health

‘Obesogenic environment: We live very sedentary lifestyles, paired with fast food culture’

Rates of obesity and overweight are spiralling due to a “monumental societal failure” to tackle the problem, with more than half of adults and almost a third of children and young people set to be affected by 2050, according to a new study published in The Lancet. That represents more than 3.8 billion adults and 746 million children and adolescents. As we commemorate World Obesity Day, FRANCE 24’s Genie Godula welcomes Dr. Karen Coulman, Senior Research Fellow and Obesity Specialist Dietitian at the University of Bristol.
#Health #Obesity #WorldObesityDay

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Cut sugar in-take to fight obesity, say doctors

Hyderabad: Healthcare experts on Tuesday called on people to curtail sugar in-take to fight obesity as a study conducted by AIG Hospitals found that 80 per cent of IT professionals in Hitec City were overweight.
AIG Hospitals also announced the launch of a dedicated website for its Centre for Obesity and Metabolic Therapy, providing expert consultations and treatment information.
Speaking at a panel discussion organised by AIG Hospitals on the health risk caused by obesity, Dr Ramakrishna said: “In order to reduce weight, cutting down on sugars is essential. About 10-20 per cent reduction in weight can be seen if we stop eating sugars. It also helps prevent cardiovascular diseases. This includes all kinds of sugars, brown, jaggery, and artificial sweeteners.”
The panel discussion was organised on the occasion of World Obesity Day.
With obesity being tagged as an epidemic and a multifactorial disease impacting all bodily functions, doctors talked about the causes, prevention, management and treatment of obesity. The panel featured specialists from gastroenterology, cardiology, pulmonology, psychology and others.
“The impact of obesity on lungs is huge as it increases the risk of immune disregulation. Obese people are more at risk of getting pneumonia, influenza, and other infections. The rate of mortality increased among obese people who get these diseases, as observed during Covid period,” said Dr Vishwanath.
People with obesity also deal with sleep problems. With fat deposited in lungs and neck, people are unable to breathe while sleeping. With abdominal fat, the diaphragm is unable to move. It also causes a cascade of inflammatory problems. Therefore, it is important to get 6-8 hours of deep sleep.
Doctors also mentioned that obese people are more predisposed to get cancers. Additionally, 40 per cent of children in government schools have non-alcoholic fatty liver disease (NAFLD), highlighting the urgency of action.
Maintaining a healthy, balanced diet is key to avoiding obesity and related diseases. Doctors mentioned that intermittent fasting, where people can have proper health meals during 8 hours in the day and then not eat anything for the next 16 hours, works better than fasting on alternate days.
A major discrepancy in nutrition is lack of fruits and vegetables in the Indian diet. While the recommendation is 500 gm of vegetables per day, an individual only consumes 50 gms of vegetables per day. Not knowing what to eat, people just end up going hungry to avoid gaining weight and lose out on nutrition as well.
The human body also needs at least one gram of protein per kilogram of body weight. The psychological aspect of obesity is that most people are surrounded by a toxic food environment, where junk food is easily available and is encouraged. Avoiding such exposure is necessary.
Hyderabad police commissioner C.V. Anand stressed that obesity is influenced by more than just food choices. He also launched FitCop, an app with 18,000 enrolled officers. The initiative identified 300-400 officers at risk for lifestyle diseases.

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Rapamycin Restores Leptin Sensitivity and Leads to Fat Loss in Obese Mice

Worldwide obesity rates have more than doubled since 1990, with nearly a billion people now falling into the category. Though a complex interplay of genes, diet, and environment contribute, 90% of cases have leptin resistance in common.
In lean individuals, fat cells produce the hormone leptin, which suppresses appetite. But in most individuals with obesity, this signal fails to register. Why this happens has been a mystery for more than three decades, ever since Jeffrey M. Friedman’s laboratory at the Rockefeller University cloned the leptin gene in 1994.

