Tag: obesity

Categories : Metabolic DisordersTags :

Significant Gaps between Obesity Science and Patient Care

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As research continues to produce evidence about the underlying causes of obesity and optimal strategies to treat and manage obesity have evolved, there are disparities in application of the latest scientific advances in the clinical care for people with obesity. Widespread adoption of current findings, consistency of care and expertise in obesity care varies by health care professional and institution. These findings are detailed in a new American Heart Association scientific statement, “Implementation of Obesity Science Into Clinical Practice,” published in the journal Circulation.

“Obesity is undeniably a critical public health concern in the U.S. and around the world, affecting nearly all populations and straining our health care systems,” said Deepika Laddu, Ph.D., FAHA, chair of the statement writing committee and a senior research scientist at Arbor Research Collaborative for Health in Ann Arbor, Michigan. “As a major risk factor for heart disease, obesity has significantly hindered progress in reducing heart disease rates. Despite advancements in understanding the complexities of obesity and newer treatment options, major gaps remain between obesity research and real-world implementation in clinical practice.”

Studies show intensive lifestyle therapy is considerably more effective for weight loss than brief advice from a health care professional. However, general educational information is offered more frequently by health professionals rather than referrals to classes, programs or tangible resources for lifestyle changes. One study revealed that only 16% of health care professionals had working knowledge about evidence-based lifestyle treatments for obesity, including diet and nutrition, physical activity and intensive behavioral therapy referral. Other barriers to addressing weight loss are exacerbated by socioeconomic and racial or ethnic inequities. People of diverse races and ethnicities and people who are covered by Medicare or Medicaid are less likely to be referred to weight management programs or to have them covered by insurance.

For about 30 years, the prevalence of obesity in the US and around the world has been escalating. Recent estimates indicate more than 40% of US adults ages 20 and older are living with obesity, according to the US Centers for Disease Control and Prevention.

Research has led experts to unlock the multifactorial causes of obesity, including sociological and physiological determinants of health. Treatments for obesity have also evolved with more strategies for lifestyle modifications, medication therapy and bariatric surgery – but each treatment approach comes with challenges.

“While significant strides have been made in advancing the science to help us understand obesity, there remains a considerable gap between what we know and what happens in the doctor’s office,” said Laddu. “Health care professionals and health care systems need to find better ways to put what we know about obesity into action so more people can get the right support and treatment. Adopting new technologies and telemedicine, making referrals to community-based weight management programs to encourage behavioural change, providing social support and increasing reach and access to treatments are just some of the promising methods we could implement to unlock successful, evidence-based obesity care.”

Weight loss medications

Glucagon-like peptide-1 (GLP-1) agonists, such as high-dose semaglutide and tirzepatide, are the most recently FDA-approved medications for long-term weight management, and both are associated with an average weight loss of more than 10% at six months in clinical studies. However, despite half of adults in the U.S. meeting the BMI criteria for obesity and being eligible for these medications, a small proportion of this population is currently taking them.

Weight loss surgery

In the decades since bariatric (weight loss) surgery was first introduced as an option for people with severe obesity, there have been advances in the expertise and safety of the procedures, as well as an increased understanding of the health benefits that often result after bariatric surgery. A comprehensive review of studies focused on weight loss surgeries showed that patients who underwent bariatric surgery had lower risks of cardiovascular disease and decreased risks for multiple other obesity-associated conditions, including Type 2 diabetes and high blood pressure. One challenge facing health care professionals is ensuring that the populations with the greatest needs have access to bariatric surgery in terms of costs, resources and social support.

The statement describes strategies that both address these challenges and improve how obesity-based research is incorporated into clinical care. The statement also identifies the need to develop solutions across populations in order to manage obesity at the community level. Potential improved public health policies and future research to expand patient care models and optimize the delivery and sustainability of equitable obesity-related care are suggested.

