Tag: overweight

Categories : Cardiovascular Disease Metabolic DisordersTags :

Semaglutide Cuts CVD Events by 20% in People with Obesity or Overweight but not Diabetes

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In a large, international clinical trial, people with obesity or overweight but not diabetes taking semaglutide for more than three years had a 20% lower risk of cardiovascular disease outcomes and lost an average of 9.4% of their body weight.

Semaglutide, a GLP-1 medication primarily prescribed for people with Type 2 diabetes, is also FDA-approved for weight loss in people with obesity.

These results were shared in a late-breaking science presentation at the American Heart Association’s Scientific Sessions 2023 and the full manuscript was also published in The New England Journal of Medicine.

“This news is very encouraging for people with overweight or obesity because no treatment specifically directed at the management of obesity and overweight in people without Type 1 or Type 2 diabetes has been tested in a randomised trial and been shown to influence cardiovascular outcomes,” said lead study author A. Michael Lincoff, MD.

While prior research has confirmed the benefits of semaglutide in managing blood sugar, decreasing cardiovascular disease events and reducing weight in people with Type 2 diabetes, this study specifically investigated the potential impact of semaglutide on cardiovascular disease in people with overweight or obesity and cardiovascular disease who did not have either Type 1 or Type 2 diabetes.

In this randomised, controlled, double-blind trial, participants were assigned to take either 2.4mg of semaglutide (the FDA-approved semaglutide dose for weight management) or a placebo once a week, which is higher than the FDA-approved semaglutide dose limit for Type 2 diabetes of 2.0mg/week. Each person in the study used a ‘pen’ to inject the medicine or placebo into a skin fold in their stomach, thigh or upper arm each week on the same day, and the dose started at 0.24mg and gradually increased every four weeks up to 2.4mg, and mean follow-up for all participants was 40 months.

In addition to taking either semaglutide or placebo for the trial, all participants also received standard of care treatment for cardiovascular disease, such as cholesterol modifying medications, antiplatelet therapies, beta blockers or other treatments. The authors note that heart disease diagnoses varied among the participants, therefore, treatment was adjusted to meet each individual’s diagnosis and needs, as well as the treatment guidelines in their country of residence.

The study, which ran from October 2018 through June 2023, indicated the following:

  • There was a 20% reduction in the risk of heart attacks, strokes or death due to cardiovascular disease in the participants who took semaglutide, compared to the participants in the placebo group.
  • In the semaglutide group, the participants’ body weight was reduced, on average, by 9.4% compared to a reduction of 0.9% among the adults in the placebo group.
  • There were no new safety concerns found in the study, which researchers note is encouraging since the SELECT trial is the largest and longest (4.5 years) trial of semaglutide in adults without Type 1 or Type 2 diabetes.
  • The number of serious adverse events was lower in the semaglutide group. Previous studies of medications of the GLP-1 receptor agonist class have shown an association with gallbladder disorders, and in SELECT, there was a slightly higher rate of gallbladder disorders in the semaglutide vs placebo group (2.8% vs 2.3%, respectively).
  • Semaglutide was stopped more frequently than placebo for gastrointestinal intolerance, a known side effect of this class of medications; however, there was no higher rate of serious gastrointestinal events.
  • The researchers noted that this medication did not lead to an increased rate of pancreatitis, which has been a concern with prior medications of this type.
  • Of note, other weight-loss medications that are not GLP-1 receptor agonists have been associated with increased risks of psychiatric disorders or cancer; these risks were not elevated with semaglutide in the SELECT trial.

“It’s been estimated that within about ten years, over half of the world’s population will have overweight or obesity,” said Dr Lincoff. “And while GLP-1 medications are frequently prescribed for patients with vascular disease and Type 2 diabetes, there is a significant number of people who do not have Type 1 or Type 2 diabetes but do have vascular disease and overweight or obesity for whom these medications are often not available due to access to care issues, insurance coverage or other factors. This population may now potentially benefit from semaglutide, and importantly, our results indicate the magnitude of cardiovascular risk reduction with semaglutide among people without Type 1 or Type 2 diabetes is the same as what we have seen in people with Type 2 diabetes. Our findings expand the opportunity to treat patients who have overweight or obesity and existing heart disease without Type 1 or Type 2 diabetes, and we have a chance to significantly reduce their risk of a secondary cardiovascular event including death.”