But now Friedman, MD, PhD, together with Bowen Tan, Kristina Hedbacker, PhD, and other researchers in Friedman’s Laboratory of Molecular Genetics have discovered a neural mechanism involved in leptin resistance, and identified a way to reverse it in mice using the mTOR inhibitor rapamycin. The team found that rapamycin restores leptin sensitivity to diet-induced obese (DIO) mice, leading to significant loss of fat with only minimal effects on muscle.
“Before our research, the cause of obesity in diet-induced obese mice was unknown, leaving a critical gap in our understanding of how leptin resistance develops and how it can be reversed,” said Tan, a graduate student in Friedman’s lab. “Even though Jeff Friedman discovered this powerful hormone back in 1994, its full potential to help people lose weight hasn’t been realized because most obese patients have acquired resistance to leptin,” added Hedbacker, a research specialist at Howard Hughes Medical Institute and a member of Friedman’s lab. “It’s really exciting to think that there may be means for addressing this.”
Senior author Friedman, together with co-first authors Tan, Hedbacker, and colleagues reported on their work in Cell Metabolism, in a paper titled, “A cellular and molecular basis of leptin resistance,” in which they suggest their findings establish “.. a key pathogenic mechanism leading to obesity.”

“Obesity is the cardinal feature of metabolic syndrome and a worldwide public health problem,” the authors wrote. Long before plant agriculture and animal domestication provided more reliable access to nutrients, humans routinely faced starvation. That’s when the leptin circuit evolved. Neurons in the hypothalamus—the brain’s energy-balance regulator—pick up satiety signals from fat, which secretes leptin. A high amount of the hormone signals that there are adequate fat stores and the energy tank is full, while a low leptin level indicates that the body is running on fumes. “In lean animals, adipose tissue mass is tightly controlled by the hormone leptin (LEP), which functions as the afferent signal in a negative feedback loop that maintains energy balance,” the authors explained. “LEP reduces appetite, in part by activating α-MSH (POMC)-expressing neurons in the arcuate nucleus (ARC) of the hypothalamus.”
Our brains retain this system for regulating food consumption, even as conditions around it have drastically changed, with more people having access to high-calorie foods than ever before. Data suggest that as weight is gained and leptin levels continually rise, the brain gradually stops responding to leptin. “This phenomenon is analogous to insulin resistance, which is the most common cause of diabetes and a condition that develops over time, due, in part, to chronically elevated insulin levels,” Hedbacker said. “Similarly, most people with obesity have high leptin, but reception of their leptin signaling is blocked. This makes it very difficult to lose weight because the brain does not receive the appropriate signal of how much fat is stored.”
With this in mind, Tan and Hedbacker set out to identify biomarkers in the 10% of patients with obesity who are leptin-sensitive and could potentially benefit from leptin treatment. They looked at both leptin-sensitive and leptin-resistant mice. “Similar to most humans with obesity, diet-induced obese (DIO) mice have high leptin levels and fail to respond to the exogenous hormone, suggesting that their obesity is caused by leptin resistance, the pathogenesis of which is unknown,” the authors noted.
What they discovered sent them down an unexpected path. The scientists found that in leptin-resistant mice, the levels of two essential amino acids are dysregulated in response to leptin. These two amino acids, methionine and leucine, are known activators of a signaling molecule called mTOR (mammalian target of rapamycin). Leptin-sensitive animals showed no such dysregulation.
“With this as a starting point, we found that mTOR is hyperactive in specific brain regions and cell types in obese animals,” Tan said. For their study the researchers tested the effects of the mTOR inhibitor rapamycin in four groups of mice: leptin-sensitive mice fed a low-calorie chow diet, mimicking people who remain lean; mice fed a high-fat diet that developed leptin resistance, similar to people who develop obesity; and two sets of obese mice that were leptin-deficient but responsive to the hormone. These mice were fed either the low-calorie chow diet or the high-fat diet. “Our finding that LEP sensitivity was inversely associated with plasma levels of mTOR activators led us to hypothesize that mTOR activation might diminish LEP sensitivity in DIO mice. We evaluated this possibility by treating DIO mice with rapamycin (RAP), a specific mTOR inhibitor,” they explained.
The results were striking: “Obese mice fed a high-fat diet and treated with the mTOR inhibitor rapamycin lost significant amounts of weight, which—similar to leptin treatment in leptin-sensitive animals—was primarily due to a decrease in the amount of adipose tissue,” Tan said. The authors further noted, “We found that RAP, a specific mTOR inhibitor, reduces body weight in DIO mice but not in mice with defects in LEP signaling or low circulating levels of the hormone.”