Specific approaches are highlighted in the statement to help bridge the gap between the science about obesity and clinical care, such as:

  • To reach and successfully impact populations in need, health care professionals may consider how social determinants of health, including insurance type, household income, race and ethnicity, environment, health literacy, access to health-promoting resources and social supports all influence the likelihood of successful patient treatment.
  • Education for health care professionals explaining the complex origins and clinical consequences of obesity is discussed. Such training should emphasize information about diagnosis, prevention and treatment of obesity. Despite the high prevalence of obesity around the world, there is a lack of education programs centered on obesity for medical professionals.
  • Further evaluation of health policy changes that health care systems and insurance plans can implement and scale in order to make obesity treatment affordable for patients, especially those at high risk for adverse outcomes such as cardiovascular disease.
  • A framework for delivering obesity care into clinical practice settings is reviewed, as well as efforts by some professional societies for developing interventions that make obesity treatment more accessible.

“The statement emphasises the importance of a comprehensive approach across different levels of health care delivery and public policy, along with the adoption of feasible, evidence-based strategies in clinical settings,” said Laddu. “It also underscores the need for future research and policy changes to improve current patient care models and ensure equitable access to obesity-related care for people in underrepresented groups.”

The scientific statement also provides possible solutions for how to help people in their day-to-day lives, including interventions with digital technology and access through telemedicine. However, more research is needed in obesity science and treatment. Limited understanding of the cost-effectiveness of obesity prevention and the long-term health outcomes for established therapies has hindered the implementation of obesity science into clinical settings. Cross-collaborative obesity science research between stakeholders and health economists may serve as the bridge to developing and scaling cost-effective prevention programs.

Source: American Heart Association

Categories : Metabolic Disorders VaccinesTags :

Metabolic Health before Flu Vaccination Determines Its Effectiveness

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A four-week healthy diet improved the effectiveness of a flu vaccine given to obese mice

Photo by Gustavo Fring on Pexels

Scientists at St. Jude Children’s Research Hospital have shown that improving metabolic health in obese mice before vaccination, but not after, protects against influenza virus.

Metabolic health (normal blood pressure, blood sugar and cholesterol levels, among other factors) influences the effectiveness of influenza vaccinations. Vaccination is known to be less effective in people with obesity compared to those with a healthier body mass index (BMI), but St. Jude Children’s Research Hospital scientists have found that the difference is attributable not to obesity itself, but rather metabolic dysfunction. In a study published in Nature Microbiology, the researchers found that switching obese mice to a healthy diet before flu vaccination, but not after, completely protected the models from a lethal dose of flu, despite BMI.

“We found that the vaccines worked effectively if at the time of vaccination an animal is metabolically healthy,” said corresponding author Stacey Schultz-Cherry, PhD, St. Jude Department of Host-Microbe Interactions and Center of Excellence for Influenza Research and Response co-director. “And the opposite was also true: regardless of what the mice looked like on the outside, if they had metabolic dysfunction, the vaccines did not work as well.”

Prior research has shown that 100% of obese mice succumbed to influenza after exposure, even after vaccination. Contrary to the scientists’ original expectations, when mice who were vaccinated while obese returned to a healthy weight, outcomes did not improve. These now outwardly healthy mice still all succumbed to disease when exposed to the real virus. Only switching to a healthy diet four weeks before vaccination improved survival, with drastic effect, despite high BMI.

“We were excited to see this effect because mice with obesity are so susceptible to severe disease and succumbing to the infection,” Schultz-Cherry said. “Getting 100% survival with the vaccine where we had only seen 0% survival was impressive.” The improved survival suggests the researchers have discovered a greater underlying principle determining influenza vaccine efficacy.

Metabolic dysfunction hinders the immune system

While studying how metabolic function influences influenza vaccine responses, the scientists found that poor metabolic health causes immune system dysfunction. T cells, the primary immune cells involved in anti-viral responses, failed to act in animals that had been in an unhealthy metabolic state at the time of vaccination, even during later viral exposure. Even when the animals ate a healthy diet after vaccination and maintained a normal BMI, the anti-flu T cells were “frozen” in that dysfunctional state.

However, a healthy diet before vaccination improved T-cell function, which resulted in a robust anti-flu response during later exposure.

