Greaux Healthy Releases Childhood Obesity Prevention Toolkit

Childhood obesity is a growing concern across the nation, with Louisiana ranking third in the country for prevalence. Addressing this public health crisis requires a multifaceted approach rooted in evidence-based care and practical resources. Recognizing this urgent need, Greaux Healthy, a public service initiative powered by LSU’s Pennington Biomedical Research Center in collaboration with the State of Louisiana, has launched the Childhood Obesity Prevention, Evaluation, and Treatment Toolkit.

This comprehensive resource is designed to equip healthcare providers with the latest scientific evidence and actionable strategies to prevent, evaluate, and treat childhood obesity and its related comorbidities. Developed in alignment with the 2023 American Academy of Pediatrics (AAP) clinical practice guidelines, the toolkit serves as a quick-reference guide that can be seamlessly integrated into various pediatric healthcare settings across Louisiana.

A practical, evidence-based approach

The Childhood Obesity Prevention, Evaluation, and Treatment Toolkit synthesizes the latest research into a streamlined resource, offering clear and practical guidance for healthcare professionals. Dr. Amanda Staiano, Director of Pennington Biomedical’s Pediatric Obesity and Health Behavior Laboratory and a key contributor to the toolkit, highlights its significance:

The comprehensive nature of this toolkit provides pediatricians with a quick reference for evaluating childhood obesity and its comorbidities and approaches for treating children and adolescents with overweight and obesity, all grounded in scientific evidence.

The toolkit’s user-friendly format allows providers to efficiently integrate scientifically validated protocols into their clinical routines, ensuring early intervention and improved health outcomes for children.

Key features of the toolkit

  • Rapid Evaluation Protocols: Simplified guidelines for assessing obesity and associated health risks.
  • Step-by-Step Treatment Strategies: Evidence-based recommendations for behavioral counseling, pharmacotherapy, and referrals for advanced care when needed.
  • Family-Centered Tools: Resources to support sustainable lifestyle changes for children and their families.

 

Pennington Biomedical Medical Investigator Dr. Stewart T. Gordon, FAAP, underscores the importance of the toolkit in addressing a statewide health challenge:

The Greaux Healthy team looks forward to working with all Louisiana pediatric health care professionals — including pediatricians, family physicians, nurse practitioners, physician assistants, dieticians, behavioral health providers, nurses, and health educators — to improve access to prevention, evaluation, and treatment of childhood obesity.

A call to action

Dr. John Kirwan, Executive Director of Pennington Biomedical, reinforces the urgency of this initiative:

Waiting or delaying treatment is not an option when it comes to childhood obesity. Our goal is to provide health care providers with the tools they need to make informed decisions and offer comprehensive, effective treatment to improve the health and future of our children.

With childhood obesity being a chronic disease affecting thousands of Louisiana children, the launch of this toolkit marks a critical step forward in improving pediatric healthcare. By equipping providers with the necessary resources, Greaux Healthy and Pennington Biomedical are fostering a healthier future for children and families across the state.

Healthcare professionals are encouraged to utilize this free, evidence-based resource to enhance their clinical practice and help combat childhood obesity effectively. You can download it here.

Your responses and feedback are welcome!

Source: “New toolkit empowers health care providers with evidence-based strategies for childhood obesity prevention and treatment,” Medical XPress, 2/20/25
Image by Katrin Bolotsova/Pexels

Oprah Through the Years, Part 17

This post picks up from where an earlier one left off: with Oprah Winfrey in the late 1980s. She was an incredibly popular show-biz figure and media icon, whose global fame spread partly because of her wide variety of interests. Her opinions were respected, her tastes admired, and droves of people relied upon her judgment in such matters as which books to read. Fans responded to her empathy, spontaneity, generosity, and numerous other attractive personal qualities, and related to her like a sister or dear friend.

People, especially women, trusted Oprah and felt understood by her. As both a television host and a sympathetic surrogate friend, she must have felt strong pressure to cover the issue of overweight and everything connected with it, because such a large portion of her audience was dealing with the specter of obesity, and needed help. At the same time, a person in her position would be well-advised to tread carefully, and avoid promoting the anti-obesity culture or appearing as an anti-obesity crusader. Coming from her, any hint of blame or shame could alienate the audience.

An ancient shadow

These conditions resembled an ancient philosophical and theological conflict that so many individuals and institutions over the centuries had to face, and somehow reconcile: how to love the sinner but hate the sin. How to deplore the existence of too much fat, without insulting those who grew too much fat and then suffered for it.

Oprah was not yet the mega-wealthy star she would eventually become, but one thing was clear, and worth repeating :

All the fame and the success doesn’t mean anything if you can’t fit into the clothes. If you can’t fit into your clothes, it means the fat won. It means you didn’t win.

Also, on the personal level, for Oprah to actively campaign against obesity was at the same time to wage war against herself. This was especially evident in the aftermath of the much-regretted 1988 “wagon of fat” TV appearance. To continue wearing those skinny jeans, it would only be necessary to remain on a liquid diet for the rest of her life.