Among the study limitations were including adults with prior cardiovascular disease, thereby not investigating primary prevention of cardiovascular disease (people with no history of a heart attack, stroke and/or peripheral artery disease). In addition, 28% of the study participants were female, which is not proportionate to the number of women with cardiovascular disease and overweight or obesity in the general population.

Additional analyses will include identifying the mediators of the cardiovascular benefit to determine to what extent the results were driven by reduction of metabolically unhealthy body fat, positive impacts on inflammation or blood sugar, direct effects of the medication itself on plaque build-up in the arteries, or a combination of one or more variables.

Source: American Heart Association

Categories : Gender GeneticsTags :

Researchers Identify Sex-specific Genes for Obesity

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Researchers have added several genes, which appear to affect obesity risk in certain sexes and ages, to the list of genes which influence weight gain. The study, published in the journal Cell Genomics, may shed light on new biological pathways that underlie obesity and highlight how sex and age contribute to health and disease.

“There are a million and one reasons why we should be thinking about sex, age, and other specific mechanisms rather than just lumping everyone together and assuming that disease mechanism works the same way for everyone,” says senior author John Perry, a geneticist and professor at the University of Cambridge. “We’re not expecting people to have completely different biology, but you can imagine things like hormones and physiology can contribute to specific risks.”

To untangle sex’s role in obesity risk, the research team sequenced the exome (the protein-coding part of the genome) of 414 032 adults from the UK Biobank study. They looked at variants, or mutations, within genes associated with body mass index (BMI) in men and women, respectively. Five genes influencing BMI in women and two in men were identified.

Among them, faulty variants of three genes – DIDO1, PTPRG, and SLC12A5 – are linked to higher BMI in women, up to nearly 8 kg/m² more, while having no effect on men. Over 80% of the women with DIDO1 and SLC12A5 variants had BMI-indicated obesity. Those carrying DIDO1 variants had stronger associations with higher testosterone levels and increased waist-to-hip ratio, both risk indicators for obesity-related complications like diabetes and heart disease. Others with SLC12A5 variants had higher odds of having type 2 diabetes compared with non-carriers. These findings highlight previously unexplored genes that are implicated in the development of obesity in women but not men.

Perry and his colleague then repeated their method to look for age-specific factors by searching for gene variants associated with childhood body size based on participants’ recollections. They identified two genes, OBSCN and MADD, that were not previously linked to childhood body size and fat. While carriers of OBSCN variants had higher odds of having higher weight as a child, MADD variant carriers were associated with smaller body sizes. In addition, the genetic variants acting on MADD had no association with adult obesity risk, highlighting age-specific effects on body size.

“What’s quite surprising is that if you look at the function of some of these genes that we identified, several are clearly involved in DNA damage response and cell death,” says Perry. Obesity is a brain-related disorder, whereas biological and environmental factors act to influence appetite. “There’s currently no well-understood biological paradigm for how DNA damage response would influence body size. These findings have given us a signpost to suggest variation in this important biological process may play a role in the aetiology of obesity.”

Next, the research team hopes to replicate the study in a larger and more diverse population. They also plan to study the genes in animals to peer into their function and relationship with obesity.

“We’re at the very earliest stages of identifying interesting biology,” says Perry. “We hope the study can reveal new biological pathways that may one day pave the way to new drug discovery for obesity.”

Source: Science Daily

Categories : Metabolic Disorders PaediatricsTags :

Childhood TV Watching Linked to Metabolic Syndrome in Adulthood

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A new study has added to the evidence that excessive TV watching as a child can lead to poor health in adulthood. The research, published this week in the journal Pediatrics, found that children who watched more television were more likely to develop metabolic syndrome as an adult.

Metabolic syndrome is a cluster of conditions including hypertension, hyperglycaemia, excess body fat, and abnormal cholesterol levels that lead to an increased risk of heart disease, diabetes and stroke.

