Tag: weight management

New WHO Guideline Advises Against Non-sugar Sweeteners for Weight Management

The World Health Organization (WHO) has released a new guideline on non-sugar sweeteners (NSS), which recommends against using NSS to control body weight or reduce the risk of noncommunicable diseases (NCDs).

This comes as WHO conducts its first review of obesity management guideline in more than two decades. Last week, Francesco Branca, WHO director of nutrition and food safety, had also warned that weight-loss drugs such as Wegovy are “not a silver bullet” in tackling obesity.

The recommendation is based on the findings of a systematic review of the available evidence which suggests that use of NSS does not confer any long-term benefit in reducing body fat in adults or children. Results of the review also suggest that there may be potential undesirable effects from long-term use of NSS, such as an increased risk of type 2 diabetes, cardiovascular diseases, and mortality in adults.

“Replacing free sugars with NSS does not help with weight control in the long term. People need to consider other ways to reduce free sugars intake, such as consuming food with naturally occurring sugars, like fruit, or unsweetened food and beverages,” says Francesco Branca, WHO Director for Nutrition and Food Safety. “NSS are not essential dietary factors and have no nutritional value. People should reduce the sweetness of the diet altogether, starting early in life, to improve their health.”

The recommendation applies to all people except individuals with pre-existing diabetes and includes all synthetic and naturally occurring or modified non-nutritive sweeteners that are not classified as sugars found in manufactured foods and beverages, or sold on their own to be added to foods and beverages by consumers. Common NSS include acesulfame K, aspartame, advantame, cyclamates, neotame, saccharin, sucralose, stevia and stevia derivatives.

The recommendation does not apply to personal care and hygiene products containing NSS, such as toothpaste, skin cream, and medications, or to low-calorie sugars and sugar alcohols (polyols), which are sugars or sugar derivatives containing calories and are therefore not considered NSS.

Because the link observed in the evidence between NSS and disease outcomes might be confounded by baseline characteristics of study participants and complicated patterns of NSS use, the recommendation has been assessed as conditional, following WHO processes for developing guidelines. This signals that policy decisions based on this recommendation may require substantive discussion in specific country contexts, linked for example to the extent of consumption in different age groups.

The WHO guideline on NSS is part of a suite of existing and forthcoming guidelines on healthy diets that aim to establish lifelong healthy eating habits, improve dietary quality and decrease the risk of NCDs worldwide.

Source: WHO

How to Prevent Dangerous Weight Loss in COVID Patients

Photo by Stephen Andrews on Unsplash

COVID infection often causes adipose atrophy, weight loss and cachexia, which significantly contribute to poor quality of life and mortality. Now, researchers at Karolinska Institutet have discovered that SARS-CoV-2 infection fuels blood vessel formation in fat tissues, thus revving up the body’s thermogenic metabolism. Blocking this process with an existing drug curbed weight loss in mice and hamsters that were infected with the virus, according to the study published in the journal Nature Metabolism.

“Our study proposes a completely new concept for treating COVID associated weight loss by targeting the blood vessels in the fat tissues,” says corresponding author Yihai Cao, professor at Karolinska Institutet.

The researchers examined how different types of fat, including brown fat and visceral and subcutaneous white fat, reacted when exposed to SARS-CoV-2 and how it impacted weight in mice and hamsters. They found that the animals lost significant amounts of weight in four days and that this weight loss was preceded by the activation of brown fat and the browning of both types of white fat. These fat tissues also contained more microvessels and high levels of a signaling protein called vascular endothelial growth factor (VEGF), which promotes the growth of new blood vessels.

Similar mechanisms in humans

The researchers observed the same mechanisms in human tissue samples from four patients who died of COVID, suggesting the findings could be clinically relevant for humans.

When the animals were treated with an anti-VEGF drug, the animals recovered most of their lost weight and their fat tissues exhibited fewer microvessels.

“Antiangiogenic drugs are currently used in the clinic to treat various types of cancers,” Yihai Cao says. “It’s possible these drugs could also be helpful in treating COVID-related problems such as excessive weight loss and metabolic changes, thus improving the quality of life and survival for these patients. Of course, we will need more research to validate if our preclinical findings also hold up in human trials.”