The winds of change

A couple of years later, she told a magazine reporter about the four months of enforced starvation that preceded the wagon stunt and confessed, “I thought I was cured. And that’s just not true. You have to find a way to live in the world with food.” At which point, she did a 180-degree turn and decided to never diet again. By 1992, her weight had reached a peak 237 pounds, too much for a 5’7″ frame to carry. At some point she met trainer Bob Greene and they had a conversation which she recalled years later for her O magazine.

He asked why she was overweight; she replied that she loved food. This was not the exact answer Greene was hoping to elicit, however, and it was quite some time before Oprah was comfortable with admitting that the purpose of eating so much food was to numb her emotions.

As we have mentioned, the investigation into any one person’s obesity needs to include several aspects of family and individual history. Of course their habitual dietary practices are a big factor, but so are their other customary activities, including purposeful exercise. Also to be considered are the psychosocial environment, medications, and their idiosyncratic pattern of weight loss and gain.

Oprah had never consulted a psychiatrist, but subsequent conversations with Greene turned out to be, in her words, “priceless therapy.”

Your responses and feedback are welcome!

Source: “The Highs and Lows of Oprah Winfrey’s 50-Year Weight Loss Journey,” MSN.com, 2024
Source: “Top 10 Oprah Moments,” TIME.com, 05/25/11
Source: “Oprah Winfrey’s Weight Loss Journey,” EOnline.com, 03/24/24
Image by Pat Hartman

New Study Finds Self-Guided Family-Based Treatment Effective for Childhood Obesity

Childhood obesity is a growing concern worldwide, with one in five children in the U.S. affected. In southern Italy, four in 10 children are overweight despite it being the birthplace of the highly praised Mediterranean Diet. And South Korea is now has the highest obesity rate in East Asia among children and adolescents. And that’s just in the news this week. The list grows and grows.

While traditional obesity treatment methods have been effective, they often come with significant barriers, such as time commitment, cost, and access to specialized care. However, a new clinical trial from UC San Diego suggests that a self-guided version of Family-Based Treatment (FBT) could be a game-changer, offering a more accessible, affordable, and equally effective alternative.

What is family-based treatment?

FBT is a well-established approach to treating childhood obesity that involves working closely with families to promote healthier behaviors. Traditionally, healthcare professionals guide families through a structured program focused on encouraging physical activity, teaching healthy eating habits, and developing age-appropriate behavioral skills.

The new study from UC San Diego’s Center for Healthy Eating and Activity Research (CHEAR) found that self-guided FBT provides the same benefits while reducing the time, cost, and scheduling constraints associated with clinician-led programs.

A more flexible, cost-effective approach

Dr. Kerri Boutelle, senior study author and director of CHEAR, highlighted the limitations of traditional FBT:

While effective, it can be time-intensive, expensive, and offered at limited times, making it difficult for many families to participate.

In contrast, self-guided FBT condenses the program significantly. Instead of the traditional 26 hours of treatment over six months, the self-guided model requires only five hours of treatment within the same timeframe. Families complete 20-minute sessions every other week without the need for a trained clinician, making it a viable option for busy households and those facing financial challenges.

The importance of family involvement

Unlike adult obesity, which is often addressed individually, research shows that a family-based approach is most effective for children. Traditional FBT typically involves parents and their children (ages 8-15) in small group sessions, fostering a supportive environment. However, Dr. Boutelle’s research suggests that direct work with parents — rather than relying on group sessions or extensive clinician involvement — is the key to success.

She said:

While some families may benefit from the standard approach, providing more flexible and accessible alternatives like self-guided FBT can help us make a wider impact on childhood obesity.

Dr. Boutelle emphasized that this model allows treatment to be delivered in medical offices, enabling physicians and healthcare providers to support families without requiring extensive training.

Addressing the complexity of childhood obesity

Obesity in children is a multifaceted issue influenced by diet, physical activity, genetics, and environmental factors. Key contributors include:

  • Diet: High consumption of sugary drinks, processed foods, and large portion sizes.
  • Physical Activity: Sedentary lifestyles, excessive screen time, and limited exercise.
  • Genetics: Some children may be genetically predisposed to weight gain.
  • Environment: Accessibility to unhealthy foods, lack of safe spaces for physical activity, and social norms promoting sedentary habits.

 

With obesity linked to serious health concerns such as type 2 diabetes, high blood pressure, and mental health issues, accessible and effective treatments are crucial. The self-guided FBT model offers a promising solution, making evidence-based care more widely available to families who might otherwise struggle to access traditional programs.

Looking ahead

The findings from UC San Diego’s research underscore the need for innovative approaches to tackling childhood obesity. By offering a flexible, cost-effective, and family-centered solution, self-guided FBT has the potential to reach more families and create lasting health improvements for children nationwide.

As Dr. Boutelle puts it:

There’s no reason to require extensive in-person treatment when we can achieve the same results in a way that fits into families’ lives more easily. Our goal is to ensure that more children receive the help they need without unnecessary barriers.

