Showing posts with label healthy living. Show all posts
Showing posts with label healthy living. Show all posts

Thursday, July 23, 2026

Globally, people are living longer, but spending more years in poor health

Food for thought! That sounds about right? This is a serious quality of life issue!

How much are individuals to be blamed e.g. for knowingly living significantly unhealthy lives?

What are the extra/additional healthcare costs associated with this?

"People around the world are living longer than ever before but spending more of those additional years in poor health, according to a new Global Burden of Disease (GBD) study published in The Lancet Public Health. ...

Researchers found that the global morbidity gap widened in almost all countries and territories analyzed between 1990 and 2023. Globally, while the share of life spent in poor health increased, trends varied by country, and a smaller number of countries saw this share decline.

Within a generation, the global morbidity gap widened by nearly two years, increasing from 8.8 years in 1990 to 10.7 years in 2023.
Globally, people spent an average of 14.5% of their lives in poor health in 2023, up from 13.6% in 1990.
Instead of occurring only in the final years of life, the widening morbidity gap was observed across the adult lifespan, suggesting that people are spending more years living with disease and disability throughout adulthood. ..."

From the abstract:
"Summary
Background
As survival improves globally, the central public health challenge increasingly shifts from extending life to extending healthy lifespan. The compression of morbidity hypothesis proposes that effective prevention and care will delay disability more than death, reducing the morbidity gap—ie, the duration or proportion of life spent in poor health.
We aimed to comprehensively estimate changes in the morbidity gap globally, regionally, and nationally from 1990 to 2023, by sociodemographic development levels and sex, and analysed leading diseases and injuries and their underlying risk factors contributing to years lived in poor health.

Methods
Using Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2023 estimates of life expectancy and healthy life expectancy (HALE) at birth for 204 countries and territories from 1990 to 2023, we calculated the morbidity gap as life expectancy minus HALE, and the proportional morbidity gap as this difference divided by life expectancy.
Results are presented globally, by GBD super-region and country, Socio-demographic Index (SDI) quintile, and sex.
We decomposed the morbidity gap into cause-specific and risk-specific contributions, assigning to each cause group its proportional share of years lived with disability (YLD), adjusted for comorbidity to avoid double counting disability for co-occurring conditions. We report mean estimates and 95% uncertainty intervals (UIs) derived from 250 or more draws from posterior distributions.

Findings
From 1990 to 2023, the global morbidity gap increased from 8·8 years (95% UI 6·7–11·2) to 10·7 (8·2–13·7), an increase of 1·9 years (1·3–2·6), or 21·9% (16·0–27·9), with point estimates suggesting widening morbidity gaps in 203 of 204 countries and territories.
Globally in 2023, an average of 14·5% of life was spent in poor health, compared to 13·6% in 1990. From 1990 to 2023, across locations, age-specific morbidity gaps widened across the adult life course, rather than concentrating in the final years of life.
In 2023, morbidity gaps were largest in the high SDI quintile and smallest in the low SDI quintile.
Countries with longer life expectancies had larger morbidity gaps and both had a positive relationship with SDI; however, the relationship between life expectancy and the proportional morbidity gap was less clear.
A small number of chronic, largely non-fatal causes were the primary contributors to the morbidity gap, with musculoskeletal disorders (especially low back pain), mental disorders (depressive and anxiety disorders), sense organ diseases (age-related hearing loss), unintentional injuries (falls), and other non-communicable diseases together accounting for 57·4% of unhealthy years in 2023, globally.
High fasting plasma glucose, high body-mass index, and child and maternal malnutrition were the leading risk factors contributing to the global morbidity gap.

Interpretation
The expansion of the morbidity gap across nearly all locations indicates that improvements in survival have consistently outpaced reductions in non-fatal health loss across geographies, SDI levels, and sexes, with most populations now spending a decade or more of life in poor health across the lifespan.
Progress towards healthy ageing should therefore be assessed not only by reduced mortality, but also by declines in years lived in poor health, with emphasis placed on extending healthspan. ..."

People are living longer, but spending more years in poor health


Figure 1 Morbidity gap by GBD super-region (A) and SDI quintile (B), 1990–2023



Figure 2 Comparison of the morbidity gap (A, B) and proportional morbidity gap (C, D) versus life expectancy across countries and territories, 1990 (A, C) and 2023 (B, D)


Monday, January 12, 2026

Doctor reveals two simple tests that predict how well you’ll age

Recommendable! I am also a strong believer that balancing exercises are very important as you age like standing on one leg and stretching your other leg etc.

