation, which is known for its effects on premature skin aging. More recent epidemiological findings suggest that (1) associations of PM can be altered by UV radiation with stronger PM associations at lower levels of UV, and (2) there is an association of tropospheric ozone with wrinkle formation, independent of NO, PM, and UV. The association between traffic-related air pollution and skin aging has been well-established. More recent epidemiological studies focused on the associations with ozone as well as interactions with of ambient air pollution with UV radiation, a research area that is becoming more important with the increase of global warming.

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Ambient air pollution and daily hospital admissions for respiratory system-related diseases in a heavy polluted city in Northeast China.

PMID: 

Environ Sci Pollut Res Int. 2020 Jan 13. Epub 2020 Jan 13. PMID: 31933086

Abstract Title: 

Ambient air pollution and daily hospital admissions for respiratory system-related diseases in a heavy polluted city in Northeast China.

Abstract: 

Respiratory disease admission has been increasing in the recent 5 years due to heavy air pollutions and bad weather conditions in China. We investigated the short-term association of ambient air pollution with daily counts of hospital admissions due to respiratory infection diseases with stratified analysis by age (0-18, 19-65, and> 65 years old), gender (male, female), season (spring, summer, autumn, winter), and disease type (lung infections, asthma, COPD (chronic obstructive disease), URI (upper respiratory infections)) in heavy polluted city of Shenyang in China. Daily ambient air pollution concentrations, weather conditions, and hospital admission counts for 53 months (from November 1, 2013 to March 25, 2018) were extracted from related authorities in electronic databases. Associations between outdoor air pollution levels and hospital admissions were estimated for time lags of 0-7 days using quasi-Poisson additive regression models, adjusted for meteorological variables, holidays, day of week, and season, as well as eliminating autocorrelations. Single pollutant analysis results showed lung infection diseases were related to all pollutant concentration change with no lag effects. After adjusting for otherpollutants and confounding factors, we found NOwas associated with daily admissions of lung infections (ER = 6.75%, 95% CI 1.24, 12.55), asthma (ER = 20.36%, 95% CI 4.26, 38.95; lag day 5, ER = 18.48%, 95% CI 2.83, 36.51), and COPD (ER = 13.27%, 95% CI 0.46, 27.71); CO was associated with lung infections and asthma with lag effects on lag days 1 and 4; and PMwas associated with COPD admissions on lag day 6. Respiratory hospital admissions in female over 65 years old and autumn were more associated with increased air pollutant levels. Our study results might add more detail evidences for relationship studies between air pollution exposure and respiratory diseases and contribute to the precise respiratory disease prevention and air pollution control strategies.

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This study suggests air pollution as a risk factor for rheumatoid arthritis.

PMID: 

Int J Environ Res Public Health. 2020 01 8 ;17(2). Epub 2020 Jan 8. PMID: 31936295

Abstract Title: 

Influence of Ambient Air Pollution on Rheumatoid Arthritis Disease Activity Score Index.

Abstract: 

Rheumatoid arthritis (RA) is a chronic autoimmune of an unknown etiology. Air pollution has been proposed as one of the possible risk factors associated with disease activity, although has not been extensively studied. In this study, we measured the relationship between exposure to air pollutants and RA activity. Data on RA patients were extracted from the Kuwait Registry for Rheumatic Diseases (KRRD). Disease activity was measured using disease activity score with 28 examined joints (DAS-28) and the Clinical Disease Activity Index (CDAI) during their hospital visits from 2013 to 2017. Air pollution was assessed using air pollution components (PM 10 , NO 2 , SO 2 , O 3 , and CO). Air pollution data were obtained from Kuwait Environmental Public Authority (K-EPA) from six different air quality-monitoring stations during the same period. Multiple imputations by the chained equations (MICE) algorithm were applied to estimate missing air pollution data. Patients data were linked with air pollution data according to date and patient governorate address. Descriptive statistics, correlation analysis, and linear regression techniques were employed using STATA software. In total, 1651 RA patients with 9875 follow-up visits were studied. We detected an increased risk of RA using DAS-28 in participants exposed to SO 2 and NO 2 withβ = 0 . 003 (95% CI: 0.0004-0.005, p

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Association between maternal exposure to ambient PM10 and neural tube defects.