Using data from 879 participants of the Dunedin study, researchers found those who watched more television between the ages of 5 and 15 were more likely to have these conditions at age 45.

Television viewing times were asked at ages 5, 7, 9, 11, 13 and 15. On average, they watched just over two hours per weekday.

“Those who watched the most had a higher risk of metabolic syndrome in adulthood,” says Professor Bob Hancox, who led the study.

“More childhood television viewing time was also associated with a higher risk of overweight and obesity and lower physical fitness.”

Boys watched slightly more television than girls and metabolic syndrome was more common in men, than women (34% and 20% respectively). The link between childhood television viewing time and adult metabolic syndrome was seen in both sexes however, and may even be stronger in women.

There was little evidence that watching less television as an adult reduced the association between childhood television viewing and adult health.

“While, like any observational study, researchers cannot prove that the association between television viewing at a young age directly causes adult metabolic syndrome, there are several plausible mechanisms by which longer television viewing times could lead to poorer long-term health.

“Television viewing has low energy expenditure and could displace physical activity and reduce sleep quality,” he says.

“Screentime may also promote higher energy intake, with children consuming more sugar-sweetened beverages and high-fat dietary products with fewer fruit and vegetables. These habits may persist into adulthood.”

The results are important because screen times have increased in recent years with new technologies.

“Children today have far more access to screen-based entertainment and spend much more time being sedentary. It is likely that this will have even more detrimental effects for adult health.

“These findings lend support to the World Health Organization recommendation that children and young teenagers should limit their recreational screen time.”

Source: University of Oregon

Categories : Metabolic DisordersTags :

Excess Weight is a Greater Mortality Risk than BMI Alone Suggests

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Excess weight or obesity raises mortality risk by between 22% to 91%, a significantly higher rate than previously believed, while the mortality risk of being slightly underweight has likely been overestimated, according to new research published in the journal Population Studies.

The analysis of nearly 18 000 participants counters prevailing wisdom that excess weight boosts mortality risk only in extreme cases, and it also challenges the use of body mass index (BMI) to investigate health outcomes due to its inherent biases. After accounting for those biases, it estimates that about 1 in 6 deaths in the US are related to excess weight or obesity.

“Existing studies have likely underestimated the mortality consequences of living in a country where cheap, unhealthy food has grown increasingly accessible, and sedentary lifestyles have become the norm,” said author Ryan Masters, associate professor of sociology at CU Boulder. “This study and others are beginning to expose the true toll of this public health crisis.”

Challenging the obesity paradox

While numerous studies show that heart disease, high blood pressure and diabetes (which are often associated with being overweight) elevate mortality risk, very few have shown that groups with higher BMIs have higher mortality rates.

Instead, in what some call the “obesity paradox,” most studies show a U-shaped curve: Those in the “overweight” category (BMI 25–30) surprisingly have the lowest mortality risk. Those in the “obese” category (30–35) have little or no increased risk over the so-called “healthy” category (18.5–25). And both the “underweight” (< 18.5) and extremely obese (> 35) are at increased risk of death.

“The conventional wisdom is that elevated BMI generally does not raise mortality risk until you get to very high levels, and that there are actually some survival benefits to being overweight,” said Masters, a social demographer who has spent his career studying mortality trends. “I have been suspicious of these claims.”

He noted that BMI, which doctors and scientists often use as a health measure, is based on weight and height only and doesn’t account for differences in body composition or how long a person has been overweight.

“It’s a reflection of stature at a point in time. That’s it,” said Masters, noting that Tom Cruise (at 170cm and an extremely muscular 91kg at one point), had a BMI of 31.5, famously putting him in the category of “obese.” “It isn’t fully capturing all of the nuances and different sizes and shapes the body comes in.”

Taking these nuances, Masters accessed data from the National Health and Nutrition Examination Survey (NHANES) the from 1988 to 2015, analysing 17 784 people, including 4468 deaths.

He discovered that a full 20% of the sample characterised as “healthy” weight had been in the overweight or obese category in the decade prior. When set apart, this group had a substantially worse health profile than those in the category whose weight had been stable.