Sunday, September 21, 2025

Exercise metabolite Lac-Phe curbs appetite naturally in mice, humans, and racehorses

Good news!

"Researchers led by scientists at Baylor College of Medicine (BCM) have unraveled just how an exercise-induced signaling metabolite, N-lactoyl-phenylalanine (Lac-Phe), travels a unique pathway to the brain and impacts the activity of one, and then two different neurons. It triggers a chain of events that ultimately suppresses appetite ..."

"... The researchers previously discovered that Lac-Phe is the most increased metabolite – a product of the body’s metabolism – in blood after intense exercise, not just in mice but also in humans and racehorses. The team’s previous work showed that giving Lac-Phe to obese mice reduced how much they ate and helped them lose weight without negative side effects. But until now, scientists didn’t fully understand how Lac-Phe works to suppress appetite. ...

The researchers studied two types of brain cells in mice. One type was AgRP neurons, which stimulate hunger and are in the arcuate nucleus of the hypothalamus. The other type was PVH neurons in the paraventricular nucleus of the hypothalamus. These neurons help suppress hunger.

AgRP and PVH neurons work together. Normally, AgRP neurons send signals that inhibit PVH neurons, making you feel hungry. But when AgRP neurons are turned off, PVH neurons become more active, reducing appetite.

He lab members and colleagues discovered that Lac-Phe directly inhibits AgRP neurons, which in turn activates PVH neurons. This chain of events resulted in mice eating less. The animals’ behavior remained normal, suggesting that Lac-Phe doesn’t cause unpleasant side effects. ..."

From the abstract:
"N-Lactoyl-phenylalanine (Lac-Phe) is a lactate-derived circulating metabolite that reduces feeding and obesity, but the molecular mechanisms that underlie the metabolic benefits of Lac-Phe remain unknown.
Here we show that Lac-Phe directly inhibits hypothalamic neurons that express Agouti-related protein (AgRP), resulting in an indirect activation of anorexigenic neurons in the paraventricular nucleus of the hypothalamus (PVH).
Both AgRP inhibition and PVH activation are required to mediate Lac-Phe-induced hypophagia. 
Lac-Phe-mediated inhibition of AgRP neurons occurs through activation of the ATP-sensitive potassium (KATP) channel, whereas inhibition of the KATP channel blunts the effects of Lac-Phe to suppress feeding.
Together, these results reveal the molecular and neurobiological mechanisms by which Lac-Phe mediates metabolic improvements and suggest this exercise-induced metabolite might have therapeutic benefits in various human diseases."

Exercise metabolite Lac-Phe curbs appetite naturally

Saturday, August 09, 2025

The emerging Science of Health Behind Feeling Great

Food for thought! How do we measure a happy and healthy life? Or why is medicine the dismal science?

I am not sure that the comparison of human health with a battery (see image below) was a good choice. This does not make me feel great! 😊

"... Studies have shown that how healthy we feel is often a surprisingly good predictor of how long we’ll live — sometimes even better than clinical tests. That’s led scientists to suspect that behind our gut instincts are real biological signals that modern medicine just hasn’t learned to detect yet. If researchers could identify the factors that give rise to these feelings of vitality, they say, it could change how we take care of ourselves. ...

Until recently, the prospect of defining and measuring health as a distinct biological state — rather than merely inferring it in the absence of disease — was seldom discussed in medical circles. ...

In a new paper ... they lay out the most detailed framework to date for understanding optimal health — or “intrinsic health,” as they call it — offering both a conceptual foundation and a roadmap for how scientists might learn to measure it. ...

intrinsic health is a “field-like state,” a kind of emergent property that arises from the dynamic interplay of systems involved in energy processing and communication across all levels of physiology — from molecular signaling within cells to coordination amongst organs. When energy is flowing freely and metabolic pathways are buzzing with crosstalk, they argue, we enter a state of “dynamic equilibrium” that enables our bodies to adapt seamlessly to changes in our environment ..."