“The T cells were better able to do their job in the metabolically healthy mice at the time of vaccination,” Schultz-Cherry said. “It wasn’t a matter of the numbers of them or the types of them. It was their functional activity. There were plenty of them in the lungs, not working. The healthy diet switched them from not working to functioning properly, but only if the switch occurred before vaccination.”

The earlier healthy diet also improved inflammation. Pro-inflammatory cytokines are upregulated in obese animals. Schultz-Cherry’s team found that models also returned to a lower basal cytokine level when switched to a healthy diet before vaccination.

“A healthy diet lowered some of the systemic meta-inflammation in these animals, and they regained some of the epithelial innate immune responses,” said Schultz-Cherry. “We started seeing better signalling of things like interferons, which we know is problematic in obesity and in general saw the immune system starting to function the way that it should.”

Improving metabolic health may improve influenza vaccine effectiveness

“What we found and are emphasising is that it’s not the phenotype of obesity that matters; it’s really about metabolic health,” Schultz-Cherry said. “It’s metabolic health at that moment of vaccination that really makes a difference.”

The study was restricted to mice, but it does open research opportunities to improve influenza vaccine efficacy in humans. The findings suggest methods of improving metabolic health may also improve subsequent influenza vaccinations. Given the recent introduction of metabolic improvement drugs, especially glucagon-like peptide 1 (GLP-1) agonists, there may be potential for a cooperative effect.

“We don’t know for sure, but if the outcome of using GLP-1 drugs is weight loss and improved metabolic health, we would hypothesise that it will help,” Schultz-Cherry said. “But we do know that we can do better protecting our vulnerable populations, and this study is a start for understanding how.”

Source: St. Jude Children’s Research Hospital

Categories : Metabolic DisordersTags :

A Single Gene Causes Mitochondria to ‘Fragment’ in Obesity

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These coloured streaks are mitochondrial networks within fat cells. Researchers from UC San Diego discovered that a high-fat diet dismantles mitochondria, resulting in weight gain. Credit: UC San Diego

While lifestyle factors like diet and exercise play a role in the development and progression of obesity, scientists have come to understand that obesity is also associated with intrinsic metabolic abnormalities. Now, researchers from University of California San Diego School of Medicine have shed new light on how obesity affects our mitochondria, the all-important energy-producing structures of our cells.

In a study published January 29, 2023 in Nature Metabolism, the researchers found that when mice were fed a high-fat diet, mitochondria within their fat cells broke apart into smaller mitochondria with reduced capacity for burning fat. Further, they discovered that this process is controlled by a single gene. By deleting this gene from the mice, they were able to protect them from excess weight gain, even when they ate the same high-fat diet as other mice.

“Caloric overload from overeating can lead to weight gain and also triggers a metabolic cascade that reduces energy burning, making obesity even worse,” said Alan Saltiel, PhD, professor in the Department of Medicine at UC San Diego School of Medicine. “The gene we identified is a critical part of that transition from healthy weight to obesity.”

Obesity occurs when the body accumulates too much fat, which is primarily stored in adipose tissue. Adipose tissue normally provides important mechanical benefits by cushioning vital organs and providing insulation. It also has important metabolic functions, such as releasing hormones and other cellular signaling molecules that instruct other tissues to burn or store energy.

In the case of caloric imbalances like obesity, the ability of fat cells to burn energy starts to fail, which is one reason why it can be difficult for people with obesity to lose weight. How these metabolic abnormalities start is among the biggest mysteries surrounding obesity.

To answer this question, the researchers fed mice a high-fat diet and measured the impact of this diet on their fat cells’ mitochondria, structures within cells that help burn fat. They discovered an unusual phenomenon. After consuming a high-fat diet, mitochondria in parts of the mice’s adipose tissue underwent fragmentation, splitting into many smaller, ineffective mitochondria that burned less fat.