With ongoing efforts to expand awareness and accessibility, self-guided FBT could soon become a standard tool in the fight against childhood obesity.

Your responses and feedback are welcome!

Source: “UC San Diego clinical trial: Family-based treatment best for obese children,” SDNews.com, 2/14/25
Image by Agung Pandit Wiguna/Pexels

Genes, From Must to Maybe — Continued

Up until recently, genes and epigenetic variations have dictated how the inheritance of obesity works. Sure, they “contribute to obesity by influencing the function of metabolic pathways in the body and regulating neural pathways and appetite centers.” Certainly, they “influence insulin resistance, dyslipidemia, inflammation, hypertension, and ectopic fat deposition.”

Of course, genetic mutations “can be inherited in an autosomal dominant or autosomal recessive manner and are influenced by genetic mechanisms of deletion, genetic imprinting, and translocation.” So far all these factors, as described in the book Genetics and Obesity, have been unrelentingly true.

Multiplicity of causation

But, as previously discussed, genes and their complex epigenetic mutations no longer hold the monopoly on defining or deciding fate for all humans, all the time.

First, science learned a lot about how epigenetic modifications happen during the development of the fetus. Of course, such a possibility had been suspected. But we have come a long way from the days when, for instance, the grotesque physique of the so-called Elephant Man was blamed on his pregnant mother having been frightened by the sight and behavior of an elephant.

The advance of science caused such beliefs to be dismissed as mere superstition. Then, science progressed even further to discover that disorders actually can grow from the horrors of war and other emotionally devastating roots.

Things that can happen

Epigenetic development, including changes to the insulin metabolism of a fetus, can be influenced by maternal over-nutrition and also by maternal under-nutrition. For the unborn child such disturbance can be a survival adaptation, but once born and exposed to other nutrition sources, it can lead to inescapable difficulty in survival.

The authors of Genetics and Obesity mention how…

The rising prevalence of obesity and type 2 diabetes in developing countries like India and sub-Saharan Africa confounded epidemiologists for the longest time and is now known to have its origins explained by the theory of fetal programming.

Another source of trouble, quite understandably, is maternal exposure to toxins like those introduced by cigarette smoking, and other endocrine-disrupting chemicals now recognized as obesogens. Maternal stress, caused by such events as natural disasters and their grievous consequences, is strongly suspected. Fetal metabolic derangement can stem from the mother being very young, or seriously underweight, or suffering from diabetes.

Multifactorial, again

The nourishment absorbed by a person as a baby and as a small child are both, of course, very influential in either a positive or negative way. Treatment with antibiotics in the first year of life has been linked to subsequent obesity, as well as non-alcoholic fatty liver disease and other conditions later in life. Even paternal over-nutrition, low protein intake, pre-diabetes, and other conditions can affect a child’s development. Mind you, this is the father! These causes have recently been looked at much more closely than ever before.

Then, there is syndromic obesity, so named because it results from syndromes with such distinctive names as Prader-Willi, WAGR, SIM1, Bardet-Biedl, and Fragile X. Also, there is monogenic obesity, which “generally involves mutations in the leptin signaling pathway leading to suppression of anorexigenic and activation of orexigenic pathways.” Furthermore, around 60% of inherited obesity is now understood to be of polygenic origin, affecting appetite control, energy balance, and many other factors.

Your responses and feedback are welcome!

Source: “Genetics and Obesity,” NIH.gov, 07/31/23
Source: “Joseph Merrick — The Elephant Man,” LondonMuseum.org, undated
Image by Cory Doctorow/Attribution-ShareAlike 2.0 Generic

Genes, From Must to Maybe

DNA is the instruction book that directs the activities of cells. Epigenetics is the field of knowledge about the heritable changes in the workings of genes, and more importantly, about how their actions can be modified without disturbing the DNA sequence itself.

The epigenome consists of all the genes in the body, plus everything else that influences them for better or worse; and it is malleable. Here is a quotation from the National Human Genome Research Institute:

The epigenome consists of chemical compounds that modify, or mark, the genome in a way that tells it what to do, where to do it, and when to do it. Different cells have different epigenetic marks. These epigenetic marks, which are not part of the DNA itself, can be passed on from cell to cell as cells divide, and from one generation to the next.

Shockingly, over recent decades, it has begun to look as though a person’s genetic makeup does not actually imply inexorable Fate, but resembles something more like a set of very strong suggestions. Even without crazy science-fictional editing tools like CRISPR (clustered interspaced short palindromic repeats), unsatisfactory genes can be outsmarted and over-ruled by the human organism itself.

Moreover, the person who inhabits the body is clueless about the remodeling project. It seems nothing short of miraculous, that thousands of genetic diseases are now seen as potentially fixable by a one-time CRISPR treatment. But all along, Nature has been busy re-arranging the genetic furniture. This quotation is from the Cleveland Clinic:

[The epigenome] changes over time. That can be both good and bad. It’s good in the sense that things like nutritious food, exercise and manageable stress can result in epigenetic changes that can promote health. But other factors like processed foods, smoking and lots of stress can cause epigenetic changes that can harm health.