From the abstract:
"The health sciences largely focus on disease. However, the interconnected determinants of diseases suggest that we need a science of health, a framework to examine the biology of homeodynamics in a changing environment and how this affects the health we value.
We build on first principles and recent discoveries on biological system dynamics to develop the concept of intrinsic health, a field-like state emerging from the dynamic interplay of energy, communication, and structure within the organism, giving rise to robustness/resilience, plasticity, performance, and sustainability. Intrinsic health is a quantifiable property of individuals that declines with age and interacts with context. We propose a measurement framework and describe how it will contribute to achieving the shared goals of medicine and public health."

The Secret Science Behind Feeling Great | Columbia Magazine "Columbia biologists propose a more holistic framework for measuring health — asking not what ails you, but what makes you thrive."



Fig. 2. A comparison of evolutionary fitness and intrinsic health.


Fig. 3. Intrinsic health as a field-like state.
(A) Intrinsic health emerges from the energy, communication, and structure of the body at multiple interacting hierarchical levels, from molecular to organismal.


Fig. 4. A measurement framework for intrinsic health.


Friday, June 20, 2025

Thai athlete, 105, in league of his own at World Masters Games

Good news! Stay fit and you will be in a class of your own outcompeting everyone else! 😊
"As the only competitor in his age group, the 105-year-old former school principal won gold at all four events." 

Monday, March 31, 2025

Goodbye Chips & Soda? Inside Mexico’s Junk Food Ban For Schools with Palki Sharma

Government prohibition is usually the dumbest thing to do and it often does not work! Is it not foremost the responsibility of parents to make sure that children eat healthy?

Sunday, February 16, 2025

GLP-1 class of weight loss and diabetes drugs dial down alcohol and nicotine cravings in alcoholics

Good news! However, is it the medication itself or the effect of the medication on the patient in terms of successful and significant weight loss, feeling better, better self image and self esteem etc.?

"... This new study is the results of one of six clinical trials  ... In a double-blind randomized nine-week trial, 48 US adults (71% female) with a mean age of 39.9 years were assigned either semaglutide (0.25 mg/week for four weeks, 0.5 mg/week for four weeks and 1.0 mg for one week) or a placebo at weekly clinic visits.

What the researchers found was that while there was a reduction in some – but not all – clinical measures of alcohol use, the drug significantly impacted participants' desire to reach for a drink. For anyone wanting, but struggling, to cut back, not necessarily quit altogether, blocking alcohol cravings could be a game-changer in developing healthier habits. ...

"For weekly drinking outcomes, medication effects on number of drinks per calendar day were nonsignificant; however, semaglutide significantly reduced alcohol craving and drinks per drinking day, also interacting with treatment week to predict reductions in heavy drinking days," the researchers noted. "Consequently, the proportion of participants with zero heavy drinking days increased significantly in the semaglutide group across the two-dose phases."

The smokers in the trial receiving semaglutide also saw a change in habits. Overall, the smokers on semaglutide went from an average of 14 cigarettes per day to eight per day. ..."

From the key points and abstract:
"Key Points
Question
Does the glucagon-like peptide 1 (GLP-1) receptor agonist semaglutide reduce alcohol consumption and craving in adults with alcohol use disorder (AUD)?
Findings
In this randomized clinical trial, relative to placebo, low-dose semaglutide reduced the amount of alcohol consumed during a posttreatment laboratory self-administration procedure. Over 9 weeks of treatment, semaglutide led to reductions in some but not all measures of weekly consumption, significantly reduced weekly alcohol craving relative to placebo, and led to greater relative reductions in cigarettes per day in a subgroup of participants with current cigarette use.
Meaning 
These results justify larger clinical trials of incretin therapies for AUD.