The team then investigated which cell types in the brain were the target of rapamycin, focusing on a dozen cell types in the hypothalamus, where leptin is known to act. Using single-cell sequencing, Tan found that rapamycin treatment exerted significant effects on neurons in the hypothalamus that express a gene known as POMC. These neurons are known to mediate leptin’s weight-reducing effects. “We then employed snRNA-seq to show that RAP treatment of DIO, but not lean mice, specifically induced gene expression in POMC neurons that promote LEP signaling and melanocortin production,” they wrote. “Further studies showed that POMC neurons and melanocortin signaling are necessary for RAP’s weight-reducing effects and that increased mTOR activity in POMC neurons is sufficient to cause LEP resistance.”
Added Hedbacker, “We found that rapamycin reduced mTOR in POMC neurons and restored their receptivity, essentially resensitizing the animals to leptin and leading to a decreased size of fat depots relative to muscle mass.” Defects in POMC-expressing neurons are also known to cause leptin resistance and obesity, Friedman noted, adding, “it was satisfying to find that an acquired form of leptin resistance targets this same pathway.”
By showing that it is possible to restore leptin signaling, the findings could potentially lead to new obesity treatments. “In summary, we show that LEP resistance in DIO animals is caused by increased mTOR activity in POMC neurons and that RAP reduces obesity by re-sensitizing endogenous LEP signaling in these cells,” the authors wrote. “These findings thus have important implications for our understanding of the pathogenesis of obesity and potential therapeutic applications.”
Loss of fat mass without muscle mass is characteristic of leptin treatment, but it’s unusual for weight loss in general. For example, weight loss achieved by dieting or treatment with highly effective anti-obesity medications such as Ozempic leads to a significant loss of both fat and muscle. “Reversing LEP resistance could also have clinical implications, particularly because LEP spares lean body mass in contrast to the new peptide-based therapeutics that can cause significant loss of lean mass,” the scientists pointed out.
Future research in Friedman’s lab will explore why a high-fat diet elevates mTOR signaling in the brain. The lab will also try to develop means for inhibiting mTOR specifically in POMC neurons to avoid potential side effects of systemic rapamycin use, which is linked to glucose intolerance and potentially diabetes.
“The development of brain-specific rapalogs provides a possible means to selectively reduce mTOR activity in the brain, and it might also be possible to develop cell-specific mTOR modulators,” the investigators noted. “Alternatively, the development of means for cell-specific delivery of RAP to POMC neurons could provide new avenues for treating obesity or maintaining weight loss.”
The post Rapamycin Restores Leptin Sensitivity and Leads to Fat Loss in Obese Mice appeared first on GEN – Genetic Engineering and Biotechnology News.

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“Shunt-ing” down obesity with novel endogenous metabolites

Obesity is a growing public health issue that has recently been transformed through the advent of new medicines. However, our understanding of the pathways and mechanisms that regulate energy balance in mammals is still developing. Recent discoveries on this front include an exciting new finding that there exists a novel class of metabolites in humans and mice that can regulate obesity in rodents.

