Study Finds That Severe Childhood Obesity Can Cut Life Expectancy in Half

Severe childhood obesity can drastically reduce life expectancy, cutting it nearly in half, according to a recent global study conducted by Stradoo GmbH, a life sciences consultancy in Munich. This research provides detailed insights into how the age of onset, severity, and duration of childhood obesity affect long-term health and life expectancy.

Long-term impact of childhood obesity

Presented at the European Congress on Obesity (ECO) in Venice, Italy, the study findings quantified the impact of various aspects of childhood obesity on long-term health for the first time. It was led by Dr. Urs Wiedemann along with colleagues from universities and hospitals across Europe and the United States.

The researchers found that the earlier a child develops obesity, the more severe the long-term effects. For instance, a child living with severe obesity at age four, who does not lose weight, has a life expectancy of just 39 years — about half the average life expectancy.

The findings in detail

“While it’s widely accepted that childhood obesity increases the risk of cardiovascular disease and related conditions such as type 2 diabetes (T2D), and that it can reduce life expectancy, evidence on the size of the impact has been patchy,” said Dr. Wiedemann. She added:

A better understanding of the precise magnitude of the long-term consequences and the factors that drive them could help inform prevention policies and approaches to treatment, as well as improve health and lengthen life.

The researchers developed an early-onset obesity model to estimate the effect of childhood obesity on cardiovascular disease, related conditions like T2D, and life expectancy. This model included four key variables: age of obesity onset, obesity duration, irreversible risk accumulation (a measure of irreversible health effects even after weight loss), and severity of obesity.

Critical factors

The severity of childhood obesity was measured using BMI Z-scores, which indicate how much an individual’s Body Mass Index (BMI) deviates from the norm for their age and sex. For example, a four-year-old boy with a BMI Z-score of 3.5, indicating severe obesity, has a life expectancy of just 39 years if he does not lose weight.

Data for the model were drawn from 50 existing clinical studies on obesity and related comorbidities, involving over 10 million participants worldwide. Approximately 2.7 million of these individuals were between two and 29 years of age.

The risks of severe childhood obesity

The model shows that earlier onset and more severe childhood obesity elevate the likelihood of developing related health issues later in life. For instance, a child with a BMI Z-score of 3.5 at age four has a 27% likelihood of developing type 2 diabetes by age 25 and a 45% chance by age 35. In contrast, a child with a BMI Z-score of 2 at age four has a 6.5% chance of developing type 2 diabetes by age 25 and 22% by age 35.

Higher BMI Z-scores at an early age also lead to a lower life expectancy. For instance, a BMI Z-score of 2 at age four without subsequent weight reduction reduces life expectancy from about 80 years to 65 years. The life expectancy drops further to 50 years for a BMI Z-score of 2.5 and 39 years for a BMI Z-score of 3.5.

Implications for early weight loss

Comparisons with other studies and expert opinions confirmed the model’s accuracy. Moreover, the model demonstrated the positive impact of weight loss on life expectancy and long-term health. For example, a child with severe early onset obesity (BMI Z-score of 4 at age four) has a life expectancy of 37 years and a 55% risk of developing T2D by age 35. If the child loses weight, reducing the BMI Z-score to 2 by age six, life expectancy increases to 64 years, and the risk of T2D drops to 29 percent.

“The early onset obesity model shows that weight reduction has a striking effect on life expectancy and comorbidity risk, especially when weight is lost early in life,” said Dr. Wiedemann.

Addressing childhood obesity

The model has some limitations. It does not account for the causes of obesity, genetic risk factors, ethnic or sex differences, or the interactions between different comorbidities. However, the impact of childhood obesity on life expectancy is profound.

Dr. Wiedemann said:

It is clear that childhood obesity should be considered a life-threatening disease. It is vital that treatment isn’t put off until the development of type 2 diabetes, high blood pressure, or other ‘warning signs’ but starts early. Early diagnosis should and can improve quality and length of life.

The bottom line

The findings of this study underscore the urgent need for early intervention in cases of childhood obesity. Preventative measures and timely treatments are crucial to improving the long-term health and life expectancy of affected children. As our understanding of the long-term consequences of childhood obesity deepens, so too must our commitment to tackling this critical public health issue from an early age.

Your responses and feedback are welcome!

Source: “Severe childhood obesity can cut life expectancy in half,” Earth.com, 05/16/24
Source: “Young children with persistent severe obesity could have half average life expectancy, study finds,” The Guardian, 05/14/24
Image by Christopher Williams on Unsplash

Fooling the Body With Filler

While bariatric surgery makes the stomach smaller, so less food will fit inside, a patient dedicated to non-compliance can definitely stretch that pouch back out again. Another method seeks to reduce the space available for food, not by tailoring the stomach itself into a smaller receptacle, but instead by filling it with non-food.