In addition to discovering this metabolic effect, they also discovered that it is driven by the activity of single molecule, called RaIA. RaIA has many functions, including helping break down mitochondria when they malfunction. The new research suggests that when this molecule is overactive, it interferes with the normal functioning of mitochondria, triggering the metabolic issues associated with obesity.

“In essence, chronic activation of RaIA appears to play a critical role in suppressing energy expenditure in obese adipose tissue,” said Saltiel. “By understanding this mechanism, we’re one step closer to developing targeted therapies that could address weight gain and associated metabolic dysfunctions by increasing fat burning.”

By deleting the gene associated with RaIA, the researchers were able to protect the mice against diet-induced weight gain. Delving deeper into the biochemistry at play, the researchers found that some of the proteins affected by RaIA in mice are analogous to human proteins that are associated with obesity and insulin resistance, suggesting that similar mechanisms may be driving human obesity.

“The direct comparison between the fundamental biology we’ve discovered and real clinical outcomes underscores the relevance of the findings to humans and suggests we may be able to help treat or prevent obesity by targeting the RaIA pathway with new therapies,” said Saltiel “We’re only just beginning to understand the complex metabolism of this disease, but the future possibilities are exciting.”

Source: EurekAlert!

Categories : Cardiovascular Disease Metabolic DisordersTags :

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

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By HualinXMN – Own work, CC BY-SA 4.0

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 : Metabolic DisordersTags :

Obesity Reduces the Rate at Which Energy is Burnt

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A new study published in the journal Obesity found that people at a healthy weight use more energy during the day, when most people are active and eat, while those who have obesity spend more energy during the night, when most people sleep. The study, from Oregon Health & Science University, also found that during the day, those with obesity have higher levels of insulin – a sign that the body is working harder to use glucose.

“It was surprising to learn how dramatically the timing of when our bodies burn energy differed in those with obesity,” said the study’s first author, Andrew McHill, PhD, an assistant professor in the OHSU School of Nursing and the Oregon Institute of Occupational Health Sciences at OHSU. “However, we’re not sure why. Burning less energy during the day could contribute to being obese, or it could be the result of obesity.”

Obesity is defined as having a Body Mass Index, or BMI, of 30 or more. Being overweight or obese increases the risk for health conditions such as high blood pressure and Type 2 diabetes.

Schedules and when people sleep, eat and exercise can also affect health, by either complementing or going against the body’s natural, daily rhythms. Every 24 hours, people experience numerous changes that are triggered by the human body’s internal clock. These changes normally occur at certain times of the day in order to best serve the body’s needs at any given hour.

McHill and the study’s senior author, Steven A. Shea, PhD, director of the Oregon Institute of Occupational Health Sciences at OHSU, focus their research on how circadian rhythms and sleep impact the human body. McHill leads the OHSU Sleep, Chronobiology and Health Laboratory.

While previous research has suggested circadian rhythm misalignment affects energy metabolism and glucose regulation, those studies have largely involved participants who have a healthy weight. To explore this further, McHill, Shea and colleagues organized a study that included people of different body sizes.

A total of 30 participants took part in the study, which involved them staying at a specially designed circadian research lab for six days. The study followed a rigorous circadian research protocol involving a schedule designed to have participants be awake and sleep at different times throughout each day.

After each period of sleep, volunteers were awakened to eat and participate in a variety of tests for the remaining time of each day. One test had participants exercise while wearing a mask that was connected to a machine called an indirect calorimeter, which measures exhaled carbon dioxide and helps estimate energy usage. Blood samples were also collected to measure glucose levels in response to an identical meal provided during each day.

Next, the research team plans to explore eating habits and hunger in people who are obese, as well as those who have a healthy weight. That new study will also follow up on a 2013 study, led by Shea, that found circadian clocks naturally increase food cravings at night.

Source: Oregon Health & Science University

Categories : Genetics Metabolic DisordersTags :

Twin Study Reveals Epigenetic Signature for Obesity

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A susceptibility to gain weight may be written into the epigenetic information of human cells, a Washington State University study indicates.

