Obesity and Ageing

Significant link between obesity and cognitive decline revealed by Chinese research

A recent study conducted in China has established a significant connection between obesity and the deterioration of brain health, suggesting that individuals with obesity may suffer from a reduction in brain volume akin to the effects seen after 12 years of ageing.

Researchers from Tsinghua University and Capital Medical University Affiliated Beijing Friendship Hospital undertook a comprehensive study spanning 16 years, during which they monitored the body mass index (BMI) and brain health of over 1,000 Chinese adults across various age groups. The findings of this research were derived from neuroimaging data, which highlighted a distinct association between obesity and several markers of cognitive decline. These markers include diminished brain volume, an increase in white matter lesions, and compromised microstructural integrity of the brain.

In the context of China’s health standards, an individual with a BMI exceeding 24 is categorised as having overweight, and obesity is defined at a BMI threshold of 28. The study, published in the journal Health Data Science, notes a critical finding: individuals under the age of 45 with a BMI over 26.2 exhibit brain volume reductions equivalent to the natural age-related decline observed over 12 years.

This research was spotlighted by the state media outlet Life Times, which stressed the study’s recommendation for younger individuals to maintain a BMI below 26.2 to safeguard their cognitive health. The report emphasised the absence of health benefits in being overweight, stating, “There is no healthy overweight person.”

The implications of obesity on brain health are not unique to China. A related study published in 2023 by a Lancet sub-journal, involving 10,000 participants from across Asia, corroborated these findings. This study illustrated that an increase of 0.27 kilograms in visceral fat correlates with 0.7 years of cognitive ageing for the average person.

Concerns are growing regarding the future health landscape of the Asia-Pacific region, as the authors of the study forecast a surge in dementia cases coinciding with increasing obesity levels and an ageing population. The region, which currently sees approximately 4 million new dementia cases annually—accounting for 40% of the global incidence—is also witnessing a rise in obesity rates that surpass the global average by about 7%.

A separate 2023 study, encompassing nearly 15.8 million adults from more than 240 Chinese cities, reported that 34.8% of the subjects had overweight and 14.1% were classified as having obesity. The study further noted a higher propensity for obesity and overweight conditions among men compared to women, with affected individuals more likely to suffer from health issues such as fatty liver disease, prediabetes, and hypertension.

Sun Dejin, a neurologist from Shenzhen Third People’s Hospital, shared insights with Life Times regarding the severe impact of obesity on cognitive functions. According to Sun, obesity leads to notable cognitive impairments, including deteriorations in thinking, learning, and memory capabilities. He warned that if these cognitive declines are not addressed, they could progress to dementia, posing severe risks to overall health and well-being.

This body of research collectively underscores the critical need for managing obesity to mitigate its profound effects on brain health and cognitive function.

Study reveals heart damage risks in sedentary children

A recent study has highlighted alarming trends in heart health among children and young adults, revealing that excessive sedentary behaviour, commonly referred to as being a ‘couch potato’, could lead to an enlarged heart. This condition significantly increases the risk of heart attacks, strokes, and premature mortality.

Researchers have identified that sedentary habits account for up to 40% of the total increase in heart size from the ages of 17 to 24. The study also discovered that limited physical movement contributes to the enlargement of teenagers’ hearts independently of other contributing risk factors such as obesity or hypertension.

Andrew Agbaje, an associate professor of clinical epidemiology and child health at the University of Eastern Finland in Kuopio, referred to childhood and teenage sedentary behaviour as a “ticking time bomb.” Agbaje, in a recent press release, stressed the severity of the health threats posed by inactivity during youth. “There is growing evidence that childhood sedentariness is a serious health threat that warrants urgent attention,” he stated.

Conversely, the study noted that children who participate in regular light physical activity can mitigate the risk of heart enlargement significantly. Such activities have been found to reduce the increase in heart mass by 49%. “Engaging in three to four hours of light physical activity daily is an effective countermeasure to sedentary habits,” Agbaje explained.

Activities beneficial for cardiovascular health include playing outdoor games, walking pets, running errands on foot, cycling to local destinations, strolling in parks, gardening, and playing casual sports like basketball, soccer, and frisbee.

The study also observed that children who engage in more intense workout routines might see an approximate 5% increase in heart mass, which is attributed to strengthening of the heart muscle rather than harmful enlargement.