Various epigenetic changes affect the metabolism, the aging process, brain disorders, inflammatory and autoimmune diseases, the tolerance for neoplasms, and even susceptibility to substance use disorders. It comes as no surprise that these alterations also make a difference around the heritability of obesity. Here are words from the book Genetics and Obesity, by Ekta Tirthani, Mina S. Said, and Anis Rehman:

About 50% of the time, obesity in childhood is carried into adulthood in a phenomenon known as “tracking.” Around 250 genes are now associated with obesity. The FTO gene on chromosome 16 is the most important and carries the highest risk of the obesity phenotype.

So, this is a serious matter, and what are we doing about it? Genetically predisposed obesity can now be treated with “early lifestyle interventions, bariatric surgery, and medications.” Better yet, the discipline of endocrinology “can help treat and control diabetes and other cardiometabolic parameters that cause epigenome changes passed on from generation to generation.”

Out in the world, however, researchers do need to deal with some complications:

In genome-wide association studies done so far, most subjects have European ancestry. However, 47% or the vast majority of patients grappling with the burden of obesity in the United States are of African-American and Hispanic/Latino descent.

Obviously, other countries might also face such problems when attempting to study variegated populations. But the future of the field shows incredible promise in the areas of obesity and metabolic disorders. For instance,

The use of histone deacetylators is now being suggested […] for its use in lifestyle medicine, and research in this field is ongoing. Methylation Quantitative Trait Locus (meQTL) studies are now being used to further epigenetic studies. New Nutri-pharmacogenomic studies are expanding our understanding of how nutrition affects genetics.

The heritability of obesity is easier than many other characteristics to observe and verify with the naked eye. It also is relevant to a very large chunk of the population, and thus likely to attract research grants and generate useful publicity. It should not be a chore to convince the public and the relevant institutions and funding sources of the vital importance of this kind of research, and of the financial support necessary to make it all happen.

Your responses and feedback are welcome!

Source: “National Human Genome Research Institute,” Genome.gov, undated
Source: “Epigenetics,” ClevelandClinic.org,” undated
Source: “Genetics and Obesity,” NIH.gov, 07/31/23
Image by National Human Genome Research/Public Domain

Oversize Bodies and Itty-Bitty Genes, Continued

Nature is able to circumvent expectations and even reason, and science should not be blamed for underestimating that possibility, because cause and effect are not always blatantly obvious. Previously we mentioned a Netherlands study showing that “men who were still in the womb when their mothers experienced malnutrition tended to have children with a tendency to become overweight adults.”

In other words, the effect carries on into the third generation. Such weirdness can be explained by accepting that genes do not interact only with one another, but with such environmental factors as temperature, acidity, and nutrients, as well as elements that are not yet recognized.

War, separation from loved ones, and many other types of stress can cause a person’s physiology to change in ways that are heritable, while their genetics remain unchanged. In Greek, “epi” means over, on top of, or in addition to. In this case, it signifies that cell function can change in a way that will be stable and is heritable, while the DNA sequence remains unchanged. This happens because of the world around us, when “our environment influences our genes by changing the chemicals attached to them,” and sometimes because of choices we make such as “what we eat, our physical activity level, access to resources and more.”

All this implies that, since some characteristics are changeable, we are better off figuring out how to play a deliberate and purposeful role, rather than heedlessly accept whatever random experiments some corporation wants to perform on us, and especially in preference to letting things happen to us through our own neglect. Sadly, depending on one’s gender, age, parental status, state of health, and many other factors, the average grownup does not like to think too much about this whole subject.

What moms do matters

Many women like to learn about the best veggies to eat while pregnant, but very few would enjoy an in-depth analysis of how their habits during and even before pregnancy quite possibly messed up the lives of their existing children. Guilt alone is oppressive enough, but guilt for something that can never be taken back or corrected is a potentially catastrophic burden. For a mother in that position, blame can come from three directions: herself, the child, and the biological father. If the child is born with, for instance, a problem that her smoking habit probably caused, there is the recipe for a lifetime of misery.

With maternal smoking alone, possible consequences include miscarriage, premature birth, stillbirth, placental abruption, placenta previa, low birth weight, and increased risk of defects like cleft lip and cleft palate. The fetus might not get enough oxygen, and lung problems are a possibility. There could be abnormal bleeding during pregnancy or delivery. Even after a seemingly successful delivery, the chance of Sudden Infant Death Syndrome is increased.

It transcends the personal

There is another problem. The entire health insurance industry is already a nightmare for patients and families to deal with. When a baby shows up with medical problems, a thorough study of all the epigenetic possibilities could cause a horrific situation. If detectives were to compile cases against mothers who, for instance, smoked cigarettes while pregnant, this could lead to, among other consequences, court battles capable of consuming fortunes and lifetimes.

