RNC – Health Page

Twelve-year-olds in the U.S. live in a world where smartphone access feels almost unavoidable, yet the decision to give a device at this age carries far more weight than some parents realize. Many families assume that a phone is simply a tool for convenience or safety, but the emerging data signals something deeper: Early access appears to shape how your child sleeps, handles stress, and interprets their social world. Those early patterns influence confidence, learning, emotional steadiness, and even how your child relates to their own body. When a child enters the digital world before they have the emotional and neurological maturity to handle constant stimulation, their developing brain may adapt to an environment that never truly shuts off. That shift is thought to affect how they regulate attention, manage relationships, and interpret social pressure. You see the results in subtle ways first — restlessness, heavier reliance on screens for comfort, later bedtimes — but the long-term patterns reveal why this conversation deserves your full attention. Your decisions about device access influence far more than screen habits; they shape foundational systems tied to sleep, mood balance, and healthy development. Early Phone Ownership Shapes Health in Powerful Ways A study published in Pediatrics investigated how early smartphone access influences depression, obesity, and sleep disruption in adolescents.1 The researchers set out to understand whether owning a smartphone at a younger age places a child on a different health trajectory than peers who don’t have these devices. They analyzed data from 10,588 children in early adolescence, an age defined by rapid emotional growth and heightened sensitivity to social feedback. The findings showed higher odds of depression, obesity, and insufficient sleep among those who owned a smartphone at age 12 compared to those who did not. • Health risks rise dramatically when phones enter a child’s life too soon — According to the study, adolescents who owned smartphones at age 12 had a 31% higher risk of depression, a 40% higher risk of obesity, and a 62% higher likelihood of insufficient sleep compared to peers without phones. When you translate that into your child’s daily life, it means earlier ownership may shift mood, appetite, and energy patterns in ways that researchers say build with each earlier year of ownership — though the cited study followed outcomes only through age 13, not into adulthood.2 • The earlier a child gets a phone, the more those risks build year after year — Each year earlier that a child received a smartphone increased the odds of obesity by 9% and insufficient sleep by 8%. The researchers described this pattern as a “per-year effect,” meaning the timing itself matters, not just the presence of a phone. This is consistent with the idea that delaying smartphone access may reduce cumulative risk, similar to how delaying exposure to other health-related stressors is thought to support long-term health. • New smartphone access is linked to sharply diverging health paths — Among adolescents who did not own a smartphone at age 12, those who acquired one over the following year had a 57% higher likelihood of reporting clinical-level psychopathology and a 50% higher likelihood of insufficient sleep at age 13. Even after adjusting for their baseline mental health, these differences held steady. This means the shift wasn’t simply explained by preexisting issues. The researchers describe this as an association, not proof that phone acquisition alone caused the change in behavioral and emotional patterns that followed. • Sleep disruption from early phone exposure is a significant concern — While the study didn’t analyze specific app use or timing, insufficient sleep associated with phone ownership often reflects stimulation, nighttime alerts, late-night scrolling, and exposure to blue light, which disrupts melatonin, a hormone that regulates sleep-wake cycles. Melatonin is primarily produced in your mitochondria in response to near-infrared light exposure, and healthy evening melatonin release depends partly on winding down light and screen exposure before bed. When melatonin drops in the evening, your child takes longer to fall asleep and experiences more fragmented rest. This pattern may reinforce fatigue-driven eating, lower movement, and mood instability. • Smartphones expose children to increased social stressors — Smartphones expose adolescents to constant social feedback loops, including comparison, peer evaluation, and subtle forms of social exclusion. These experiences may influence cortisol — your body’s main stress hormone — which plays a role in energy balance, appetite, sleep quality, and emotional resilience. When your child receives this type of stimulation before their brain has matured, stress patterns may form that are more difficult to unwind later. Early Access to Smartphones May Alter Emotional Development in Lasting Ways A related study published in the Journal of Human Development and Capabilities evaluated how childhood smartphone ownership influences emotional stability and psychological well-being in young adulthood.3 The researchers used data from the Global Mind Project, a worldwide mental health database, to determine whether the age a child receives a smartphone shifts measurable outcomes years later. The study population included 18- to 24-year-olds across multiple global regions, offering a broad view of how early smartphone exposure aligns with later emotional outcomes. • Early phone ownership predicts deeper emotional struggles in young adulthood — Individuals who received a smartphone before age 13 experienced more suicidal thoughts, higher aggression, lower emotional resilience, and weaker self-worth as young adults. Girls reported the greatest emotional strain, while boys showed increased instability and reduced empathy compared to peers who received smartphones later. Young adults who had smartphones earlier in childhood also experienced more symptoms described as “detachment from reality,” which means trouble staying grounded in real-world interactions and emotional experiences. Early ownership was also associated with hallucinations, or perceiving things that aren’t present. The authors explained that these patterns were consistent across geographic regions, emphasizing that the phenomenon is not restricted to any single culture or social environment. • The role of technology-driven stressors in worsening mental health — As the authors stated, emotional deterioration was linked to “social media access, cyberbullying, disrupted sleep, and poor family relationships,” all of which were more common among early smartphone recipients. Cyberbullying refers to harassment or humiliation through digital platforms, and this form of stress often carries deeper psychological weight because it follows the child everywhere, without a break. Early access also increased exposure to algorithm-driven content, which reinforces comparison, insecurity, and compulsive scrolling patterns that affect emotional regulation. • The earlier the phone, the worse the long-term results — The researchers noted a clear gradient: the younger the child at the time of ownership, the greater the severity of mental health symptoms in adulthood.4 The threshold at age 13 appeared especially important because neurological development at that age includes growth in impulse control and emotional regulation. When a child enters digital environments without these capacities in place, their coping systems may become shaped more by overstimulation than by healthy interpersonal feedback. • Girls lose resilience and boys lose calm when phones arrive too early — Females who received smartphones before age 13 showed the largest drops in self-worth, confidence, and emotional resilience. These traits involve the ability to handle stress, recover from setbacks, and maintain a stable sense of identity. For boys, the steepest changes involved emotional volatility, lower calmness, and reduced empathy. Early smartphone exposure disrupted the specific emotional strengths each group typically develops during adolescence. • How family dynamics influence risk — According to the researchers, poor family relationships intensified the negative effects of early smartphone ownership, suggesting that children with less support experienced the steepest emotional declines. When a child receives a smartphone early without strong relational anchors, the device may become a significant emotional reference point, shaping beliefs, behaviors, and coping skills. It’s worth noting that both studies discussed here are observational: They show associations between the timing of smartphone ownership and later health and mental health outcomes, not proof that smartphone ownership by itself causes these outcomes. The Journal of Human Development and Capabilities researchers note this as a limitation of their own work, even as they argue the scale of the potential impact justifies a precautionary approach. Practical Steps to Protect Your Child’s Health in a Digital World Your child’s brain and body respond to their environment more than you might realize, and early smartphone access may shape sleep, stress, and emotional development in ways that influence their long-term well-being. That means your solutions have to target not only early smartphone exposure but also the root causes identified in the research: disrupted sleep, overstimulation, reduced movement, and constant exposure to digital social pressure. To take back control, structure your child’s environment with clear boundaries that support healthy rhythms. Straightforward steps create real progress without turning your home into a battleground. 