Abstract
Importance
Preclinical, observational, and pharmacoepidemiology evidence indicates that glucagon-like peptide 1 receptor agonists (GLP-1RAs) may reduce alcohol intake. Randomized trials are needed to determine the clinical significance of these findings.
Objective
To evaluate the effects of once-weekly subcutaneous semaglutide on alcohol consumption and craving in adults with alcohol use disorder (AUD).
Design, Setting, and Participants
This was a phase 2, double-blind, randomized, parallel-arm trial involving 9 weeks of outpatient treatment. Enrollment occurred at an academic medical center in the US from September 2022 to February 2024. Of 504 potential participants assessed, 48 non–treatment-seeking participants with AUD were randomized.
Intervention
Participants received semaglutide (0.25 mg/week for 4 weeks, 0.5 mg/week for 4 weeks, and 1.0 mg for 1 week) or placebo at weekly clinic visits.
Main Outcomes and Measures 
The primary outcome was laboratory alcohol self-administration, measured at pretreatment and posttreatment (0.5 mg/week). Secondary and exploratory outcomes, including prospective changes in alcohol consumption and craving, were assessed at outpatient visits.
Results
Forty-eight participants (34 [71%] female; mean [SD] age, 39.9 [10.6] years) were randomized. Low-dose semaglutide reduced the amount of alcohol consumed during a posttreatment laboratory self-administration task, with evidence of medium to large effect sizes for grams of alcohol consumed (β, −0.48; 95% CI, −0.85 to −0.11; P = .01) and peak breath alcohol concentration (β, −0.46; 95% CI, −0.87 to −0.06; P = .03). Semaglutide treatment did not affect average drinks per calendar day or number of drinking days, but significantly reduced drinks per drinking day (β, −0.41; 95% CI, −0.73 to −0.09; P = .04) and weekly alcohol craving (β, −0.39; 95% CI, −0.73 to −0.06; P = .01), also predicting greater reductions in heavy drinking over time relative to placebo (β, 0.84; 95% CI, 0.71 to 0.99; P = .04). A significant treatment-by-time interaction indicated that semaglutide treatment predicted greater relative reductions in cigarettes per day in a subsample of individuals with current cigarette use (β, −0.10; 95% CI, −0.16 to −0.03; P = .005).
Conclusions and Relevance
These findings provide initial prospective evidence that low-dose semaglutide can reduce craving and some drinking outcomes, justifying larger clinical trials to evaluate GLP-1RAs for alcohol use disorder."

Ozempic dials down alcohol cravings for people wanting to cut back

Popular weight loss, diabetes drug shows promise in reducing cravings for alcohol (original news release) "USC-led trial confirms side effect: Semaglutide, better known as Ozempic and Wegovy, could also help people cut down on their alcohol intake."





Sunday, December 15, 2024

Never stop working out especially when you are older

Good news! No made up excuses for older people! 😊

As the well known adage says, if you don't use it you lose it!

"Regular exercise has been associated with lower risk of death. Martinez-Gomez et al. investigated whether this association is affected by age, analyzing data from more than 2 million individuals 20 to 97 years of age. The results showed that the negative correlation between physical activity and mortality is present in all age groups and becomes stronger in older individuals. By contrast, the association between mortality risk and other modifiable health factors, including smoking, education level, alcohol consumption, body weight, hypertension, and diabetes, decreases with age. How much these effects are due to the exercise itself or are confounded by healthier individuals being able to do exercise remains to be disentangled."

From the key points and abstract:
"Key Points
Question  Does age modify the associations between physical activity and all-cause mortality?

Findings
In this cohort study using a pooled analysis of 4 multi-country megacohorts including more than 2 million individuals aged 20 to 97 years, the beneficial association between meeting the physical activity recommendation (eg, 150 minutes per week of moderate-intensity physical activity) and mortality was greater as age increased. For other modifiable health factors, the associations were remarkably smaller as age increased.

Meaning
The magnitude of the association between physical activity and mortality risk remains mainly consistent across the adult lifespan; therefore, promotion of physical activity is essential at all stages of adult life.

Abstract
Importance  Physical activity (PA) guidelines recommend the same amount of PA through adulthood to live longer.

Objective
To explore whether there is an age-dependent association between PA and all-cause mortality and to investigate the age-dependent associations between other modifiable health factors (high educational level, not smoking, not regularly consuming alcohol, healthy body weight, and living without hypertension and diabetes) and mortality.

Design, Setting, and Participants
This cohort study used a pooled analysis of 4 population-based prospective cohorts (National Health Interview Survey, 1997-2018; UK Biobank, 2006-2010; China Kadoorie Biobank, 2004-2008; and Mei Jau, 1997-2016). Data were analyzed from June 2022 to September 2024.

Exposures  
Self-reported leisure-time PA.

Main Outcomes and Measures
The primary outcome was deaths identified through follow-up linkage to national death registries. Analyses were performed for the total sample and by age groups (20-29, 30-39, 40-49, 50-59, 60-69, 70-79, and ≥80 years). Cox proportional hazards regression models with stratification by study were used to calculate mortality hazard ratios and their 95% CIs for the pooled dataset and by age group.