What about childhood obesity, and a mother’s liability if her child turns out to be dangerously obese? A report titled “The Effect of Maternal Overweight and Obesity Pre-Pregnancy and During Childhood in the Development of Obesity in Children and Adolescents: A Systematic Literature Review” examined 11 studies on the subject. Some looked at maternal overweight or obesity before conception, and found “consistent positive associations with childhood obesity,” while others reported “positive associations between childhood obesity and maternal overweight/obesity during childhood.” The paper goes on to say,

This review has confirmed the multifactorial etiology of childhood obesity, indicating that maternal overweight and obesity has an important role in the development of childhood obesity, regardless of its occurrence (i.e., before the child’s conception or during childhood).

Still, the book we discussed, Genetics and Obesity, named factors that can overrule the gene pool and cause positive deviations. Bariatric surgery affects micro-RNA and can cause epigenetic changes. A staunchly maintained exercise schedule “can cause widespread changes in DNA methylation.” So can fasting.

And if positive epigenetic modification is what we want, it can be obtained with prebiotics and probiotics and even with fecal transplants to build up and perk up the gut microbiome. In other words, a conscientious prospective mother can plan ahead, and quit smoking or lose weight or otherwise “clean up her act” and provide a safe and welcoming womb for a fetus to inhabit.

(To be continued…)

Your responses and feedback are welcome!

Source: “Epigenetics,” ClevelandClinic.org, undated
Source: “Genetics and Obesity,” NIH.gov, 07/31/23
Source: “Smoking During Pregnancy,” WebMD.com, 10/04/24
Source: “The Effect of Maternal Overweight and Obesity Pre-Pregnancy and During Childhood in the Development of Obesity in Children and Adolescents: A Systematic Literature Review,” NIH.gov, 12/02/22
Image by The 5th Ape/Attribution 2.0 Generic

Can New Weight-Loss Drugs Surpass The Current Ones?

Are the weight loss medications currently on the market possibly being overused or not used as intended? Yes and yes. The article published in Axios, “Wegovy and Ozempic stars dim amid overuse concerns,” quotes a few specialists voicing their concern. One of them is Peter Antall, chief medical officer of digital chronic health company Lark. He says,

There is almost like a backlash kind of a sentiment going on… I don’t believe that we’re having second thoughts about the power of the medication. But I think the shine is coming off how they’re being used in real practice… That’s where many of us are concerned.

Another expert is obesity specialist and gastroenterologist Dr. Christopher McGowan, who penned his opinion in MedPage Today. He explained why his “perspective has shifted based on real-world experience.” Dr. McGowan is “deeply concerned about how GLP-1 medications are being used.” He writes:

The benefits of these drugs cannot be denied when they are taken as intended — meaning indefinitely. But what happens to the body and mind when these medications are discontinued? This is where the problem lies…

Noting that “from an efficacy standpoint, these drugs ‘work’,” but only for those who can “afford, tolerate, and sustain GLP-1.” They lose weight and enjoy other benefits such as improvements in various conditions, including kidney disease, sleep apnea, osteoarthritis — the list goes on. However, Dr. McGowan’s parting words send a chill:

 I fear we will look back on this era — after patients have spent tens of thousands of dollars, endured uncomfortable and sometimes serious side effects and experienced recurring weight gain and resurgent food noise — and ask: Even if these drugs ‘work,’ did they really work? Or did they ultimately harm our patients, our society, and our economy? It’s a sobering thought, but one I fear is all too real.

New kids on the block

Pharmaceutical companies are fully aware of current concerns and are actively testing a new wave of weight-loss medications, or planning more trials for the current ones, with a goal of enhancing their effectiveness and offering additional health benefits beyond shedding pounds.

Current treatments like Ozempic and Wegovy, which contain semaglutide — a GLP-1 receptor agonist that helps regulate blood sugar and appetite, are expensive, require weekly injections, and must be taken long-term to prevent weight regain. Drug makers hope that new alternatives will overcome these challenges. Plus, the global market keeps expanding and the demand is surging, so we are sure Big Pharma sees the dollar signs as well.

Let’s take a quick look at what medications we should expect to improve, and what the manufacturers and the researchers plan for them in 2025, as outlined in a recent article published in Nature.

Tirzepatide

Tirzepatide, marketed as Mounjaro and Zepbound, activates both GLP-1 and another hormone, GIP, which plays a role in fat metabolism. In clinical trials, it helped participants lose up to 20% of their body weight over 72 weeks, outperforming semaglutide, which leads to about 15% weight loss in a similar timeframe. Additionally, tirzepatide reduced heart weight, lowered fat around the heart, improved mobility, and decreased blood pressure and inflammation.

A major trial set to conclude in 2025 will explore its impact on heart disease in people with obesity and diabetes.

Retatrutide

Developed by Eli Lilly, retatrutide stimulates GLP-1, GIP, and glucagon receptors, showing even greater potential than existing drugs. In trials, participants lost an average of 24% of their body weight over 11 months. This medication also helped regulate blood sugar in diabetics and is now in phase III trials, expected to conclude by 2026.