1. Delay smartphone access until your child shows strong emotional regulation skills — You may help support healthy development when you match device access to your child’s maturity rather than their age alone. If your child struggles with big emotions, impulsive choices, or social overwhelm, delaying a smartphone may help protect their confidence and long-term emotional health. When you present this as a skill your child is growing into rather than a hard restriction, they see that the goal is to make them stronger, not to punish them. 2. Keep smartphones out of the bedroom at all times — Protect your child’s sleep by removing nighttime triggers that may disrupt melatonin, disrupt sleep cycles, and interfere with emotional stability. This important boundary gives their nervous system a break from alerts, scrolling, and blue light. I recommend setting a family rule that all devices stay in a shared spot outside bedrooms, and taking regular phone breaks to manage smartphone dependence and give their mind a rest. 3. Limit wireless device use and reduce your child’s exposure to EMFs — Your child’s developing brain is thought to be more sensitive to wireless radiation than an adult’s, as their thinner skull bones are believed to offer less protection. If your child is constantly surrounded by wireless devices, they’re exposed to EMF levels that could disrupt mood regulation, impair focus, and raise risks of neurological problems over time. I recommend treating wireless access as something used only when absolutely needed, not as a default. To support your child’s long-term well-being, swap wireless connections for wired ones, turn off Wi-Fi when it’s not in use, and keep phones away from their body entirely. If your child reaches for a smartphone out of habit, build a simple routine together that replaces wireless use with safer alternatives. Treat it like a daily challenge they get to master, which strengthens their sense of control and lowers their total EMF load without creating conflict. 4. Create a predictable home routine that anchors sleep, movement, and downtime — You build stability by giving your child a rhythm that balances stimulation with recovery. If your child thrives on structure, set repeating anchor points throughout the day: morning sunlight, set meal times, walking breaks, and an early wind-down routine. These anchors may help support healthy regulation of stress hormones and support mood resilience, especially for children who are regularly exposed to digital environments. 5. Use device rules that strengthen family connection instead of fueling conflict — Consistent rules give your child a clear framework, and that makes daily life smoother for both of you. Useful boundaries include things like no phones before school, no devices in bedrooms, and screen-free hours in the evening. If your child pushes back, involve them in choosing the exact times or places where phones stay off-limits. You might agree on a “family tech-off night,” or designate a basket where phones go when everyone is home. Once they see why these rules matter — and once they help decide them — they’ll feel respected instead of controlled, and that shift may lower conflict while raising personal accountability. This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen. FAQs About Early Smartphone Use Q: Why is age 12 such a sensitive time for smartphone ownership? A: Age 12 sits in a window of rapid emotional and neurological development. The research suggests that receiving a smartphone at 12 or earlier is associated with disruptions in sleep, stress responses, and emotional balance. Earlier ownership also is associated with shifts in eating patterns, attention, and emotional coping skills in ways that appear to build year after year. Q: What health risks rise when a child gets a smartphone too early? A: Children who own a smartphone at age 12 face higher risks of depression, obesity, and insufficient sleep. These shifts influence confidence, learning, appetite regulation, and stress responses. For children who didn’t have a phone at 12, getting one between ages 12 and 13 was associated with sharply higher odds of clinical-level emotional symptoms by age 13. Q: How does early smartphone access affect long-term mental health? A: Young adults who received smartphones before age 13 reported more suicidal thoughts, lower emotional resilience, weaker self-worth, and symptoms of detachment from reality. Girls showed the greatest drops in confidence and resilience, while boys showed more emotional instability and reduced empathy. Q: Why is sleep disruption such a key part of the problem? A: Smartphones interfere with melatonin, the hormone that controls sleep-wake cycles. Nighttime scrolling, alerts, and bright screens delay sleep, fragment rest, and increase fatigue. Poor sleep then affects appetite, weight, stress tolerance, and emotional regulation. Q: What practical steps help protect my child? A: Delay smartphone access until your child demonstrates strong emotional regulation, keep phones out of bedrooms, limit wireless and EMF exposure, create a predictable daily rhythm, and use simple device rules that encourage cooperation rather than conflict. These steps target the root causes — overstimulation, sleep disruption, and emotional overload — and may support healthier long-term development.

For decades, xanthan gum has slipped into the food supply with almost no scrutiny. Manufacturers add it to gluten-free breads, salad dressings, sauces, ice cream, protein shakes, and countless packaged foods because it thickens, stabilizes, and improves texture without changing flavor. Many people don’t think twice when they see it on an ingredient label. Yet that confidence rests on surprisingly little long-term safety data, and most of what does exist focuses on surface-level markers — weight, blood sugar, cholesterol — that can look perfectly normal while something deeper goes wrong. Xanthan appears across so many product categories that anyone eating a modern processed diet likely consumes it multiple times a day without realizing it. People with swallowing disorders may take in even more, since xanthan gum-based thickeners are standard in clinical nutrition. The question scientists have largely failed to ask is what happens inside the digestive tract when that kind of exposure continues week after week. An animal study finally looked in the right place, and what the researchers found beneath the surface contradicted everything the conventional safety profile would predict. Next, I’ll break down exactly what they discovered and why those changes deserve your attention. Xanthan Gum Triggered Hidden Inflammation in the Colon The study, published in PLOS One, investigated what happened when adult Wistar rats consumed xanthan gum every day for 10 weeks.1 The researchers examined the colon itself, measuring inflammatory chemicals, immune cell activity, gut barrier proteins, and changes in the gut microbiome. They also tested three different xanthan gum doses designed to reflect different patterns of human consumption, from people who regularly eat processed foods to those who rely on xanthan gum-based thickeners because of swallowing disorders. The researchers wanted to determine whether continuous exposure altered the intestinal environment. That’s important because changes inside your digestive tract often develop long before routine blood work reveals a problem. • The colon became inflamed even though the animals looked healthy on the outside — After 10 weeks, the rats showed no significant differences in body weight, food intake, body fat, blood glucose, triglycerides, cholesterol, or HDL cholesterol compared to animals that didn’t receive xanthan gum. If a doctor looked only at those numbers, everything would appear normal. Yet microscopic examination of the colon told a very different story. The researchers found that xanthan gum promoted “an inflammatory state” across all doses and concluded that “dietary xanthan gum induced moderate-grade inflammation and modified the colon gut barrier.” • Immune cells accumulated inside the intestinal wall as xanthan gum intake continued — When researchers examined colon tissue under the microscope, they found inflammatory cells had infiltrated the intestinal wall, especially in the groups receiving the medium and highest xanthan gum doses. Most of these cells were lymphocytes, a type of white blood cell involved in long-lasting immune responses rather than short-lived reactions. The researchers also assigned inflammation scores based on the severity of tissue changes. Compared to the control animals, both the medium- and highest-dose groups had significantly higher scores, confirming that the inflammatory response was measurable rather than simply a microscopic observation. • Proteins that help control what passes through your intestinal lining shifted in the wrong direction — Researchers found greater amounts of Claudin-2 in the xanthan gum groups. Claudin-2 is a protein that acts like adjustable caulking between intestinal cells; it controls how tightly those cells seal together. When Claudin-2 levels rise above normal, the seal loosens, allowing substances to slip through the intestinal lining that would normally stay inside the digestive tract. The researchers also observed higher levels of inflammatory signaling molecules known to increase Claudin-2 and weaken the gut barrier, creating conditions that reinforce inflammation instead of allowing the tissue to recover. • The gut microbiome changed in subtle but meaningful ways — Xanthan gum didn’t significantly alter the dominant bacterial groups known as Firmicutes and Bacteroidetes or the overall diversity of the microbiome. Even so, the highest-dose group developed significantly higher levels of Elusimicrobiota, a relatively rare group of gut bacteria that scientists are still working to understand, while the medium-dose group showed a trend toward more Patescibacteria, another uncommon group of microbes often found in complex microbial communities. These shifts matter not because scientists fully understand what these bacteria do, but because they didn’t occur in isolation — statistical analysis linked them directly to the inflammatory markers and barrier protein changes happening in the same tissue, suggesting the microbiome was responding to the inflammatory environment xanthan gum created rather than changing randomly. • The findings offer a biological explanation for earlier concerns about xanthan gum — The researchers explained that their results support previous reports linking xanthan gum-containing thickeners with serious intestinal problems such as necrotizing enterocolitis — a life-threatening condition in which intestinal tissue becomes severely inflamed and begins to break down — in premature infants. Although this study involved adult rats, it identified specific biological changes, including chronic inflammation, altered gut barrier proteins, and microbiome shifts, that help explain why long-term xanthan gum exposure deserves closer attention. These findings come from an animal study. Additional research is needed to determine whether the same effects occur in humans. How to Reduce Your Xanthan Gum Exposure at the Source If your goal is a healthier gut, the smartest place to start is with the foods that introduce the problem in the first place. The research in this article showed changes in the colon after long-term xanthan gum exposure, not because of a nutrient deficiency but because of repeated intake of a common food additive. That means your greatest opportunity is to reduce the amount that enters your diet every day instead of searching for something that simply masks the effects afterward. 