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Tag: Obesity

  • Common Plastics May Contribute to Obesity, Infertility, and Asthma

    Common Plastics May Contribute to Obesity, Infertility, and Asthma

    Recent studies show that chemicals in everyday plastics may silently cause long-term health issues. Early-life exposure has been associated with obesity, infertility, and cognitive impairments.
    Chemicals in everyday plastics may be fueling obesity, infertility, and asthma that begin in childhood. Experts warn urgent action is needed to protect future generations. Image Credits: Shutterstock

    Recent studies show that chemicals in everyday plastics may silently cause long-term health issues. Early-life exposure has been associated with obesity, infertility, and cognitive impairments.

    Researchers note that while minor lifestyle adjustments can help, long-term protection will demand decisive global measures.

    Growing Worries Over Early-Life Plastic Exposure

    Experts at NYU Langone Health warn that exposure to chemicals in common plastic products during childhood may pose serious health risks that persist into adulthood.

    This finding is based on a comprehensive review of hundreds of recent studies published in The Lancet Child & Adolescent Health.

    Research Connecting Plastic Chemicals to Health Issues

    In their recent analysis, researchers review decades of evidence showing that additives in industrial and household plastics may increase the risk of disease and disability, particularly with early-life exposure. The review focuses on three key chemical groups: phthalates, which add flexibility; bisphenols, which provide rigidity; and perfluoroalkyl substances (PFAS), which make products heat- and water-resistant.

    The studies tracked thousands of pregnant individuals, fetuses, and children, linking these chemicals to long-term health issues such as heart disease, obesity, infertility, and asthma.

    “Our research highlights how plastics contribute to the early development of numerous chronic diseases that persist into adolescence and adulthood,” said study lead author and pediatrician Leonardo Trasande, MD, MPP. “To ensure children remain healthy and live longer lives, we must take strong action to reduce the use of these materials,” added Trasande, the Jim G. Hendrick, MD, Professor of Pediatrics at NYU Grossman School of Medicine.

    How Common Products Emit Dangerous Chemicals

    Trasande points out that these chemicals are present in many everyday products, such as food packaging, cosmetics, and paper receipts. Research shows that repeatedly using, heating, or treating plastics in certain ways can release microplastic particles and nanoparticles, which people then ingest.

    Studies also suggest that chemicals in plastics can trigger excessive immune responses (inflammation) and disrupt hormones that control vital biological processes. Scientists further believe these substances may affect brain development, with numerous studies linking early exposure to lower IQ and conditions like autism and attention deficit hyperactivity disorder (ADHD).

    Ways Families Can Minimize Exposure

    In addition to highlighting the risks, the Lancet review offers strategies for reducing plastic use and safeguarding public health.

    “There are easy and affordable measures parents can take to limit their children’s exposure to plastics,” said Trasande, director of NYU Grossman School of Medicine’s Division of Environmental Pediatrics and NYU Langone Health’s Center for the Investigation of Environmental Hazards.

    He recommends swapping plastic food containers for glass or stainless steel and avoiding microwaving or dishwashing plastic items to significantly reduce exposure.

    Trasande also highlights the important role of pediatricians and other healthcare providers in guiding families to make safer choices. He urges clinicians to work with schools and community organizations to educate children and teens about the potential risks of plastic exposure.

    Regulatory Measures and International Initiatives

    At the policy level, the authors call for stricter regulations to reduce nonessential plastic use, especially in low-income communities that already face significant health disparities.

    The review coincides with the latest United Nations negotiations in Geneva on the Global Plastics Treaty, an emerging agreement aimed at limiting worldwide plastic pollution, with over 100 countries backing legally binding production caps.

    Trasande emphasizes that the findings highlight the urgent need for a strong global treaty to protect both human health and the environment. He notes that while the economic influence of the plastics industry is often seen as an obstacle to new regulations, the health-related costs of plastic exposure are substantial, with his team estimating around $250 billion annually in the United States alone.

    Plastics and Their Impact on Healthcare

    The Global Plastics Treaty will be a central focus at NYU Langone Health’s 2025 Plastics, Human Health, and Solutions Symposium. Experts will discuss the latest microplastics research, recent policy updates, and the critical role of regulations in tackling this escalating public health issue.

    While the review underscores the health risks associated with plastics, the authors emphasize that the material remains vital in many medical applications. Plastics are used in equipment like ventilators and feeding tubes for premature infants, nebulizers for children with asthma, and masks that help prevent the spread of infectious diseases. The researchers clarify that their findings do not challenge the importance of plastics in healthcare but rather highlight the need to reduce unnecessary use in everyday items.

