What New Research Says About Childhood Growth and BMI

For decades, pediatric health experts have relied on a concept known as “adiposity rebound” to help assess a child’s future risk of obesity. Traditionally, this stage, when body mass index (BMI) begins to rise again after early childhood, has been viewed as a potential warning sign. But new research published in The Journal of Nutrition is challenging that long-held belief and offering a more nuanced understanding of how children grow.

A look at childhood growth patterns

The study analyzed data from 2,410 children and adolescents ages 2 to 19 who participated in the National Health and Nutrition Examination Survey (NHANES) between 2021 and 2023. Researchers observed a familiar trend: BMI decreases in early childhood, then begins to rise again around age 6 — the classic “adiposity rebound.”

However, there was a surprising twist. While BMI increased, another important measurement, the waist-to-height ratio, continued to decline. This metric is considered a more accurate indicator of body fat, particularly abdominal fat.

The implication? The rise in BMI during this stage may not signal increased fat at all. Instead, it may reflect healthy growth in lean tissues like muscle and bone.

Why BMI alone may be misleading

BMI has long been used as a simple screening tool because it relies on such basic measurements as height and weight. But it has a significant limitation, as it cannot distinguish between fat mass and fat-free mass. This distinction is especially important in children, whose bodies are constantly changing.

Lead researcher Andrew Agbaje emphasized this concern, saying:

Recent global consensus statements on redefining and diagnosing obesity have recommended that obesity should not be diagnosed with BMI alone but confirmed with non-invasive measures such as waist-to-height ratio.

He also said:

This new study buttresses the misleading use of BMI in children whose body composition rapidly changes during growth and the potential for attributing physiological functions to pathology, which might lead to unnecessary interventions. Waist-to-height ratio should be incorporated as the first inexpensive measure in diagnosing pediatric obesity with BMI used as a confirmatory tool due to its imprecision.

Introducing the “body composition reset”

One of the most compelling ideas to emerge from the study is what researchers call a “body composition reset.” This term describes the natural shift toward lean tissue development during early childhood. Rather than indicating a buildup of fat, the increase in BMI may actually reflect a healthy phase of growth, one that supports strength, bone development, and overall physical maturation. This finding challenges the assumption that an earlier adiposity rebound automatically signals a higher risk of obesity later in life.

Why waist-to-height ratio matters

Unlike BMI, the waist-to-height ratio focuses on fat distribution, particularly abdominal fat, which is more closely linked to health risks such as heart disease, Type 2 diabetes, high blood pressure, liver disease, and bone fractures. Because it is less influenced by muscle growth, this measurement provides a clearer picture of whether a child is carrying excess body fat.

A shift in pediatric obesity screening

The study adds to a growing body of evidence suggesting that BMI should not be used in isolation when evaluating children’s health. Incorporating waist-to-height ratio could help clinicians better distinguish between normal growth and true obesity risk, avoid unnecessary labeling or interventions, and provide more accurate, individualized care, among other things.

Recognition for innovative research

Agbaje’s contributions to pediatric cardiometabolic health have not gone unnoticed. He is the inaugural recipient of the American Society for Nutrition Foundation/Novo Nordisk Foundation Flemming Quaade Award, which honors early-career physicians making significant strides in obesity prevention and management. The award will be presented again at NUTRITION 2026, scheduled for July 25–28, 2026, in National Harbor, Maryland.

So, in a nutshell, a single number like BMI cannot tell the whole story. The new approach may reduce the chances of misclassifying healthy developmental changes as medical concerns. For parents, it should serve as a reassuring message that not every change in BMI signals a problem. Sometimes, it simply reflects a child growing exactly as they should.

Your responses and feedback are welcome!

Source: “Study Challenges Decades-Old Puzzle About Childhood Body Fat,” American Society for Nutrition, 4/23/26
Source: “Adiposity Rebound or Fat-Free Mass Anabolism in Children…,” The Journal of Nutrition, 3/9/26
Image by beyzahzah/Pexels

Genetics May Shape the Future of GLP-1 Medications

Childhood obesity treatment is entering a new and highly personalized era. As GLP-1 receptor agonists gain traction as effective tools for weight management in adolescents, emerging research suggests that genetics may play a key role in determining who benefits most (and who experiences side effects).