This work was done at Peking University First Hospital in Beijing, China:

Oral intragastric expandable capsules taken twice daily before meals reduce body weight in adults with overweight or obesity…

The tactic can cause “mild gastrointestinal adverse events,” but it has the advantage of being a non-invasive, non-permanent intervention. Another desirable feature is a lack of the many side effects that pharmacological methods too often trigger. Oral and intragastric, the capsule enters the mouth and lands in the stomach where it “expands to fill about one quarter of average stomach volume and then passes through the body.”

In the Chinese study, it took 24 weeks (six months, or half a year) for study participants to lose as little as 5% of baseline body weight, which seems paltry compared to some other methodologies.

Much more remains to be discovered about this way of doing things, because of the limitations of this small study in which only fewer than 4% of the subjects had type 2 diabetes. Also, they are characterized as “relatively young,” so they did not experience metabolic or cardiovascular effects that might kick in later. Here is an interesting detail:

Gastrointestinal disorders were reported in 25.0% of participants in the intragastric expandable capsule group compared with 21.9% in the placebo group, with most being transient and mild in severity.

To put it another way, a quarter of the participants taking the real stuff experienced unpleasant side effects — and so did almost as many of the subjects taking imaginary medicine. When people ingest something that is totally inert and inactive, and yet are visited by adverse results, that is the nocebo effect. “A nocebo effect can occur if a person takes a real or active medicine, and can also occur if they are given a placebo.”

Both placebo and nocebo effects are fascinating areas in which a whole lot of additional investigation is obviously needed. There is a lot going on in this realm, including controversy over the ethics. One article says,

Unfortunately, guidance for informing trial participants about trial intervention harms, in a way that is ethical, understandable, and does not produce nocebo effects, is currently under-researched. A recent study suggested that information provided to trial participants often fails to tell them what they wish to know, and that it is presented in a way that is difficult to understand.

What is this stuff, anyway?

Intragastric expandable capsules consist of two naturally derived components, food-grade carboxymethylcellulose cross-linked with citric acid, forming a three-dimensional polymer matrix that rapidly absorbs water and occupies the volume of the stomach and small intestine when administered orally with water before a meal, subsequently producing satiety. Each capsule contains no less than 10 000 highly absorbent cellulose-based hydrogel particles…

Dietary fiber comes in two varieties: soluble and insoluble. Soluble dietary fiber has long been recommended for its stomach-filling effect. It has been found to slow gastric emptying, increase perceived satiety, and significantly aid in appetite regulation. But its usefulness appears to depend on such variables as molecular size and solubility, and food matrix.

In addition, “Viscous soluble dietary fibres are believed to be more capable of inducing satiety compared to non-viscous soluble dietary fibres.” So apparently, “soluble fibres are not all created equal.” One vital area for additional research is the possibility that combinations of soluble fibers might be even more effective than any single type.

Your responses and feedback are welcome!

Source: “Premeal Stomach-Filling Capsule Effective for Weight Loss,” MDedge.com, 02/13/24
Source: “Placebo effect,” Vic.gov.au, undated
Source: “Harmful placebos,” Ox.ac.uk, 12/11/18
Source: “Efficacy and safety of intragastric expandable oral capsules in adults with overweight or obesity,” Doi.org 01/22/24
Source: “Unravelling the Effects of Soluble Dietary Fibre Supplementation on Energy Intake and Perceived Satiety in Healthy Adults,” NIH.gov, 01/06/19
Image by Edward Russell/CC BY 2.0 DEED

Upgrade the Parenting Tools

We have been exploring the realm of role modeling, also known as setting a good example. Anyone who tries it will discover that the magic word really is “example,” as in “Show, don’t tell.” Not nagging, not preaching, not blaming others for their lax habits. The more you talk about it, the less effective the lesson is. A good habit is to be quietly demonstrated over and over again, and eventually, a parent can be pleasantly surprised at what a young person has incorporated into his or her own life.

If there is a discussion about why the family is going on a three-mile hike, it’s better to keep it general. We don’t have to make a big deal out of how the excursion is supposed to help prevent a certain family member from getting fat. Not everything that can be said ought to be said.

Sometimes, we become exasperated with adult friends, for being so sloppy, careless, and neglectful of their health. But if their parents didn’t teach them good ways, how are they supposed to know? Let’s not let our kids grow up to be bad examples! Who wants that? Nobody.