Masters pointed out that a lifetime carrying excess weight can lead to illnesses that, paradoxically, lead to rapid weight loss. If BMI data is captured during this time, it can skew study results.

“I would argue that we have been artificially inflating the mortality risk in the low-BMI category by including those who had been high BMI and had just lost weight recently,” he said.

Meanwhile, 37% of those characterised as overweight and 60% of those with obese BMI had been at lower BMIs in the decade prior. Notably, those who had only recently gained weight had better health profiles.

“The health and mortality consequences of high BMI are not like a light switch,” said Masters. “There’s an expanding body of work suggesting that the consequences are duration-dependent.”

By including people who had spent most of their life at low-BMI weight in the high-BMI categories, previous studies have inadvertently made high BMI look less risky than it is, he said.

When he looked at differences in fat distribution within BMI categories, he also found that variations made a huge difference in reported health outcomes.

Exposing a public health problem

Collectively, the findings confirm that studies have been “significantly affected” by BMI-related bias.

When re-crunching the numbers without these biases, he found not a U-shape but a straight upward line, with those with low BMI (18.5–22.5) having the lowest mortality risk.

Contrary to previous research, the study found no significant mortality risk increases for the “underweight” category.

Previous studies attributed 2 to 3% of UA adult deaths to high BMI, but his study estimates an eight times higher rate.

Masters said he hopes the research will alert scientists to be “extremely cautious” when making conclusions based on BMI. But he also hopes the work will draw attention to what he sees not as a problem for individuals alone to solve but rather a public health crisis fuelled by an unhealthy or “obesogenic” environment in the US.

“For groups born in the 1970s or 1980s who have lived their whole lives in this obesogenic environment, the prospects of healthy aging into older adulthood does not look good right now,” he said. “I hope this work can influence higher-level discussions about what we as a society can do about it.”

Source: University of Colorado at Boulder

Categories : Gender Metabolic DisordersTags :

Why Obesity’s Health Impacts are Worse for Males

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Toilet sign male and female
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A newly published study in iScience sheds light on the biological underpinnings in sex differences in obesity-related disease, with researchers observing “striking” differences in the cells that build blood vessels in the fatty tissue of male versus female mice.

Men are more likely than women to develop conditions associated with obesity such as cardiovascular disease, insulin resistance and diabetes, says study leader Professor Tara Haas at York University.

“People have used rodent models to study obesity, and the diseases that are associated with obesity – like diabetes – but they’ve typically always studied male rodents, because females are resistant to developing the same kinds of diseases,” says Haas. “We were really interested in exploring that difference because, to us, it spoke of something really fascinating happening in females that protects them.”

In earlier work, Haas and her team saw that when mice become obese, females grow a lot of new blood vessels to supply the expanding fat tissue with oxygen and nutrients, whereas males grow a lot less. For this study, Haas and her co-authors focused on differences in the endothelial cells that make up the building blocks of these blood vessels in fat tissue.

The team used software to help sift through thousands of genes to zero in on the ones that would be associated with blood vessel growth. They discovered that processes associated with the proliferation of new blood vessels were high in the female mice, whereas the males had a high level of processes associated with inflammation.

“It was very striking the extent of inflammation-associated processes that were prevalent in the males,” Haas recalls. “Other studies have shown that when endothelial cells have that kind of inflammatory response, they’re very dysfunctional, and they don’t respond to stimuli properly.”

York PhD student Alexandra Pislaru, who works in Haas’ lab and is a co-first author of the study, participated in this project as part of her dissertation.

“It is exciting to observe the continuing resilience that female endothelial cells display even when stressed by a long-term high-fat diet,” Pislaru says. “The findings from our study can help researchers to get a better understanding of why obesity manifests differently in men and women.”

The researchers also examined the behaviour of the endothelial cells when they were taken out of the body and studied in petri dishes.

“Even when we take them out of the body where they don’t have the circulating sex hormones or other kinds of factors, male and female endothelial cells still behave very differently from each other,” Haas explains.

Female endothelial cells replicated faster, while male endothelial cells displayed greater sensitivity to an inflammatory stimulus. By comparing with previously published data sets, the researchers found endothelial cells from aged male mice also displayed a more inflammatory profile compared to female cells.