This evolving intersection of obesity medicine and precision health could transform how providers treat pediatric patients. But it also raises important questions about cost, access, and equity.

The rise of GLP-1 medications in pediatric care

GLP-1 (glucagon-like peptide-1) receptor agonists, including semaglutide and liraglutide, have rapidly become a cornerstone of modern obesity treatment. Originally developed for type 2 diabetes, these medications help regulate appetite, slow digestion, and improve blood sugar control. In adolescents with obesity, clinical trials have demonstrated significant reductions in body mass index (BMI), often far exceeding results from lifestyle interventions alone.

A major study published in The New England Journal of Medicine found that teens treated with semaglutide experienced an average 16% reduction in BMI over 68 weeks. These results have fueled growing adoption in pediatric care and prompted updated treatment guidelines from the American Academy of Pediatrics, which now include pharmacotherapy as part of comprehensive obesity management.

While GLP-1 medications have shown impressive results, not all patients respond the same way. Some adolescents lose significant weight, while others see more modest changes, or struggle with side effects like nausea and vomiting. Recent research highlights a possible explanation: genetic variation. Studies suggest that certain genetic differences may influence how the body regulates appetite and metabolism, how strongly GLP-1 receptors respond to medication, and the likelihood and severity of gastrointestinal side effects.

In fact, new findings reported by Reuters indicate that specific genetic markers may be linked to both greater weight loss outcomes and increased side effect risk in patients taking GLP-1 drugs. This opens the door to a more tailored approach, where treatment decisions are guided not just by BMI or medical history, but by a patient’s genetic profile.

What is personalized (precision) medicine?

Personalized medicine, also known as precision medicine, is an approach that uses individual factors like genetics, environment, and lifestyle to guide healthcare decisions. The National Institutes of Health defines precision medicine as a way to “optimize medical care by tailoring it to individual characteristics.”

In the context of pediatric obesity, this could mean identifying which children are most likely to benefit from GLP-1 medications, predicting who may experience side effects before treatment begins, and adjusting dosages or selecting alternative therapies based on genetic insights. This approach has the potential to make treatment more effective, safer, and more efficient.

Potential benefits for pediatric patients

If successfully implemented, genetically guided obesity treatment could offer several advantages:

1. Improved Outcomes. Children could receive medications that are more likely to work for their specific biology, increasing the chances of meaningful weight loss and improved health.
2. Reduced Trial-and-Error. Providers could avoid prescribing medications that are less likely to be effective, saving time and reducing frustration for families.
3. Better Side Effect Management. Identifying genetic risk factors for side effects may help clinicians proactively manage or avoid adverse reactions.
4. More Efficient Use of Healthcare Resources. Targeted treatment could reduce unnecessary costs associated with ineffective therapies.

Ethical and equity considerations

While the promise of personalized medicine is compelling, it also introduces new challenges, particularly around access and equity, such as cost barriers, a risk of widening disparities, and data privacy concerns. Genetic testing can be expensive, and insurance coverage is inconsistent. Combined with the already high cost of GLP-1 medications, this could limit access for many families.

Also, communities already disproportionately affected by childhood obesity, such as low-income and minority populations, may have the least access to advanced testing and treatments. And, the Centers for Disease Control and Prevention continues to report higher obesity rates among underserved populations, making equitable access a critical concern. Plus, genetic testing raises questions about how sensitive health data is stored, shared, and protected (especially for children).

The integration of genetics into pediatric obesity treatment represents a major step toward more individualized, science-driven care. However, experts emphasize that medication, personalized or not, should always be part of a broader, holistic approach.

As research continues, the key challenge will be ensuring that innovation does not outpace accessibility. Personalized treatment has the potential to improve outcomes, but only if it is available to all children who need it.

Your responses and feedback are welcome!