The proof-of-concept study with a set of 22 twins found an epigenetic signature in buccal cells appearing only for the twins who were obese compared to their thinner siblings. The findings could lead to the development of a simple cheek swab test for an obesity biomarker and enable earlier prevention, the researchers said.

“Obesity appears to be more complex than simple consumption of food. Our work indicates there’s a susceptibility for this disease and molecular markers that are changing for it,” said Michael Skinner, a WSU professor of biology and corresponding author of the study published in the journal Epigenetics.

The study focused on twins to help eliminate the role of genetics and instead focus on epigenetics, molecular processes which are separate from DNA but influence how genes are expressed. The fact that the epigenetic signature was found in cheek cells rather than fat cells also suggests that the obesity signature is likely found throughout the human system.

The signature’s systemic nature also suggests that something may have occurred early in one twin’s life that triggered obesity susceptibility, Skinner added. It’s also possible that it was inherited by one twin and not the other.

For this study, Skinner worked with lead author Glen Duncan, director of the Washington State Twin Registry based at WSU, to identify 22 twin pairs, both identical and fraternal, who were discordant for obesity: one sibling had a body mass index (BMI) of 30 or higher, the standard for obesity defined by the Centers of Disease Control and Prevention, while the other sibling was in the normal range of 25 and below.

The research team analysed cells from cheek swabs provided by the twins. In the cells from the twin siblings who were obese, they found similar epigenetic changes to DNA methylation regions, areas where molecular groups made of methane attach to DNA, regulating gene expression or turning genes on or off.

The study would need to be replicated with larger groups of people to develop a biomarker test for obesity, the authors said.

The goal would be able to identify people earlier in life before they become obese so health care providers might help create interventions such as lifestyle changes, medication or both, said Duncan.

“Ultimately we would like to have some kind of preventative measure instead of our usual approach which is treatment,” he said. “It’s a simple fact that it’s better to prevent a disease, then try to treat it after you have it.”

Source: Washington State University

Categories : Diet and Nutrition PaediatricsTags :

Study Classifies Four Eating Eating Behaviours of Children

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Children fall broadly into four eating categories, according to new research at Aston University, and parents feed their children differently depending on those categories.

The four categories identified by Dr Abigail Pickard and the team in the School of Psychology are ‘avid’, ‘happy’, ‘typical’, and ‘fussy’. The results, which showed specific temperaments and carer feeding patterns associated with overeating, are published in the journal Appetite.

In the UK, around a fifth of children are overweight or obese when they begin school, rising to around a third by the time they leave primary school at age 11. The team sought to identify eating behaviour patterns and how these are associated with temperament, feeding practices and food insecurity, as a way to predict which children are more at risk of becoming overweight.

Typical eaters made up 44% of the children in the study, while fussy eaters accounted for 16%. But of greatest interest to the team was that around one in five young children in the study were found to show “avid eating,” including greater enjoyment of food, faster eating speed, and weaker sensitivity to internal cues of ‘fullness’. The behaviours that distinguish children with avid eating from those who show ‘happy’ eating (17.7% of children in the study), who have similarly positive responses to food, are wanting to eat (or eating more) in response to the sight, smell or taste of palatable food, and a higher level of emotional overeating. In combination, these eating behaviours can lead to overeating and subsequent weight gain.

Dr Pickard and the team have also shown that there are significant differences in children’s temperament and caregivers’ feeding practices between each of the four eating behaviour patterns. Children with avid eating are more likely to be active and impulsive, and their caregivers are more likely to give them food to regulate their emotions or to restrict food for health reasons. Children with avid eating were also less food secure than children who showed happy or typical eating behaviours.

Principal investigator of the project, Professor Jackie Blissett, said: “Whilst feeding practices are key intervention targets to change children’s eating behaviour and child weight outcomes, there has been little evaluation of how feeding practices interact with children’s food approach behaviours to predict eating behaviour.”