This research followed nearly 1,700 participants in the UK from the age of 11 to 24. To monitor their physical activity levels, participants wore motion-tracking devices around their waists for periods ranging from four to seven days at ages 11, 15, and 24. Initial data showed that children spent an average of six hours a day in sedentary activities, which alarmingly increased to nine hours by young adulthood.

The study further incorporated echocardiograms taken at ages 17 and 24 to assess heart structure and function, revealing significant insights into the impact of lifestyle on cardiac health.

Published on the 7th of May, 2024 in the European Journal of Preventive Cardiology, this study underscores the critical need for integrating more physical activity into the daily routines of young people to combat the adverse effects of a sedentary lifestyle on heart health.

Obesity and high-fat diets linked to swift vascular ageing in the brain

A new study conducted in mice traces how obesity and a high-fat diet may accelerate ageing in the blood vessels that supply blood to the brain. The work is being presented this week at the American Physiology Summit, the flagship annual meeting of the American Physiological Society (APS), in Long Beach, California. 

The findings suggest that obesity and a poor diet can cause damage to accumulate in the blood vessels, reducing the supply of oxygen to parts of the brain and ultimately leading to cognitive decline. The study could help scientists find ways to intervene and preserve brain function in people with obesity, which is estimated to affect about 42% of U.S. adults. 

“This project highlights the critical roles of vascular components and cellular ageing in cognitive deterioration, pinpointing novel potential therapeutic targets for dementia prevention and treatment,” said Sharon Negri, PhD, the study’s first author and a postdoctoral research fellow in the laboratory of Stefano Tarantini, PhD, in the Department of Neurosurgery at the University of Oklahoma Health Sciences Center. 

Previous research has found strong links between mid-life obesity and an increased risk of cognitive decline and dementia later in life. The scientists sought to uncover the mechanisms behind this association, with a particular focus on the role of diet and vascular health. 

To do this, the researchers studied the impact of a high-fat diet on blood flow to the brain and memory performance in aged mice with obesity. By using a special mouse model, they were also able to measure cellular senescence, a process when cells stop dividing and making new cells. Cellular senescence increases with ageing and contributes to a variety of ageing-associated diseases. 

“Obesity may cause the cells in blood vessels in the brain to age faster and reach senescence. If a link between obesity and cellular senescence is established, it could open up new lines of investigation aimed at exploring therapeutic avenues to prevent or slow down the progression of senescence, with the potential to mitigate obesity-related health issues, including cognitive decline.” – Sharon Negri, PhD, study’s first author

The results showed that after three months, mice fed a high-fat diet had increased cellular senescence and reduced density of healthy blood vessels in the brain, as well as evidence of impaired learning in a maze test, compared with normal-weight mice fed a standard diet. In addition, the scientists found that removing the senescent cells using Navitoclax, an investigational cancer drug that selectively kills senescent cells, improved features of the brain vasculature. 

If further experiments confirm that it is possible to reverse the detrimental effects of senescence, Negri and Tarantini next plan to evaluate whether various lifestyle interventions could help to prevent or reduce obesity-induced cognitive impairment.

Obesity during youth could double the risk of multiple sclerosis in later life, research suggests

Children grappling with obesity might face a significantly higher likelihood of being diagnosed with multiple sclerosis (MS) in adulthood, according to recent research findings.

Multiple sclerosis is a condition that impacts the brain and spinal cord, leading to a wide array of potential symptoms, including challenges with vision, coordination in the arms or legs, sensation, or balance. As a lifelong affliction, MS can sometimes lead to severe disability.

These insights are set to be shared at the European Congress on Obesity, taking place in Venice this May, and stem from research conducted by the Karolinska Institute in Stockholm.

Prior studies have hinted at a connection between an elevated body mass index (BMI) during adolescence and a heightened risk of MS. However, the majority of these analyses relied on retrospective approaches and self-reported data, which could introduce biases.

The recent investigation aimed to prospectively assess the risk of MS development among a significant cohort of children with obesity in comparison to their counterparts in the broader population. To this end, the researchers turned to the Swedish Childhood Obesity Treatment Register, also known as Boris. This database stands as one of the globe’s most extensive records dedicated to the treatment of childhood obesity.

