Posted on Exercise

‘Weekend warrior’ exercise pattern may equal more frequent sessions for lowering cognitive decline

The research concludes that just one or two sessions of physical activity at the weekend—a pattern of exercise dubbed ‘weekend warrior’—may be just as likely to lower the risk of cognitive decline, which can often precede dementia, as more frequent sessions.

And it may be more convenient and achievable for busy people, suggest the researchers.

They say it’s important to identify potentially modifiable risk factors for dementia because a 5-year delay in onset might halve its prevalence. They add that nearly all the evidence to date comes from studies in high-income countries.

They, therefore, drew on two sets of survey data from the Mexico City Prospective Study: the first, which took place between 1998 and 2004, and the second, which took place between 2015 and 2019. 

Some 10,033 people (average age 51) completed both surveys, and their responses were included in the analysis.

For the first survey, respondents were asked whether they exercised or played sports, and if so, how many times a week and for how long (in minutes). 

Four groups were derived from the responses: the no-exercisers, the ‘weekend warriors’ who exercised/played sports once or twice a week, the regularly active who did so three or more times a week, and a combined group comprising weekend warriors and the regularly active.

The Mini-Mental State Exam (MMSE) assessed cognitive function during the second survey. A score of 22 or less out of 30 defined MCI.

In all, 7945 respondents said they didn’t exercise; 726 fulfilled the definition of a weekend warrior; 1362 said they exercised several times a week; and 2088 made up the combined group.

During an average monitoring period of 16 years, 2400 cases of MCI were identified. MCI prevalence was 26% among non-exercisers, 14% among weekend warriors, and 18.5% among the regularly active. 

After taking account of potentially influential factors including age, educational attainment, smoking, nightly sleep, diet and alcohol intake, weekend warriors were 25% less likely to develop MCI than the no exercisers, while the regularly active were 11% less likely to do so. Those in the combined group were 16% less likely to do so.

When MCI was defined as an MMSE score of 23 or below, 2856 cases were identified. And MCI prevalence rose to 30% among the no exercisers, 20% among the weekend warriors, and 22% among the regularly active.

Compared with the no exercisers, weekend warriors were 13% less likely to develop MCI, while the regularly active and those in the combined group were 12% less likely to do so. The results were similar for both men and women.

The researchers estimated that, in theory, 13% of cases might be avoided if all middle aged adults exercised at least once or twice a week. 

This is an observational study, so no firm conclusions can be drawn about causal factors. And the researchers acknowledge various limitations to their findings. For example, the survey respondents might not have been truly representative of  middle aged adults and there were no objective measures of physical activity.

But there are several possible explanations for the seemingly protective effect of exercise on brain health, they explain.

“For example, exercise may increase brain-derived neurotrophic factor concentrations [molecules that support the growth and survival of neurons] and brain plasticity. Physical activity is also associated with greater brain volume, greater executive function, and greater memory,” they write.

“To the best of our knowledge, the present study is the first prospective cohort study to show that the weekend warrior physical activity pattern and the regularly active physical activity pattern are associated with similar reductions in the risk of mild dementia,” they continue.

And they go on to suggest that the findings “have important implications for policy and practice because the weekend warrior physical activity pattern m

Posted on Patient Talk

COVID-19 sharply boosts risk for blood-fat disorders

A new study conducted by researchers at Albert Einstein College of Medicine, which involved over 200,000 adults, found that the COVID-19 pandemic led to a 29% increase in the risk of developing dyslipidemia. This condition is characterized by abnormal blood lipid (fat) levels. Seniors and individuals with type 2 diabetes were particularly affected, facing nearly double the risk of developing dyslipidemia. This condition is a significant risk factor for cardiovascular diseases, including heart attacks and strokes. The research was published in the print edition of The Journal of Clinical Investigation.

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“Considering the widespread impact of the pandemic, the increased risk of dyslipidemia is a global concern,” said study leader Gaetano Santulli, M.D., Ph.D., an associate professor of medicine and molecular pharmacology at Einstein. “Based on our findings, we recommend that individuals have their lipid levels monitored regularly and consult with their healthcare providers about treatment options for dyslipidemia if detected. This is especially important for elderly individuals and patients with diabetes.” He emphasized that this advice is relevant for all adults, not just those formally diagnosed with COVID-19, as many people may have been infected without realizing it.

To provide context for these findings, it is estimated that 53% of U.S. adults had dyslipidemia before the pandemic. If COVID-19 has caused a 29% increase in the incidence of dyslipidemia, this would suggest that approximately 68% of Americans may now be at risk for having lipid abnormalities.

