A Seminar, and So Much More

The source document here is a podcast transcript that combines the best features of two genres. The official title is “Fatness and the Body – Episode 2: Being fat or having obesity: combining social constructivism and biomedical research on childhood obesity.” On the other hand, much of the content is less like a scientific paper and more like talking with an erudite friend, in the quietest corner of a Saturday night house party.

The scholarly content comes from Adam Mickiewicz University, a research center which, under various administrations and with a few name changes, has existed in Poznan, Poland, since 1611. This episode is part of a larger program, Unit for Biocultural Variation and Obesity. Author Zofia Boni is absolutely tireless in her pursuit of both usable facts and of ways to present them to the concerned public.

It’s multifactorial

Her academic career has emphasized anthropology, socialist studies, feminist scholarship, epidemiology, climate science, demography, and other areas of interest, all to capture the big picture regarding childhood obesity. She notes that for children and youth, typical BMI calculations are not used, but rather percentiles and databases correlated to the child’s sex…

[…] and either according to the WHO standards, you can end up with around 30% of 8 year olds in Poland having overweight and obesity, or if you end up using the standards which are the oldest ones, then it’s around 20%… And among those numbers, it is assumed that around 3 to 4% are children with obesity.

In other words, “overweight” and “obesity” are shifty characters who refuse to stand still and have their pictures taken for the record. Boni recommends a viewpoint outside the North America-centric one, from which to gaze at the past decade or so from the perspective of a European graduate student asking questions about the distinction between obesity and fatness, which is always awkward terrain both methodologically and ethically. Furthermore, why does the distinction even matter, and not incidentally, who gets to decide?

Two faces

Boni, the excellent student, is comfortable seeking facts, precision, and certainty; while at the same time, it is almost as if someone else’s brain shares her skull:

So what I want to take from those perspectives in my own future research is on the one hand, recognizing that fatness is alright, so that people are thin and fat as they are small and tall, and not pathologizing or stigmatizing it, but then also recognizing that obesity has very troubling health consequences and physical and physiological consequences. And that there is such a disease as obesity. This is in a way connected I guess, but not every fat person has obesity, right?

Throughout years of research, the author has concentrated on two questions: How and why did obesity make the shift from being chiefly a personal problem, all the way to becoming a matter of public concern? And how do actual people, especially children, experience not only obesity, but the role of public enemy into which some factions of society often try to cast them?

Your responses and feedback are welcome!

Source: “Fatness and the Body’ Episode 2,” Podcasts.ox.ac.uk
Image by RaniRamli/Pixabay

Studies Suggest GLP-1 Medications May Help Slow Progression of Some Cancers

GLP-1 medications have become widely known for their role in treating type 2 diabetes and supporting weight loss. Now, emerging research suggests these drugs may offer another important benefit: helping slow the progression of certain obesity-related cancers, as well as breast cancer.

A new study presented at the 2026 annual meeting of the American Society of Clinical Oncology (ASCO) found that patients taking GLP-1 receptor agonists after a cancer diagnosis experienced significantly lower rates of cancer progression and death compared to patients taking other diabetes medications.

GLP-1 receptor agonists, which include medications commonly prescribed for diabetes and obesity management, have attracted growing scientific interest in recent years. Researchers have increasingly explored whether the drugs’ effects extend beyond controlling blood sugar and promoting weight loss.

According to Dr. Marcin Chwistek, chief of supportive oncology and palliative care at Fox Chase Cancer Center and an ASCO expert in supportive care, GLP-1 medications may influence several biological pathways linked to cancer development and progression. Researchers believe the drugs’ anti-inflammatory and immune-regulating effects could play a role in improving outcomes for cancer patients.

What the studies found

The research team analyzed health records from more than 12,000 patients diagnosed with one of seven obesity-related cancers at stages 1, 2, or 3. The investigators compared patients who began taking GLP-1 medications after their cancer diagnosis with similar patients who were treated with a different class of diabetes drugs known as DPP-4 inhibitors, or gliptins.