1. Find the hidden sources of xanthan gum before you eat them — Try a one-week label audit. Xanthan gum appears in a wide variety of foods, including gluten-free breads, tortillas, wraps, salad dressings, sauces, gravies, soups, protein powders, meal replacement shakes, nondairy products, ice cream, frozen meals, and many packaged snacks. Make it a habit to read ingredient labels before you buy packaged foods. Every time you spot xanthan gum, choose a different product that doesn’t contain it whenever possible. You might be surprised by how often it appears. Once you recognize where it hides, avoiding it becomes much easier and eventually turns into second nature. A simple rule of thumb: spend most of your shopping time around the perimeter of the grocery store where fresh foods are located, and less time in the center aisles where xanthan gum is most likely to appear. 2. Build your meals around fresh whole foods instead of products that rely on stabilizers — The easiest way to avoid xanthan gum is to eat foods that don’t need it in the first place. Fresh fruits, properly prepared vegetables, whole-food carbohydrate sources that fit your digestive tolerance, high-quality animal protein, and simple homemade meals eliminate many processed food additives. I also recommend avoiding the highly processed foods that commonly contain xanthan gum along with other unwanted ingredients. That includes many packaged sauces, gluten-free convenience foods, protein bars, frozen meals, salad dressings, and similar products. Cooking more of your own meals gives you complete control over every ingredient. If a recipe calls for xanthan gum as a thickener, try whole-food alternatives instead — pureed cooked potato or vegetables, or a simple reduction, can often achieve the texture you need without any additive at all. 3. Support your gut instead of overwhelming it with more processed foods — If your digestion already feels off, don’t assume adding more fiber or more processed “health foods” solves the problem. Focus first on removing foods that repeatedly irritate your digestive tract, including not only xanthan gum but also seed oils, which are high in linoleic acid (LA); they weaken your colon’s protective lining and make it harder for beneficial bacteria to thrive. Begin with simple, easy-to-digest meals that minimize excessive fermentation and reduce the release of endotoxins — toxic compounds produced when certain gut bacteria break down. This gives your intestinal lining a better environment to recover. As your digestion becomes more consistent, gradually increase your carbohydrate intake using foods that your gut handles comfortably. Start with whole fruit and well-cooked starches such as white rice, which provide glucose to fuel your cells without placing excessive demands on an already stressed digestive system. Next, introduce root vegetables, followed by non-starchy vegetables, then starchy vegetables such as squash and sweet potatoes. Save beans, legumes, and minimally processed whole grains for last, and only if your digestion remains stable. Most adults thrive on about 250 grams of carbohydrates per day. 4. Choose fats that support better metabolic health instead of processed seed oils — Xanthan gum often appears in the same packaged foods that contain seed oils. Those oils add another unnecessary burden to your metabolism. I recommend replacing soybean, corn, sunflower, safflower, cottonseed, grapeseed, and canola oils with more stable fats such as grass fed butter, ghee, or tallow. Avoid nuts and seeds as they’re also high in LA. FAQs About Xanthan Gum and Colon Inflammation Q: Does this study prove xanthan gum is harmful to people? A: No. This research was conducted in rats, not humans, so it doesn’t prove the same effects occur in people. However, it showed that long-term xanthan gum consumption caused measurable inflammation, changes to proteins that regulate the gut barrier and shifts in the gut microbiome, giving scientists a biological reason to study its long-term effects in humans more closely. Q: Why didn’t routine health measurements reveal a problem? A: The rats maintained normal body weight, blood sugar, cholesterol, and other metabolic markers throughout the study. The concerning changes only became apparent when researchers examined the colon tissue under a microscope, showing that gut inflammation can develop long before standard health measurements change. Q: What happened to the intestinal lining after long-term xanthan gum intake? A: Researchers found increased amounts of proteins associated with a leakier intestinal barrier, along with higher levels of inflammatory signaling molecules. Together, these changes suggest the colon became less effective at keeping unwanted substances inside the digestive tract and more prone to ongoing inflammation. Q: Where is xanthan gum commonly found in the food supply? A: Xanthan gum is widely used as a thickener and stabilizer in processed foods. Common sources include gluten-free breads and tortillas, salad dressings, sauces, soups, protein powders, meal replacement shakes, frozen meals, nondairy products, ice cream, and many packaged snack foods. Reading ingredient labels is the easiest way to identify and avoid it. Q: What’s the most effective way to reduce your exposure to xanthan gum? A: Focus on replacing packaged foods with fresh, whole foods whenever possible. Preparing more meals at home, checking ingredient labels before you buy packaged products and choosing alternatives that don’t contain xanthan gum are practical ways to reduce your daily exposure while also cutting back on many other processed food additives. This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen. Test Your Knowledge with Today’s Quiz! Take today’s quiz to see how much you’ve learned from yesterday’s Mercola.com article. During rapid weight loss with GLP-1 medications, what type of tissue may also be lost along with fat? Bone tissue Muscle tissue Glucagon-like peptide-1 (GLP-1) medications can lead to muscle loss along with fat loss, which may reduce strength and lower resting metabolism. Learn more. Nerve tissue Skin tissue

Antidepressants have a long, documented history of side effects while taking them. For example, they’ve been associated with blurry vision, increased anxiety, constipation, sleep disturbances, and loss of libido. Research suggests roughly 1 in 3 antidepressant users in primary care may no longer benefit from the drugs and could be ready to stop — and among those who do stop, about 56% report withdrawal symptoms.1 However, withdrawal symptoms are a real trade-off, and for some people they become severe enough that they resume the medication in an effort to feel functional again. Long-Term Antidepressant Withdrawal Is Well-Documented A study published in Epidemiology and Psychiatric Sciences set out to learn what happens after people stop taking antidepressants. Specifically, the researchers investigated a condition known as post-acute withdrawal syndrome (PAWS), where symptoms continue long after someone stops their medication.2 This paper was the first systematic review with a meta-narrative synthesis of its kind focusing solely on antidepressants like selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs). Of the 1,286 records screened, seven studies met the selection criteria: three analyses of online self-reports from peer-support groups, one randomized controlled trial, one case series, one case report, and one prospective cohort study — an evidence base that the authors themselves describe as limited. They also didn’t focus on patients in the early stages of stopping antidepressants — they focused on those experiencing symptoms months, or even years, after stopping. • The effect of PAWS on your brain health — The researchers noted that PAWS involves a multitude of symptoms, including “dizziness, vertigo, tremor, nausea, insomnia, fatigue, mood dysregulation, anxiety, panic, irritability and agitation.” In severe cases, those in withdrawal report suicidal thoughts and behavior.3 • Symptoms can last for a long time — According to the studies reviewed, lingering symptoms lasted anywhere from 1.5 to 166 months (around 13.8 years). That upper figure is an outlier at the far end of a wide range, and it comes largely from online self-reports rather than controlled follow-up. Doctors usually tell patients that stopping antidepressants will be uncomfortable for a week or two, but this data tells a very different story. • Paroxetine was linked to the most problems — The most consistent risk factor identified across these studies was long-term use of paroxetine, though the authors caution that most of the included studies could not speak to this question. According to the researchers: “Two of the included studies indicate that in particular long-term paroxetine use may carry an increased risk of PAWS, but most studies were uninformative on this subject. One analysis of online self-reports further showed that the duration of tapering was positively correlated with the duration of withdrawal symptoms, suggesting that patients experiencing more persistent withdrawal symptoms try to taper more slowly.” • PAWS is not a relapse — It’s not your original depression coming back. PAWS has its own distinct pattern, and the symptoms often feel different than the ones that led you to take antidepressants in the first place. That distinction is key because it helps explain why people may be misdiagnosed as having a “relapse,” when in fact they’re going through withdrawal:4 “[I]t appears that in both clinical research and practice, protracted and persistent withdrawal