Source: “Once-Weekly Semaglutide in Adolescents with Obesity,” The New England Journal of Medicine, 11/2/22
Source: “Semaglutide Treatment Effect in People With Obesity — STEP TEENS,” American College of Cardiology, 12/20/22
Source: “Genetics may help explain why results from weight-loss jabs vary, say scientists,” The Guardian, 4/6/26
Source: “Researchers move closer to matching patients with GLP-1 drug that works best for them,” Reuters, 11/19/25
Source: “The Promise of Precision Medicine,” NIH, undated
Source: “New CDC Data Show Adult Obesity Prevalence Remains High,” CDC, 9/12/24
Image by Tara Winstead/Pexels

Is There an Ultra-Processed Foods Coverup?

Today’s post carries on from “The Nutrition That Never Arrived,” which discusses the work of Dr. Dhruv Khullar, as well as his referencing of Dr. Kevin Hall’s highly-regarded study of ultra-processed foods.

The alarming aspect of this topic is that, almost exactly one year ago, CBS News published a piece titled “RFK Jr. aides accused of censoring NIH’s top ultra-processed food scientist.” That scientist of course was Dr. Hall, described therein as “The National Institutes of Health’s top researcher on ultra-processed foods.”

Hall had announced that, after 21 years at his dream job, he was retiring early because, apparently, the NIH is no longer a place where unbiased science can be conducted. The details are rather shocking, according to journalist Alexander Tin:

Hall told CBS News that he was blocked by the department from being directly interviewed by a reporter from The New York Times, asking about recent research on how ultra-processed foods can be addictive.

Apparently, the NIH leadership did not want any comparison made between being hooked on ultra-processed foods and, for instance, your average meth habit — unless the disease manifests in exactly the same way and causes exactly the same effects as hard-drug addiction.

Hall was allowed to reply to The Times with written answers which “were then edited and sent to the reporter without his consent.” This behavior, needless to say, is normally considered highly unacceptable among professionals in the fields of both medicine and journalism.

Then the situation deteriorated even further when the government denied tampering with Hall’s words, and accused him of untruthfulness about the interference, and acted like the material wasn’t very good or worth being concerned about. Hall, however, maintained that his work on the effects of ultra-processed food on carefully observed subjects…

[…] was the largest study of its kind and no previous study had the same level of dietary control, much less admitted them to a hospital to ensure diet adherence…

Meanwhile, the NIH officials maintained that no censorship was in effect, and that any attempt to portray the government’s position as false would be deliberate distortion. In order to avoid being contradicted, the government agency also prevented Hall from participating in a conference on the subject.

At the same time, Susan Mayne, who had formerly been in charge of the food safety and nutrition center run by the Food and Drug Administration, spoke up for Hall’s research.

This whole controversy surprised many observers because just a few months earlier, reporters were writing passages like this one, published in January of 2025 in The New Yorker:

The dirty little secret is that no one really knows what caused the obesity epidemic. It’s the biggest change to human biology in modern history. But we still don’t have a good handle on why.

That was Dhruv Khullar, quoting what had been said to him by Dariush Mozaffarian, a dean at the Tufts School of Nutrition Science and Policy. The implication is that ultra-processed foods have “probably contributed to rising obesity rates,” although other factors also are involved — like changes in the human microbiome and general metabolism, as well as (probably) epigenetics.

Of course, as always, the possibility exists that the situation is influenced by factors that have not even been suspected yet.

(To be continued… )

Your responses and feedback are welcome!

Source: “RFK Jr. aides accused of censoring NIH’s top ultra-processed food scientist,” CBS News, 04/17/25
Source: “Why Is the American Diet So Deadly?,” The New Yorker, 01/06/25
Image by geralt/Pixabay

The Rise of GLP-1 Medications in Pediatric Obesity: Breakthrough or Barrier?

Childhood obesity remains one of the most urgent public health challenges in the United States, affecting roughly one in five children and adolescents. According to the Centers for Disease Control and Prevention, the prevalence of obesity among U.S. youth is about 19.7%, with higher rates among certain racial, ethnic, and low-income populations.

While lifestyle interventions, such as improved nutrition, increased physical activity, and behavioral counseling, have long been the foundation of treatment, a new class of medications is rapidly transforming the field: GLP-1 receptor agonists. These drugs are generating both excitement and debate, especially as their use expands into pediatric care.

So, are GLP-1 medications a true breakthrough, or do they risk widening existing gaps in care?