The results were notable. Patients using GLP-1 medications showed a meaningful reduction in cancer progression across several solid tumor types. The strongest benefits were observed among patients with lung, breast, colon, and liver cancers. In these groups, patients taking GLP-1 drugs were approximately 38% to 50% less likely to develop stage 4 or metastatic disease compared with those receiving alternative diabetes treatments.

The study also found that GLP-1 use was associated with a 33% lower risk of death from any cause. Among all cancer types examined, breast cancer patients appeared to experience the greatest survival benefit. Researchers reported that GLP-1 users with breast cancer had a 45% lower risk of death compared to similar patients taking other diabetes medications.

These findings suggest that the medications may have an impact not only on cancer progression but also on overall survival.

Scientists are still working to understand the mechanisms behind these results. One possibility is that GLP-1 medications help reduce chronic inflammation, which has long been linked to both obesity and cancer development. Inflammation can create an environment that supports tumor growth and spread.

Researchers also point to the drugs’ effects on the immune system. By influencing immune responses, GLP-1 medications may help the body better control cancer progression.

Weight loss itself may also contribute to improved outcomes, since excess body weight is a known risk factor for several types of cancer. However, additional research will be needed to determine exactly how these medications may influence cancer biology.

The study has been presented at ASCO’s annual meeting but has not yet been published in a peer-reviewed medical journal. Research presented at scientific conferences often undergoes additional review and validation before becoming part of standard medical practice.

Another study found that women who used GLP-1 medications had a significantly lower risk of developing breast cancer than those who did not use the drugs. The study reviewed health data from more than 110,000 women ages 45 to 80 and found that GLP-1 users were about 30% less likely to be diagnosed with breast cancer. The findings were also presented at the 2026 ASCO annual meeting by Dr. Elizabeth McDonald of the University of Pennsylvania’s Perelman School of Medicine and were simultaneously published in JCO Oncology Practice.

Dr. McDonald said:

GLP-1 medications are intriguing from a cancer research perspective because they weren’t designed for cancer therapy, but they do affect many different targets and pathways associated with cancer development, so we’re eager to study them in this context.

Your responses and feedback are welcome!

Source: “GLP-1 Meds May Help Slow the Spread of Certain Obesity-Related Cancers,” HealthDay, 5/27/26
Source: “GLP-1s May Reduce Metastatic Progression of Certain Obesity-Related Cancers,” ASCO, 5/21/26
Source: “GLP-1 use linked to lower breast cancer incidence in large cohort study,” PennMedicine.org, 6/2/26
Source: “GLP-1 Agonists Are Associated With a Significant Reduction in Breast Cancer Incidence in Women,” JCO Oncology Practice, 6/2/26
Image by Darina Belonogova/Pexels

Early-Life Junk Food Rewires the Brain

A growing body of research continues to show that what children eat can have lifelong consequences. Now, a new study published in Nature Communications suggests that eating a high-fat, high-sugar junk food diet during early life may permanently alter the brain’s appetite and reward systems, increasing the risk of overeating well into adulthood. The findings offer new insight into how childhood nutrition affects long-term health and reveal that the gut microbiome may hold the key to reversing some of the damage.

Researchers investigated how consuming a high-fat, high-sugar diet early in life impacts eating behaviors later on, even after switching to a healthier diet in adulthood. The study found that early exposure to junk food can leave a lasting imprint on the brain, essentially rewiring hunger and reward pathways in ways that persist over time.

Perhaps most concerning, the changes remained even after the subjects returned to a healthy weight and healthier eating patterns. This suggests that the effects of poor childhood nutrition go beyond temporary weight gain and may fundamentally influence how the brain regulates appetite.

One of the study’s most striking discoveries was that males and females responded differently to the unhealthy diet. Researchers found that females appeared to be more vulnerable to the long-term effects of junk food consumption. In females, the diet reduced leptin receptors in the brain.

Leptin is a hormone responsible for signaling fullness and helping regulate food intake. When leptin signaling is disrupted, the brain may struggle to recognize when enough food has been consumed, increasing the likelihood of overeating.