Help is out there

It’s always a good idea to look around and learn what sort of free educational help is available from churches, schools, institutions, universities, and government bodies. Depending on the program and its intended audience, parents might learn how to cook basic healthful meals, how to prepare homemade “baby food,” how to understand the nutrition labels on food products, how to accurately judge whether a child is hungry or just bored or seeking attention, and many other very useful skills.

There are some things that many of us just never had the opportunity to hear about — for instance, as previously mentioned, it might require a dozen failed introduction attempts before a child will accept a new food. But the mere awareness of such a random fact can be incredibly encouraging.

Here is a thoughtful quotation from a pediatrician:

As parents, we have to set an example and to promote within our families healthy eating and healthy exercise. However, children are beset on all sides by their non-parental environment as well, which includes access to cheap, high-caloric foods; glitzy advertisements; a raft of screen and video entertainment; low-nutritional value school lunches; and on and on. Parents can be perfect role models, and still lose in this effort. But at least they stack the odds more favorably for their kids.

And we are reminded that when it comes to role models, kids are much more likely to be influenced by their own contemporaries:

Whether it is reassessing what foods we offer in vending machines, in the school cafeteria or at school celebrations, we need to set up the school environment so that the healthy choice becomes the “easy” choice and the “cool” choice. When kids see their peers and role models eating healthy, hydrating, and exercising, they are more likely to engage in those behaviors themselves.

That was educator Crystal Lim on the role that can and should be played by school districts and administrators, in creating a healthy school environment.

The astonishing track record of P.E.T.

Dr. Thomas Gordon’s Parent Effectiveness Training has been an incredible benefit to millions of families. With luck, a class might be found, but all the material is online for free anyway. P.E.T. examines the limitations of control, the power of attention, the difference between being authoritative and authoritarian, the emotional climate of the home, and a whole lot of other concepts that are equally valid whether the offspring are infants or teenagers.

Responsibility, labeling, genuine needs, rewards, responsibility, acceptance, problem ownership, active listening, conflict resolution, and many other topics are covered while the ideas around them are shown to be actionable and effective.

It is quite possible that the word “obesity” is never mentioned in any of the Gordon material. What you get instead is the map to a doable lifestyle, where many of the conditions that lead to childhood obesity simply don’t exist.

Your responses and feedback are welcome!

Source: “69% of Doctors Say Parents are Completely or Mostly to Blame for Childhood Obesity,” PRNewswire.com, 08/26/15
Source: “This Childhood Obesity School Program Works Best,” Futurity.org, 02/20/23
Source: “Free Parent Resources,” GordonTraining.com, undated
Image by Frédérique Voisin-Demery/CC BY 2.0 DEED

New Research Highlights Importance of Sugar Source in Childhood Obesity

New research presented at the European Congress on Obesity (ECO) in Venice, Italy, has shed light on a critical aspect of childhood nutrition: the source of sugar. The study, conducted by Junyang Zou and colleagues from the University of Groningen and University Medical Center Groningen, challenges conventional wisdom regarding sugar consumption and its relationship to childhood obesity.

The type of sugar might matter more than the amount

The study, which examined data from the GEKCO Drenthe study, a longitudinal investigation tracking children born in the northern Netherlands, scrutinized the impact of sugar consumption from various sources on weight gain and the development of obesity. Surprisingly, the research suggests that the type of sugar consumed may be more influential than the total amount.

Contrary to common assumptions, the study found that the overall quantity of sugar consumed during early childhood did not correlate with weight status at age 10 or 11. However, the source of sugar emerged as a significant factor.

Zou elaborated:

The high consumption of sugary foods is considered a risk factor for childhood overweight and obesity and so children are advised to consume less sugar-rich foods, such as confectionery, cakes and sugar-sweetened drinks, and eat more fruit and unsweetened dairy products, such as milk and yogurt.

But while fruit and unsweetened dairy products are considered healthy, they contain high amounts of intrinsic sugars — sugar that occurs naturally in the food, rather than being added. We wanted to know if the source of sugar, added versus intrinsic, as well as the amount, affects the likelihood of developing overweight or obesity.

The research underscores the importance of distinguishing between intrinsic sugars and added sugars found in processed treats and beverages. While both fruit and unsweetened dairy products contain intrinsic sugars, they also offer essential nutrients and may confer protective effects against obesity.

Study results in more detail

Drawing upon data from the GECKO Drenthe study — an extensive longitudinal investigation tracking children born between 2006 and 2007 in the northern Netherlands — Zou and colleagues meticulously analyzed the dietary habits of 817 children who maintained a healthy weight at age 3. The findings yielded compelling insights into the diverse sources of sugar and their distinct effects on weight status.