The team reviewed data pertaining to children between the ages of two and 19 who were enrolled in the registry from 1995 to 2020. This information was then juxtaposed with data from the general population of children.

In total, the study took into account data from over 21,600 children who commenced obesity treatment at an average age of 11, alongside more than 100,000 children without obesity.

Throughout an average tracking period of six years, MS was diagnosed in 28 children from the group with obesity (representing 0.13% of this cohort) and 58 children from the group without obesity (0.06%).

The average age at which MS was diagnosed remained similar across both groups, with diagnoses typically occurring around the age of 23.

While acknowledging certain limitations in their study, the researchers underscored: “Despite the limited follow-up time, our findings accentuate that childhood obesity amplifies the risk of developing early-onset MS by more than double.”

The study’s lead researchers, Associate Professor Emilia Hagman and Professor Claude Marcus, commented: “Obesity during childhood induces a low-grade, yet chronic inflammation, which likely elevates the risk of developing various conditions, including MS.”

They further elucidated that such chronic low-grade inflammation is believed to elevate the risk of other conditions, such as asthma, arthritis, type 1 diabetes, and certain cancers. Notably, they highlighted that weight loss can diminish inflammation, thereby potentially reducing the risk of developing these diseases.

Study highlights obesity’s role in blood condition leading to multiple myeloma blood cancer

The possible interplay between lifestyle factors such as smoking, insufficient sleep, and obesity, and their influence on a blood condition that can lead to a specific type of blood cancer, warrants further investigation, according to experts.

Recent findings published in “Blood Advances” suggest that certain modifiable risk factors, notably smoking and obesity, might elevate the risk of developing monoclonal gammopathy of undetermined significance (MGUS). This condition often precedes multiple myeloma, a form of blood cancer.

Dr. David Lee, an internal medicine resident at Massachusetts General Hospital and co-author of the study, emphasised the urgency of this research. He noted that despite significant advancements in multiple myeloma treatments, it remains incurable and is often diagnosed after considerable damage to the patient’s organs. He added, “Our research group is focused on investigating risk factors and aetiology of MGUS to better understand who may be at increased risk for developing MGUS and its progression to multiple myeloma.”

MGUS is characterised by abnormally high levels of a protein called M protein in the blood. While in most instances MGUS does not cause problems, there is an annual 1% risk of progression from MGUS to myeloma, a cancer affecting plasma cells.

Myeloma results in an accumulation of a type of white blood cell in the bone marrow, leading to tumour formation throughout the bones. The most significant risk factor for developing myeloma is age, particularly affecting those over 45. The disease is more prevalent in men and is twice as likely to occur in black individuals compared to white individuals. Furthermore, having overweight or obesity has been identified as a risk factor for myeloma.

Dr. Brian Durie, Chief Scientific Officer of the International Myeloma Foundation and a haematologist and oncologist at Cedars-Sinai Medical Center, who was not part of the study, highlighted a known correlation between MGUS, myeloma, and obesity. He explained, “There’s also a correlation between obesity and a lot of other things, other kinds of cancer, other kinds of issues with your immune system.”

The study indicated that obesity might be associated with a 73% higher likelihood of having MGUS compared to those without obesity. However, the researchers cautioned that while there is a notable connection, it does not definitively prove causation.

Dr. Gary Schiller, a clinical investigator in multiple myeloma and hematologic malignancies at the University of California Los Angeles, also not involved in the study, suggested alternative explanations for the presence of MGUS. He explained that MGUS is relatively common, especially in older populations, and its occurrence might coincide with other factors like increased body mass index and reduced sleep quality. Schiller cautioned against hastily interpreting these associations as causal relationships.

Schiller and others have investigated the influence of obesity on the progression of MGUS, exploring theories involving hormones with anti-inflammatory properties that might be deficient in individuals who have overweight. However, he asserts that the current evidence does not firmly support these hypotheses.

The authors of the study believe their findings could be instrumental in guiding future research into the role of modifiable risk factors in cancer risk. Lee stressed the importance of understanding the relationship between MGUS and these risk factors to develop effective preventative health strategies against diseases like multiple myeloma.

Durie pointed out the current lack of sufficient data to confirm that lifestyle modifications in response to these risk factors would significantly impact MGUS or myeloma outcomes. Nonetheless, he mentioned animal studies that suggest this area is worth future exploration.