The unhealthy diet also interfered with how females processed essential amino acids such as tryptophan and arginine, which play important roles in mood, metabolism, and brain function. Males, on the other hand, experienced disruptions in immune-sensing pathways and steroid metabolism, showing that junk food can affect biological systems differently depending on sex. These findings may help researchers better understand why some individuals are more susceptible to obesity and eating disorders later in life.

While the long-term brain changes linked to junk food are concerning, the study also uncovered a promising possibility: targeted gut microbiome therapies may help reverse some of the damage. Researchers successfully used both probiotics and prebiotics to improve eating behaviors and restore gut-brain communication pathways.

Probiotics, including Bifidobacterium longum, appeared to directly reduce overeating behaviors while causing minimal disruption to the existing gut ecosystem. Meanwhile, prebiotics helped improve the overall gut environment and supported healthier communication between the gut and the brain.

The findings reinforce the growing understanding that the gut microbiome plays a major role in mental and physical health. Often referred to as the “gut-brain axis,” this communication network connects digestive health with brain function, appetite regulation, mood, and metabolism. Researchers suggest that targeting the microbiome could potentially serve as a “reset button” for unhealthy eating patterns that begin in childhood.

There are several reasons why limiting junk food during childhood is so important. One is nutritional deficiencies. Children require vitamins, minerals, protein, fiber, and healthy fats to support proper physical and cognitive development. Diets dominated by processed foods often fail to provide these essential nutrients, potentially impacting growth, immunity, and brain development.

Another reason is the increased risk of weight gain and obesity. Then there are effects on learning and behavior, as research has linked diets high in sugar and unhealthy fats with poorer concentration, mood swings, and behavioral difficulties in children. Let’s not forget dental health problems. Sugary snacks and beverages can increase the risk of cavities and tooth decay. Since children’s teeth are still developing, frequent exposure to sugary foods can have lasting consequences for oral health.

Finally, children who regularly consume junk food may become less interested in healthier options like fruits, vegetables, whole grains, and lean proteins. These habits can continue into adulthood, increasing the risk of chronic disease over time.

As scientists continue exploring the connection between nutrition, the gut, and the brain, one message is becoming increasingly clear: What children eat today may influence their health and eating behaviors for decades to come.

Your responses and feedback are welcome!

Source: “Childhood Junk Food May Rewire The Brain For Life, Reveals Study,” NDTV.com, 5/28/26
Source: “Bifidobacterium longum and prebiotic interventions restore early-life high-fat/high-sugar diet-induced alterations in feeding behavior in adult mice,” Nature Communications, 2/24/26
Source: New Study Discovers That a Junk-Food Diet Rewires the Brain,” Inc.com, 5/24/26
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Rethinking the “Adiposity Rebound”

For decades, doctors and researchers have relied on a concept known as the “adiposity rebound” to help explain childhood growth patterns and predict future obesity risk. But new research is now challenging that long-standing belief, suggesting that the rise in body mass index (BMI) seen in early childhood may have far less to do with body fat than previously thought.

The findings, presented by Andrew Agbaje at the European Congress on Obesity and published in The Journal of Nutrition, argue that the so-called adiposity rebound may actually reflect healthy muscle and lean tissue development rather than an increase in fat mass.

What is the “adiposity rebound”?

The adiposity rebound theory dates back to 1984, when French researcher Marie Françoise Rolland-Cachera and colleagues described a predictable pattern in childhood BMI growth. Typically, BMI rises rapidly during infancy, declines through the preschool years, and then begins increasing again around ages 4 to 6. Researchers believed this second rise, the “rebound,” represented a return of body fat accumulation.

Over time, studies suggested that children who experienced this rebound earlier in life were more likely to develop obesity during adolescence and adulthood. As a result, the timing of adiposity rebound became widely discussed in pediatric health and obesity prevention. Many clinicians viewed an early rebound as a warning sign that could justify lifestyle interventions focused on diet, physical activity, and weight management.