symptoms are frequently misdiagnosed as a relapse of the primary mental health condition (typically depression) or new emergent mental disorders, the latter being specifically embedded in the concept of persistent post-withdrawal disorders,” the study authors said. • Stopping medication versus continuing usage — One noteworthy finding is that people who tapered off their antidepressant usage still had more recorded withdrawal symptoms than those who stayed on the medication. The researchers cited a 2021 randomized controlled trial (RCT) published in The New England Journal of Medicine. Here, 478 patients were split into two groups — maintenance and discontinuation. By the end of 52 weeks, 135 people in the discontinuation group experienced withdrawal symptoms, and 92 in the maintenance group.5 Going deeper into the findings, the researchers noted:6 “In this study, 39 weeks after patients had started tapering citalopram, fluoxetine, sertraline or mirtazapine, the number of recorded withdrawal symptoms was still significantly increased compared to patients maintained on their antidepressant medication. Of note, in the design of this RCT, the popular antidepressant drugs paroxetine and venlafaxine were deliberately excluded, because, as written by the authors, both are known to cause marked withdrawal symptoms when treatment is discontinued.” • Effective treatment of PAWS is needed — After analysis, the researchers suggest that more RCTs are needed regarding PAWS. However, they recommend that the focus need to be on effective treatments, since there is little information regarding this topic: “[R]igorous long-term RCTs are required to test the efficacy of treatment and management strategies. These studies would inform clinicians about effective interventions to mitigate the severity and duration of this impairing syndrome, as to date not a single clinical intervention has been formally evaluated.” PAWS Is More Common Than You Think A meta-analysis published in The Lancet Psychiatry investigated 79 studies — 44 RCTs and 35 observational studies — with a total of 21,002 participants. The review encompasses different treatment settings, and types of antidepressants, offering a bird’s eye view of PAWS.7 • Many are affected once medication is stopped — The team found that 31% of people who stop antidepressants experience some kind of withdrawal symptom. Severe ones were less common — 2.8% of everyone who discontinued an antidepressant, compared with 0.6% of those who discontinued placebo. According to the analysis, symptoms typically began within a few days of stopping the drug, but in many cases, they didn’t fully resolve for weeks. In addition, the presence of symptoms wasn’t necessarily linked to how long someone had taken the medication — a meta-regression found no significant association between withdrawal incidence and duration of antidepressant treatment, which ranged across the included studies from one to 156 weeks. • What the 31% means once placebo is accounted for — The authors’ bottom-line estimate is lower than the raw figure. Subtracting the symptoms reported after placebo discontinuation, they put the incidence of genuine antidepressant withdrawal at “approximately 15%, affecting 1 in 6 to 7 patients who discontinue their medication” — a figure they say should inform patients “without causing undue alarm.”8 • Expectation alone can produce symptoms — People who stopped a placebo still reported symptoms at a rate of 17%, or roughly 1 in 6. The authors describe these as non-specific or “discontinuation-like” symptoms, consistent with a nocebo effect in which the expectation of discomfort produces real symptoms. • Severity and type of symptoms weren’t uniform — Specifically, desvenlafaxine, venlafaxine, imipramine, and escitalopram were associated with the highest frequency of symptoms, while imipramine, paroxetine, and desvenlafaxine or venlafaxine were associated with greater symptom severity. In contrast, drugs like fluoxetine (Prozac), which linger longer in the bloodstream, showed a much lower rate of withdrawal complaints. The researchers also suggested that the half-life of these drugs (how long they remain in the body) plausibly affects not just the severity of the symptoms, but their time of appearance as well. • What the evidence says about tapering — Notably, this featured meta-analysis itself found no difference between studies that tapered the drug and studies that stopped it abruptly (31% versus 29%). The authors nonetheless point to separate research on how tapering is done:9 “Tapering of antidepressants is recommended in most guidelines, and there is research suggesting that prolonged and hyperbolic tapering of antidepressants will substantially reduce (although not completely exclude) withdrawal effects and increase the likelihood of successful discontinuation of antidepressants.” The same authors add that hyperbolic tapering has also been criticized and, because its pragmatic feasibility is limited, may not be indicated for every patient. Critics Say the Effects of Antidepressants Are Being Downplayed Antidepressants are one of Big Pharma’s moneymakers. According to a market analysis report from Precedence Research, the global antidepressant market was valued at $19.53 billion in 2025, with North America contributing 47% of market revenue in 2024.10 That said, the labeling that acknowledges these side effects was imposed by regulators rather than volunteered by industry. Since mid-October 2004, the U.S. Food and Drug Administration (FDA) has required manufacturers to place a black box warning on all antidepressants distributed in the United States, stating that the medications “increase the risk of suicidal thinking and behavior (suicidality) in children and adolescents with major depressive disorder (MDD) or other psychiatric disorders.” The expanded warnings section adds that anxiety, agitation, panic attacks, insomnia, irritability, hostility, impulsivity, akathisia, hypomania and mania “have been reported in adult and pediatric patients” treated with these drugs.11 Despite these warnings, industry-aligned research continues to characterize these effects as minor — a framing that critics say understates the harm patients report. • Using science to give an air of legitimacy — In a report by investigative journalist Maryanne Demasi, Ph.D., she criticizes a 2025 JAMA Psychiatry meta-analysis of 50 studies and 17,828 participants12 which concluded that the mean number of discontinuation symptoms one week after stopping was “below the threshold for clinically significant discontinuation syndrome” — a finding widely reported as showing that withdrawal is only “mild.”13 One of the reasons Demasi did her analysis is because of the prestige behind the journal. When it releases an influential study, consumers and medical practitioners tend to accept that the findings are true and accurate. • Media is brought in to help — Demasi argues that industry-aligned researchers mobilized mainstream media to push a narrative that antidepressants can be slowly stopped and, as mentioned above, only produce mild side effects in doing so: “The authors mobilised a rapid media campaign to shape the public narrative, with the Science Media Centre issuing expert commentary to ‘reassure both patients and prescribers’ that most withdrawal symptoms were ‘not clinically significant.’” • The methodology is flawed — Digging deeper into the issue, Demasi broke down the logic of the JAMA Psychiatry meta-analysis. According to her findings, the studies used in the review are either biased or poorly designed. For example, she pointed out that the study followed patients for just two weeks — this isn’t applicable to antidepressant users in America, as half of them have already been taking these medications for more than five years. Demasi continues: “Worse, many trials enrolled patients already taking antidepressants — then abruptly withdrew them before randomisation. As a result, those assigned to placebo experienced withdrawal symptoms that blurred the difference between treatment and control groups, artificially minimising the harms.” • Industry funded most of the included studies — Demasi noted that most of the studies included in the meta-analysis were funded by the pharmaceutical industry. Furthermore, the researchers excluded medications such as paroxetine and escitalopram, which are already strongly linked to severe PAWS. For context, the Lancet Psychiatry meta-analysis cited earlier ran its own funding subgroup analysis and found little difference between industry-funded and independently funded studies (31% versus 28%), so funding alone does not account for the range of estimates in this literature.14 • A firsthand account of PAWS — In an interview with National Public Radio (NPR),15 a Canadian patient named Phillipa Munari described taking Effexor (venlafaxine) for 10 years. When she decided to stop taking it, problems started to appear even with the help of a doctor to taper it off. According to Munari, she developed nerve pain, as well as chronic pain in her neck and shoulders. To make matters worse, she also had severe anxiety — all of which she didn’t have before. In an effort to manage her health issues, she went back to taking Effexor and then weaned off it again, much more slowly the second time. • The effects of PAWS can be lasting — Munari shared that after her second round of Effexor (with a better tapering plan), her nerve pain and fatigue improved. However, the anxiety worsened. She describes about two years of severe symptoms and roughly four more years beyond that before she felt fully recovered. Exercise Is a Powerful Support for Your Mental Health If you’ve been feeling the blues lately, it’s worth knowing that a pill isn’t the only avenue — supporting the very systems that have been thrown off balance matters, too. And one of the most accessible ways to do that is getting regular exercise. In addition, decisions about starting or stopping a medication will need to be made with a qualified health care provider. Exercise is not just a mood booster. Research suggests it may help support brain plasticity, nervous system regulation, and energy production at the cellular level. Barring any serious injury or physical ailment, I believe that it’s one of the best ways to support your mental health because it’s free and something