The potential of modifiable risk factors in influencing health outcomes is significant, according to Durie. He suggested that efforts to reduce obesity could potentially improve outcomes for patients, emphasising the personal relevance and potential impact of such changes.

Both Durie and Schiller advise individuals with obesity and other risk factors not to be overly concerned about developing MGUS or myeloma. Durie noted, “The vast majority of patients with MGUS will never develop myeloma.” He stressed that for many, the risk of progression is low, and they are more likely to succumb to unrelated causes.

Schiller echoed these sentiments, highlighting the immediate and more pressing health risks associated with obesity, such as hypertension, diabetes, and cardiovascular diseases. He argued that these more immediate health concerns should take precedence over the potential risk of MGUS in the context of obesity.

Obesity triggers neurodegeneration by inducing brain insulin resistance

In a pivotal study conducted by Mroj Alassaf and colleagues at the Fred Hutchinson Cancer Research Center in the United States, a novel connection between obesity and the onset of neurodegenerative diseases, such as Alzheimer’s, has been uncovered.

The research, employing the biological model of the common fruit fly, indicates that diets high in sugar, which are commonly associated with obesity, lead to insulin resistance within the brain. This resistance hampers the brain’s capacity to eliminate cellular waste, which in turn elevates the risk of neurodegenerative conditions.

The findings, released on November 7 in the open-access publication PLOS Biology, promise to be influential in the development of medical interventions aimed at mitigating the chances of neurodegenerative disease onset.

While the correlation between obesity and neurodegenerative diseases like Alzheimer’s and Parkinson’s has been acknowledged in scientific circles, the causal mechanisms at play have eluded researchers until now.

The team’s research delved into this conundrum by leveraging the genetic and physiological parallels between fruit flies and humans. Building on prior knowledge that a diet rich in sugar instigates insulin resistance in the peripheral tissues of fruit flies, the focus now shifted to their neural tissues. The study zoomed in on glial cells, as abnormalities in microglia are recognised contributors to neuronal decay.

The study measured the protein PI3k—a biomarker for insulin sensitivity in cells. The high-sugar diet was found to diminish PI3k levels in glial cells, suggesting a state of insulin resistance. The team also examined the fruit fly’s version of microglia, known as ensheathing glia, responsible for clearing out neuronal waste, including deteriorating axons.

These glial cells exhibited depleted levels of Draper, a protein integral to their waste-removal function, indicating a compromised ability. Subsequent experiments demonstrated that artificially reducing PI3k levels not only caused insulin resistance but also led to decreased Draper levels in the ensheathing glia. Moreover, when the team inflicted damage on olfactory neurons, the ensheathing glia of sugar-fed flies failed to clear the resulting neuronal debris due to their unresponsive Draper levels.

The researchers conclude by stating that their work with fruit flies has established that high-sugar diets induce insulin resistance in glial cells, which disrupts their neuronal cleanup role. This study sheds light on the potential pathways through which diets leading to obesity may elevate the risk of neurodegenerative diseases.

Rising obesity levels may intensify menopause symptoms and reduce hormone therapy efficiency, preliminary study indicates

The global surge in obesity, with an estimated 13% of adults now grappling with the condition, is a growing concern. A recent report suggests that obesity prevalence is higher among women than men (15% vs. 11%), with a more pronounced incidence in developed nations. Particularly in the United States, data from the Centers for Disease Control and Prevention (CDC) reveals that in 2020, 41.9% of individuals aged 20 and over were categorised as having obesity.

The far-reaching health implications of obesity are well-documented, encompassing a higher propensity for heart attacks, strokes, type 2 diabetes, respiratory ailments, and musculoskeletal issues.

A nascent study unveils a potential additional concern: obesity might amplify the severity of menopausal symptoms and compromise the effectiveness of hormone therapy aimed at alleviating these symptoms. The study’s lead author, Dr. Anita Pershad from the Eastern Virginia Medical School, shared her insights stating, “The core inference from our study is that obesity might exacerbate a woman’s menopausal symptoms while concurrently diminishing the relief provided by hormone therapy (HT).”

However, Dr. Kara McElligot, a NAMS-certified menopause practitioner and medical advisor at Mira, underscored the preliminary nature of this investigation, which encompassed a mere 119 participants and was executed retrospectively via chart review, thus inheriting a higher risk of bias.