On average, these children consumed 112 grams of sugar daily, comprising a blend of natural and added sugars. Among the primary sources identified were sugar-sweetened beverages, dairy products, sugary snacks, and fruits. Surprisingly, while total sugar intake at age 3 did not exhibit a significant correlation with BMI at ages 10 and 11, the source of sugar emerged as a critical determinant of weight status.

Notably, children who derived a higher proportion of their sugar intake from whole fruits demonstrated lower BMI scores and experienced less weight gain as they approached adolescence. Similarly, those who consumed more sugars from unsweetened liquid dairy products, such as milk, exhibited a reduced risk of developing obesity or overweight status.

Conversely, sugar intake from sugary snacks was associated with higher BMI scores, underscoring the detrimental impact of added sugars found in processed foods. Despite the study’s observational nature, the findings offer valuable insights into the nuanced relationship between sugar consumption and childhood obesity.

The bottom line

The research presented at the ECO highlights the critical role of sugar sources in the development of obesity during childhood. It also underscores the imperative of reevaluating dietary recommendations to prioritize nutrient-rich sources of sugar, such as fruits and unsweetened dairy products, while minimizing the consumption of sugary snacks and beverages. By empowering parents, healthcare professionals, and policymakers with evidence-based insights, we can chart a course toward a healthier future for our children — one sweet choice at a time.

Your responses and feedback are welcome!

Source: “Understanding the role of sugar sources in development of childhood obesity,” News-Medical.net, 05/13/24
Source: “Kids’ Obesity Risk Depends on Source of Sugar, Not the Amount,” Newsweek, 05/13/24
Image by Myriam Zilles on Unsplash

Be a Role Model Every Day

Imitation is the sincerest form of flattery, and that fact is both one of the most destructive and one of the most redemptive features of human nature. So we need to take the advice of Julia Olech, who wrote,

Be a role model: Children often mimic adults, so show them you also choose healthy options. When you make good food choices and limit your junk food intake, they’re more likely to do the same.

Parenting is difficult, so hard sometimes that parents conveniently forget the basic “home truths.” One of those inconvenient verities is that our children watch our every move. Not only that, but all too often, they imitate what we do. How else are they supposed to learn to be human? From the media? Really? Don’t we believe that we present a better example than some of the nonsense that appears on TV and in video games?

To be fair, a lot of parents do a pretty good job of keeping their kids separated from random violence, irresponsibility, stupidity, and other undesirable traits. If you are one of those conscientious citizens, congratulations. There is, however, another very important principle involved. In addition to protecting kids from bad influences, you — yes you, Mom, Dad, Grandma, Grandpa, older sibling, etc. — need to provide the counterbalancing good influences.

Who is that in the mirror?

A now-defunct website called BlissTree.com once published a piece claiming that 75% of parents ignore the problem of overweight in their children. Doubtless, other authors would find research claiming different percentages. At any rate, that writer made the argument that 50 years ago, there were bakeries and fast-food outlets and television, but the childhood obesity rate was less than one-third of today’s, so how can we blame “society” for making our kids fat?

That argument of course is not sturdy, because a lot of things are here now that were not present then, like antibiotics in the water and plastic in the food. At any rate, the point the author mainly intended to make was that no matter how much we would like to blame “society” for everything that goes wrong, eventually, we have to ‘fess up and acknowledge that society is us. We are a society, especially at home. After all, who do our kids see the most, especially in the early years? Their caregiving relatives, aka role models.

What ought we to demonstrate?

Corny as it sounds, a daily workout of some kind is something it wouldn’t hurt for children to witness their parents doing. Carolyn Williams, Ph.D., R.D., says, for example,

Moderate-intensity exercise actually decreases appetite by increasing the hormone that suppresses appetite and decreasing the hormone that triggers hunger… A strenuous workout frames the next 24 to 36 hours in a positive health perspective, meaning you’re more likely to make good food choices, monitor portions, and resist temptations.

But it doesn’t have to be all noisy and sweaty, it can be as gentle as a regular session of chair yoga — as long as the young’uns catch some kind of a notion. The subliminal messages are,

— You are valuable, and the physical machine that you live inside of deserves good care.
— Your routine does not need to be strenuous or lengthy.
— Just do this nice thing for yourself every day.

An area worth putting some effort into

What really needs to be nipped in the bud is the whole picky-eater scene. Dr. Suanne Kowal-Connelly told The New York Times,

Children look up to us, they model our behavior and notice what we enjoy. Parents should serve children the same foods they eat, though in smaller portions, and not offer something else saying, for example, “There are chicken nuggets in the freezer if you don’t like the broccoli I made.”