that you can do right away. • • Exercise compares favorably with standard care — In an umbrella review of 97 reviews covering 1,039 trials and 128,119 participants, published in the British Journal of Sports Medicine, researchers reported that physical activity was extremely beneficial for symptoms of depression, anxiety, and distress — about 1.5 times more effective than counseling or the leading medications. As noted by the lead author Ben Singh, Ph.D.:16 “Physical activity is known to help improve mental health. Yet despite the evidence, it has not been widely adopted as a first-choice treatment … Higher-intensity exercise had greater improvements for depression and anxiety, while longer durations had smaller effects when compared to short and mid-duration bursts.” • Any exercise is better than nothing — Singh noted that moving your body, no matter how you do it, is beneficial. He explains:17 “We also found that all types of physical activity and exercise were beneficial, including aerobic exercise such as walking, resistance training, Pilates, and yoga. Importantly, the research shows that it doesn’t take much for exercise to make a positive change to your mental health.” • Start with a walk — While it’s tempting to start off with an intense session at the gym, you can already gain plenty of benefits by going for a walk. In my interview with Dr. James O’Keefe, he noted that it’s a great way to boost your fitness — an average of 10,000 steps a day is associated with meaningful benefits. It’s also a moderate-intensity activity that is difficult to overdo for most people, which makes it sustainable as a daily habit. Aim for about an hour of walking a day. • Strength training complements walking — Lifting weights is another beneficial strategy that goes hand in hand with your daily walks, however, it’s important that you don’t overdo it. According to O’Keefe, observational data suggest the additional mortality benefit appears to flatten,18 and may reverse, beyond roughly 130 to 140 minutes of total strength training per week: “I’ve always been a fan of strength training … But again, the devil is in the details about the dosing. When you look at people who do strength training, it adds another 19% reduction in all-cause mortality on top of the 45% reduction that you get from one hour of moderate exercise per day. When I strength train, I go to the gym and spend anywhere from 20 to 40 minutes, and … I try to use weights that I can do 10 reps with … After that, you’re feeling sort of like spent and … it takes a couple of days to recover. If you do that two, at the most three, times a week, that looks like the sweet spot for conferring longevity.” • There are other useful strategies to support your mood — While exercise is effective, it’s not the only option available. I recommend supporting your gut with fermented foods (preferably homemade), given how closely gut health is intertwined with your brain function. In addition, getting deep, restorative sleep is important for your mental health. Managing stress, as well as resetting your body’s internal clock by getting sun exposure within about 20 minutes of waking up, will also help support your mental and physical well-being. For an in-depth explanation of these tips, read “Depression Accelerates Physical Illness and Increases Disease Risk.” Frequently Asked Questions (FAQs) About Post-Acute Withdrawal Syndrome Q: What is Post-Acute Withdrawal Syndrome (PAWS) and how common is it after stopping antidepressants? A: PAWS refers to long-lasting withdrawal symptoms that occur after discontinuing antidepressants such as selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs). These symptoms include dizziness, anxiety, tremors, insomnia, fatigue, and even suicidal thoughts.According to a 2024 meta-analysis from The Lancet Psychiatry, 31% of people who stop taking antidepressants report some form of withdrawal symptom — falling to approximately 15%, or about 1 in 6 to 7, once the symptoms reported after placebo discontinuation are subtracted. A separate 2025 systematic review of seven studies, drawn largely from online self-reports and case reports, found persistent symptoms lasting anywhere from one and a half months to about 13.8 years at the extreme. Q: Are PAWS symptoms just a relapse of depression or something different? A: No. PAWS symptoms are distinct from a relapse of depression. While often misdiagnosed as a return of the original mental health condition, PAWS has its own symptom profile and course. This misdiagnosis can lead to unnecessary reinstatement of medications and further confusion for patients. Q: Which antidepressants are most associated with severe withdrawal symptoms? A: In The Lancet Psychiatry meta-analysis, desvenlafaxine, venlafaxine, imipramine and escitalopram were associated with the highest incidence of withdrawal symptoms, and imipramine, paroxetine, and desvenlafaxine or venlafaxine with the greatest severity. In contrast, longer-acting drugs like fluoxetine are associated with fewer issues. Tapering rather than stopping abruptly is recommended in most clinical guidelines, though that same meta-analysis found no difference in withdrawal incidence between studies that tapered and studies that stopped abruptly. Q: Is the pharmaceutical industry downplaying the risks of antidepressant withdrawal? A: Critics say yes. Investigative reporting by Maryanne Demasi, Ph.D., argues that pharmaceutical companies minimize the severity of withdrawal symptoms. A 2025 meta-analysis published in JAMA Psychiatry found discontinuation symptoms fell below the threshold for clinical significance — widely reported as “mild” — but critics argue this rested on short follow-up, industry-funded research that excluded high-risk drugs, and poorly designed trials. Media campaigns, they say, further reinforced this framing. Q: What supportive strategies are being discussed for antidepressant withdrawal? A: No intervention has yet been formally tested for antidepressant withdrawal itself — the 2025 systematic review notes that “to date not a single clinical intervention has been formally evaluated” for PAWS, and calls for long-term trials. Separately, and for symptoms of depression and anxiety rather than withdrawal specifically, an umbrella review reported that physical activity was about 1.5 times more effective than counseling or the leading medications. Activities like walking, strength training, yoga, and Pilates were all beneficial — even light exercise can make a meaningful difference. Any plan for tapering or stopping an antidepressant need to be made with a qualified health care provider. This article is for informational purposes only and does not constitute medical advice. Consult a qualified health care provider before making changes to your health regimen.

Heart disease feels like a permanent feature of modern life, but it wasn’t always that way. In the late 1800s, coronary heart disease was uncommon, and most people died from infections rather than chronic vascular problems. Today, coronary heart disease sits at the center of cardiovascular mortality, bringing with it chest pain, breathlessness, fatigue, and sudden heart attacks that often appear after years of silent damage. That contrast alone raises a basic question you deserve an honest answer to: What fundamentally changed? The usual explanations focus on longer lifespans, better diagnostics, or individual behavior. I don’t find those answers sufficient. When I examined long-term mortality data, one pattern stood out: Something changed the internal environment of human arteries long before heart attacks became common. One change stands out because it happened quickly, affected nearly everyone, and reshaped what people ate every single day. My paper, “Seed Oils as a Hypothesized Contributor to Heart Disease: A Narrative Synthesis,” published in the journal Cureus on January 21, 2026, explains why the widespread adoption of industrial seed oils deserves closer scrutiny.1 It synthesizes over 200 references showing that the rapid adoption of LA-rich industrial seed oils in the early 1900s preceded the surge in coronary heart disease deaths by 10 to 20 years — the exact timeframe needed for atherosclerotic plaques to develop — and that LA oxidation generates the same inflammatory aldehydes like 4-HNE now implicated in oxidative damage to the lining of blood vessels. Coronary heart disease doesn’t begin with a heart attack. It begins quietly, with changes inside blood vessels that build year after year. To understand why heart disease became so widespread — and how you can change your own trajectory — you need to see how one dietary shift altered the internal environment of your arteries over time. I break down that evidence step by step in my paper, which you can read in full below. >>>>> Click Here <<<<< You can also download a simplified version of this paper, rewritten in layman-friendly terms for easier understanding of the science. >&get;>>> Click Here <<<<< How Seed Oils Quietly Reshaped Heart Disease Risk Here’s what the data revealed when I traced the timeline. My paper set out to identify what changed before heart disease rates surged in the early 20th century. Instead of focusing on short-term risk markers, I analyzed historical mortality records, U.S. Department of Agriculture (USDA) food supply data, and decades of mechanistic research to align dietary shifts with the slow biology of artery disease. • A clear dose-response pattern emerged across countries — As shown in the figure above, countries with higher per-capita linoleic acid (LA) availability consistently showed higher rates of coronary heart disease during the mid-20th century. Nations consuming the most LA, including the U.S. and Israel, experienced the highest coronary heart disease mortality, while countries that maintained traditional low-LA diets, such as Japan and Greece, had dramatically lower rates. This population-level pattern reinforces the sequence seen over time: increased seed oil exposure came first, followed years later by rising heart disease. Although this type of ecological comparison can’t prove cause on its own, the uniform gradient across very different countries highlights how sustained LA exposure aligns with long-term arterial risk when an entire food system changes at once. • Industrial diets tracked rising heart disease deaths — As