“You can’t make the assumption that both sexes are going to respond to the same series of events the same way,” says Haas. “This isn’t just an obesity related issue – I think it’s a much broader conceptual problem that also encompasses healthy aging. One implication of our findings is that there will be situations where the treatment that is ideal for men is not going to be ideal for women and vice-versa.”

While humans and mice have different genes that may be turned up or down, Haas believes the general findings would likely apply and is interested studying the same cells in humans in future research.

Source: York University

Categories : Metabolic Disorders PaediatricsTags :

New Guidelines Recommend Aggressive Intervention in Childhood Obesity

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New clinical guidelines from the American Academy of Pediatrics (AAP) advise “immediate, intensive obesity treatment to each patient” upon diagnosis of childhood obesity. Published in the journal Pediatrics, these recommendations stands in marked contrast from other, previous guidelines.

The guidelines are summarised in key action statements, some of which recommend children ages 6 and up (and sometimes 2 to 5) with overweight or obesity to intensive health behaviour and lifestyle therapy.

In children 12 and older, the guidelines advise consideration of weight-loss pharmacotherapy. In case of severe obesity (BMI ≥35 or 120% of the 95th percentile for age and sex, whichever is lower) for adolescents 13 and older, clinicians should offer referrals for evaluation for metabolic and bariatric surgery.

Author Sarah Armstrong, MD, co-director of the Duke Center for Childhood Obesity Research told Medpage Today that “This is one of the most important messages that differentiates our current clinical practice guidelines from the prior recommendations, and that is to say 15 years of data have taught us that ‘watchful waiting’ only leads to greater increase in child BMI, accumulation of comorbidities, and more challenges in trying to reverse some of this.”

The guidelines also recommend regularly screening children ages 2 years and up for obesity, and comprehensively evaluating children and adolescents with overweight and obesity for related comorbidities.

Clinicians are also advised to treat children and adolescents for overweight/obesity and comorbidities concurrently, in line with principles of the chronic care model, using a non-stigmatising approach centred around the family.

The guidelines are based on a comprehensive evidence review of controlled and comparative effectiveness trials and high-quality longitudinal and epidemiologic studies. In a pair of accompanying technical reports, the authors give detailed descriptions of the evidence review behind the development of the guidelines.

Categories : Metabolic DisordersTags :

Overweight Can be The Result of Insufficient Insulin Processing

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Obesity
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Lifestyle leading to overweight increases the risk of metabolic diseases such as diabetes – but the relationship also works in reverse, according to a new study. If insulin production is compromised, as is the case in the early stages of type 2 diabetes, this can contribute to overweight. The researchers report their findings in the journal Nature Communications.

When hormone activation goes awry

The research group, led by Dr Daniel Zeman-Meier of the University Hospital of Basel, focused on protease PC1/3 – a key enzyme in the body that transforms various inactive hormone precursors into the final, active forms. Sever endocrine disorders can result if PC1/3 does not function properly. The consequences include a feeling of uncontrollable hunger and severe overweight.

“Until now, it was assumed that this dysregulation is caused by a lack of activation of satiety hormones,” explained Dr Zeman-Meier. “But when we turned off PC1/3 in the brains of mice, the animals’ body weight did not change significantly.” The researchers concluded from this that something other than a brain malfunction must be responsible.

Incorrect activation of insulin leads to hunger and overweight

In their next step, they tested whether overweight could be caused by incorrect activation of other hormones. Among other things, PC1/3 activates insulin. “Investigating the role of insulin production as a cause of overweight was obvious,” said Dr Zeman-Meier. The researchers shut off PC1/3 specifically in the insulin-producing beta cells of the pancreas in mice. The animals consumed significantly more calories and soon became overweight and diabetic.

An important mechanism in humans

“These results are also interesting because PC1/3 is reduced in the pancreas of patients with prediabetes,” says Professor Marc Donath, research leader and final author of the study. This indicates that incorrect insulin activation could cause overweight as well as result from it.