Parents can talk about the beautiful colors of various foods and why they’re good for us — make it a learning game. A new food may have to be introduced many times — 12 or 13 — just to get children to try it.

Your responses and feedback are welcome!

Source: “Junk Food Marketing Study: What Are Kids Being Fed?,” CyberGhostVPN.com, 02/13/24
Source: “To End Childhood Obesity, Parents Need To Learn To Say ‘No’,” BlissTree.com, 01/04/12
Source: “9 Things That Make You Eat More,” Yahoo.com, 05/05/16
Source: “Using Shelter-in-Place Time to Foster Better Family Food Habits,” NYTimes.com, 04/06/20
Image by It’s No Game/CC BY 2.0 DEED

Obesity Villains, Inadequate Premises, and Unclear Conclusions

This blog has been taking a second or third look at various phenomena that have been deemed responsible for, or at least conducive to, childhood obesity. Most recently, it looked at sleep debt which, blame-wise, proves to be a very elusive target.

Today’s post checks out the remaining causes that were examined in the 2009 paper, “Ten putative contributors to the obesity epidemic,” to see how they have held up over time.

Endocrine disrupters

The targets of blame in this area are chemicals whose presence in the natural environment has increased alarmingly. Of particular concern is their effect on the embryos of mammals, including humans — although exposure is in no way beneficial to adults, either. According to the paper,

PBDE, BPA, and other EDCs exposure have been implicated as contributing to obesity in both humans and model animals, possibly by interfering with estrogen and androgen signaling… [T]he human population is widely exposed to BPA and it appears to accumulate in the fetus.

[D]isruption of the activity of estrogen and testosterone signaling by EDCs during fetal development can lead to permanent changes in reproductive organ development, which can later in life impair homeostatic systems, such as the regulation of body fat and weight.

The chemicals suspected of endocrine disruption come at us from every direction. Anyone who enjoys guilt-tripping themselves or others can ponder the personal and societal effects of consumer products, incineration, atmospheric transport, agricultural runoff, harbor contamination, industrial and municipal effluents, and pulp mills in the ever-increasing plasticization of the environment and of our very own innards.

Proving the connection in a lab is tricky, because not much is known about endocrine disruptors’ hormonal activity, and that is the problem. Some aspects are more obvious and easier to catch on to, like the effect of estrogen on white adipose tissue. Fortunately for the scientists who track this sort of thing, much evidence is easily captured, for instance, BPA that is detectable in the urine of 95% of Americans.

Pharmaceutical iatrogenesis and obesity

Many of the most widely used types of pharmaceuticals have been observed to cause a concerning amount of weight gain — including antidiabetics, antihistamines, antihypertensives, steroid hormones, contraceptives, protease inhibitors, and psychotropics. The risks extend to the damage done by poor patient compliance when the obesogenic effects show up and patients decide, “No thanks, I’d rather risk high blood pressure and mental imbalance than be fat.”

Ambient temperature and obesity

Who would have thought that a difference of one and one-half degrees could cause a significant life-altering difference? But for week-old infants, it was found that despite identical feeding, the weight of babies in 36.5-degree incubators was greater than the weight of babies in 35-degree incubators. Here is another unsettling discovery:

[W]eight gain during the first four months of life is positively correlated with childhood overweight status, and weight gain during this period is greater for infants born in the spring (and presumably reared in warmer ambient temperatures) than infants born in the fall…

In their summary and departing remarks, the authors of this paper stated their desire to see scientists “remain skeptical of simplistic conclusions about complex phenomena which public health advocates in the obesity field, in particular, seem prone to accept as complete and adequate explanations.” Why? Because…

[A]ny one explanatory theory must be viewed in the context of the constellation of plausible, interrelated, and in many cases still unproven hypotheses.

Your responses and feedback are welcome!

Source: “Ten putative contributors to the obesity epidemic,” November 2009
Image by Towfiqu barbhuiya on Unsplash

Semaglutide and Psychiatric Risk

Weight gain and its associated health risks often pose significant challenges for people with psychiatric disorders. The intersection of mental health and physical well-being necessitates careful consideration of treatment options, particularly when addressing weight management.

Semaglutide, a glucagon-like peptide-1 (GLP-1) receptor agonist, gained FDA approval in 2017 for the treatment of type 2 diabetes. It operates by mimicking the GLP-1 hormone, which regulates insulin production and influences food intake and reward mechanisms within the brain. The medication, renowned for its efficacy in weight loss, has recently come under scrutiny for its potential psychiatric side effects, prompting clinicians and patients to reevaluate its role in managing obesity, particularly in people living with serious mental illness.