Source: Karolinska Institutet

Late Night Snacks Impact Hunger, Metabolism and Adipose Tissue

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While popular diets discourage midnight snacking, few studies have examined the simultaneous effects of late eating on the weight gain trifecta regulation of calorie intake, the number of calories burnt, and molecular changes in fat tissue. Now, a new study published in Cell Metabolism has found that timing of food intake significantly impacts energy expenditure, appetite, and molecular pathways in adipose tissue.

“We wanted to test the mechanisms that may explain why late eating increases obesity risk,” explained senior author Frank A. J. L. Scheer, PhD, Director of the Medical Chronobiology Program in the Brigham’s Division of Sleep and Circadian Disorders. “Previous research by us and others had shown that late eating is associated with increased obesity risk, increased body fat, and impaired weight loss success. We wanted to understand why.”

“In this study, we asked, ‘Does the time that we eat matter when everything else is kept consistent?'” said first author Nina Vujovic, PhD, a researcher in the Medical Chronobiology Program in the Brigham’s Division of Sleep and Circadian Disorders. “And we found that eating four hours later makes a significant difference for our hunger levels, the way we burn calories after we eat, and the way we store fat.”

Vujovic, Scheer and their team studied 16 patients with a body mass index (BMI) in the overweight or obese range. Each participant completed two laboratory protocols: one with a strictly scheduled early meal schedule, and the other with the exact same meals, each scheduled about four hours later in the day. In the last two to three weeks before starting each of the in-laboratory protocols, participants maintained fixed sleep and wake schedules, and in the final three days before entering the laboratory, they strictly followed identical diets and meal schedules at home. In the lab, participants regularly documented their hunger and appetite, provided frequent small blood samples throughout the day, and had their body temperature and energy expenditure measured. To measure how eating time affected molecular pathways involved in adipogenesis, or how the body stores fat, investigators collected biopsies of adipose tissue from a subset of participants during laboratory testing in both the early and late eating protocols, to enable comparison of gene expression patterns/levels between these two eating conditions.

Results revealed that eating later had profound effects on hunger and appetite-regulating hormones leptin and ghrelin, which influence our drive to eat. Specifically, levels of the hormone leptin, which signals satiety, were decreased across the 24 hours in the late eating condition compared to the early eating conditions. When participants ate later, they also burned calories at a slower rate and exhibited adipose tissue gene expression towards increased adipogenesis and decreased lipolysis, which promote fat growth. Notably, these findings convey converging physiological and molecular mechanisms underlying the correlation between late eating and increased obesity risk.

Vujovic explained that these findings are not only consistent with a large body of research suggesting that eating later increases risk of developing obesity, but they shed new light on how this might occur. By using a randomised crossover study, and tightly controlling for behavioural and environmental factors such as physical activity, posture, sleep, and light exposure, investigators were able to detect changes the different control systems involved in energy balance, a marker of how our bodies use the food we consume.

Future studies will include more female participants. Despite only five female participants, the study was set up to control for menstrual phase, reducing confounding but making recruiting women more difficult. Going forward, Scheer and Vujovic are also interested in better understanding the effects of the relationship between meal time and bedtime on energy balance.

“This study shows the impact of late versus early eating. Here, we isolated these effects by controlling for confounding variables like caloric intake, physical activity, sleep, and light exposure, but in real life, many of these factors may themselves be influenced by meal timing,” said Scheer. “In larger scale studies, where tight control of all these factors is not feasible, we must at least consider how other behavioural and environmental variables alter these biological pathways underlying obesity risk. “

Source: Brigham and Women’s Hospital

Major Review Urges Tackling of Weight Stigma in Healthcare

Obesity
Image source: Pixabay CC0

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

Weekly Prednisone Could Reduce Obesity and Help in Muscular Dystrophy

Source: Pixabay CCO

In a study on obese mice fed a high-fat diet, receiving prednisone once weekly improved their exercise endurance and strength, and their reduced weight. The study was published in the Journal of Experimental Medicine. A previous study had found that weekly prednisone was helpful in muscular dystrophy.