What are GLP-1 medications?

GLP-1 (glucagon-like peptide-1) receptor agonists are medications that mimic a naturally-occurring hormone involved in regulating appetite, insulin secretion, and digestion. By slowing gastric emptying and increasing satiety, they help reduce food intake and promote weight loss.

Two of the most widely discussed GLP-1 medications are semaglutide and liraglutide. Originally approved for type 2 diabetes, both medications are now FDA-approved for chronic weight management in certain adolescent populations aged 12 and older. Their growing popularity reflects a broader shift toward recognizing obesity as a chronic, biologically complex disease, not simply a result of lifestyle choices.

Clinical trials have demonstrated significant results in adolescents using GLP-1 medications. A landmark study published in The New England Journal of Medicine found that teens treated with semaglutide experienced an average 16.1% reduction in BMI, compared to just 0.6% in the placebo group. Similarly, trials involving liraglutide showed meaningful reductions in BMI and improvements in metabolic health markers.

Beyond weight loss, GLP-1 medications may improve insulin resistance, blood pressure, and lipid profiles (cholesterol levels). These benefits are particularly important given that childhood obesity is strongly linked to long-term risks such as type 2 diabetes, cardiovascular disease, and even certain cancers.

Despite their clinical promise, GLP-1 medications remain out of reach for many families. Without insurance, these drugs can cost $900 to $1,300 per month, a significant financial burden. Even for insured patients, access is often delayed by prior authorization requirements, step therapy protocols, and inconsistent coverage policies.

According to the American Academy of Pediatrics, disparities in access to obesity treatment, including medications, mirror broader inequities in healthcare. Children from underserved communities, who are already at higher risk for obesity, are often the least likely to receive advanced treatments.

Additional barriers include limited availability of pediatric obesity specialists, geographic disparities in care access, and stigma surrounding obesity treatment. This raises a critical concern: Could a breakthrough therapy unintentionally widen health disparities?

While short-term outcomes are encouraging, long-term safety data in pediatric populations is still evolving.

Common side effects include nausea, vomiting, diarrhea, or constipation. In most cases, these symptoms are mild to moderate and improve over time. However, there are still unanswered questions about long-term use in developing bodies, potential impacts on growth and development, weight regain after discontinuation, and more.

Early evidence suggests that stopping GLP-1 therapy often leads to partial or full weight regain, highlighting the chronic nature of obesity and the potential need for ongoing treatment. Experts emphasize that medication should not replace foundational lifestyle interventions but instead serve as part of a comprehensive, multidisciplinary care plan.

The emergence of GLP-1 medications marks a turning point in pediatric obesity treatment. For adolescents who have struggled with traditional approaches, these therapies offer meaningful, evidence-based results, and in many cases, renewed hope. However, their full potential will only be realized if systemic barriers are addressed.

Expanding insurance coverage, improving provider access, and reducing stigma will be essential to ensuring equitable care. As research continues and policies evolve, the challenge is clear: How do we ensure that this medical breakthrough benefits all children, not just a select few?

Your responses and feedback are welcome!

Source: “Once-Weekly Semaglutide in Adolescents with Obesity,” The New England Journal of Medicine, 11/2/22
Source: “Prescriptions for Obesity Medications Among Adolescents Aged 12–17 Years with Obesity — United States, 2018–2023,” CDC, 6/5/25
Source: “Executive Summary: Clinical Practice Guideline for the Evaluation and Treatment of Children and Adolescents With Obesity,” Pediatrics, February 2023
Source: “New Institute for Clinical and Economic Review Report Shows Significant Jump in Launch Prices, Exceeding Inflation and GDP Growth,” ICER, 10/23/25
Image by Leeloo The First/Pexels

Spectacular Obesity Costs Spotlighted

This is a continuation of “Unacceptable Obesity Costs Suspected.” About a decade ago, medical specialists and public health authorities were noticing more and more suspicious correlations between a substance known as bisphenol A (BPA) and various undesirable effects on humans. Chiefly, BPA seemed to be causing childhood obesity, and in some quarters, great interest was generated in the notion of discontinuing its use in products that might ever introduce the stuff into the bodies of children, orally or via any other route.