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Decoding the complex systems of obesity

We present this special focus issue on March 4th, coinciding with World Obesity Day 2025, to show our solidarity with the World Obesity Federation and advocate for increased awareness, prevention, and treatment of obesity. We embrace this year’s World Obesity Day theme, “Changing Systems,” which challenges us to broaden our perspective from viewing obesity as solely an individual issue and recognize the wider systemic factors that contribute to the rapidly escalating rates of obesity worldwide. As researchers and as editors we often take a narrow view, focusing on specific genes, molecules, or cell signaling pathways that impact metabolism and contribute to obesity. However, with this issue, we aim to expand that view, presenting papers that highlight how body systems cooperate to impact metabolic health and, more broadly, how environmental factors, including food systems, contribute to this complex disease. By understanding the systems that influence obesity on a broader level, we can hope to optimize current disease management and to uncover novel approaches to combat it.

Decoding the complex systems of obesity Read More »

Analysis predicts a third of children worldwide will be obese or overweight by 2050

Obesity rates are set to skyrocket, with one in six children and adolescents worldwide forecast to be obese by 2050, according to a new study. But with significant increases predicted within the next five years, the researchers stress urgent action now could turn the tide on the public health crisis.

Analysis predicts a third of children worldwide will be obese or overweight by 2050 Read More »

Chronic Diseases Are Killing Kids — and Exposure to Chemicals Is Driving the Epidemic

Chronic noncommunicable diseases (NCDs) are on the rise in children. Asthma, obesity and even certain childhood cancers now occur far more frequently than they did a few generations ago. According to a major study published in The New England Journal of Medicine (NEJM) by the Consortium for Children’s Environmental Health, these diseases now rank among the leading causes of illness and death for young people.1

The study points out that environmental pollution and exposure to synthetic chemicals are widespread, suggesting that these chemicals, produced in huge quantities from fossil fuels, are key factors driving this increase.

Why Chronic Diseases in Children Are on the Rise

Chronic diseases, such as heart disease and diabetes, are often thought of as conditions that affect adults. However, the NEJM study explains that children today are developing NCDs at alarming rates.

These diseases are caused by a mix of factors, including genetics, lifestyle and environmental exposures. Synthetic chemicals appear to be a key part of this picture, especially since children face unique risks during early stages of growth.

One example the study highlights is the significant rise in childhood cancers, estimated at around 35% more cases than seen half a century ago.2 It also reports that male reproductive birth defects have doubled in frequency. These trends suggest that children’s bodies, which are still developing, are less capable of defending against chemicals found in everything from food packaging to household products.

Meanwhile, neurodevelopmental disorders affect around 1 in 6 children, and autism spectrum disorder is diagnosed in about 1 in 36 children.3 If you look at these numbers, it’s clear that what was once unusual is now becoming disturbingly common. The study contrasts this surge in child health problems with patterns in adults, where deaths and disabilities linked to certain cancers and cardiovascular diseases have decreased over time.

Better screening and treatments help explain the improvements in older populations. In children, however, environmental factors appear to be overshadowing any of the benefits that have helped adults. This gives you a clue that today’s generation of children are living in environments filled with new synthetic substances that pose unprecedented risks.

When a disease begins during childhood, it alters a child’s quality of life for decades, as many of these childhood-onset diseases carry into adulthood.

Synthetic Chemicals Are Everywhere

The NEJM paper notes that an estimated 350,000 manufactured chemicals, mixtures and plastics exist in global inventories.4 Many of these substances are derived from fossil fuels such as gas, oil and coal. Production of synthetic chemicals has grown 50-fold since 1950, is increasing by roughly 3% every year and is expected to triple by 2050.5

If you think about the sheer numbers, it’s no surprise that children come into contact with these chemicals everywhere — from plastic toys and bottles to upholstered furniture, carpeting and electronics. As noted by the authors, once these chemicals enter the market, they often spread into the air, water and soil.

Environmental pollution is now so widespread that even remote corners of the planet show signs of contamination. Because these pollutants travel long distances in air and water, you cannot assume that living far from industrial centers guarantees safety.