seed oils replaced traditional fats, coronary heart disease mortality climbed from about 137 deaths per 100,000 adults in 1900 to more than 450 per 100,000 by 1968.2,3,4 Smoking, longer lifespans, and improved diagnostics were considered, yet none aligned as closely in timing or magnitude with this rise. As shown in the figure below, U.S. trends from 1900 to 2025 show a parallel rise in coronary heart disease incidence, seed oil intake, and cigarette consumption, with heart disease peaking in the mid-20th century as industrial seed oils became widely adopted. While smoking later declined and heart disease rates fell, seed oil intake continued to climb, highlighting a long-term dietary shift that aligns with changes in cardiovascular risk at the population level. • Seed oil exposure accelerated rapidly — Intake didn’t increase gradually. Per-capita seed oil availability doubled within a few decades, rising from roughly 2.7 kilograms (about 6 pounds) to more than 5.4 kilograms (about 12 pounds) per person. Soybean oil drove much of this shift, expanding from near zero in 1909 to more than 11 kilograms (about 24 pounds) per person per year by the late 20th century. • Early adopters showed earlier disease — Urban and industrialized populations that integrated seed oils sooner experienced earlier and higher heart disease rates. Autopsy data from mid-20th-century soldiers even revealed advanced plaque in young adults where it had once been rare. These weren’t elderly patients with decades of decline — these were young men in their 20s, already showing the arterial damage of much older people. Human Tissue Composition Shifted with the Food Supply But the story doesn’t end with food supply data — it shows up in human tissue itself. The research documented a 136% increase in LA stored in body fat during the same period. This means that compared to your great-grandparents, your fat tissue today contains more than twice as much of this unstable, inflammatory fat. The primary damage wasn’t reflected in cholesterol or blood pressure changes. LA oxidizes easily, breaking down into reactive compounds that directly injure blood vessels. These oxidized fragments are chemically “sticky” — they attach to proteins and DNA in ways that trigger immune responses and damage cells. Think of oxidation like rust forming on metal. When LA oxidizes inside your body, it essentially “rusts,” creating damaged molecules that irritate and injure your artery walls. • Toxic lipid byproducts fueled plaque formation — As shown in the figure above, fats from LA-rich seed oils become incorporated into circulating LDL particles, where they are far more prone to oxidative damage than more stable fats. Once oxidized, these LDL particles irritate the inner lining of your arteries, switching on inflammatory signals that draw immune cells into the vessel wall. Those cells absorb the damaged cholesterol and swell into “foam cells,” forming the earliest layers of plaque. As oxidized fats continue to accumulate, the plaque grows, the artery wall stiffens, and the protective cap over the plaque weakens, raising the risk of sudden rupture and clot formation over time. • Slow plaque growth hid the damage for decades — Atherosclerosis typically takes 10 to 20 years to become clinically visible. Seed oil intake rose well before heart attacks and sudden cardiac deaths became common, matching the known timeline of arterial injury. • Other risk factors amplified but did not initiate disease — Smoking intensified oxidative injury but did not start the process. Improved diagnostics explained detection, not disease creation. Refined sugar worsened metabolism, yet its rise didn’t match the early heart disease inflection. • Inflammation kept artery damage switched on — When seed oil fats break down inside your arteries, they essentially trick your immune cells into treating damaged cholesterol as a threat to engulf — but the cells can’t digest it. Those cells start soaking up damaged cholesterol and turn into bloated “foam cells,” which are the first building blocks of artery plaque. At the same time, inflammatory signals stay active and allow injured cells to linger instead of clearing out, letting plaque grow and harden over time. • Modern eaters inherit decades of LA exposure — Even if you don’t cook with seed oils, LA is baked into the modern food supply through packaged foods and restaurant meals. That constant exposure supplies the raw material for ongoing oxidative injury inside your arteries. Once you can see and measure your LA intake, heart disease stops looking like fate and starts looking like what it is: a slow injury you can prevent. How to Address the Real Problem If you take one thing from this research, let it be this: Heart disease did not surge because human biology suddenly failed. I look at it as a slow injury driven by a modern fat intake your body wasn’t designed to handle. When you lower the oxidative burden on your arteries, you may help support arterial stability and reduce further damage accumulation year after year. This section focuses on removing the root driver first, not masking downstream symptoms. 1. Cap your LA intake in the 2 to 3 gram range per day — This is the foundation. Excess LA from seed oils loads your tissues with highly unstable fats that break down into inflammatory byproducts. Focus on keeping daily intake between 2 and 3 grams because that aligns far more closely with pre-industrial exposure. (Going much lower than 2 grams a day also isn’t recommended, as your mitochondria still requires LA in small amounts.) To put that in perspective, one tablespoon of soybean oil contains about 7 grams of LA — more than double your daily limit. A single serving of potato chips fried in vegetable oil can contain 3 to 5 grams. To significantly lower your LA exposure, eliminate soybean, corn, sunflower, safflower, canola, and cottonseed oils entirely. Once these oils are gone, you sharply reduce the raw material that may contribute to arterial inflammation and plaque formation. 2. Track your LA intake so progress becomes visible — Invisible problems stay unsolved. I recommend tracking LA intake directly rather than guessing. To do so, sign up for my Pax health platform. It has a feature called the Seed Oil Sleuth, which monitors your LA intake to a tenth of a gram. That kind of feedback builds confidence and consistency. You see exactly how daily choices affect long-term risk, which makes the changes stick. 3. Stop relying on restaurant food and fried meals — If you eat out often, this step matters. Restaurants almost universally rely on seed oils because they’re cheap and shelf-stable. Fried foods and sautéed dishes expose those oils to high heat, which accelerates oxidation before the food even reaches you. When you cook at home, you regain control over the fats entering your bloodstream, and that may help lower oxidative stress inside your arteries. 4. Replace seed oils with stable traditional fats — I recommend you cook with grass fed butter, ghee, or tallow. These fats resist oxidation and do not fragment into toxic byproducts under heat. When you switch fats, you’re not just avoiding harm — you’re helping support a calmer biochemical environment inside your blood vessels. 5. Avoid high-LA animal foods like chicken and pork — This step surprises many people. These animals store dietary LA directly in their tissues. That means you absorb it secondhand. Choose grass fed beef or lamb instead, which naturally contain far lower LA levels. This swap lowers your exposure without forcing you to reduce protein intake or calories. For instance, conventional chicken thighs contain about 2 to 3 grams of LA per serving, while grass fed beef contains roughly 0.1 to 0.2 grams. When you address the cause — unstable industrial fats accumulating in your tissues — you stop fighting your biology and start working with it. Over time, that shift may change how your arteries respond to stress, inflammation, and aging itself. Because LA accumulates in tissues over years, reducing intake is a long-term strategy. Human trial data on specific timelines for improvement are limited, so individual results are likely to vary, with any benefit to inflammatory markers potentially accumulating gradually over years as tissue LA stores deplete. FAQs About Seed Oils and Heart Disease Q: Why weren’t seed oils a problem in the past? A: Seed oils were not widely consumed before the early 1900s. Traditional diets relied on butter, tallow, and lard, which are far more stable fats. The rapid industrial introduction of seed oils dramatically increased LA exposure in a very short period, creating conditions the human body hadn’t adapted to over evolutionary time. For most of human history, LA intake was estimated at 1% to 2% of calories. By the late 20th century, it had risen to 7% to 8% — a change that happened in decades rather than the millennia required for biological adaptation. Q: What makes LA from seed oils harmful to arteries? A: LA is highly unstable. When it breaks down, it forms reactive compounds that may damage blood vessel walls, keep inflammation switched on, and may accelerate plaque buildup. Over decades, this ongoing injury is thought to alter the structure and function of arteries in ways that may raise heart disease risk. Q: If I don’t cook with seed oils, am I still exposed? A: Yes. LA is embedded in the modern food supply. Packaged foods, restaurant meals, sauces, dressings, and fried foods almost always rely on seed oils. Even without using them at home, daily exposure adds up unless intake is intentionally reduced. Q: How does reducing LA help heart health over time? A: Lowering LA intake may reduce the raw material that contributes to oxidative damage inside arteries. Over time, some research suggests this may support a calmer internal environment, though evidence that it meaningfully slows plaque accumulation or restores vascular resilience in humans is still preliminary. Q: What’s the most effective first step to reduce risk? A: The most effective first step is tracking and limiting LA intake to between 2 and 3 grams per day. Once intake becomes visible and measurable, heart disease may feel less inevitable and more like something you can actively influence by reducing chronic exposure rather than chasing symptoms. This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen.