The research, though yet to be peer-reviewed, was showcased at the 2023 Annual Meeting of The Menopause Society in Philadelphia, held between September 27 and 30. The study, spanning five years, meticulously reviewed the medical records of 119 women visiting a menopause clinic. These women were segregated into two cohorts based on their Body Mass Index (BMI)—those with a BMI above 30 were categorised as having obesity, while those below this threshold formed the other group.

The evaluation revealed no substantial disparity between the groups concerning age, the extent of menopause, hormone therapy utilisation, and acceptance. However, a significant finding emerged: women with obesity exhibited a higher propensity to report symptoms such as vasomotor symptoms (hot flashes), genitourinary/vulvovaginal symptoms, mood fluctuations, and diminished libido.

Dr. Sherry Ross, a seasoned OB/GYN at Providence Saint John’s Health Center in Santa Monica, elucidated a plausible cause, positing that women with obesity might experience intensified hot flashes and night sweats as fatty tissues could act as insulators, retaining heat within the body. Another theory proposes that obesity might trigger hormonal imbalances, thus engendering elevated oestrogen levels which, in turn, could exacerbate menopausal symptoms.

Dr. Ashley Parr, D.O., OB/GYN at The Women’s Hospital at MemorialCare Saddleback Medical Center, concurred with this notion, adding that the oestrogen-producing capability of fat cells could potentially alter the hormonal equilibrium of women with obesity during menopause, even post the cessation of ovarian function.

Moreover, the research identified a diminished likelihood of symptomatic relief post systemic and/or localised hormone therapy among women with obesity, compared to their counterparts without obesity. Dr. Pershad disclosed ongoing inquiries into the ambiguous efficacy of hormone therapy among women with obesity.

She further discussed exploring alternative designs and administration routes to potentially enhance hormone therapy effectiveness. Concurrently, Dr. Parr highlighted that obesity-associated risks for other health conditions like heart disease and breast cancer could deter the choice of hormone replacement, prompting considerations for non-hormonal treatment alternatives such as SSRIs, SNRIs, and vaginal oestrogen based on the specific symptoms sought to be addressed.

Dr. McElligot delineated the conceivable reasons behind the diminished effectiveness of hormone therapy in women with obesity, referring to various factors influencing the severity and experience of oestrogen deficiency, with obesity being a prime contender. She also brought attention to liver drug metabolism studies that reveal variations in circulating drug quantities based on BMI among adults, shedding light on the possible need for revising hormone therapy dosing recommendations to cater to the distinct metabolic dynamics presented by obesity.

Revitalising weight loss: The miraculous power of “beige fat” in reversing age-related weight gain

Discovering the ability to activate the body’s own fat-burning mechanisms and counteract age-related metabolic changes might seem like an unattainable dream, but researchers at Cornell University’s Division of Nutritional Sciences are working towards making it a reality. Their recent study explores the potential of a specific type of fat cells known as “beige fat” to reverse the effects of a slowing metabolism.

In mammals, including humans, two main types of fat exist: white adipose tissue (WAT), which stores excess calories, and brown adipose tissue (BAT), which burns calories to generate heat and regulate body temperature. The study sheds light on the therapeutic possibilities of a third type of fat called beige fat, a subtype of WAT. Beige fat shares characteristics with both white and brown fat, possessing thermogenic properties similar to brown fat and the ability to regulate blood sugar levels and reduce fatty acids associated with conditions like arterial hardening and heart disease.

The formation of beige fat occurs when adipose progenitor cells, a type of stem cell found within white fat, are stimulated by prolonged exposure to cold temperatures. However, as individuals age, their response to this stimulus weakens, leading to an imbalance favouring the production of white fat.

“Seasonal changes in beige fat occur in young humans, but an older person would have to stand outside in the snow in their underwear to achieve those same effects,” explains Dan Berry, an assistant professor in the Division of Nutritional Sciences at Cornell University.

Previous research by Berry revealed that the ageing process inhibits the formation of beige fat cells in response to cold temperatures.

The study’s lead author, Abigail Benvie, a doctoral student researcher in Berry’s lab, explains that the ultimate goal of their research is to find ways to stimulate metabolic pathways without subjecting individuals to prolonged cold exposure. Researchers successfully suppressed this pathway in ageing mice and stimulated the production of beige fat cells in areas where only white fat would typically form.