Results
A heterogeneous sample of 2 011 186 individuals (mean [SD] age, 49.1 [14.3] years; age range, 20-97 years;
1 105 581 women [55.0%]) were included. After a median (IQR) follow-up of 11.5 (9.3-13.5) years, 177 436 deaths occurred. The association between PA and mortality in the total sample showed a nonlinear dose-response pattern, but age modified this association (P for interaction <.001); PA was consistently associated with a lower risk of mortality across all age groups, but the reduction in risk was greater in older vs younger age groups, especially at high levels of PA. The hazard ratio for mortality associated with meeting the recommended PA in the total sample was 0.78 (95% CI, 0.77-0.79). This inverse association between meeting PA recommendations and mortality was somewhat greater as age increased (P for interaction <.001). Age also modified the associations of the other modifiable health factors with mortality (all P for interaction <.001), but the magnitude of associations was greater in younger vs older age groups.

Conclusions and Relevance
In this pooled analysis of cohort studies, the association between PA and mortality risk remained consistent across the adult lifespan, which contrasts with other modifiable health factors, for which associations with mortality risk diminished with age. Given these findings, the promotion of regular PA is essential at all stages of adult life."

In Other Journals | Science

Thursday, December 12, 2024

Living Longer, but Not Healthier - the health span-lifespan gap

Bad news!

Caution is advised when comparing health data across countries. E.g. that the US supposedly has the largest heatlh span-life span gap might be a statistical artifact, because there is better data available in the US than for other countries.

"Lifespans are increasing worldwide, but those extra years are not necessarily healthier, finds a large new study published in JAMA Network Open.

The health span-lifespan gap—the difference between how long people live and how long they live in good health—has widened over the past two decades among 183 WHO member states, reports Yahoo Life. 
On average, people live 9.6 fewer healthy years than their total lifespan, with a larger gap for women. In the U.S., the gap is 12+ years. 
The health span deficit is linked to the cumulative effects of aging itself, researchers say—but also the uptick in chronic diseases like heart disease and diabetes, and mental health issues. 
A tale of two countries: Meanwhile, a new report from the Bloomberg American Health Initiative finds that the U.S. trails England and Wales in life expectancy by 2.7 years—and that four preventable causes of death drive the disparity: cardiovascular disease, overdoses, motor vehicle crashes, and gun violence, per a commentary in The Hill."

From the abstract:
"Abstract
Importance  Health-adjusted life expectancy, a measure of healthy longevity, lags longevity gains, resulting in a healthspan-lifespan gap.
Objective
To quantify the healthspan-lifespan gap across the globe, investigate for sex disparities, and analyze morbidity and mortality associations.
Design, Setting, and Participants
This retrospective cross-sectional study used the World Health Organization (WHO) Global Health Observatory as the global data source and acquired national-level data covering all continents. The 183 WHO member states were investigated. Statistical analysis was conducted from January to May 2024.
Exposures
Data represent 2 decades of longitudinal follow-up.
Main Outcomes and Measures
Changes in life expectancy and health-adjusted life expectancy, as well as the healthspan-lifespan gap were quantified for all participating member states. Gap assessment was stratified by sex. Correlations of the gap with morbidity and mortality were examined.
Results
The healthspan-lifespan gap has widened globally over the last 2 decades among 183 WHO member states, extending to 9.6 years. A sex difference was observed with women presenting a mean (SD) healthspan-lifespan gap of 2.4 (0.5) years wider than men (P < .001). Healthspan-lifespan gaps were positively associated with the burden of noncommunicable diseases and total morbidity, and negatively with mortality. The US presented the largest healthspan-lifespan gap, amounting to 12.4 years, underpinned by a rise in noncommunicable diseases.
Conclusions and Relevance
This study identifies growing healthspan-lifespan gaps around the globe, threatening healthy longevity across worldwide populations. Women globally exhibited a larger healthspan-lifespan gap than men."

Global Health NOW: Living Longer, but Not Healthier; Afghanistan to Ban Women From Nursing, Midwifery; and Decrypt the Halls



Figure 1.  Global Life Expectancy, Health-Adjusted Life Expectancy, and Healthspan-Lifespan Gap


Thursday, May 02, 2024

Scientists work out the many effects of endurance exercise at the cellular level affecting all tissues and they vary by sex

Good news! Exercise more!

"... new research shows that the body’s response to exercise is more complex and far-reaching than previously thought. In a study on rats, a team of scientists from across the United States has found that physical activity causes many cellular and molecular changes in all 19 of the organs they studied in the animals. ..."

