Posted on Cardiovascular disease, Exercise

Prolonged sitting can sabotage health, even if you’re young and active

Millennials sit more than 60 hour per week, fueling heart disease risk and accelerating aging
Millennials sit more than 60 hours per week, fueling heart disease risk and accelerating ageing.

Recent research from CU Boulder and the University of California, Riverside, reveals that millennials are spending over 60 hours a week sitting due to long commutes, back-to-back Zoom meetings, and evenings spent streaming and scrolling through social media. This sedentary lifestyle could increase their risk of heart disease and accelerate other signs of ageing.

The study of over 1,000 individuals from Colorado, including 730 twins, is one of the first to investigate how prolonged sitting affects health metrics such as cholesterol levels and body mass index (BMI) in young adults.

Research shows that simply meeting the minimum physical activity guidelines—approximately 20 minutes of moderate exercise each day—is insufficient to offset the risks associated with spending most of our waking hours sitting.

“Our research indicates that reducing the sitting time during the day, engaging in more vigorous exercise, or implementing a combination of both may be essential for lowering the risk of premature ageing in early adulthood,” stated the study’s senior author, Chandra Reynolds, a professor in the Department of Psychology and Neuroscience as well as the Institute for Behavioral Genetics.

After the COVID pandemic, Bruellman noticed that he and others his age were sitting more. He set out to learn more about the consequences.

“Young adults often believe they are immune to the effects of aging. They think, ‘My metabolism is excellent, so I don’t need to worry until I reach my 50s or 60s,’” said Bruellman. “However, what you do during this crucial stage of life is important.”

A walk after work isn’t enough.

The authors analyzed data from participants aged 28 to 49, with an average age of 33, from CU’s Colorado Adoption/Twin Study of Lifespan Behavioural Development and Cognitive Ageing (CATSLife), which has followed twins and adopted individuals since Childhood.

Participants reported sitting almost 9 hours daily, with some sitting as much as 16 hours. On average, they reported between 80 and 160 minutes of moderate physical activity weekly and less than 135 minutes of vigorous exercise weekly. The authors note that these results are likely better than national averages due to Colorado’s active lifestyle.

The researchers looked at two key heart and metabolic ageing measures: total cholesterol/high-density lipoprotein and body mass index (BMI). The study found that the more one sat, the older one looked. Adding a little moderate activity on top of a long day of sitting did little to buffer these impacts.

Young adults who sat 8.5 hours per day and performed at or below current exercise recommendations could enter a “moderate to high risk” category for cardiovascular and metabolic disease, the authors said.

“Taking a quick walk after work may not be enough,” said Reynolds. “While this is increasingly apparent with age, we show that associations are already emerging in early adulthood.”

Adding vigorous activity did have a buffering effect.

For instance, those who exercised vigorously (think running or cycling) for 30 minutes daily had cholesterol and BMI measures that looked like those of individuals five to 10 years younger who sat as much as they did but didn’t exercise.

However, even vigorous activity could not fully buffer the negative impacts of prolonged sitting, the study concluded.

Same genes, different lifestyles

Identical twins are handy to study because they share 100% of their genes, making it easier to rule out genetic factors that might contribute to different health outcomes and zero in on lifestyle differences.

When looking at a subset of twins with different sitting and physical activity habits, the researchers found that replacing sitting with exercise seemed to improve cholesterol better than simply adding exercise to a full day of sitting.

The bottom line, the researchers said, is to try to do both.

To reduce sitting time at work, use a standing desk, take breaks, and organize walking meetings. If possible, do something that gets you out of breath for at least 30 minutes per day, or be a “weekend warrior” and get in longer, vigorous workouts when you can, said Bruellman.

He hopes the study will prompt policymakers to revisit physical activity guidelines and specify how much sitting is too much.

Meanwhile, Reynolds encourages young adults to take steps now that could shape their future:

“This is the time to build habits that will benefit health over the long term.”

Posted on Osteoporosis, Rheumatoid arthritis

Two key genes identified linking rheumatoid arthritis and osteoporosis

Two key genes, ATXN2L and MMP14, that are most strongly linked to both diseases

Of the many genes involved in rheumatoid arthritis and osteoporosis, the researchers identified two essential genes, ATXN2L and MMP14, most strongly linked to both diseases—credit Lo et al.

Rheumatoid arthritis is a prevalent condition that affects approximately 17 million people globally. This disease occurs when the immune system mistakenly attacks the joints, leading to pain, swelling, and damage to the cartilage and bones. Additionally, individuals with rheumatoid arthritis are at an increased risk of developing osteoporosis, a more serious condition that can arise from the bone damage caused by the immune response as well as from certain medications used to treat the disease.