At the same time, concern grew about the costs that the use of this industrial chemical exacted from society in terms of both human suffering and financial impact. A ton of money was being spent to repair the ravages of BPA on kids, and on young people and adults who had encountered it in early life. Of course, it didn’t do adults any good either, even if, as children, they had managed to escape it.

Neither the first warning nor the last

Late in 2016, amid a climate of escalating suspicion, The Lancet published a report that brought up in no uncertain terms the price tag, in actual money, for tolerating BPA. By then, research had determined that the cost of disease and dysfunction caused by endocrine-disrupting chemicals, familiarly known as EDCs, amounted to more than 1% of the European Union’s annual gross domestic product, familiarly known as its GDP. (In American dollars, this amounted to the equivalent of around $217 billion.)

According to the report,

Exposure to EDCs varies widely between the USA and Europe because of differences in regulations and, therefore, we aimed to quantify disease burdens and related economic costs to allow comparison… Estimates were made based on population and costs in the USA in 2010. Costs for the European Union were converted to US$ (€1=$1·33).

In the United States, the costs accruing to EDCs were calculated to be around 2.33% of the gross domestic product, or around $340 billion. Experts utilized studies from the fields of epidemiology and toxicology to reckon the “probabilities of causation for 15 exposure–response relations between substances and disorders.” The scientists also had much to say about American societal expenses. They determined that…

The difference was driven mainly by intelligence quotient (IQ) points loss and intellectual disability due to polybrominated diphenyl ethers (11 million IQ points lost and 43,000 cases costing $266 billion in the USA vs 873,000 IQ points lost and 3290 cases costing $12.6 billion in the European Union).

The pesticides containing the dangerous chemicals were much more responsible in Europe, implying a need for improved screening there, for “chemical disruption to endocrine systems and proactive prevention.” The known effects of these chemicals on various body systems were already quite concerning, but the discoveries about their ability to wipe out IQ points definitely suggested a need for more awareness in that department. In 2018, PubMed had this to say about a small study:

This is the first study reporting the presence of bisphenols in two distinct regions of the human brain. Bisphenols accumulation in the white matter-enriched brain tissue could signify that they are able to cross the blood-brain barrier.

More recent publications

Another report (among many) supported the idea that exposure to BPA analogues is strongly connected with not only obesity, but also other undesirable health effects, especially in children. Then another one caused a stir by confirming that…

[…] endocrine-disrupting chemicals negatively affect a wide range of systems throughout the human body and have consequences at every life stage.

By now, professionals interested in this question were accustomed to hearing BPA and its relatives described as “forever chemicals,” meaning that once present in the body, they refuse to leave. The chemicals were deemed responsible not only for obesity but also for diabetes and reproductive disorders in both sexes.

On the policy front, the good news was that some substances had been banned; the bad news was that equally harmful chemicals were recruited to take their places. In no sane vocabulary could this be defined as progress.

Two years ago, a Spanish study of 106 children between ages 5 and 10, about half each of girls and boys, indicated that BPA “impacts the gut microbiome of children differently, with normal-weight children showing greater bacterial diversity compared to those who are overweight or obese.” In other words, this endocrine disruptor affects the gut microbiome adversely, leading to a variety of undesirable results.

Yet, the situation is very complicated, with many unclear connections and relationships among various factors. Still, enough is known to create certainty that this chemical and others like it should ideally be kept out of the body altogether — especially in the case of children and even more particularly where babies are concerned.

Your responses and feedback are welcome!

Source: “Exposure to endocrine-disrupting chemicals in the USA: a population-based disease burden and cost analysis,” TheLancet.com, December 2016
Source: “Possible Obesogenic Effects of Bisphenols Accumulation in the Human Brain,” Ncbi.nlm.nih.gov, 05/29/18
Source: “Bisphenol A Analogues in Food and Their Hormonal and Obesogenic Effects: A Review,” Ncbi.nlm.nih.gov, 09/06/19
Source: “Common Plastic Chemical Linked to Increased Childhood Obesity Risks,” SciTechDaily.com, 03/09/24
Images by Kalle_89 and OpenClipart-Vectors/Pixabay