"... amounting to over 35,000 biological molecules that respond and adapt to endurance exercise over time, including tissues from organs not usually associated with exercise. ...
While molecular changes were seen in all tissues, the way in which each tissue responded was unique. ..."

From the abstract:
"Regular exercise promotes whole-body health and prevents disease, but the underlying molecular mechanisms are incompletely understood. Here, the Molecular Transducers of Physical Activity Consortium profiled the temporal transcriptome, proteome, metabolome, lipidome, phosphoproteome, acetylproteome, ubiquitylproteome, epigenome and immunome in whole blood, plasma and 18 solid tissues in male and female Rattus norvegicus over eight weeks of endurance exercise training. The resulting data compendium encompasses 9,466 assays across 19 tissues, 25 molecular platforms and 4 training time points. Thousands of shared and tissue-specific molecular alterations were identified, with sex differences found in multiple tissues. Temporal multi-omic and multi-tissue analyses revealed expansive biological insights into the adaptive responses to endurance training, including widespread regulation of immune, metabolic, stress response and mitochondrial pathways. Many changes were relevant to human health, including non-alcoholic fatty liver disease, inflammatory bowel disease, cardiovascular health and tissue injury and recovery. The data and analyses presented in this study will serve as valuable resources for understanding and exploring the multi-tissue molecular effects of endurance training and are provided in a public repository (https://motrpac-data.org/)."

Scientists work out the effects of exercise at the cellular level | Broad Institute Prolonged physical activity in rats results in profound changes to RNA, proteins, and metabolites in nearly all tissues, providing clues to many human health conditions.


Fig. 1: Summary of the study design and multi-omics dataset.


Fig. 5: Training-induced immune responses.


Fig. 6: Training-induced changes in metabolism.


Thursday, April 20, 2023

Clear chemical connection between physical activity and brain health

Amazing stuff! Use it or loose it!

"... Now, scientists have shown in cell studies that the connection may be more direct, which opens the door to more targeted physical therapies for brain health and potential treatment of neurodegenerative conditions. ...
The scientists ... were able to demonstrate through mice muscle cells how their contraction caused hippocampal neurons to fire off larger and more frequent electrical signals. Within days, these stronger and healthier signals became more synchronized, mimicking neural organization in the brain. ..."

"... To isolate the chemicals released by contracting muscles and test them on hippocampal neurons, the researchers collected small muscle cell samples from mice and grew them in cell culture dishes in the lab. When the muscle cells matured, they began to contract on their own, releasing their chemical signals into the cell culture.
The research team added the culture, which now contained the chemical signals from the mature muscle cells, to another culture containing hippocampal neurons and other support cells known as astrocytes. Using several measures, including immunofluorescent and calcium imaging to track cell growth and multi-electrode arrays to record neuronal electrical activity, they examined how exposure to these chemical signals affected the hippocampal cells.
The results were striking. Exposure to the chemical signals from contracting muscle cells caused hippocampal neurons to generate larger and more frequent electrical signals — a sign of robust growth and health. Within a few days, the neurons started firing these electrical signals more synchronously, suggesting that the neurons were forming a more mature network together and mimicking the organization of neurons in the brain. ...
“Ultimately, our research may contribute to the development of more effective exercise regimens for cognitive disorders such as Alzheimer's disease,” ..."

From the highlights and abstract:
"Highlights
• Contracting muscle media enhances hippocampal neuronal activity.
• Contracting muscle media expedites synaptic maturation.
• Contracting muscle media accelerates accumulation of filamentous actin at synapses.
• Contracting muscle media induces significant astrocyte and neuron proliferation.
• Astrocytes release factors that inhibit muscle media-induced neuronal activity.
Abstract
Exercise supports brain health in part by enhancing hippocampal function. The leading hypothesis is that muscles release factors when they contract (e.g., lactate, myokines, growth factors) that enter circulation and reach the brain where they enhance plasticity (e.g., increase neurogenesis and synaptogenesis). However, it remains unknown how the muscle signals are transduced by the hippocampal cells to modulate network activity and synaptic development. Thus, we established an in vitro model in which the media from contracting primary muscle cells (CM) is applied to developing primary hippocampal cell cultures on a microelectrode array. We found that the hippocampal neuronal network matures more rapidly (as indicated by synapse development and synchronous neuronal activity) when exposed to CM than regular media (RM). This was accompanied by a 4.4- and 1.4-fold increase in the proliferation of astrocytes and neurons, respectively. Further, experiments established that factors released by astrocytes inhibit neuronal hyper-excitability induced by muscle media, and facilitate network development. Results provide new insight into how exercise may support hippocampal function by regulating astrocyte proliferation and subsequent taming of neuronal activity into an integrated network."