The APA poster on psychiatric comorbidities

Heidi Anne Duerr, MPH, reported for Psychiatric Times on a case study that was presented at the 2024 American Psychiatric Association Annual Meeting. The study shed light on the complexities of using semaglutide in patients with psychiatric comorbidities.

Presented in the poster titled “Semaglutide-Induced Suicidal Ideation in a Patient with Psychiatric Comorbidities: A Case Report,” study author Raju Kakarlapudi and colleagues recounted the upsetting experience of a 42-year-old female patient dealing with morbid obesity and type 2 diabetes mellitus alongside bipolar I disorder and posttraumatic stress disorder (PTSD).

The patient’s difficult journey

Bariatric surgery, a common weight loss intervention, was deemed unsuitable due to the patient’s psychiatric history. Consequently, semaglutide, marketed as Ozempic, emerged as a viable alternative to help the patient manage weight. However, within a mere three weeks of starting the medication, the patient started exhibiting “significant psychiatric disturbances including abrupt behavioral alterations and protracted nihilistic delusions.” Disturbingly, she even attempted self-strangulation on multiple occasions. Subsequent discontinuation of semaglutide led to the disappearance of these behavioral changes.

Additional research uncovered this

Kakarlapudi and colleagues said that…

The primary aim [was] to augment awareness regarding the potential adverse effects associated with Ozempic utilization, both among the general populace and within the psychiatric community.

Kakarlapudi et al. conducted an extensive literature review using Google Scholar, uncovering approximately 60 documented cases of suicidal ideation and seven suicide attempts linked to semaglutide use. Interestingly, many patients reported an improvement in depression upon discontinuation of the drug, suggesting a potential association between semaglutide and depressive symptoms that could precipitate suicidal ideation.

What we were told back in January

Interestingly, it was widely reported last January that health agencies in the U.S. and Europe have conducted thorough reviews and found no evidence linking thoughts of suicide or self-harm to semaglutide. The European Medicines Agency concluded after a nine-month review that there is no causal association between GLP-1 receptor agonists and suicidal thoughts or actions. Similarly, the Food and Drug Administration (FDA) in the U.S. reached a similar conclusion after examining reports to its adverse event reporting system. That only goes to show that more research is needed while we proceed with caution when it comes to using these weight loss medications.

The bottom line

The authors of the case study underscored the need for further research to elucidate the underlying mechanisms by which semaglutide may exacerbate psychiatric symptoms and precipitate suicidal ideation. By identifying specific proteins and enzymes implicated in these adverse effects, clinicians can better mitigate risks and tailor treatment strategies to individual patient needs.

Your responses and feedback are welcome!

Source: “Annual Meeting: Poster Investigates the Link Between Semaglutide and Suicidal Ideation,” Psychiatric Times, 05/07/24
Source: “Ozempic isn’t linked to suicidal thoughts, U.S. and European health agencies find,” NBC News, 4/15/24
Image by Hans Reniers on Unsplash

Sleep Debt, an Obesity Villain Suspect

According to “Ten putative contributors to the obesity epidemic,” the factor known as “sleep debt” has not really made its case as a major obesity villain. The multiple authors say,

For all of these putative causes, we believe further research is warranted. For some such as sleep debt, research is warranted to determine whether the factor is indeed contributing to obesity levels.

For some, such as sleep debt or ambient temperature effects, studies involving manipulation of these factors in human randomized controlled trials to evaluate effects (if any) on weight seem warranted, and indeed some such studies are underway.

To put the question colloquially, is sleep debt actually “a thing”? Interesting cases to consult would be those of people who have suffered sleep deprivation as one aspect of a planned, calculated agenda of interrogation and/or punishment. But in that extreme instance, food deprivation and several other factors would have been present, so such individuals would make unhelpful experimental subjects. When undergoing sleep deprivation, they were not concurrently in a position to experience weight gain.

Still, the “Sleep Debt and Obesity” section takes up a rather large proportion of the “Ten putative contributors” paper, which includes 231 instances of the keyword itself.

Does sleep duration affect the biological mediators of energy homeostasis and appetite? Apparently, yes. Over the past five decades or so, among humans of diverse ages and nations, and among animals, the connection between decreased sleep and obesity has been increasingly noted. But there is more to it than that. Depending on other variables, sleep deprivation seems capable of causing either weight loss or weight gain.

Sleep, or a deficit of it, affects ghrelin, leptin, galanin, orexin, thyroid stimulating hormone, glucose, insulin, peptides, and no doubt other important chemicals produced by the body. Sleep debt is associated with an appetite for masses of energetic high-carbohydrate foods.