PMID: 

Int J Hyg Environ Health. 2020 Jan 24 ;225:113453. Epub 2020 Jan 24. PMID: 31986338

Abstract Title: 

Association between maternal exposure to ambient PMand neural tube defects: A case-control study in Liaoning Province, China.

Abstract: 

BACKGROUND: The potential association between maternal exposure to ambient PMand offspring neural tube defects (NTDs) is a contentious issue. This study aims to evaluate the aforementioned association at a provincial level in China.METHODS: A total of 2736 cases and 7950 randomly selected healthy infants included in the Maternal and Child Health Certificate Registry of Liaoning Province and delivered between 2010 and 2015 were recruited. Daily PMconcentrations were obtained from all available monitoring stations located within the study area. A multivariable logistic regression model was established to calculate the adjusted odds ratios (ORs) and 95% confidence intervals (CIs).RESULTS: PMexposure was significantly associated with the risk of NTDs during the three months preconception (per 10 μg/mincrement: OR = 1.10, 95% CI 1.07-1.14; per standard deviation [27 μg/m] increment: OR = 1.29, 95% CI 1.18-1.41; highest tertile: OR = 1.61, 95% CI 1.37-1.91) and the first trimester (highest tertile: OR = 1.57, 95% CI: 1.31-1.87). When focusing on shorter exposure windows, similar associations were observed for PMexposure from the third month before pregnancy to the third month after pregnancy. Sensitivity analyses using propensity score matching yielded consistent findings.CONCLUSIONS: Maternal exposure to PMis positively associated with NTDs during the critical period of fetal neural tube development. However, due to the limitation of the exposure assessment as well as potential residual confounding, further research is warranted to confirm our findings.

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Long-term exposure to total and source-specific ambient ambient air pollution may increase diabetes mellitus risk.

PMID: 

Environ Int. 2020 Mar ;136:105493. Epub 2020 Jan 25. PMID: 31991234

Abstract Title: 

All-source and source-specific air pollution and 10-year diabetes Incidence: Total effect and mediation analyses in the Heinz Nixdorf recall study.

Abstract: 

BACKGROUND: An increasing number of studies have been published recently on the association between ambient air pollution (AP) and incident diabetes mellitus (DM), but studies investigating source-specific AP toxicity and potential mediating pathways are rare. We investigated the associations of all-source, traffic-specific, and industry-specific outdoor AP exposure with 10-year incidence of DM and potential mediation via inflammation-associated biomarkers.METHODS: Data from participants of the prospective Heinz Nixdorf Recall cohort study who attended the baseline (t; 2000-2003), 5-year follow-up (t; 2006-2008), and 10-year follow-up (t; 2011-2015) examinations was used. For participants without DM at baseline (determined using information on physician diagnosis and glucose-lowering medication), residential long-term exposure (total, traffic-specific, and industry-specific) to particulate matter (PM, PM), nitrogen dioxide (NO), and accumulation mode particle number concentration (PN) were estimated using a chemistry transport model. Covariate-adjusted modified Poisson regression models with robust standard errors were applied to estimate relative risks (RR) for the associations between baseline AP and incident DM at t. Mediation analyses for adiponectin, high-sensitivity C-reactive protein (hsCRP), and interleukin-1 receptor antagonist (IL-1RA) were conducted to estimate natural direct and indirect effects.RESULTS: Of the 4,814 participants at t, 2,451 participants (mean baseline age: 58.2 years) were included in the main analysis. Interquartile range (IQR) increases in total PMand PNwere associated with increased risk of DM (e.g., RR: 1.25 [95% Confidence Interval (CI): 1.02, 1.53] per 3.8 µg/mPM). Whereas traffic-specific exposures were associated with DM risk for all air pollutants (e.g., RR: 1.24 [95% CI: 1.06, 1.46] per 0.3 µg/mPM), significant associations for industry exposures were limited to NOand PN(e.g., RR: 1.24 [95% CI: 1.03, 1.49] per 230 particles/mL PN). Potential mediation of the association between AP and DM was observed for adiponectin but not for hsCRP and IL-1RA.CONCLUSION: Our study shows that long-term exposure to total and source-specific ambient AP may increase DM risk, with consistent results observed across traffic-specific exposures. Decreases in adiponectin may play a potential role along the causal pathway.

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