Experts believe that combination therapies like retatrutide could be particularly effective, as obesity is a complex condition that benefits from targeting multiple biological pathways.

Orforglipron

Unlike Ozempic, which requires injection, orforglipron is a daily pill that mimics GLP-1’s effects. In early trials, it led to a 10% weight loss over 26 weeks while improving blood pressure and reducing circulating fat molecules.

Eli Lilly anticipates completing phase III trials in 2025, with potential U.S. regulatory approval in 2026. Experts suggest that if oral drugs like orforglipron prove effective, they could disrupt the market by offering a more convenient and cost-effective option.

MariTide

Amgen’s experimental drug MariTide, which stimulates GLP-1 while inhibiting GIP activity, is designed to be taken via monthly injections. In a 52-week study, it resulted in up to 20% weight loss. Unlike other treatments, MariTide appears to help maintain weight loss for months after stopping the medication, an issue seen with semaglutide and tirzepatide.

This potential for sustained results could make it a more attractive option for patients reluctant to commit to lifelong treatment.

CagriSema

Novo Nordisk’s CagriSema, a blend of semaglutide and cagrilintide, has shown superior weight-loss outcomes compared to its individual components. A 68-week study saw participants lose approximately 23% of their body weight.

Muscle preservation and metabolic treatments

Several companies are exploring synthetic amylin-based therapies, which help regulate appetite and blood sugar while preserving muscle mass — an advantage over GLP-1 drugs, which can lead to muscle loss. Novo Nordisk’s amycretin, a combination of GLP-1 and amylin, led to a 22% weight reduction in just 36 weeks.

Another experimental drug, enobosarm, developed by Veru, was found to preserve muscle in older adults with obesity when combined with Wegovy. Future studies may investigate how to help older or frail individuals lose weight while maintaining muscle strength and preventing osteoporosis.

Emerging therapies targeting cannabinoid receptors, which influence hunger, have shown early promise, with more research expected in 2025.

The bottom line

Looking ahead, researchers hope to shift the focus from simple weight loss to a broader understanding of obesity as a metabolic disease. Some believe that the next major breakthrough could come from a treatment that addresses inflammation, a key factor in obesity — though results from human trials are still a long way off.

Even if these new treatments aren’t widely available in 2025, researchers believe that the coming year will provide key insights into which therapies will be most effective and accessible in the near future.

Your responses and feedback are welcome!

Source: “The weight-loss drugs being tested in 2025: will they beat Ozempic?,” Nature, 2/6/25
Source: “Wegovy and Ozempic stars dim amid overuse concerns,” Axios, 2/11/25
Source: “I No Longer Think GLP-1s Are the Answer,” MedPage Today, 1/30/25
Image by Chokniti Khongchum/Pexels

Oversize Bodies and Itty-Bitty Genes

The big complicating factor here is epigenetics, for which the Cleveland Clinic offers an elegant definition:

Epigenetics is the study of how our environment influences our genes by changing the chemicals attached to them. What we eat, our physical activity level, access to resources and more affect those chemicals, in turn shaping our health.

As it turns out, a lot of aspects of the human condition which were assumed to be hardwired, or totally determined by genes, are actually malleable, whether or not we currently understand the processes behind how all of this works.

So, on one level, the genes we inherit say “This is how it’s gonna be.” Then, the science of epigenetics comes along and says, “Except when it isn’t, and boy oh boy, do we ever still have a lot to learn about that!”

Today we consult the National Library of Medicine for an overview of contemporary knowledge and thinking about the relationship between obesity and genetics. The authors are Ekta Tirthani, Mina S. Said (both of Rochester General Hospital), and Anis Rehman (Northern Virginia Medical Center). There is, to use a non-technical and totally accurate phrase, a lot going on. The only factor that is a bedrock certainty is maternal health — and just to deal with that one aspect requires “a team of obstetricians, pediatricians, nutritionists, geneticists, psychologists.”

Diagnosis of genetic and/or epigenetic origins of obesity

Here is an abbreviated version, just the highlights, of the authors’ explanation of how to figure this out in any individual case, and it is no walk in the park:

Endocrine causes of obesity […] must be ruled out early with history, physical examination, and lab work. Syndromic obesity can sometimes be distinctly diagnosed based on the presence of physical features… After basic lab work is done […] physicians can check leptin, insulin, and proinsulin levels. If all the above blood work is negative genetic testing can be carried out.

This is where it gets really complicated, involving arcane lab work that is only available in a few advanced facilities, and costs a bundle because of the expensive equipment required, along with the detailed high-level knowledge in obscure fields. But wait, there is more.

Research is necessary into the individual’s family history and personal history, as well as several other areas of life: psychosocial environment, habitual dietary practices, everyday activities, purposeful exercise, medications, and the subject’s (or patient’s) unique pattern of weight gain and loss thus far.

Two drugs are FDA-approved for treating genetically caused obesity, while several others (like the semaglutide and liraglutide we hear so much about) are working hard to prove their worth in that arena.