GLP-1 medications have transformed how millions of people lose weight, but the number on the scale tells only part of the story. When appetite drops and pounds disappear quickly, it’s easy to assume everything is moving in the right direction. Yet experienced clinicians are raising a pointed question: what exactly are you losing? If the answer includes a significant share of muscle along with fat, the consequences reach far beyond appearance. Muscle supports your strength, balance, mobility, and metabolism, and once it disappears, rebuilding it demands far more effort than preserving it in the first place. At the same time, as prescriptions have surged, so have reports of medication-related problems reaching poison centers across the U.S. National data reveal a striking increase in reported exposures following approval of these drugs for weight management. A growing share of those cases proved serious enough to require professional medical evaluation. The patterns behind those reports point less to a flaw in the medications themselves and more to gaps in education, dosing errors, and a population of newer users still learning how to handle the drugs safely. Those trends highlight an important shift in the conversation. Success with these medications isn’t simply about losing pounds. It’s about preserving your health, protecting your metabolism, and avoiding preventable problems along the way. That starts with understanding why the quality of your weight loss matters every bit as much as the amount. Muscle Loss Changes the Story Behind Weight Loss In an MSN news report published in June 2026, interventional cardiologist Dr. Sanjay Bhojraj, who has more than 20 years of clinical experience, challenged the common belief that every pound lost on GLP-1 medications like Ozempic represents better health.1 Instead, he emphasized that the way you lose weight determines whether your health improves or declines. It’s worth noting that his comments come from a news interview and reflect his clinical perspective rather than findings from a formal study. His message centered on a simple but often overlooked point: Successful treatment involves much more than taking a weekly injection. It requires a complete strategy that includes nutrition, exercise, and a realistic plan for maintaining results after the medication ends. Instead of asking yourself only, “How much weight have I lost?” Bhojraj encourages you to ask a better question: “What exactly did I lose?” That shift in thinking changes the entire conversation because losing muscle carries very different consequences than losing excess body fat. • Eating less doesn’t automatically make you healthier — One of Bhojraj’s strongest warnings addressed a mistake he frequently sees among patients who rely on appetite suppression alone. As he explained, “Not all weight loss on GLP-1 medications is healthy weight loss,” adding that “the biggest mistake I see? People confuse eating less with getting healthier.” Your body still requires enough protein and regular physical activity while you lose weight. If your calorie intake drops sharply but your protein intake falls with it, your body begins breaking down muscle tissue to meet its energy needs. • Protein and strength training help tell your body to protect muscle — Bhojraj explained that GLP-1 medications reduce appetite, but they don’t automatically protect lean body mass. Lean body mass refers to everything in your body that isn’t fat, including your muscles, bones, and organs. Muscle represents the largest part of that lean tissue and deserves special attention during weight loss. His advice was straightforward. Prioritize adequate dietary protein while following a resistance-training program. Resistance training means exercises that force your muscles to work against a load, such as weight machines, free weights, resistance bands, or even your own body weight through movements like pushups, squats, and lunges. Those activities send your body a powerful signal that your muscles remain necessary and deserve to stay. A practical way to monitor your progress is to track more than body weight. Notice whether everyday tasks become easier, whether you continue lifting similar weights in the gym, and whether your balance and stability remain strong. Those improvements provide evidence that you’re protecting the muscle that supports healthy aging instead of sacrificing it during rapid weight loss. • Losing muscle slows the engine that burns calories every day — Bhojraj highlighted another consequence that many people overlook. Rapid weight loss frequently includes a significant amount of lean muscle loss, which he compares to sarcopenia — the loss of muscle tissue faster than the body replaces it. Strictly, sarcopenia describes age-related muscle loss, while lean mass lost during rapid weight reduction is a related but distinct problem. Either way, the same two habits help protect muscle: adequate protein and resistance exercise. Muscle requires energy even while you rest, which means people with more muscle naturally burn more calories throughout every day. When muscle disappears, your resting metabolic rate falls. Resting metabolic rate simply means the calories your body burns to keep your heart beating, lungs working, and organs functioning even while you sit or sleep. This explains why some people struggle after stopping GLP-1 medication. A slower metabolism means your body requires fewer calories than before. If old eating habits return while calorie needs have dropped, regaining weight becomes much easier. • Digestive health deserves attention throughout treatment — Another important point from Bhojraj’s discussion is that appetite suppression alone doesn’t equal complete metabolic health. He specifically included digestion among the factors people often ignore while focusing exclusively on the scale. Digestion affects how efficiently your body breaks down food and absorbs the protein, vitamins, and minerals required to support muscles and normal body functions. Simply eating less without paying attention to food quality leaves your body with fewer building blocks to repair and maintain healthy tissue. One useful habit is to review your routine every week instead of waiting until problems appear. Ask yourself whether you consistently eat enough protein, complete resistance exercise, tolerate meals comfortably, and maintain your energy throughout the day. Those simple checkpoints help you judge your progress using real measures of health instead of relying only on body weight. The urgency to lose weight quickly doesn’t only affect what happens inside your body. It also shapes how quickly people take up the medications, and national data from poison centers track how sharply reported problems have grown alongside that uptake. Poison Center Reports Revealed How Rapidly GLP-1 Problems Grew A nationwide analysis, published in the Journal of Medical Toxicology, tracked how GLP-1 medication exposures changed after approval for weight loss.2 To understand how GLP-1 medication problems changed after semaglutide received U.S. Food and Drug Administration (FDA) approval for chronic weight management in 2021, researchers analyzed 10,033 exposures reported to the National Poison Data System between 2012 and 2023. Semaglutide, sold under the brand names Ozempic and Wegovy, is the GLP-1 medication at the center of that growth. The researchers focused on who experienced medication-related problems, what types of exposures occurred, and how often those events required medical care. Because the National Poison Data System collects reports from poison centers throughout the U.S., it provides a broad picture of real-world medication problems rather than the tightly controlled conditions found in clinical trials. That makes the findings especially valuable because they reflect what happens after medications reach everyday patients. • Reported exposures more than doubled after weight-loss approval — The researchers identified 3,113 GLP-1 exposures before July 2021 and 6,920 afterward, meaning reports increased more than twofold following semaglutide’s approval for obesity treatment. Semaglutide-related poison center calls accelerated by an additional 9.9% every quarter after approval, confirming that the increase represented far more than routine year-to-year growth. Semaglutide quickly became the medication involved in most reports. Before approval, it accounted for 24.6% of reported GLP-1 exposures. After approval, that figure jumped to 64.2%, making it the dominant product reported to poison centers. Other GLP-1 medications increased only slightly during the same period. • The average age of reported exposures dropped from 57 years before approval to 51.6 years afterward — When the authors roughly estimated the age of just the newly exposed group, the average dropped to about 47.5 years — though they called this an approximation, and the data can’t tell whether someone was taking the drug for diabetes or for weight loss. Women also represented a much larger share of reported exposures, increasing from 68.9% before approval to 78.2% afterward. Those changes reflect how the medications expanded beyond their original role in diabetes treatment. As more adults without diabetes began using GLP-1 drugs for obesity, poison center reports shifted toward a younger population that differed from the earlier patient group. • Most reports involved dosing mistakes rather than intentional overdoses — Researchers found that therapeutic errors, meaning people accidentally took the medication incorrectly, accounted for the majority of reported exposures in both periods — 85.6% before approval and 81.0% afterward, a slight decline as a share even as the raw number rose. Examples include taking the wrong dose, injecting the medication too often, or misunderstanding how to use the injection pen. The pattern also shifted toward first-time or short-term use. Acute exposures, meaning