Moreover, these substances are found in everyday items like household cleaners, shampoos and lotions, and repeated exposure from multiple products adds up over time. Disturbingly, as noted in the NEJM paper, unlike pharmaceuticals, most synthetic chemicals are not required to prove they are safe before they are sold.6

Fewer than 20% have been tested for toxicity, and even fewer have been studied for their possible effects on infants and children.7 This lack of oversight leads to a situation where health impacts often only become clear once a generation of children has already been exposed. Because chemical production is profitable, the industry resists stricter regulations that could slow down or limit growth.

Further, government agencies often lack the authority or resources to require comprehensive premarketing testing.8 This leaves you in the dark about what’s in the products you buy. By the time scientists uncover harmful effects, many kids have already been exposed for years on end. Delaying action on childhood health can lead to serious issues — like asthma, developmental delays, or even cancer — emerging years after the damage is done.

The Evidence Behind Chemicals and Disease in Children

The NEJM paper illustrates that the link between chemicals and children’s health issues is not just based on theory. Researchers have tied several childhood diseases to specific synthetic chemicals over the years.

Some of the most striking evidence comes from well-documented events: the tragedy at Minamata, Japan, for example, where mercury-contaminated fish eaten by pregnant women led to severe neurologic damage in babies, or the cases of mothers taking diethylstilbestrol (DES) who remained healthy themselves while their daughters faced a higher risk of reproductive cancers.9

These episodes demonstrated that chemicals cross the placenta and cause serious harm to babies even if the mother appears fine. Another incident was the thalidomide disaster, where pregnant women in the 1950s and early 1960s took a sedative that caused severe limb defects in more than 10,000 infants worldwide. Thalidomide was a turning point in understanding that children and fetuses are especially sensitive to chemicals even at low or short-term exposures.10

These events helped shape the field of environmental pediatrics, giving researchers a framework to investigate how and why chemicals harm children during key windows of development. Today, scientists use prospective birth-cohort studies to measure chemical exposures in pregnant women and follow their children’s health for many years.

Such studies have revealed links between phthalates — found in plastics and personal care products — and male reproductive disorders, and between certain pesticides or flame retardants and lower IQ scores or neurodevelopmental issues.

When multiple studies in different locations find similar patterns, the evidence becomes hard to dismiss. In many cases, parents show no obvious harm, yet their children suffer health consequences linked to chemical exposures that occurred in the womb. Further, harms can appear at different times in life. Some birth defects or cancers show up early, but others, such as obesity, fertility problems or cardiovascular disease, arise years later.

The NEJM study underscores that this delayed effect makes it easy to miss the true cause. If your child develops asthma at age 7 or 8, it’s not obvious if a chemical exposure in infancy or even before birth played a role. This timing gap suggests that the full impact of today’s environment doesn’t become clear for decades, which is why stronger prevention efforts are so important.

Why Today’s Laws Are Failing Children

The NEJM paper also offers a sobering look at the limitations of current regulations. The federal Toxic Substances Control Act (TSCA) in the U.S. was meant to protect the public and the environment from “unreasonable risks,” but experts say it has not lived up to that promise.

One major shortcoming is that companies producing new chemicals do not have to prove these substances are safe before putting them on the market. Instead, government regulators must prove a chemical is harmful, which is a slow and costly process.11

You might assume that once a hazard is known, authorities would step in quickly. However, very few chemicals have actually been banned or heavily restricted in the nearly 50 years since TSCA first became law. Many that were suspected of causing harm lingered for years while manufacturers disputed the science or withheld data under the banner of “trade secrets.”

As noted by the authors, chemical companies receive government subsidies and enjoy broad legal protections, giving them few incentives to reduce production or invest in safer alternatives.12

In the European Union, the Registration, Evaluation, Authorization and Restriction of Chemicals (REACH) framework promises more rigorous oversight. Unfortunately, REACH also falls short, the study highlights, in part because it allows industry-supplied data to serve as a basis for safety, with minimal quality checks from independent labs.13

Thus, while Europe has banned or restricted more chemicals than the U.S., the overall outcome remains similar: tens of thousands of substances in use with limited real-world testing and oversight. Most policies also consider chemicals one at a time, overlooking the fact that you and your children are exposed to a “soup” of chemicals every day. They also rarely account for children’s greater vulnerability.