    Read the original article on: SciTechDaily

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  • Monthly Injection Reduces Body Weight by 16% in Landmark Obesity Study

    Monthly Injection Reduces Body Weight by 16% in Landmark Obesity Study

    It’s estimated that nearly half of all adults worldwide are overweight, and 16% are living with obesity
    Kaboompics.com / Pexels

    A new drug developed by California-based pharmaceutical company Amgen has shown strong potential as an effective obesity treatment. In a completed phase II trial, participants receiving a once-monthly injection of the drug—called MariTide—lost up to 16% of their body weight within a year.

    That level of weight loss is similar to the average results seen with the widely used weekly medication Ozempic. However, a once-a-month injection may be easier for patients to maintain and could be more practical for those in remote areas with limited access to frequent medical deliveries.

    The phase 2 trial included 592 adults over the age of 18 with a body mass index (BMI) over 30. Some participants were not only obese but also living with Type 2 diabetes.

    Monthly Injections Led to Up to 16% Weight Loss—Far Exceeding Placebo Results

    The findings were promising: those in the treatment group who received an injection every four weeks lost an average of 12.3% to 16.2% of their body weight after one year. In comparison, participants in the placebo group saw only a 2.5% average weight loss.

    Participants who had both obesity and diabetes experienced only slightly less weight loss than those without diabetes. Notably, their weight loss hadn’t plateaued by the end of the year, suggesting continued progress might be possible with ongoing treatment. The study’s findings were published this week in The New England Journal of Medicine.

    Discovery Chapter One: Meet MariTide

    MariTide Combines Two Hunger-Regulating Mechanisms to Support Weight Loss

    So how does MariTide work? Short for Maridebart Cafraglutide, the drug uses a dual approach to influence the body’s hunger and satiety signals. One component is a glucagon-like peptide-1 receptor agonist (GLP-1 RA), which mimics a natural hormone that tells the brain when the stomach is full. This is the same mechanism used in Ozempic and helps prolong feelings of fullness, making it easier to eat less.

    MariTide also blocks the GIP receptor, unlike some drugs that activate it. Animal studies suggest that inhibiting this pathway—especially alongside GLP-1 activity—can enhance weight loss by improving brain-to-body metabolic signaling.

    Designed with a long half-life, MariTide stays in the body longer and only needs to be taken once a month. While gastrointestinal side effects were common, they eased at lower or gradually increased doses.

    A 72-week phase 3 trial is now underway to see if MariTide can outperform the ~16% weight loss seen in phase 2, and to test its effectiveness for people with heart disease and sleep apnea.

    MariTide joins a wave of new obesity treatments, including a Chinese semaglutide-class drug finishing phase III trials, three new drugs from Novo Nordisk, and a pill from Monash University targeting weight loss without muscle loss.

    Read the original article on: New Atlas

    Read more: Does Obesity Prevent or Increase Dementia Risk?

  • Does Obesity Prevent or Increase Dementia Risk?

    Does Obesity Prevent or Increase Dementia Risk?

    Several dementia advocacy organizations recommend maintaining a healthy weight to lower the risk of dementia. However, certain studies have proposed that obesity could potentially offer protection against dementia. What does scientific research reveal about this matter?
    Credit: Pixabay

    Several dementia advocacy organizations recommend maintaining a healthy weight to lower the risk of dementia. However, certain studies have proposed that obesity could potentially offer protection against dementia. What does scientific research reveal about this matter?

    The link between obesity and dementia appears strong initially, as obesity in middle age is associated with a higher risk of dementia later in life. However, complexities arise. Despite rising obesity rates, dementia rates in the West have declined. Moreover, an “obesity paradox” suggests obesity may reduce dementia risk.

    Addressing Causality Challenges with Limited Data

    Determining causality is challenging due to data limitations. Randomized trials would clarify, but they’re impractical and unethical. Thus, researchers rely on observational studies, which have biases like reverse causation and confounding.

    Recent findings highlight childhood intelligence’s role. Lower childhood intelligence correlates with higher obesity risk and poorer cognitive skills in midlife. Therefore, the link between midlife obesity and cognitive decline may be influenced by childhood intelligence, emphasizing the need for a nuanced understanding.

    So, how can we address these bias issues? One innovative approach is conducting Mendelian randomization studies, often dubbed “nature’s randomized trial.”

    In these studies, researchers divide a large population into two groups solely based on whether they possess a gene (or genes) associated with obesity. As these genes are randomly inherited, this naturally randomizes the population into two groups balanced for all factors except obesity status.

    While not without potential biases, any differences in dementia risk are attributed directly to obesity.

    Several studies, at least ten, have employed this method to investigate if obesity influences Alzheimer’s disease, the most prevalent form of dementia. Only one study has hinted at a connection between the two.

    Thus, returning to the question: does obesity truly elevate dementia risk? As scientists caution, the absence of evidence doesn’t imply evidence of absence. In other words, lacking sufficient data to confirm the link doesn’t necessarily disprove it.

    Science progresses gradually. With continued data collection and advancements in techniques, a more definitive answer to this question will eventually surface.