“These studies were done in mice. However, if these same pathways hold true in humans, then once-weekly prednisone could benefit obesity,” explained senior author Dr Elizabeth McNally.

“Daily prednisone is known to promote obesity and even metabolic syndrome – a disorder with elevated blood lipids and blood sugar and weight gain,” Dr McNally said. “So, these results, in which we intermittently ‘pulse’ the animals with once-weekly prednisone, are strikingly different. Obesity is a major problem, and the idea that once-weekly prednisone could promote nutrient uptake into muscle might be an approach to treating obesity.”

The once-weekly prednisone, a glucocorticoid steroid, promoted nutrient uptake into the muscles. The researchers also found these mice had increased adiponectin levels, an adipocyte-secreted hormone involved in protecting against diabetes and insulin resistance. Mice that were already obese from eating a high-fat diet were also found to benefit after once-weekly prednisone, experiencing increased strength, running capacity and lower blood glucose.

Most knowledge on steroids like prednisone is derived from studies of daily doses of prednisone

“We see a very different outcome when it is taken once a week,” Dr McNally said. “We need to fine tune dosing to figure out the right amount to make this work in humans, but knowing adiponectin might be one marker could provide a hint at determining what the right human dose is.”

Dr McNally described the weekly dose as “a bolus, or spike, of nutrients going into your muscle.”

“We think there is something special about promoting this spike of nutrients into muscle intermittently, and that it may be an efficient way to improve lean body mass,” she added.

“What is exciting to me about this work is the finding that a simple change in the dosing frequency can transform glucocorticoid drugs from inducers to preventers of obesity,” said corresponding author Mattia Quattrocelli. “Chronic once-daily intake of these drugs is known to promote obesity. Here we show that dosing the same type of drug intermittently – in this case, once weekly – reverses this effect, promotes muscle metabolism and energy expenditure, and curtails the metabolic stress induced by a fat-rich diet.”

Many patients take prednisone daily for different immune conditions, which has side effects including weight gain and even muscle atrophy with weakness. Investigators want to determine whether patients can get the same immune benefit with intermittent prednisone dosing, which could be much more beneficial to the muscle.

Dr McNally’s team previously found that intermittent prednisone administration was helpful for muscular dystrophy, showing once weekly prednisone improved strength, recently reporting that a pilot trial in humans with muscular dystrophy in which one weekly dose of prednisone improved lean mass.

McNally wants to identify biomarkers most critical to measure a beneficial response to prednisone.

“If we can determine how to choose the right dose of prednisone that minimises atrophy factors and maximises positive markers like adiponectin, then we can really personalise the dosing of prednisone,” she said.

The group also recently showed that weekly prednisone uses strikingly different molecular pathways to strengthening the muscle in male versus female mice, based on a new study just published in the Journal of Clinical Investigation by Isabella Salamone, a graduate student in Dr McNally’s lab.

The benefits of weekly prednisone are linked to circadian rhythms, according to another new study published in Science Advances. Human cortisol and steroid levels spike early in the morning before awakening.

“If you don’t give the drug at the right time of day, you don’t get the response,” Quattrocelli said. “In mice, we obtained good effects with intermittent prednisone in muscle mass and function when we dose them at the beginning of their daytime. Mice have a circadian rhythm inverted to us, as they generally sleep during the daytime and are active at night. This could mean that the optimal dosing time for humans during the day could be in the late afternoon/early evening, but this needs to be appropriately tested.”

Conducting these studies in mice is a major limitation, Dr McNally said.

“While we are encouraged by the pilot study in humans with muscular dystrophy, mouse muscles have more fast-twitch fibres than humans, and slow-twitch muscle could be different,” Dr McNally said. “More studies are needed to try to better understand whether these same mechanisms work in human muscles.”

Source: Northwestern University

Bringing Back Thiazolidinediones – Without the Weight Gain

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By uncovering the subtle difference between two varieties of a protein, researchers from the Pennsylvania may have discovered how to eliminate the weight gain side effects of thiazolidinediones, which were once widely-used diabetes drugs. These findings, published in Genes & Development, could lead to more effective treatment from modified thiazolidinediones, which many likely avoid in its current form due to side effects.

