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Latest research: 7 hours of sleep per day is the best "maintenance product", too much/little sleep time will accelerate aging

On the morning of March 16, the Chinese Sleep Research Association announced the annual theme of World Sleep Day in Beijing, "healthy sleep for all". The "2023 White Paper on Chinese Residents' Sleep" released at the meeting showed that the overall sleep quality of Chinese residents is poor, with an average sleep time of 6.75 hours after midnight and an average number of 1.4 awakenings. This is far from the ideal sleep duration and quality. In the field of medicine and health, "phenotypic age" , which is often used as a predictor of various diseases and a biomarker for evaluating aging, refers to a person's physiological age, determined by their physical characteristics and functions rather than their actual age. Research shows that age based biomarkers can be used as reliable indicators for individuals suffering from certain health diseases, such as cardiovascular disease, type II diabetes, nervous system diseases and other chronic disease phenotypes, which can provide more accurate information than actual age or single markers (such as telomere). Although these studies provide some evidence for the relationship between sleep and age-related phenotypic changes, more research is still needed to fully understand this relationship. A study conducted by the Tsinghua University team You et al. analyzed the sleep patterns of 48,762 American adults and the phenotypic age reflected by multiple biomarkers, and found an interesting inverted U-shaped relationship: 7 hours of sleep per day is the optimal "care product" for the human body, and too little or too much sleep time will accelerate the increase of phenotypic age. In addition, this study cleverly incorporated exercise into the scope of discussion, revealing the subtle but crucial relationship between exercise and sleep. According to the data from NHANES, the research team investigated the trend of sleep duration and the relationship between sleep duration and phenotypic age. In different annual cycles, most people's sleep duration is 6-9 hours. Moreover, since the 2015-2016 cycle, the proportion of short sleep and very short sleep has shown a downward trend, while the proportion of long sleep has shown an upward trend. When the researchers used the crude model and Model 1 to evaluate sleep duration as a continuous variable, they found no significant correlation between it and phenotypic age. However, in the fully adjusted model, there was a significant correlation between continuous sleep duration and phenotypic age (Model 2, p=0.031). Compared with the normal sleep group, short sleep duration was positively correlated with phenotypic age in the crude model and model 1 (crude model, p=0.050; model 1, p

2024

03/21

A healthier diet can help slow down aging and reduce the risk of dementia

  The MIND diet is a well-known healthy eating pattern that combines the Mediterranean diet with a diet that reduces the risk of high blood pressure.   Recently, Yian Gu, Daniel Belsky and others from Columbia University published a research paper entitled "Diet, Pace of Biological Aging, and Risk of Dementia in the Framingham Heart Study" in the journal Annals of Neurology.   The study found that a healthy diet slows down the rate of biological aging and is associated with a reduced risk of dementia and death. The slowed biological aging rate plays a partial mediating role in the association between a healthy diet and a reduced risk of dementia. Monitoring the rate of aging may help prevent dementia.   In the study of dementia, the focus on nutrition is usually on the impact of specific nutrients on the brain, while this study tests the hypothesis that a healthy diet can prevent dementia by slowing down the overall biological aging rate of the body.   In this study, the research team used data from the second cohort of the Framingham Heart Study, which began in 1971. Participants were aged 60 years or older, had no dementia, and recorded dietary, epigenetic, and follow-up data. They conducted 9 follow-ups approximately every 4-7 years. During each follow-up, data collection included physical examination, lifestyle-related questionnaires, blood sampling, and neurocognitive testing starting in 1991.   Of the 1,644 participants included in the analysis, 140 developed dementia and 471 died during the 14-year follow-up period. To assess their aging rate, the research team used an epigenetic clock, DunedinPACE, to evaluate the rate of decline in a person's body as they age through epigenetics.   Healthy diet can prevent dementia, but the protective mechanism is not clear. Previous studies have linked diet and dementia risk to accelerated biological aging. This study tested the hypothesis that multisystem biological aging is a mechanism of diet-disease association. The study determined that higher adherence to the MIND diet slowed the rate of aging as assessed by the Dunedin PACE and reduced the risk of dementia and death. In addition, in the mediation effect analysis, the slowed Dunedin PACE accounted for 27% of the diet-disease association and 57% of the diet-mortality association.   The MIND diet is a well-known healthy eating pattern that combines the Mediterranean diet with a diet that reduces the risk of high blood pressure.   Overall, the results of this study suggest that the slowing of aging speed plays a partial mediating role in the relationship between a healthy diet and a reduced risk of dementia, and monitoring the aging speed may help prevent dementia. However, a large part of the association between diet and dementia remains unexplained, possibly reflecting a direct link between diet and brain aging that does not overlap with other organ systems. Therefore, further investigation of brain-specific mechanisms is needed in well-designed mediating studies.