This research not only offers potential solutions for age-related weight gain and associated health conditions but also provides insights into the molecular mechanisms underlying beige fat formation. The study’s co-authors, including graduate students Derek Lee, Benjamin M. Steiner, and Siwen Xue, as well as Yuwei Jiang from the University of Illinois at Chicago, plan to further investigate the identified pathway and explore other molecular regulators of beige fat formation. With a $2.2 million, five-year grant from the National Institutes of Health, Berry’s lab aims to deepen our understanding of how these regulators change in levels and activity during the ageing process.

The study, published in the journal Nature Communications, represents a significant step forward in harnessing the potential of beige fat to combat age-related weight gain and improve metabolic health.

Obesity associated with diminished bone strength, particularly in men

Despite the protective implication often associated with high body weight in terms of fracture risk, recent studies suggest that obesity may in fact raise the risk of fractures, particularly in men with high body fat content.

A comprehensive examination of dual x-ray absorptiometry (DXA) data from a broad spectrum of over 10,000 U.S. individuals revealed an intricate connection between body weight and bone density. Dr. Rajesh Jain and Dr. Tamara Vokes, both from the University of Chicago, discussed these complex findings in the Journal of Clinical Endocrinology & Metabolism.

The duo discovered that each 1 kg/m2 increase in lean mass index correlated with a 0.19 higher T-score in people below 60 years of age. However, every corresponding increase in fat mass index was associated with a 0.10 decline in T-score, with a significant statistical difference (P<0.001).

Their research indicated that while lean mass positively impacted bone mineral density (BMD) equivalently in both genders, the deleterious effect of fat mass was more pronounced in men, leading to a 0.13 lower T-score per additional 1 kg/m2, compared to a 0.08 drop in women (P<0.001 for interaction).

“Our analysis of a large, heterogeneous population presenting a wide range of BMI indicated a clear negative correlation between bone density and fat mass, and a positive correlation with lean mass,” Jain and Vokes stated.

The researchers highlighted that despite lean mass exhibiting a stronger overall impact than fat mass, the detrimental effects of fat on BMD were significantly more evident in men and individuals with excessive fat content.

These insights hold critical clinical implications as they suggest obesity could contribute to declining BMD in patients traditionally not perceived as high fracture risk, and who therefore might not typically undergo DXA screening.

Contrasting previous studies constrained by small sample sizes or referral bias, Jain and Vokes’ findings reflect broader U.S. population data. They emphasise that obesity does not provide immunity against low BMD, advocating for clinicians to assess bone density, especially when other risk factors are present.

To reach their conclusions, the researchers assessed data from the National Health and Nutrition Examination Surveys conducted from 2011 to 2018. This dataset encompassed body composition and DXA measurements for 10,814 individuals aged 20 to 59.

Using linear regression models with total body BMD as the dependent variable, the researchers scrutinised the impact of lean and fat mass, accounting for age, gender, race/ethnicity, height, and smoking status. Notably, they highlighted the challenge of disentangling the interconnected influences of fat and lean mass on bone density.

Prior studies exploring the impact of fat mass on bone density reported varying results due to differing statistical methods and are somewhat outdated, the researchers pointed out. Moreover, the current study benefited from a densitometer with a higher weight limit, allowing for the examination of more severe obesity cases.

However, the study had limitations, including its focus on adults below 60 years, leaving room for potentially different body composition and bone mass relationships in older individuals. It also didn’t evaluate factors besides sex hormones that might elucidate the observed gender differences in the link between fat mass and bone density.

Despite women generally having a higher proportion of body fat, fat accumulation patterns differ by gender, with women typically storing fat in the hip and thigh areas, and men in the trunk and abdomen. Jain and Vokes acknowledged that differences in fat distribution might influence BMD, although their study could not conclusively prove this.

Obesity in childhood and puberty linked to higher risk of blood clots in later life

According to a new study by the University of Gothenburg, being overweight during childhood and early adulthood increases the risk of developing blood clots in later years. The study analysed the health data of 37,000 men and their early body mass index (BMI) and any blood clots that developed as they got older. The researchers found that both overweight in childhood and overweight in young adulthood increased the risk of venous blood clots later in life, with overweight in young adulthood proving to be a more influential factor than childhood overweight. While most blood clots occur in the legs and are not dangerous, they can become life-threatening if they travel to the lungs and cause a pulmonary embolism.