How humans do it

The truly delightful thing about people is our ability to generate self-perpetuating cycles of damage. Eat too much; get fat; lose sleep over your increasing obesity; stress out and eat more food and the wrong kinds of it; get fatter, etc.

Sleep debt has been attributed to “insomnia, stress, social pressures, desire to get more work accomplished, night-shift work, medications used to treat colds, allergies, pain and cardiovascular problems, and modern-living habits such as late-night TV viewing and use of the internet.” Those add up to a lot of variables, making it much more difficult to track the consequences of sleep deprivation in the wild. But it is said that…

Epidemiological research studies as well as wide-scale polling by the National Sleep Foundation (NSF) suggest that American adolescents and adults are chronically sleep deprived.

The NSF survey found that “individuals that self-reported to be short sleepers (less than 6 hours a night on workdays) were significantly more likely to be obese than those that self-reported to be normal or long sleepers (8 hours or more on workdays).”

There has been controversy over the effects of physical activity. An entire area of curiosity on this topic has to do with sleep apnea and other sleep-related breathing disorders. Then, there is a confusing relationship between too much sleep, not enough sleep, and mortality rates, and the additional relationship between those factors and obesity. Also, according to a major study, “African Americans had substantially higher obesity rates than did European Americans,” and…

The possibility that differences in sleep duration can contribute to the higher incidence of obesity among minority populations is supported by a recent finding by Hale and Do (2007). In this study of over 32,000 adults in the United States, the investigators found a higher risk of short (<6) and of long (>9) sleep hours, both extremes attributed to increased rate of health problems, in black vs. white respondents.

A notable conclusion from numerous studies all over the world is that “Sleep debt may have the most potent and adverse effects on body weight in children and adolescents.”

Your responses and feedback are welcome!

Source: “Ten putative contributors to the obesity epidemic,” ncbi.nlm.nih.gov, November 2009
Image by Jon Tyson on Unsplash

Obesity Villains Examined

Over the years, Childhood Obesity News has pointed the finger at numerous villains who share varying degrees of culpability for obesity. Many of these have been the same entities mentioned in “Ten putative contributors to the obesity epidemic.”

Its roster of 22 authors included Dr. Joe C. Eisenmann who by now has accumulated 30 years of experience as a coach, professor, researcher, educator, applied sport scientist, and strength and conditioning coach. Children’s health, fitness, and athletic development are his missions, and “tested, trained, energized” are his watchwords.

For his own website, Dr. Eisenmann has written that,

The benefits of exercise on the child and teenage brain include:

– improved concentration, cognition, memory and academic performance
– better self-esteem
– stress reduction
– decreased likelihood of mental health issues like anxiety and depression
– decreased severity of ADHD symptoms and autism spectrum disorder

An immature, growing brain needs to assemble itself from a lot of moving parts, and research has shown that taking into account the needs of both structure and function, physical exercise plays an enormous part in helping it to do so.

Returning to the subject of obesity villains, what newsworthy candidates did the multi-author project mention? Regarding epigenetics, there is said to be basic in vitro evidence, animal evidence, and epidemiological evidence that the area is worth scrutinizing:

Animal models and human data illustrate that dysregulation of epigenetic processes can cause obesity. Recent molecular studies provide an additional link by showing that genes critical to energy balance are regulated by epigenetic mechanisms…

If the intrauterine environment of an obese woman induces developmental adaptations in her developing fetus that then predispose her offspring to obesity, feed-forward transgenerational amplification of obesity could result.

The subheading “Intrauterine and intergenerational effects” is ticked for animal evidence, ecological correlation evidence, and epidemiological evidence. Speaking of bariatric surgery patients, the report says, “Children born after maternal weight loss have a lower risk for obesity than do their siblings born before maternal weight loss.” This leads to an area called metabolic imprinting, suggesting that body weight could be regulated by epigenetic means.

Another factor discussed here before is “assortative mating,” the tendency of humans to become intimately involved with others who have similar characteristics. But they also become involved with others who have very different characteristics, and lust has always been like that. Also, it pretty much guarantees that if two obese people have a child, that child is likely to be obese.

It also implies that an overweight person is more likely to ask an overweight person on a date, having learned from experience that potential partners of normal weight don’t really consider themselves as potential partners. According to folk wisdom, it takes a lot of personality to overcome a serious weight differential. Still, as the paper indicates,

The consequences of assortative mating are complex and dependent on the “genetic architecture” of a particular trait. Given that obesity is a complex polygenic trait, models of assortative mating are quite complex.

Your responses and feedback are welcome!