“One small, undiscovered difference between the two forms of a single protein proved to be extremely significant,” said study senior author Mitchell Lazar, professor at the University of Pennsylvania. “Our findings suggest a way to improve on the mechanism of action of thiazolidinedione drugs, which holds promise for eliminating the side effect of weight gain.”

After their introduction in the 1990s, thiazolidinediones, which include rosiglitazone, soon enjoyed widespread use in diabetes. Since then, they have fallen out of favour due to their side effects. This has led some researchers to investigate whether new compounds could be developed that retain these drugs’ therapeutic effects while having fewer side effects.

In their study, Prof Lazar and his team approached this problem by studying thiazolidinediones’ target, PPARgamma (PPARγ), a protein which helps control fat cell production. The scientists examined two lines of mice: One greatly deficient in one form of the protein, PPARγ1, the other greatly deficient in PPARγ2. In the mice, the scientists showed that activating PPARγ1 or PPARγ2 with a thiazolidinedione had an anti-diabetic effect in each case, protecting mice from the metabolic harm of a high-fat diet.

However, the researchers discovered that activation of these two forms has subtly different downstream effects on gene activity. Specifically, in the PPARγ1-deficient mice (in which most of the present PPARγ takes the form of PPARγ2), the thiazolidinedione treatment caused no weight gain.

The finding therefore suggests that it may be possible to realize the benefits of thiazolidinediones without the weight gain side effect, by selectively activating PPARγ2 and not PPARγ1.

“We’re now studying in more detail how PPARγ1 and PPARγ2 work and how they differ, in the hope of finding ways to selectively activate PPARγ2,” Prof Lazar said.

Source: University of Pennsylvania

Getting Adequate Sleep Results in Reduced Calorie Intake

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Getting adequate sleep could be key to fighting growing rates of obesity around the world, according to a study published in JAMA Internal Medicine, which focused solely on improving sleep duration in overweight individuals.

Understanding the underlying causes of obesity and how to prevent it is the best way to fight obesity, according to first author Dr Esra Tasali. “The current obesity epidemic, according to experts, is mostly explained by an increase in caloric intake, rather than lack of exercise,” she said.

In a randomised clinical trial with 80 adults, published in JAMA Internal Medicine, researchers found that young, overweight adults who habitually slept fewer than 6.5 hours a night were able to sleep for 1.2 hours longer after a personalised sleep hygiene counselling session. The sleep intervention was intended to extend time in bed duration to 8.5 hours and, compared to controls, the increased sleep duration also reduced participants’ overall caloric intake by an average of 270 kcal (calories) per day.

“Over the years, we and others have shown that sleep restriction has an effect on appetite regulation that leads to increased food intake, and thus puts you at risk for weight gain over time,” said Tasali. “More recently, the question that everyone was asking was, ‘Well, if this is what happens with sleep loss, can we extend sleep and reverse some of these adverse outcomes?”

The study examines the effects of sleep extension on caloric intake but also does so in a real-world setting, with no influence on participants’ diets. Participants slept in their own beds, tracked their sleep with wearable devices, and otherwise followed their normal lifestyle without any instructions on diet or exercise.

“Most other studies on this topic in labs are short-lived, for a couple of days, and food intake is measured by how much participants consume from an offered diet,” said Tasali. “In our study, we only manipulated sleep, and had the participants eat whatever they wanted, with no food logging or anything else to track their nutrition by themselves.”

Instead, to objectively track participants’ caloric intake, investigators relied on the “doubly labelled water” method to track change in energy stores, which uses isotopes of hydrogen and oxygen in drinking water. “This is considered the gold standard for objectively measuring daily energy expenditure in a non-laboratory, real-world setting and it has changed the way human obesity is studied,” said Professor Dale A. Schoeller, senior study author and pioneer of the method.

Overall, individuals who increased their sleep duration were able to reduce their caloric intake by an average of 270 kcal per day – which would translate to roughly 12 kg of weight loss over three years if the effects were maintained over a long term.