a single incorrect dose or one-time mistake, increased from 47.2% before approval to 58.7% afterward, while acute-on-chronic exposures, meaning problems that developed during ongoing regular use, declined. This supports the researchers’ conclusion that many reports involved newer users who were still learning how to use the medication correctly. • More people needed medical evaluation even though many symptoms remained mild — The investigators found that the proportion of patients managed in or referred to a health care facility increased from 23% before approval to 33.5% afterward, representing a 46% higher likelihood of requiring professional evaluation. Note that this category counts people who were already at a health care facility when the call was placed as well as those referred to one, so it is broader than “required professional evaluation.” At the same time, the study reported that most exposures still produced relatively mild gastrointestinal symptoms. Even so, digestive symptoms sometimes became severe enough to require medical attention because repeated nausea and vomiting increase the risk of dehydration, meaning your body loses more water and minerals than it replaces. One death was reported across the 10,033 exposures — a patient who had undergone liposuction and developed colonic ischemia — and the authors state that causality cannot be determined from a single report. They concluded that improved patient counseling and clearer poison center guidance may help reduce preventable therapeutic errors and unnecessary emergency evaluations. • They are equally clear about what their data cannot do — Poison center reports “cannot establish causality,” and the study is descriptive pharmacovigilance rather than evidence that these medications caused the outcomes reported. Two cautions the authors themselves raise are worth keeping in mind alongside these numbers. Because these drugs drew intense media and social media attention, the authors write that the rise in call volume “likely reflects a combination of rapid expansion in the user base and variable degrees of stimulated reporting.” This means some of the increase reflects more people picking up the phone, not only more people having problems. At the same time, because reporting to poison centers is voluntary, the data may understate how often these problems actually occur. Build the System That Regulates Your Appetite Naturally Your body already contains the machinery to regulate appetite, burn fat, and protect muscle without a weekly injection. The problem isn’t that the system is broken beyond repair. The problem is that modern diets and lifestyle habits have suppressed the signals it depends on. GLP-1 medications reduce appetite, but they also introduce risks that range from muscle loss to medication errors and other complications. Rather than replacing your body’s own appetite-regulating system with an injection, I recommend restoring the biological processes that already exist. Your colon naturally produces GLP-1 through specialized cells called L-cells,3 and those cells are thought to respond to butyrate,4 a short-chain fatty acid made by beneficial gut bacteria. When your microbiome functions the way it was designed, it helps regulate appetite, blood sugar, and metabolism while you preserve your strength instead of sacrificing it. 1. Remove the foods that prevent your gut from recovering — I recommend eliminating seed oils, such as soybean, corn, canola, sunflower, and safflower oil, because their high linoleic acid (LA) content degrades the gut environment that beneficial bacteria depend on to thrive. Excess LA is also thought to impair your colon cells’ ability to use butyrate for energy, weakening the protective lining of your digestive tract. Use more stable traditional fats instead, such as tallow, ghee, or grass fed butter. Keep your LA intake below 5 grams per day, and ideally closer to 2 grams, to give your microbiome the opportunity to recover and begin producing the compounds that support healthy appetite regulation. 2. Heal your digestion before increasing fiber — If you struggle with bloating, abdominal discomfort, or irregular bowel habits, avoid loading your diet with large amounts of fermentable fiber all at once. Begin with simple, easy-to-digest meals that reduce excessive fermentation while your intestinal lining recovers. As digestion becomes more predictable, gradually increase carbohydrates using foods your body tolerates well. Whole fruit and well-cooked white rice provide glucose for cellular energy without overwhelming an already stressed microbiome. Next, add root vegetables, followed by non-starchy vegetables and then starchy vegetables such as squash and sweet potatoes. Leave beans, legumes, and minimally processed whole grains until last, and only if your digestion remains comfortable. Most adults do best with roughly 250 grams of carbohydrates each day once metabolic health improves. 3. Feed the bacteria that produce butyrate — Once your gut becomes more stable, begin adding foods that nourish butyrate-producing microbes. Cooked-and-cooled white potatoes and green bananas contain resistant starch, a type of carbohydrate that reaches your colon intact and serves as food for beneficial bacteria. As those microbes multiply, butyrate production increases, your gut barrier becomes stronger, and your body regains the natural metabolic signals that help regulate appetite and blood sugar. A useful detail: You don’t have to eat potatoes cold to get the benefit. Cooking, cooling, and then gently reheating them retains most of the resistant starch, so a rewarmed baked potato or a pan of leftover roasted potatoes still feeds those beneficial bacteria effectively. 4. Protect your muscle while your metabolism recovers — Preserving muscle deserves as much attention as losing fat. Prioritize adequate protein and regular resistance exercise throughout your weight-loss journey. Aim for 0.6 to 0.8 grams per pound (1.32 to 1.76 grams per kilogram) of ideal body weight, with one-third coming from collagen-rich sources like slow-cooked meats or bone broth. Weight training, resistance bands, and bodyweight exercises all help tell your body to hold onto muscle instead of breaking it down for energy. Strong muscles also keep your metabolism higher, making it easier to maintain your progress over the long term. 5. Judge success by how your body performs, not just by what you weigh — I encourage you to look beyond pounds lost. Your strength, daily movement, energy, and ability to handle everyday activities without strain tell you far more about your metabolic health than any number on a scale. Those measurements tell you whether your metabolism is becoming healthier or simply becoming smaller. I explain how to restore your body’s own GLP-1 production through nutrition and metabolic support in my book, “Weight Loss Cure: Melt Fat Naturally with Your Own GLP-1,” where I outline practical strategies for rebuilding the biological systems that regulate appetite naturally. FAQs About GLP-1 Medications and Weight Loss Q: Why isn’t all weight loss on GLP-1 medications considered healthy? A: The scale doesn’t distinguish between fat and muscle. If a significant portion of your weight loss comes from muscle, your metabolism slows, your strength declines, and maintaining your results becomes more difficult. Protecting muscle through adequate protein intake and resistance exercise is just as important as losing excess body fat. Q: Why did poison center reports involving GLP-1 medications increase so quickly? A: As these medications became widely prescribed for weight management, reports to poison centers rose sharply. Many cases involved accidental dosing mistakes rather than intentional overdoses, especially among newer users who were still learning how to administer the medications correctly. The study’s authors add that intense media attention probably encouraged more people to call, so part of the rise reflects reporting behavior rather than a rise in problems alone — though because reporting to poison centers is voluntary, the data still likely understate how often these problems actually occur. Q: What’s the biggest mistake people make while taking GLP-1 medications? A: Focusing only on eating less instead of improving overall health. Appetite suppression alone doesn’t preserve muscle, support digestion, or build habits that last after the medication stops. A long-term plan includes nutritious meals, regular strength training, and attention to metabolic health. Q: If I decide not to use a GLP-1 medication, how can I support healthy appetite control? A: Restoring a healthy gut microbiome helps your body regulate appetite naturally. Removing foods that disrupt gut health, healing digestion, feeding beneficial bacteria, and preserving muscle all support the biological systems involved in healthy metabolism instead of relying on an injectable medication. Q: How should I measure progress if the scale isn’t the whole story? A: Look at more than your body weight. Improvements in strength, energy, balance, endurance, and your ability to perform everyday activities provide a much better picture of whether your metabolism and overall health are moving in the right direction. Your goal is lasting health, not simply a lower number on the scale. This article is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before making changes to your health regimen. Test Your Knowledge with Today’s Quiz! Take today’s quiz to see how much you’ve learned from yesterday’s Mercola.com article. Why is fluorine added to some medicines? To increase vitamin content and bioavailability To change the medicine’s color To improve stability or how it moves through the body Fluorine can help medicines resist breakdown, remain stable, or move through the body differently, but it usually does not provide the therapeutic effect. Learn more. To provide the medicine’s main therapeutic effect