She explained that despite the knowledge of the influence of feeding practices on children’s weight, current public health advice is generic and does not reflect variability in children’s appetites. Parents and caregivers can be left feeling frustrated when trying to manage their child’s food intake. By defining the four eating behaviour profiles, this research project, which is funded by the Economic and Social Research Council and co-developed by Professor Claire Farrow, Dr Clare Llewellyn, Dr Moritz Herle, Professor Emma Haycraft and Dr Helen Croker will make it easier to identify the best feeding practices for each eating pattern and provide tailored, effective advice for parents.

Dr Pickard said: “Parents can use this research to help them understand what type of eating pattern their child presents. Then based on the child’s eating profile the parent can adapt their feeding strategies to the child. For example, children in the avid eating profile may benefit more from covert restriction of food, i.e., not bringing snacks into the home or not having foods on display, to reduce the temptation to eat foods in the absence of hunger. Whereas, if a child shows fussy eating behaviour it would be more beneficial for the child to have a balanced and varied selection of foods on show to promote trying foods without pressure to eat.”

The team has planned further research investigating avid eating behaviour and will invite the caregivers and their children into the specialist eating behaviour lab at Aston University to get a better picture of what avid and typical eating behaviours look like in a real-life setting. All the findings will be integrated and the researchers will work with parents to develop feasible and helpful feeding guidelines to reduce children’s intake of palatable snack foods.

Source: Aston University

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 : Genetics Metabolic DisordersTags :

Abdominal Fat Accumulation may not be as Great a Diabetes Risk as Previously Thought

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Conventional wisdom holds that abdominal fat accumulation increases the risk for type 2 diabetes. But surprising new findings from the University of Virginia School of Medicine suggest that naturally occurring genetic variations in our genes can lead some people to store fat at the waist but also protect them from diabetes.

The unexpected discovery, which is published in eLife, provides a more nuanced view of the role of obesity in diabetes and related health conditions. It also could pave the way for more personalised medicine, such as prioritising weight loss for patients whose genes put them at increased risk but place less emphasis on it for patients with protective gene variants, the researchers say.

“There is a growing body of evidence for metabolically healthy obesity. In this condition, people who would normally be at risk for cardiovascular diseases and diabetes because they are obese are actually protected from adverse effects of their obesity. In our study, we found a genetic link that may explain how this occurs in certain individuals,” said researcher Mete Civelek, PhD, of UVA’s Center for Public Health Genomics. “Understanding various forms of obesity is important to tailor treatments for individuals who are at high risk for adverse effects of obesity.”

As medicine grows more sophisticated, understanding the role of naturally occurring gene variations will play an important role in ensuring patients get the best, most tailored treatments. The new work by Civelek and his team, for example, indicates that variants can simultaneously predispose some people to store fat at the abdomen, thought to put them at increased risk for metabolic syndrome, while also protecting them from type 2 diabetes. (Metabolic syndrome raises the risk for diabetes, stroke and other serious health issues.)

One of the metrics doctors use to determine if a patient has metabolic syndrome is abdominal obesity. This is often calculated by comparing the patient’s waist and hip measurements. But Civelek’s research suggest that, for at least some patients, it may not be that simple, with doctors using genetic testing to guide patients to good health.

“We found that among the hundreds of regions in our genomes which increase our propensity to accumulate excess fat in our abdomens, there are five which have an unexpected role,” said Yonathan Aberra, the lead author of the study and a PhD candidate at UVA’s Department of Biomedical Engineering, a joint program of the School of Medicine and School of Engineering. “To our surprise, these five regions decrease an individual’s risk for type 2 diabetes.”

In addition to producing surprising findings, Civelek’s research provides important new tools for his fellow researchers seeking to understand the complexities of gene variations. The sophisticated approach Civelek and his collaborators developed to identify the relevant variants and their potential effects will be useful for future research into metabolic syndrome and other conditions.

The tools could also prove invaluable in the development of new and better treatments for metabolic syndrome, the scientists say.

“We now need to expand our studies in more women and people from different genetic ancestries to identify even more genes that underlie the metabolically health obesity phenomenon,” Civelek said. “We plan to build on our findings to perform more experiments to potentially identify a therapeutic target.”

Source: University of Virginia Health System

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