Perhaps the most surprising aspect of the study was the intervention’s simplicity. “We saw that after just a single sleep counselling session, participants could change their bedtime habits enough to lead to an increase in sleep duration,” said Dr Tasali. “We simply coached each individual on good sleep hygiene, and discussed their own personal sleep environments, providing tailored advice on changes they could make to improve their sleep duration. Importantly, to blind participants to sleep intervention, recruitment materials did not mention sleep intervention, allowing us to capture true habitual sleep patterns at baseline.”

Even though the study did not systematically assess factors that may have influenced sleep behaviour, “limiting the use of electronic devices before bedtime appeared as a key intervention,” said Dr Tasali.

Following just a single counselling session, participants increased their average sleep duration by over an hour a night. Despite prescribing no other lifestyle changes, most participants had a large decrease in how much they ate, with some participants’ intake reduced by 500kcal per day.

The subjects were only involved in the study for a total of four weeks, with two weeks for gathering baseline information about sleep and caloric intake, followed by two weeks to monitor the effects of the sleep intervention.

“This was not a weight-loss study,” said Dr Tasali. “But even within just two weeks, we have quantified evidence showing a decrease in caloric intake and a negative energy balance – caloric intake is less than calories burned. If healthy sleep habits are maintained over longer duration, this would lead to clinically important weight loss over time. Many people are working hard to find ways to decrease their caloric intake to lose weight – well, just by sleeping more, you may be able to reduce it substantially.”

Source: University of Chicago Medicine

Chewing Food Thoroughly Helps in Weight Management

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Previous research has shown that the age-old advice of chewing food thoroughly helps protect against weight again obesity, and now a study has revealed why this is so.

Typically, the chewing process reportedly enhances the energy expenditure associated with the metabolism of food and increases intestinal motility all add up to an increased heat generation in the body, known as diet-induced thermogenesis (DIT). However, how prolonged chewing induces DIT in the body remains unclear. A study published in the journal Scientific Reports answers these questions.

DIT increases energy expenditure above the basal fasting level – a factor known to prevent weight gain. The team previously found that slow eating and thorough chewing not only increased DIT but also enhanced blood circulation in the splanchnic region of the abdomen. Although these studies linked chewing-induced-DIT with increased digestion and absorption-related activity in the abdomen, they left scopes for further exploring a few crucial points.

Senior author Prof Hayashi Naoyuki Hayashi from Waseda University explained: “We were unsure whether the size of the food bolus that entered the digestive tract contributed to the increase in DIT observed after slow eating. Also, do oral stimuli generated during prolonged chewing of food play any role in increasing DIT? To define slow chewing as an effective and scientific weight management strategy, we needed to look deeper into these aspects.”

To find the answers, the researchers designed their new study to exclude the effect of the food bolus by involving liquid food. The entire study included three trials conducted on different days. Volunteers swallow 20mL liquid test food normally every 30 seconds as a control trial. In the second trial, the volunteers kept the same test food in their mouth for 30 seconds without chewing, allowing longer tasting before swallowing. In the third trial they studied the effect of both chewing and tasting; the volunteers chewed the 20mL test food for 30 seconds at a frequency of once per second and then swallowed it. The variables such as hunger and fullness, gas-exchange variables, DIT, and splanchnic circulation were duly measured before and after the test-drink consumption.

While there was no difference in hunger and fullness scores among the trials, as Prof Hayashi describes: “We found DIT or energy production increased after consuming a meal, and it increased with the duration of each taste stimulation and the duration of chewing. This means irrespective of the influence of the food bolus, oral stimuli, corresponding to the duration of tasting food in the mouth and the duration of chewing, increased DIT.” Gas exchange and protein oxidation too increased with the duration of taste stimulation and chewing, and so did blood flow in the splanchnic celiac artery. Since this artery supplies blood to the digestive organs, upper gastrointestinal tract motility also increased in responsivense to chewing.

The study demonstrated that energy expenditure through thorough chewing, though small, could help reduce obesity and metabolic syndrome.

With robust evidence behind it, slow eating and thorough chewing could be the latest recommendations for managing weight.

Source: Waseda University