2024

03/20

New mechanism for more than 30 years! New oral antihypertensive drug approved by FDA

On March 19th, the FDA official website showed that Aprocitentan (trade name Tryvio) developed by Idorsia was approved for the treatment of refractory hypertension patients.   Aprocitentan is a novel oral dual endothelin A/B receptor (ETA/ETB) antagonist that effectively inhibits the binding of ET-1 to ETA and ETB. It is the active metabolite of masitentan and has a longer half-life (48 h vs. 14 h). The FDA approval was mainly based on the positive results of the Phase III PRECISION study. The study is a multi-center, blinded, randomized Phase III clinical trial, which is divided into three phases:   The first phase is a 4-week double-blind period, during which 730 patients were randomly assigned to the 12.5mg (n=243), 25mg (n=243) aprocitentan groups or the placebo group (n=244);   The second phase is a 32-week (4-36 weeks) single-blind period, during which patients receive 25 mg of aprocitentan (n=704) treatment; The third phase is a 12-week (36-48 weeks) double-blind drug withdrawal period, during which patients are randomly reassigned to the 25 mg aprocitentan group (n=307) or the placebo group (n=307) in a 1:1 ratio.   The primary and key secondary endpoints of the study were the changes in systolic blood pressure from baseline to week 4 and week 40, respectively. At baseline, 63% of patients had received at least four antihypertensive medications.   The results showed that the study achieved the primary endpoint, which was that the reduction in sitting systolic blood pressure (SiSBP) in patients treated with aprocitentan was significantly greater than that in patients treated with placebo. Specifically, after 4 weeks of treatment with aprocitentan, the SiSBP in patients significantly decreased, and the differences between the 12.5mg and 25mg groups were -3.8mmHg (p=0.0042) and -3.7mmHg (p=0.0046), respectively, compared to the placebo group.   In addition, the study also achieved a key secondary endpoint, with patients receiving apocitentan treatment showing a sustained reduction in SiSBP compared to the placebo group during weeks 36-40, with a difference of -5.8 mmHg (p

2024

03/19

A large-scale study found that every bite of pork, beef, and mutton may increase the risk of cancer.

  The results showed that regular consumption of red meat and processed meat increases the risk of colorectal cancer. The study also identified two genes, HAS2 and SMAD7, which can change the level of cancer risk based on the consumption level of red or processed meat. Recently, researchers from the Keck School of Medicine at the University of Southern California published a research paper entitled "Genome-Wide Gene–Environment Interaction Analyses to Understand the Relationship between Red Meat and Processed Meat Intake and Colorectal Cancer Risk" in the journal "Cancer Epidemiology, Biomarkers & Prevention".   This large-scale study shows that regular consumption of red meat and processed meat increases the risk of colorectal cancer. People with higher intake of red meat and processed meat have a 30% and 40% increased risk of colorectal cancer, respectively.   In addition, the study also identified two genes, HAS2 and SMAD7, which can change cancer risk levels based on the consumption level of red or processed meat.   In this study, researchers analyzed data from 27 European colorectal cancer risk studies, including 29,842 colorectal cancer patients and 39,635 non-cancer patients. Participant intake of red and processed meat was collected through dietary questionnaires, and genetic data was analyzed to explore the association between red and processed meat intake and colorectal cancer.   The researchers divided the participants into four groups based on their intake of red meat (beef, pork, and lamb) and processed meat (bacon, sausage, luncheon meat, and hot dogs).   The analysis found that compared with the group with the lowest intake of red meat, the risk of colorectal cancer in the group with the highest intake of red meat increased by 30%; compared with the group with the lowest intake of processed meat, the risk of colorectal cancer in the group with the highest intake of processed meat increased by 40%. Next, the researchers analyzed the genetic data to determine whether there was a genetic variant that could alter the risk of colorectal cancer in people who eat more red meat.   Researchers have discovered two genes, HAS2 and SMAD7, that change cancer risk levels based on red or processed meat consumption levels.   For HAS2 gene, about 66% of the population carries HAS2 gene variants, and compared with the lowest red meat intake group, the highest red meat intake group has a 38% increased risk of colorectal cancer. For the SMAD7 gene, about 74% of the population carries two copies of the SMAD7 gene variant. For people with two copies of the variant, compared to those with the lowest intake of red meat, those with the highest intake of red meat have an 18% increased risk of developing colorectal cancer. Individuals with only one copy of the most common variant or two copies of less common variants have significantly higher cancer risks, at 35% and 46%, respectively. Researchers said that this finding indicates that different genetic variations may lead to different risks of colorectal cancer in individuals who consume red meat, and reveals why red meat and processed meat increase the risk of colorectal cancer.   However, the researchers emphasized that the current study did not prove a causal relationship between these genetic variations.   In short, the results suggest that regular consumption of red and processed meat increases the risk of colorectal cancer. The study also identified two genes, HAS2 and SMAD7, which change cancer risk levels based on the consumption level of red or processed meat.

2024

03/18

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