Even when obesity is passed down through the genes, various interventions can make a difference. The implementation of many different interventions can eliminate, at least partially, the validity of “I can’t help myself, it’s genetic” as a rationale. Sometimes the problem is clearly not genetic.

Or is it? An entire branch of philosophy could be based on arguing that, ultimately, everything and anything in the realm of human behavior might be genetic in origin. The manuscript describes these areas in much greater detail. The interventions that are mentioned and their mechanisms include:

— Bariatric surgery can cause changes in adipocyte-derived exosomal micro-RNA and cause epigenetic changes in differential methylated regions…
— Regular exercise can cause widespread changes in DNA methylation… For patients who maintain their weight loss, the DNA methylation profiles resemble lean individuals…
— Fasting can cause changes in DNA methylation of genes…
— The use of probiotics, prebiotics, and fecal transplant can restore gut flora and cause positive epigenetic modifications…

One principle is impossible to overemphasize: Obesity is multifactorial. In this area of human health, genetic factors do not equal the Implacable Hand of Fate or any such fatalistic notion. There is, in other words, plenty of room for improvement.

(To be continued…)

Your responses and feedback are welcome!

Source: “Epigenetics,” ClevelandClinic.org, undated
Source: “Genetics and Obesity,” Genetics and Obesity, nih.gov, 07/31/23
Image by Kevin Simmons/Attribution 2.0 Generic/

Oprah Through the Years, Part 16

The previous post discussed a stressful event from when Oprah Winfrey’s career was just taking off — her interrogation and public shaming by comedian Joan Rivers who was, on that day, not very humorous at all.

We do not presume to read Oprah’s mind. But a rudimentary understanding of human psychology (and especially, personal experience with therapy) could inspire a person to imagine how the effects of such strenuous and ubiquitous harping on weight could cultivate a preoccupation with the subject that would carry into the future.

It could set up an ongoing conflict between being perpetually overweight oneself, and the seeming necessity to buy into the fat-hating, fat-shaming culture that America and many parts of the world had converted to. This is what appears to have happened to Oprah, while at the same time, over the ensuing years, she also had learning experiences and personal revelations about the harm caused by the whole anti-fat zeitgeist.

The path of twisted reasoning

It might make sense to perceive that 1985 event as something that loomed large in her subconscious, drawing her more and more into the fat-despising state of mind, while at the same time coping with the mental conflict that demanded she must of course despise herself. It would, after all, be a logical conclusion. If you are required to hate Fat, and yet also supposed to love yourself, well, that is simply too much cognitive dissonance for the mind to handle. Therefore, if you hate fat and and are fat, you must necessarily hate yourself — which somehow turns out to be easier than exploring the illogical root of the contradiction.

Aunt Joanie really cares

Also, logically, if such a prominent person as Rivers took the trouble to give advice — rough as that widely broadcast counseling session had been — it must mean that she truly cared, and only wanted the best for this TV guest who aimed for a career in entertainment. It was as if a respected aunt warned a troubled teenager that she had better straighten up and fly right, before she encountered the juvenile justice system and wound up in the reformatory.

If fat is bad, then as an honest and upright person you must hate all the fat, even your own. And if that awful stuff is part of you, you must be pretty awful. So to redeem yourself, the least you could do is become a missionary for the abolition of fat — which might account for the many shows having to do with overweight that Oprah produced and hosted over the years. Who knows? It might even connect to her later alignment with WeightWatchers, which could, uncharitably, be read not only as an investment opportunity, but also as “virtue signaling.”

In 1986, with the humiliation by Rivers still fresh, Oprah told her TV audience, “I still hate myself because of my weight.” Soon afterward came the quotation we already mentioned, which included the damning words,

If you can’t fit into your clothes, it means the fat won. It means you didn’t win.

And it’s not as if Oprah had never recognized the issue. For at least a decade, it had already loomed large in her mind. As far back as 1977, when she first consulted a diet doctor, she had been striving to win. Whenever a new fad diet came along she tried it, with consistently unsatisfactory results.

The session with Joan Rivers was later confirmed to be connected with the incident (three years later, in 1988) that Oprah eventually came to recognize as the “biggest, fattest mistake” of her career. In an article published only last year, Clare Stephens wrote,

Oprah recently acknowledged her role in perpetuating diet culture during a livestream for Weight Watchers. “I’ve been a major contributor to it.” she said… The wagon of fat has gone down in pop culture history as an example of our pathological obsession with weight loss…

[T]he wagon of fat seems like the insidious start of it all. A moment of stigmatizing fat, and telling an audience of primarily women that if they just cared enough, theirs could be set aside too, rather than attached to their bodies.

Your responses and feedback are welcome!

Source: “In 1985 Joan Rivers asked Oprah a Question,” MamaMia.com, 05/13/24
Image by Pat Hartman

Unlocking Brown Fat’s Power: A New Strategy Against Obesity

A groundbreaking study from the National Cancer Research Centre (CNIO) has revealed an innovative approach to combating obesity by enhancing the body’s natural ability to generate heat. Researchers have discovered that blocking the mitochondrial protein MCJ in brown fat significantly increases thermogenesis, leading to weight loss in obese mice and providing protection against obesity-related diseases such as diabetes. The study was recently highlighted in SciTechDaily.