The link between obesity and blood clots is already well known, but the impact of a higher BMI in childhood on the risk was unclear. The researchers examined the data of a large group of men in Sweden who were born between 1945 and 1961, looking at school records at age 8 and Armed Forces medical examinations at age 20 to establish BMI data. They then looked at blood clot data on the men up to an average age of 62.

The study found that BMI at both age 8 and age 20 can be linked to blood clots independently of each other. As adults, the researchers found that two groups were more at risk – those who had been overweight both as a child and in early adulthood, and those with a normal weight in childhood but who became overweight in early adulthood. In addition, the study found that carrying excess weight in both childhood and early adulthood increased a person’s risk of arterial thrombi, which are clots that result from constricted blood vessels with fatty deposits. However, the researchers noted that more research is needed in this area as they only found a small number of cases.
The study’s senior authors emphasised that obesity and overweight during puberty seem to have a marked impact on a person’s future risks of venous thrombi. The study has been published in the Journal of Internal Medicine.

Obesity can lead to frailty in old age, study finds

A new study has found that adults with obesity are at greater risk of experiencing frailty in later life than adults with an average body mass index (BMI).

Researchers conducted a long-term study on adult men and women in Norway and discovered that obesity puts individuals at risk of becoming frail as they age. Frailty is characterised by physical deterioration and increased vulnerability, and while it has been associated with underweight older adults, the study reveals a positive association between obesity and the risk of frailty among older adults.

The study, published in the BMJ Open journal, analysed the body mass index and waist circumference of 2,340 women and 2,169 men over the age of 45 between 1994 and 1995. The participants were followed up for a period of 21 years to determine their risk of frailty. The researchers defined physical frailty as having three or more symptoms including poor grip strength, slow walking speed, exhaustion, unintentional weight loss, and low physical activity.

The findings show that participants with “baseline obesity” were more likely to be frail or pre-frail compared to those with an average BMI. Additionally, those with high waist circumference throughout follow-up were also more likely to be pre-frail or frail compared to participants with a stable normal waist circumference trajectory. Excess weight exacerbating the decline in muscle strength and physical capacity that occurs with age, along with metabolic disorders, inflammaging, and oxidative stress associated with obesity, could contribute to the risk of frailty.

The study’s lead author, Dr. Anju Jain, emphasised the importance of early intervention to prevent and treat obesity. She noted that while weight loss can be challenging, it is possible and can have significant health benefits. She also called for more public health efforts to promote healthy eating and physical activity throughout life.

The researchers caution against viewing frailty as solely a wasting disorder and highlight the importance of routinely assessing and maintaining optimal BMI and waist circumference throughout adulthood to reduce the risk of frailty in later life.

Excess weight, obesity more deadly than previously believed

A new study from the University of Colorado Boulder, and published in the journal Population Studies, has found that the risk of death from excess weight or obesity is much higher than previously believed, with mortality rates increased by between 22% to 91%. 

The research challenges the “obesity paradox,” which suggests that only extremely high levels of excess weight are associated with increased mortality risk. The study analysed data from nearly 18,000 people and found that using body mass index (BMI) to study health outcomes can bias findings, potentially leading to underestimates of the consequences of living in an environment where unhealthy food is cheap and sedentary lifestyles are the norm. The study estimates that about one in six U.S. deaths are related to excess weight or obesity.

The research found that a full 20% of people classified as having a “healthy” weight had previously been in the overweight or having obesity category, and that these individuals had a substantially worse health profile than those in the “healthy” category whose weight had been stable. The study also found that the health and mortality consequences of high BMI are duration-dependent, meaning that people who have spent most of their lives at a low BMI but have recently gained weight may have better health profiles than those who have had overweight or obesity for most of their lives.

The study’s author, Ryan Masters, hopes that the research will alert scientists to be “extremely cautious” when making conclusions based on BMI, and will draw attention to the public health crisis of an “obesogenic” environment in the U.S. Masters noted that the prospects of healthy ageing into older adulthood do not look good for groups born in the 1970s or 1980s who have lived their whole lives in this obesogenic environment. The study estimates that about 16% of U.S. deaths are related to excess weight or obesity, a figure that is eight times higher than previous research had suggested.