Source: “Ten putative contributors to the obesity epidemic,” ncbi.nlm.nih.gov, November 2009
Source: “New Year. New Platform. New Logo,” JoeEisenmann.substack.com, 01/03/23
Source: “Exercise and Brain Health for Young People: Another Puzzle Piece to Achieving Optimal Well-Being,” Substack.com, 10/29/23
Image by Loco Steve/CC BY-SA 2.0 DEED

How GLP-1 Medications Are Changing Consumer Habits and Industry Dynamics

A paradigm shift is underway in the world of food and beverage consumption, and it’s being driven by a surprising catalyst: medications. Specifically, GLP-1 drugs, primarily used for weight loss and managing diabetes, are not only altering consumer behavior but also posing challenges to various sectors of the food industry.

Recent survey points to significant impact

A recent survey conducted by Morgan Stanley sheds light on the significant impact of GLP-1 medications on consumer spending habits, particularly in the realm of dining out and getting takeout. According to the survey, a majority of people taking GLP-1 drugs reported spending less on restaurant meals and deliveries, indicating a notable shift in their culinary preferences. In contrast, a smaller proportion indicated tightening their budgets while grocery shopping, suggesting a more nuanced effect on at-home food consumption.

Morgan Stanley analysts put it this way:

There is growing evidence that the drugs have a meaningful impact on consumer behavior and spending on groceries and restaurants… All of these dynamics suggest GLP-1 drugs’ impact across consumer sectors is set to increase as drug uptake grows and the drugs reshape behavior among a demographic group that represents a disproportionate share of calorie consumption.

Raised concerns as a consequence

The implications of this behavioral shift are reverberating across the food and beverage industry, raising concerns among stakeholders about potential revenue implications. With the market for GLP-1 drugs projected to reach a staggering $105 billion by 2030 and an estimated 31.5 million Americans expected to be on these medications by 2035, the impact on various sectors of the food industry is not to be underestimated.

However, according to CNBC, which was one of the many outlets reporting on the survey results,

[M]any food and beverage companies have reassured investors over the last few months that it’s still unclear how much those drugs will lower their revenue. Morgan Stanley also said in the survey that GLP-1s are a manageable long-term pressure on restaurants, not an “existential risk.”

Food companies survival projections

Among the most vulnerable are traditional fast-food chains and packaged food manufacturers, whose offerings often align with the high-calorie, indulgent preferences that GLP-1 medications seem to deter. Conversely, places offering healthier alternatives, such as fast-casual restaurants focusing on fresh ingredients and nutritional transparency, are better positioned to weather the storm of changing consumer habits.

In particular, brands like Cava, Chipotle, Sweetgreen, and Starbucks stand out as adaptable to the evolving consumer landscape, while legacy fast-food chains like Jack in the Box, Wendy’s, and Shake Shack may face greater pressure to innovate and cater to health-conscious clientele.

Similarly, packaged food companies like Hershey are identified as particularly vulnerable due to their reliance on traditional, calorie-dense snacks. On the flip side, companies offering healthier alternatives, such as Vital Farms and Simply Good Foods, are poised to benefit from the growing demand for nutritious options.

What foods might be out?

The survey also highlights the impact of GLP-1 medications on specific food categories, with consumers reporting reduced consumption of snacks, confections, and sugary drinks. This trend is expected to translate into a decline in the consumption of certain products, including ice cream, cakes, candies, and regular sodas, by 2035.

GLP-1 drugs are going for your vices, too

Wait, there’s more. It’s not just the food but tobacco and alcohol, too. The report suggests that users of GLP-1 drugs, including Ozempic, are reducing their consumption of tobacco and alcohol while on these medications due to appetite suppression effects. Survey data shows significant reductions in both tobacco and alcohol consumption after starting the treatment.

While caution is advised in drawing conclusions, anecdotal evidence suggests these drugs might help curb addictive behaviors. Clinical trials are underway to explore this further. Morgan Stanley predicts continued growth in the GLP-1 market, projecting a $105 billion global market by 2030, with around 31.5 million users in the U.S. by 2035.

The bottom line

The rise of GLP-1 medications is reshaping consumer habits and posing challenges to various sectors of the food and beverage industry. While some companies may face headwinds, others have the opportunity to innovate and cater to the growing demand for healthier options. As the landscape continues to evolve, adaptation and responsiveness to changing consumer preferences will be key for businesses seeking to thrive in this new era of food consumption.

Your responses and feedback are welcome!

Source: “Most people on weight loss drugs are spending less on restaurants and takeout, survey says,” CNBC, 4/20/24
Source: “Ozempic is coming for the alcohol and tobacco industries next,” Quartz, 4/23/24
Image by Jonathan Borba on Unsplash

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Profiles: Kids Struggling with Weight

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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