But PC1/3 is also important in the weight regulation of healthy individuals, Prof Donath stressed. The researchers were able to show that the gene expression of PC1/3 in the pancreas is negatively correlated with body weight in the general population — meaning that sufficient PC1/3 promotes a healthy body weight.

The finding that a defect in the beta cells is a trigger of overweight promises new therapeutic possibilities. For example, it is conceivable that medications could be used to reduce the production of immature insulin precursors, creating a new tool in the fight against overweight and diabetes.

Source: University of Basel

Categories : Ethics and Law Metabolic DisordersTags :

Major Review Urges Tackling of Weight Stigma in Healthcare

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Obesity
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Weight stigma is a negative bias known to limit both access to health services and treatments. A joint international consensus statement was recently published in Nature, aiming to end weight stigma in healthcare globally.

Researchers conducted a large review of over 3700 studies to evaluate weight stigma reduction strategies in healthcare practice and healthcare education, with a view to provide recommendations for interventions, learning, and research. The findings, published in Obesity Reviews, indicate that there is a need to move away from a weight-centric approach to healthcare.

Lead author, Dr Anastasia Kalea said: “Sadly healthcare, including general practice, is one of the most common settings for weight stigmatisation and we know this acts as a barrier to the services and treatments that can help people manage weight.

“A common misconception among medics and others, is that obesity is caused by factors within a person’s control, focusing on diet and exercise without recognition of, for instance, social and environmental determinants.

“In this review, it was clear more needs to be done to educate healthcare professionals and medical students on the complex range of factors regulating body weight, and to address weight stigma, explicitly emphasising its prevalence, origins, and impact.”

Researchers undertook a systematic review of 3773 international research articles. This included 25 weight stigma interventional initiatives, comprising a total of 3554 participants.

Weight-inclusive approaches to education in healthcare were identified as effective in challenging stereotypes and improving attitudes. They identified stigma reduction strategies in healthcare, which included ethics seminars discussing patient experiences, embedding virtual story-telling of patient case studies, or empathy evoking activities in the curriculum, such as following a calorie restricted diet or participation in clinical encounters with patients living with overweight and obesity. However, other methods such as video presentations and short lectures were not equally effective in improving attitudes in the long term.

Researchers are now calling on medical schools in both the UK and globally to ensure effective and sustained weight-inclusive teaching is embedded in medical doctor training and is added to the continuing professional development of clinicians.

Dr Kalea said: “Weight stigma needs to be addressed early on and continuously throughout healthcare education and practice, by teaching the genetic and socioenvironmental determinants of weight, by discussing the sources, impact and recognising the implications of stigma on treatment. We need to move away from a solely weight-centric approach to healthcare to a health-focussed weight-inclusive one. And it is equally important to assess the effects of weight stigma in epidemiological research.”

The urgency of tackling the obesity and overweight has been brought to the fore by evidence of the link to an increased risk from COVID.

Dr Kalea added: “Stigma reduction interventions are a current research priority. Improving the ways we educate healthcare professionals early on is a starting point, keeping the focus on our patients; we need to communicate better, listen carefully to our patients needs and let these inform our teaching and research agendas.”

Weight stigma is also known to cause ‘internalised weight bias’ (IWB), which is when a person applies negative societal or cultural beliefs about body weight to themselves. This can lead to psychological distress, depression, anxiety, low self-esteem and often leads to decreased health motivation and maladaptive coping such as avoidance of timely healthcare, social isolation, reduced physical activity and disordered eating behaviours.

Weight stigma has also been shown to increase risk of developing obesity, and healthcare is one of the most common contexts where weight stigmatisation occurs. Physicians have been reported as the second most common source of weight stigma and discrimination.

Source: University College London

Categories : Metabolic Disorders PaediatricsTags :

Sleep is Also Important in Avoiding Overweight in Babies

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While the importance has long been known, little research has examined the necessity of sufficient sleep during the first months of life. New research suggests that newborns who sleep longer and wake up less throughout the night are less likely to be overweight in infancy. Their results are published in Sleep.