In two previous studies, Dr. Santulli and his team found that COVID-19 increased the incidence of new cases of hypertension and type 2 diabetes. “In those analyses, we demonstrated that the risk of developing these disorders remained high three years after the pandemic. Additionally, we observed a concerning rise in total cholesterol levels, which warranted further investigation,” said Dr. Santulli. In the latest study, the researchers first identified the incidence of dyslipidemia among over 200,000 adults living in Naples, Italy, during the three years before the onset of the pandemic (2017-2019). They then examined the incidence of dyslipidemia in the same group during the COVID-19 period (2020-2022). This analysis excluded individuals who had been previously diagnosed with dyslipidemia or who had been taking lipid-lowering medications.

The investigators found that COVID-19 raised the risk for developing dyslipidemia in the entire study group by an average of 29%. The increase was even higher among people over age 65 and those with chronic conditions, particularly diabetes and obesity, cardiovascular disease, chronic obstructive pulmonary disease, and hypertension. The findings are the most definitive to date because other studies—most of them linking COVID-19 with modestly increased risks for blood-lipid problems—used as control groups different populations or people thought to have gone through the pandemic without becoming infected. However, significant numbers of people classified as “COVID-free” actually developed the disease but were either never tested or didn’t seek medical care.

“Our study did not attempt to determine whether participants had tested positive for COVID-19,” Dr. Santulli said. “Instead, because we had been following this group for many years prior to the pandemic, we were able to measure COVID’s overall impact on the population by simply comparing levels of dyslipidemia in the same group before and after the pandemic. Any increase in dyslipidemia incidence would almost certainly have to be the result of COVID-19.”

How COVID-19 might have increased the incidence of dyslipidemia remains unclear. One possible explanation is a finding Dr. Santulli made in an earlier study: that SARS-CoV-2 (the virus that causes COVID) disrupts the function of endothelial cells, which line the inside of blood vessels throughout the body and play a critical role in regulating blood lipids.

A separate study found that COVID-19 is a powerful risk factor for heart attacks and strokes for as long as nearly three years after an infection. “This investigation, published online a month after ours, essentially confirms our observations in this study, since dyslipidemia is a major contributor to cardiovascular disease,” said Dr. Santulli. “It also suggests that tackling dyslipidemia should reduce the risk of cardiovascular disease in those who have had COVID.”  

The researchers are now studying the effects of COVID-19 on cardiovascular-kidney-metabolic (CKM) syndrome, a recently described condition involving four connected medical problems—heart disease, kidney disease, diabetes, and obesity—all of which involve endothelial dysfunction.

Posted on autoimmune conditions, Diet, Multiple Sclerosis, Obesity

The negative effect of high-fat diet on multiple sclerosis progression

Western high-fat diet can cause chronic pain, according to UT Health San Antonio-led team

Recent research published in the journal *Glia* has uncovered important connections between dietary choices and the progression of multiple sclerosis (MS). The study, led by Patrizia Casaccia, the founding director of the Advanced Science Research Center at the CUNY Graduate Center’s Neuroscience Initiative and an Einstein Professor of Biology and Biochemistry at the same institution, investigated the role of enzymes known as ceramide synthase 5 and 6. These enzymes are linked to the harmful effects of a diet high in palm oil on neurons in the central nervous system, which may lead to an increase in the severity of MS symptoms.

Multiple sclerosis (MS) is an inflammatory autoimmune disease characterized by significant damage to the myelin sheath, which protects nerves throughout the body. Current treatments aim to control the immune system’s response, but the exact mechanisms leading to neurodegeneration in MS are still not well understood. Previous research from the Casaccia lab and others has indicated that a high-fat diet can exacerbate the severity of MS symptoms. In their study, researchers investigated potential mechanisms by which a diet high in palm oil may negatively affect neuronal health.

Neuroprotection From Palm Oil-Induced Toxicity

In the experimental autoimmune encephalomyelitis (EAE) model of inflammatory demyelination, researchers discovered that mice with diets high in palm oil had a more severe disease course.

“We hypothesized that within neuronal cells, palm oil is transformed into a toxic substance known as C16 ceramide by specific enzymes called CerS5 and CerS6,” explained principal investigator Casaccia. “This ceramide causes damage to mitochondria, depriving neurons of the energy they require to combat inflammation in the brain. Consequently, we investigated whether inactivating these enzymes could provide neuroprotection.”