Clear chemical connection between physical activity and brain health

Exercise releases chemical signals that boost brain health Beckman researchers studied how chemical signals from contracting muscles promote healthy brains. Their findings reveal how these signals help grow and regulate new brain networks while also pointing toward ways of improving brain health through exercise.


Hippocampal neurons (yellow) surrounded by astrocytes (green) in a cell culture from the study.


Saturday, March 04, 2023

Daily 11 minute brisk walk enough to reduce risk of early death

Good news and easy to do and cheap! No botox, no injections, no surgery, strange potions etc.! 

Couch potatoes get up! There is no good excuse for early death!

This is a very comprehensive meta study!

Currently, I briskly walk as a minimum about 1.5 hours and almost 7 miles per week. I feel I am in good shape! Disclosure: I was not part of this study! 😊

"In a study published today in the British Journal of Sports Medicine, the researchers say that 11 minutes a day (75 minutes a week) of moderate-intensity physical activity – such as a brisk walk – would be sufficient to lower the risk of diseases such as heart disease, stroke and a number of cancers.
Cardiovascular diseases – such as heart disease and stroke – are the leading cause of death globally, responsible for 17.9 million deaths per year in 2019, while cancers were responsible for 9.6 million deaths in 2017. Physical activity – particularly when it is moderate-intensity – is known to reduce the risk of cardiovascular disease and cancer, and the NHS recommends that adults do at least 150 minutes of moderate-intensity activity or 75 minutes of vigorous-intensity activity a week. ...
carried out a systematic review and meta-analysis, pooling and analysing cohort data from all of the published evidence. ...
In total, they looked at results reported in 196 peer-reviewed articles, covering more than 30 million participants from 94 large study cohorts, to produce the largest analysis to date of the association between physical activity levels and risk of heart disease, cancer, and early death.
The researchers found that, outside of work-related physical activity, two out of three people reported activity levels below 150 min per week of moderate-intensity activity and fewer than one in ten managed more than 300 min per week. 
Broadly speaking, they found that beyond 150 min per week of moderate-intensity activity, the additional benefits in terms of reduced risk of disease or early death were marginal. But even half this amount came with significant benefits: accumulating 75 min per week of moderate-intensity activity brought with it a 23% lower risk of early death. ...
What counts as moderate-intensity physical activity?
Moderate-intensity physical activity raises your heart rate and makes you breathe faster, but you would still be able to speak during the activity. Examples include:
Brisk walking
Dancing
Riding a bike
Playing tennis
Hiking"

Daily 11 minute brisk walk enough to reduce risk of early death | University of Cambridge One in ten early deaths could be prevented if everyone managed at least half the recommended level of physical activity, say a team led by researchers at the University of Cambridge.




Saturday, September 04, 2021

Benefits of time-restricted eating depend on age and sex

For many decades, apparently time-restricted eating never goes out of fashion! It is rediscovered every so often. 

Does not common sense suggests, to eat at certain times and e.g. not all day. That some routine in your dietary habits helps digestion and controls weight gain.

"Time-restricted feeding (TRF) is a nutritional intervention wherein food intake is limited to a consistent 8- to 10-h daily window without changes in nutritional quality or quantity. TRF can prevent and treat diet-induced obesity (DIO) and associated metabolic disease in young male mice fed an obesogenic diet, the gold standard preclinical model for metabolic disease research. ...
We show that most of the benefits of TRF are age-independent but are sex-dependent. TRF protects both sexes against fatty liver and glucose intolerance while body weight benefits are observed only in males. We also find that TRF imparts performance benefits and increases survival to sepsis in both sexes."

Benefits of time-restricted eating depend on age and sex - Salk Institute for Biological Studies Not everyone benefits equally from TRE, but TRE has important health benefits for all. Time-restricted eating (TRE), a dietary regimen that restricts eating to specific hours, has garnered increased attention in weight-loss circles. A new study by Salk scientists further shows that TRE confers multiple health benefits besides weight loss. The study also shows that these benefits may depend on sex and age.