“While an association between insufficient sleep and weight gain is well-established in adults and older children, this link has not been previously recognized in infants,” said study co-author Susan Redline, MD, MPH, senior physician in the Division of Sleep and Circadian Disorders at the Brigham. “In this study, we found that not only shorter nighttime sleep, but more sleep awakenings, were associated with a higher likelihood of infants becoming overweight in the first six months of life.”

To conduct this research, Dr Redline and colleagues observed 298 newborns born at Massachusetts General Hospital between 2016 and 2018. The infants’ sleep patterns were monitored using ankle actigraphy watches – devices that measure patterns of activity and rest over multiple days. Researchers obtained three nights’ worth of data at the one- and six-month marks while parents kept sleep diaries, recording their children’s sleep and wake episodes.

Scientists measured infant height and weight and determined their body mass index, classifying infants as overweight if they fell into or above the 95th percentile on the World Health Organization’s growth charts.

Notably, researchers found that just one extra hour of sleep was associated with a 26% decrease in overweight risk. Additionally, infants that woke up less during the night faced a lower risk of excess weight gain. Scientists speculate that having more sleep promotes routine feeding practices and self-regulation, factors that mitigate overeating.

Investigators noted an underrepresentation of African-American individuals and lower-income families in their dataset. Additionally, confounding variables, such as breastfeeding duration, could have impacted infant growth. In the future, the researchers aim to extend this study to evaluate how sleep patterns impact growth within the first two years of life and identify key factors that mediate the correlation between sleep and weight gain. They also aim to evaluate interventions for promoting healthy sleep habits.

“This study underscores the importance of healthy sleep at all ages,” said Dr Redline. “Parents should consult their pediatricians on the best practices to promote healthy sleep, like keeping consistent sleep schedules, providing a dark and quiet space for sleeping, and avoiding having bottles in bed.”

Source: EurekAlert!

Categories : Diet and Nutrition Metabolic DisordersTags :

Body Clock Disruption on High-fat Diet Leads to Obesity

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According to a new study, when rats are fed a high fat diet, this disturbs the body clock in their brain that normally controls satiety, leading to over-eating and obesity. 

This new research, published in the Journal of Physiology, may be a cornerstone for future clinical studies that could restore the proper functioning of the body clock in the brain, to avoid overeating.

It was believed that the body clock resided only in the hypothalamus, but research over the years has clarified that some control of our body’s daily rhythms (hormone levels, appetite etc) lies in several other parts of the brain and body, including a group of neurons in the evolutionary ancient brainstem, called the dorsal vagal complex (DVC).

Specifically, the DVC has been shown to moderate food intake by inducing satiety. In obesity, research has shown that daily rhythms in food intake and the release of hormones related to eating, are blunted or eliminated. It is unclear if the malfunctioning of brain centres controlling appetite is a cause or the result of obesity.

This new study found that rats on a high-fat diet, before they started to gain weight, showed changes in the DVC’s daily neuronal rhythms and its response to appetite hormones. Thus, the researchers proposed that DVC disruption causes obesity.

Two groups of rats were used: those fed a well-balanced control diet (10% kcal from fat) and a high-fat diet (70% kcal from fat). To mimic the impact of unhealthy diet on humans, the researchers introduced the new diet to adolescent rats and monitored their food intake over 24h for four weeks.

Using multi-electrode arrays, the researchers measured DVC changes over 24h, simultaneously monitoring around a hundred DVC neurons from each brainstem slice. With this, circadian changes of neuronal activity could be assessed as well as neuronal responses to metabolically-relevant hormones in each of the diet groups.

Rats being nocturnal animals is a limitation of the study. The DVC activity peaked at the end of day, the rest phase for rodents, but an active phase for humans. Thus, it remains to be established if the phase of the brainstem clock is set to day and night, or whether it depends on patterns of rest and activity. These findings however could lead to understanding how to reset the body clock and tackle obesity.

First author Dr Lukasz Chrobok said:

“I’m really excited about this research because of the possibilities it opens up to tackle the growing health issue of obesity. We still do not know what are the time cues which are able to reset or synchronise the brainstem clock. Hopefully, the restoration of daily rhythms in this satiety centre before or after the onset of obesity may provide new therapeutic opportunities.”

Source: The Physiological Society