The researchers found that genetically deleting the enzymes CerS6 and CerS5 in neurons could prevent neurodegeneration in an experimental model of MS.

“This was true even when mice were given a diet high in palmitic acid,” said Damien Marechal, a research associate with the Casaccia Lab and co-first author of the paper. “This new information highlights a specific metabolic pathway that shows how dietary fats can exacerbate MS symptoms.”

Significance for MS Patients and Clinicians

The paper’s findings have significant implications for individuals diagnosed with MS, clinicians treating patients, and neuroscientists researching the disease. The work reinforces that lifestyle choices, such as diet, can profoundly impact the course of the disease. The study’s results build on previous concepts about careful dietary decisions in managing the symptoms of MS. The findings also identify potential molecules that could help slow diet-induced symptom severity.

“Our research provides a molecular explanation for how to protect neurons from the palm-oil-dependent creation of molecules that harm them,” said Casaccia. “We hope this information can empower patients to make informed dietary decisions that could positively impact the course of the disease while identifying strategies to counteract the effect of cerS5 and cerS6 in a neuron-specific fashion.”

Posted on Cognitive dysfunction, Dementia, Diabetes, Diet, Obesity

Restricting sugar consumption in utero and in early childhood significantly reduces risk of midlife chronic disease

New research shows combined use of sodium glucose co-transporter 2 inhibitors (SGLT2is) and glucagon-like peptide-1 receptor agonists (GLP1-RAs) is likely to offer additional protection against heart and kidney disease in patients with diabetes

A new study has found that a low-sugar diet in utero and in the first two years of life can meaningfully reduce the risk of chronic diseases in adulthood. This provides compelling new evidence of the lifelong health effects of early-life sugar consumption.

A study published in the journal Science reveals that children who had sugar restrictions during their first 1,000 days after conception faced up to a 35% lower risk of developing Type 2 diabetes and a 20% reduced risk of hypertension in adulthood. The research indicates that low sugar intake by mothers during pregnancy was sufficient to lower these health risks, and maintaining sugar restrictions after birth further enhanced the benefits.

Using an unintended “natural experiment” from World War II, researchers at the USC Dornsife College of Letters, Arts and Sciences, McGill University in Montreal, and the University of California, Berkeley, examined how sugar rationing during the war influenced long-term health outcomes.

The United Kingdom introduced limits on sugar distribution in 1942 as part of its wartime food rationing program. Rationing ended in September 1953.

The researchers used contemporary data from the U.K. Biobank, a database of medical histories and genetic, lifestyle and other disease risk factors, to study the effect of those early-life sugar restrictions on health outcomes of adults conceived in the U.K. just before and after the end of wartime sugar rationing.

“Studying the long-term effects of added sugar on health presents challenges,” explains Tadeja Gracner, a senior economist at the USC Dornsife Center for Economic and Social Research and the study’s corresponding author. “It is difficult to identify situations where individuals are randomly exposed to different nutritional environments early in life and tracked over a span of 50 to 60 years. The end of rationing provided us with a unique natural experiment that helped us overcome these obstacles.”

On average, during rationing, sugar intake was about 8 teaspoons (40 grams) per day. When rationing ended, sugar and sweets consumption skyrocketed to about 16 teaspoons (80 grams) per day. 

Notably, rationing did not involve extreme food deprivation overall. Diets generally appeared to have been within today’s guidelines set by the U.S. Department of Agriculture and the World Health Organization, which recommend no added sugars for children under two and no more than 12 teaspoons (50g) of added sugar daily for adults. 

The immediate and large increase in sugar consumption but no other foods after rationing ended created an interesting natural experiment: Individuals were exposed to varying levels of sugar intake early in life, depending on whether they were conceived or born before or after September 1953. Those conceived or born just before the end of rationing experienced sugar-scarce conditions compared to those born just after who were born into a more sugar-rich environment.

The researchers then identified those born in the U.K. Biobank data collected over 50 years later. Using a very tight birth window around the end of sugar rationing allowed the authors to compare midlife health outcomes of otherwise similar birth cohorts.  

While living through the period of sugar restriction during the first 1,000 days of life substantially lowered the risk of developing diabetes and hypertension, for those later diagnosed with either of those conditions, the onset of disease was delayed by four years and two years, respectively. 

Notably, exposure to sugar restrictions in utero alone was enough to lower risks, but disease protection increased postnatally once solids were likely introduced. 

The researchers say the magnitude of this effect is meaningful as it can save costs, extend life expectancy, and, perhaps more importantly, improve quality of life.