Why researchers are questioning the theory

According to Prof. Agbaje, the problem may lie in relying too heavily on BMI as a measure of body fat. BMI is a simple calculation based on height and weight, but it cannot distinguish between fat, muscle, bone, and other lean tissues. This limitation has long been recognized in adults, especially among athletes or muscular people whose BMI may appear elevated despite having low body fat levels.

Dr. Agbaje argues that the same issue may exist in children. He says:

Puberty is a defining moment in human biology that alters the whole body, but adiposity rebound is not; it is a natural growth process unattached to any problem, whether it is early rebound or late. So the previous associations relating early BMI-based adiposity rebound to later life obesity are misleading analyses. Positive statistical associations do not always equate to biological plausibility.

New evidence points to lean mass growth

To explore what is really happening during early childhood growth, researchers examined data from 2,410 children and adolescents between ages 2 and 19 using information from the National Health and Nutrition Examination Survey (NHANES), dated 2021-2023.

Instead of focusing only on BMI, the study also analyzed waist circumference-to-height ratio (WHtR), which researchers say is a more accurate indicator of body fat distribution. The results showed a striking difference between BMI patterns and WHtR patterns.

While BMI followed the familiar trajectory, declining in early childhood before increasing again, WHtR continued to decrease for several years and never returned to the higher levels seen during toddlerhood. Researchers say this finding suggests that the BMI rebound is not actually driven by increasing fat mass. Instead, it may reflect healthy gains in muscle, lean tissue, and overall body development.

In other words, what many experts once viewed as a warning sign of obesity could actually represent a normal and beneficial stage of growth.

A “body composition reset”

Dr. Agbaje describes this period as a kind of “body composition reset” that helps prepare children for later stages of development. Rather than indicating excess fat gain, the increase in BMI after early childhood may simply reflect the body building strength, muscle mass, and lean tissue needed for continued growth.

This interpretation could dramatically change how clinicians view childhood BMI trends. For years, some interventions attempted to delay or alter adiposity rebound in hopes of reducing future obesity risk. However, Dr. Agbaje points to long-term clinical trials that found dietary interventions did not change the timing or pattern of BMI rebound. That may be because the process is not a disease mechanism at all.

The study also adds to growing discussions about the limitations of BMI as a health tool. Researchers increasingly argue that BMI alone may oversimplify body composition, especially in children whose bodies are constantly developing.

Waist-to-height ratio, by contrast, may provide a clearer picture of unhealthy fat accumulation because it focuses more directly on central body fat. Dr. Agbaje believes WHtR could become a more useful screening tool for identifying excess fat in children and adolescents moving forward.

What this could mean for parents and pediatricians

The findings do not suggest that childhood obesity is unimportant or that healthy lifestyle habits should be ignored. Instead, the research highlights the importance of accurately understanding normal growth and avoiding unnecessary concern over biological processes that may simply reflect healthy development.

If future studies confirm these findings, it could reshape how pediatricians evaluate childhood growth patterns and obesity risk. Rather than treating early BMI rebounds as a condition requiring intervention, experts may begin focusing more on overall body composition, activity levels, nutrition quality, and long-term metabolic health.

Your responses and feedback are welcome!

Source: “Scientists Say a 40-Year-Old Childhood Obesity Warning May Be Completely Wrong,” SciTechDaily, 5/15/26
Source: “Early Adiposity Rebound and the Risk of Adult Obesity,” AAP.org, 3/1/98
Source: “Effects of 20-year infancy-onset dietary counselling on cardiometabolic risk factors in the Special Turku Coronary Risk Factor Intervention Project (STRIP): 6-year post-intervention follow-up,” The Lancet, May 2020
Source: “Waist-circumference-to-height-ratio had better longitudinal agreement with DEXA-measured fat mass than BMI in 7237 children,” Nature.com, 3/5/24
Source: “Adiposity Rebound or Fat-Free Mass Anabolism in Children—Challenging a 42-Year-Old BMI Puzzle with Waist-to-Height Ratio: The ASNF-NNF 2025 Inaugural Flemming Quaade Award for Innovation in Childhood Obesity Lecture,” The Journal of Nutrition, May 2026
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