Obesity and its global impact

Obesity is a pressing global health issue, affecting over 650 million people and contributing to the rise of cardiometabolic diseases and cancer risk. The study, led by Guadalupe Sabio from CNIO and Cintia Folgueira from CNIO and the National Centre for Cardiovascular Research (CNIC), sheds light on a crucial biological mechanism that could pave the way for new therapeutic strategies.

The role of MCJ in energy metabolism

At the heart of this discovery is MCJ, a mitochondrial protein that regulates energy production within cells. The researchers found that eliminating MCJ in obese mice led to a marked increase in heat production, resulting in significant weight loss. Furthermore, the transplantation of MCJ-deficient fat tissue into obese mice also triggered weight reduction, underscoring the protein’s pivotal role in metabolic regulation.

Understanding brown fat and thermogenesis

Adipose tissue, commonly known as body fat, is not merely a passive energy reservoir but an active participant in metabolic regulation. There are two primary types of adipose tissue. White adipose tissue (WAT), which primarily stores energy. Brown adipose tissue (BAT) is rich in mitochondria and specializes in thermogenesis — the process of generating heat in response to cold and other stimuli.

The authors write in Nature Communications:

Obesity is the result of either excessive food intake or inadequate total energy expenditure. We now know that adipose tissue –body fat–, in addition to storing energy, plays a crucial role in the management of that energy by the body. Adipose tissue is a complex organ that acts as a regulator of the whole body’s metabolism, and therefore modulating its function could well be a way to combat obesity.

For years, scientists have sought ways to activate brown fat as a means to combat obesity. “Understanding how brown fat generates heat is essential if we want to leverage it as a tool against obesity,” explains Sabio. The CNIO study now identifies MCJ as a key player in this process.

A new path to weight loss and disease prevention

By blocking MCJ, brown fat burns more energy, leading not only to weight loss but also to improved metabolic health. Mice lacking MCJ in their brown fat exhibited protection against common obesity-related health issues, including diabetes and high blood lipid levels. According to lead researcher Beatriz Cicuéndez, this protection is attributed to the activation of the catabolic pathway — a vital metabolic route that enhances fat, sugar, and protein consumption to produce heat.

Future therapeutic potential

The findings highlight MCJ as a promising therapeutic target for obesity treatment. However, before moving to clinical applications, further research is necessary to assess whether MCJ plays critical roles in other tissues. Additionally, scientists are investigating how changes in fat metabolism might influence cancer progression or conditions like cachexia, a syndrome characterized by extreme muscle and fat loss.

Looking ahead

This discovery opens up exciting possibilities for developing new obesity treatments that harness the body’s natural energy-burning mechanisms. By targeting MCJ, researchers may unlock a novel approach to weight management and metabolic disease prevention, bringing hope to millions struggling with obesity worldwide.

Your responses and feedback are welcome!

Source: “Goodbye Obesity: Scientists Uncover Fat-Burning Protein Switch,” SciTechDaily, 1/27/25
Source: “Absence of MCJ/DnaJC15 promotes brown adipose tissue thermogenesis,” Nature Communications, 1/13/25
Image by Total Shape/Pexels

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Profiles: Kids Struggling with Weight

Profiles: Kids Struggling with Obesity top bottom

The Book

OVERWEIGHT: What Kids Say explores the obesity problem from the often-overlooked perspective of children struggling with being overweight.

About Dr. Robert A. Pretlow

Dr. Robert A. Pretlow is a pediatrician and childhood obesity specialist. He has been researching and spreading awareness on the childhood obesity epidemic in the US for more than a decade.
You can contact Dr. Pretlow at:

Presentations

Dr. Pretlow’s invited presentation at the American Society of Animal Science 2020 Conference
What’s Causing Obesity in Companion Animals and What Can We Do About It

Dr. Pretlow’s invited presentation at the World Obesity Federation 2019 Conference:
Food/Eating Addiction and the Displacement Mechanism

Dr. Pretlow’s Multi-Center Clinical Trial Kick-off Speech 2018:
Obesity: Tackling the Root Cause

Dr. Pretlow’s 2017 Workshop on
Treatment of Obesity Using the Addiction Model

Dr. Pretlow’s invited presentation for
TEC and UNC 2016

Dr. Pretlow’s invited presentation at the 2015 Obesity Summit in London, UK.

Dr. Pretlow’s invited keynote at the 2014 European Childhood Obesity Group Congress in Salzburg, Austria.

Dr. Pretlow’s presentation at the 2013 European Congress on Obesity in Liverpool, UK.

Dr. Pretlow’s presentation at the 2011 International Conference on Childhood Obesity in Lisbon, Portugal.

Dr. Pretlow’s presentation at the 2010 Uniting Against Childhood Obesity Conference in Houston, TX.

Food & Health Resources