    In the meantime, it’s prudent to heed the advice of dementia charities and strive to maintain a healthy weight. Doing so not only lowers the risk of various other significant health issues but might also mitigate the risk of dementia.

    Read the original article on: Science Alert

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  • Obesity Breakthrough: Losing Weight Without Eating Less

    Obesity Breakthrough: Losing Weight Without Eating Less

    Researchers have discovered how a cluster of specialized cells in the brain can cause obesity. Credit: Pixaobay

    Scientists have unraveled how a group of astrocytes, unique brain cells located in the hypothalamus, induces obesity in mice. Furthermore, their research pinpointed a medication that blocked this mechanism, resulting in weight reduction without affecting appetite or food consumption.

    The hypothalamus, a vital region in the brain responsible for regulating food intake and energy expenditure, harbors the majority of neurons involved in controlling feeding and body weight.

    Gamma-aminobutyric acid (GABA), the predominant neurotransmitter in the hypothalamus, acts on GABA A receptors. As an inhibitory neurotransmitter, GABA plays a crucial role in maintaining the body’s energy balance by determining hunger and satiety signals. When you reach a state of fullness, GABA inhibits the hunger signal, preventing overeating.

    Unraveling the Brain’s ‘Hunger Center’ and Its Role in Fat Metabolism

    The lateral hypothalamus (LH), also referred to as the lateral hypothalamic area (LHA), is recognized as the brain’s ‘hunger center.’ One of its primary roles is to stimulate feeding behavior; when activated, it induces the sensation of hunger. Although it’s known that LH neurons are connected to fat tissue and are involved in fat metabolism, their precise mechanism in regulating fat metabolism has remained unclear. New research led by the Institute for Basic Science in South Korea has investigated cells in the lateral hypothalamus of mice, with a specific focus on the role played by a particular type of cell called astrocytes in the regulation of fat metabolism.

    Within the hypothalamus, there exists a cluster of neurons that specifically expresses the alpha-5 subunit of the GABA A receptor, known as GABRA5. Furthermore, the study revealed that in diet-induced obese mice, there was a notable decrease in the pacemaker firing activity of the GABRA5 neurons. Pacemaker neurons exert influence over neuronal networks by generating intrinsic rhythmic bursts of activity.

    A Key to Controlling Weight Through Brown Fat Metabolism

    Inhibiting GABRA5 using chemogenetics in mice resulted in reduced thermogenesis in brown adipose tissue (BAT), commonly known as brown fat, leading to fat accumulation and weight gain. Reactivating the hypothalamic GABRA5 neurons, on the other hand, caused weight loss, indicating that these neurons serve as a weight regulation switch.

    Upon closer examination, researchers found that reactive astrocytes in the LH were responsible for controlling GABRA5 neuron activity. Unlike typical astrocytes that carry out metabolic and neuroprotective functions in the central nervous system, reactive astrocytes, triggered by pathological conditions, reduce these supportive roles.

    In obese mice, these reactive astrocytes exhibited elevated levels of monoamine oxidase-B (MAO-B), an enzyme involved in GABA synthesis by astrocytes. Overexpression of MAO-B inhibited the surrounding GABRA5 neurons. However, when researchers suppressed the MAO-B gene in reactive astrocytes, it reduced GABA secretion, reversing the inhibition. This, in turn, increased thermogenesis in the obese mice’s fat tissues, resulting in weight loss even when they consumed a high-calorie diet. These findings suggest that targeting the MAO-B enzyme produced by reactive astrocytes could offer an effective approach to obesity treatment without impacting appetite.

    Identifying Reactive Astrocytes as Obesity Culprits

    “Previous approaches to address obesity by targeting the hypothalamus primarily focused on neuronal pathways linked to appetite control,” explained Moonsun Sa, the lead author of the study. “To address this limitation, we shifted our attention to non-neuronal astrocytes and pinpointed reactive astrocytes as the underlying cause of obesity.”

    Monoamine oxidase-B (MAO-B) is a well-recognized therapeutic target in the treatment of Parkinson’s disease. A newly developed reversible and selective MAO-B inhibitor, KDS2010, has displayed promise as a Parkinson’s disease treatment and is currently undergoing early clinical trials. In the present study, researchers tested the effects of KDS2010 on their obese mouse models and observed that the drug resulted in a “significant reduction” in fat accumulation and weight without affecting food intake.

    “In light of the World Health Organization’s designation of obesity as the ’21st century’s emerging infectious disease,’ we see KDS2010 as a potential next-generation obesity treatment that can effectively combat obesity without suppressing appetite,” commented C. Justin Lee, the corresponding author of the study.

    This research was published in the journal Nature Metabolism, and the video below, produced by the Institute for Basic Science, showcases the study’s findings.

    A new breakthrough in obesity research allows you to lose fat while eating all you want

    Read the original article on: New Atlas

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