In the United States, individuals with diabetes face average annual medical expenses of approximately $12,000. Additionally, an earlier diagnosis of diabetes is associated with a significantly reduced life expectancy; specifically, for each decade that diagnosis occurs earlier, life expectancy decreases by three to four years.

The researchers note that these numbers underscore the value of early interventions that could delay or prevent this disease.

Experts continue to raise concerns about children’s long-term health as they consume excessive amounts of added sugars during their early life, a critical period of development. Adjusting child sugar consumption, however, is not easy—added sugar is everywhere, even in baby and toddler foods, and children are bombarded with TV ads for sugary snacks, say the researchers.

“Parents need information about what works, and this study provides some of the first causal evidence that reducing added sugar early in life is a powerful step towards improving children’s health over their lifetimes,” says study co-author Claire Boone of McGill University and University of Chicago.  

Co-author Paul Gertler of UC Berkeley and the National Bureau of Economics Research adds: “Sugar early in life is the new tobacco, and we should treat it as such by holding food companies accountable to reformulate baby foods with healthier options and regulate the marketing and tax sugary foods targeted at kids.” 

This study is the first of a larger research effort exploring how early-life sugar restrictions affected a broader set of economic and health outcomes in later adulthood, including education, wealth, and chronic inflammation, cognitive function and dementia. 

Posted on A to Z of Medical Conditions, Diabetes, Obesity

Brighter nights and darker days could lead to an early grave

Are you protecting your children’s eyes from the sun this summer?

A study of more than 13 million hours of data collected from light sensors worn by 89,000 people has found exposure to bright nights and dark days is associated with an increased risk of death.

Researchers investigated whether personal day and night light and lighting patterns that disrupt our circadian rhythms predicted mortality risk.

Published in the journal Proceedings of the National Academy of Sciences, the findings indicate that individuals exposed to high levels of light at night faced a 21% to 34% increased risk of death. In contrast, those exposed to high levels of daylight experienced a 17% to 34% decrease in their risk of death.

“Exposure to brighter nights and darker days can disrupt our circadian rhythms. This disruption can lead to various health issues, including diabetes, obesity, cardiovascular disease, mental health problems, and an increased risk of death,” explains Professor Sean Cain, a senior author and sleep expert from Flinders University.

“These new insights into the potential adverse impact of light have shown us just how important personal light exposure patterns are for your health.”

Associate Professor Andrew Phillips, co-senior author, states that nighttime light exposure disrupts circadian rhythms by shifting their timing (phase-shift) and weakening the signal (amplitude suppression) of the central circadian ‘pacemaker,’ which regulates circadian rhythms throughout the body.

“Disruption to the body’s circadian rhythms is linked to the development of metabolic syndrome, diabetes, and obesity and is also strongly implicated in the development of cardiometabolic diseases, including myocardial infarction, stroke and hypertension,” says Associate Professor Phillips.

“The observed relationships of night light exposure with mortality risk may be explained by night light disrupting circadian rhythms, leading to adverse cardiometabolic outcomes.

“Our findings clearly show that avoiding night light and seeking daylight may promote optimal health and longevity, and this recommendation is easy, accessible and cost-effective,” adds Associate Professor Phillips.

The study authors from FHMRI Sleep Health investigated the relationship between personal light exposure and the risk of all-cause and cardiometabolic mortality in 89,000 participants from the UK Biobank, aged between 40 and 69. Metrics were recorded using wrist-worn sensors, and the National Health Service collected the participants’ mortality data over an approximate follow-up period of eight years.

Sleep duration, sleep efficiency, and midsleep were estimated from motion data. At the same time, cardiometabolic mortality was defined as any cause of death corresponding to diseases of the circulatory system or endocrine and metabolic diseases.

The research also showed a disrupted circadian rhythm predicted higher mortality risk, which the authors were able to determine using computer modelling. Findings accounted for age, sex, ethnicity, photoperiod, and sociodemographic and lifestyle factors.

Lead author Dr Daniel Windred says that the findings demonstrate the importance of maintaining a dark environment during the late night and early morning hours, when the central circadian ‘pacemaker’ is most sensitive to light, and seeking bright light during the day to enhance circadian rhythms.

“Protection of lighting environments may be significant in those at risk for circadian disruption and mortality, such as in intensive care or aged-care settings,” says Dr Windred.

“Across the general population, avoiding night light and seeking daylight may lead to a reduction in disease burden, especially cardiometabolic diseases, and may increase longevity.”