In the journal APL Bioengineering from AIP Publishing, researchers from Da-Chien General Hospital, China Medical University, and Chang Gung University used analytical tools and machine learning algorithms to identify two genes associated with rheumatoid arthritis and osteoporosis. These genes could serve as diagnostic tools and potential targets for treatment.

Both diseases revolve around a key mechanism that helps regulate the body’s functions. Apoptosis, or programmed cell death, is an essential process that immune cells use to eliminate malfunctioning or unnecessary cells. However, malfunctions in this process can cause immune cells to mistakenly target random cells, often resulting in severe consequences.

“Excessive apoptosis of bone-forming cells in rheumatoid arthritis leads to joint destruction and inflammation,” stated author Hao-Ju Lo. “This same process also results in weakened bones in osteoporosis, highlighting the necessity of managing both conditions concurrently.”

Because of its central role, the researchers set out to find genes involved with apoptosis that were closely linked to both diseases. Drawing from an extensive database of genetic information, they gathered dozens of sequenced genomes from people with rheumatoid arthritis and osteoporosis to look for similarities. Combing through this mountain of genetic data was no easy task, so they turned to recently developed computational methods to narrow their search.

“We used bioinformatics tools to analyze large gene datasets, focusing on genes active in rheumatoid arthritis and osteoporosis,” said Lo. “We applied machine learning techniques, such as Lasso and Random Forest, to refine our search, identifying two key genes — ATXN2L and MMP14 — that play significant roles in both diseases.”

According to their analysis, these two genes are significantly associated with the progression of rheumatoid arthritis and osteoporosis. ATXN2L regulates processes like apoptosis, so malfunctions in this gene are likely to trigger both rheumatoid arthritis and osteoporosis. MMP14 contributes to building extracellular tissue like cartilage and could be responsible for the breakdown of joint tissue that leads to rheumatoid arthritis.

“Our analysis revealed that these genes are involved in immune regulation and bone metabolism, suggesting they could be useful markers for diagnosing or treating rheumatoid arthritis and osteoporosis,” said Lo.

With two potential targets identified, the authors plan to use these results as a starting point to develop new treatment options for patients suffering from these two linked diseases.

“We plan to validate these findings with experimental studies and explore how targeting these genes could improve treatment outcomes,” said Lo. “Our future research may also involve developing personalized therapies, leveraging AI and machine learning to predict which patients are most at risk for osteoporosis.”

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Posted on Multiple Sclerosis, Pain Management

Eleven Ways Multiple Sclerosis Causes Pain

Can multiple sclerosis cause pain? Yes, it can! This video highlights 11 common pain syndromes associated with MS, including trigeminal neuralgia, the “MS hug,” neuropathic pain, muscle spasms, and several others.

Posted on Cognitive dysfunction, Diabetes, Diet

Blood sugar control is a big factor in slowing brain aging! What about the Mediterranean diet?

The Green Mediterranean Diet Shows Promise
The Green Mediterranean Diet Shows Promise

Age-related brain atrophy refers to the gradual loss of neurons and shrinkage of brain tissue, which is a natural part of the ageing process. This condition can contribute to cognitive decline and various neurological issues. While ageing itself cannot be prevented, recent research from an 18-month dietary intervention provides hope that lifestyle and dietary changes may help slow down brain ageing.

Brain age, determined through MRI measurements of the hippocampus and lateral ventricles, reflects the biological aging of the brain, which may differ from a person’s chronological age. Chronological age is simply the number of years a person has lived, while brain age indicates the actual health of the brain. Generally, as we age, the hippocampus tends to shrink, and the lateral ventricles tend to expand, which serve as indicators of brain ageing. Some individuals may have a brain age that is younger or older than their chronological age. A younger brain age suggests better cognitive health, whereas an older brain age may indicate accelerated ageing and an increased risk of cognitive decline.

The study found that a decline in HbA1c and key markers of long-term blood sugar levels is associated with significant positive changes in specific brain regions commonly affected by age-related atrophy. It suggests that improved blood sugar control could be one of the most important factors in slowing down age-related brain changes.

Previous research has shown the benefits of the Green Mediterranean (Green-Med) diet, particularly its positive effects on blood sugar control. This diet is rich in polyphenols from plant-based sources such as Mankai—a high-protein aquatic plant—and green tea, while being low in red and processed meats. The current study reinforces these findings, suggesting that the Green-Med diet not only supports metabolic health but may also have protective effects on brain structure and function.