Because children have smaller bodies and developing organ systems, a dose that’s harmless to an adult is often harmful to a child. If a hazardous chemical stays on the market for decades, it does a lot of damage before regulators step in. By then, an entire generation has grown up exposed to a substance that could cause learning problems, respiratory issues or even increase the risk of certain cancers.

Real-World Examples and Strategies for Reducing Exposure

You might have heard about leaded gasoline. For decades, lead was added to fuel to improve engine performance, leading to widespread contamination. By the 1970s, scientists realized that it had driven up blood lead levels in children across the U.S.

The paper points out that this exposure caused a measurable drop in average IQ scores among those born in that era. When lead was finally phased out of gasoline, children’s blood lead levels fell, and average IQ scores improved.14 This example shows that when harmful substances are removed from circulation, significant public health benefits often follow.

Although it’s difficult to eliminate all exposures, there are still meaningful steps to reduce your exposure at home. Plastics are a major culprit, so replace plastic containers and bottles with stainless steel or glass, especially for foods and beverages.

If you are repainting a room, look for low- or no-VOC paint, since volatile organic compounds irritate airways and have toxic effects. Further, reduce your reliance on harsh chemical cleaning products. Even simple moves, such as using fragrance-free detergents and soaps, reduce the amount of undisclosed chemicals in your and your child’s environment.

Beyond personal choices, advocate for bigger changes. The NEJM paper makes it clear that our laws need a major overhaul.15 Contact local representatives or support organizations that push for stricter limits on chemicals in consumer goods.

In addition, look for companies that are transparent about their product ingredients. Some businesses have begun engaging in what’s called chemical footprint reporting, which means they openly track and share information about the chemicals in their supply chains.

When you shop with these brands or ask for safer products, you send a message that child health is more important than corporate secrecy. Integrative medical professionals are another helpful resource.

If your child has asthma or a developmental concern, ask your holistic pediatrician if chemical exposures are playing a role and whether they have testing, referrals or advice on reducing exposures. Open communication with your child’s health care providers makes it easier to spot early issues before they become more serious problems.

Preserving the Next Generation’s Health Through Action and Awareness

The NEJM study shows that chemicals once considered harmless endanger your child’s growth and development, especially when regulations fall behind science. NCDs, ranging from asthma to cancer, are now major threats to children worldwide, and many of these diseases have been linked to synthetic substances that saturate daily life.

Although the chemical industry wields enormous influence and profits, you have the power to question the status quo and demand safer products and environments for your children.

As production of plastics and fossil fuel-derived chemicals continues to climb, know that solutions do exist. By backing stricter laws, encouraging transparency from manufacturers and making practical changes at home, you help shift priorities toward health rather than unchecked chemical growth.

The real-life success story of phasing out leaded gasoline shows what’s possible when science, policy and public will converge. When society decides children’s well-being matters more than convenience or corporate profits, everyone benefits.

If you want a world in which kids breathe cleaner air, face fewer toxic risks and enjoy brighter futures, your involvement is essential. Even small choices add up, and your actions spark changes that give the youngest generation a better chance at a healthy life.

Chronic Diseases Are Killing Kids — and Exposure to Chemicals Is Driving the Epidemic Read More »

A third of children worldwide forecast to be obese or overweight by 2050

Obesity rates are set to skyrocket, with one in six children and adolescents worldwide forecast to be obese by 2050, according to a new study. But with significant increases predicted within the next five years, the researchers stress urgent action now could turn the tide on the public health crisis.

A third of children worldwide forecast to be obese or overweight by 2050 Read More »

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