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

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

A Putative Contributor

To catch up, please glance back at “Obesity Villains Reconsidered” and/or “Obesity Villains Exonerated.” These posts are based on a paper that cast doubt on or debunked some commonly held beliefs about the causes of obesity and supported others.

Either way, it encompassed some interesting material and provided a starting place to reassess various bits of received wisdom, because…

[…] scientists widely and readily acknowledge that multiple factors contribute to obesity including but not necessarily limited to genetic, dietary, economic, psychosocial, reproductive, and pharmacologic factors.

Among other ideas, the authors reconsidered the notion of the heavily criticized institution known as the “built environment.” In one case, they found a study that examined two racially same but economically different neighborhoods, and concluded that “levels of leisure walking and physical activity were not higher, and rates of obesity were not lower in the non-poor neighborhood with better maintenance, more sidewalks and recreational facilities.”

In another upset, the authors discovered that although high fructose corn syrup has been enthusiastically demonized, an American Medical Association position paper said “it appears unlikely that HFCS contributes more to obesity or other conditions than sucrose.” Similarly, although anti-obesity warriors hate vending machines, and devote a lot of energy to lobbying against their presence in schools, the actual evidence against the machines as obesity villains is underwhelming:

Our point is merely that we do not have conclusive evidence that the big two or their individual elements are the preeminent contributors to obesity. Despite the lack of solid evidence that clearly demonstrates the “culprits” are chiefly responsible for the obesity epidemic, researchers are quick to blame them even in the public eye…

Such confidence in one “culprit” is then often contradicted by public health proponent[s] advancing their favored target for intervention.

Due to the “complex reality” of the situation, the authors point out that some factors are not actionable in any practical way. For instance, a lot of adults have gotten fat because they quit smoking. But no responsible member of any profession would suggest that anyone should resume the nicotine habit for the sake of weight control.

Regarding the role of bacterial products in regulating metabolism and body weight, a category that has been explored is infection, because…

[…] the possible contribution of infections in the etiology of human obesity is often overlooked. Canine distemper virus (CDV) was the first reported obesity promoting virus… In mice infected with CDV, obesity develops after acute infection has abated and when no virus is detectable.

Also, there is a suspicion that the role played by bacterial products in metabolism and body weight regulation has not been considered. In this area of investigation, a lot of crazy things have been observed. For instance, take visceral fat in chickens. “Paradoxically, the increased adiposity due to SMAM-1 [an avian adenovirus] infection was accompanied by a reduction in serum cholesterol and triglycerides.”

Ad-36 is a human adenovirus capable of increasing adiposity not only in chickens but in non-human primates. In one experiment, it is said to have “increased whole-body insulin sensitivity and enhanced expression of genes involved in the adipogenic and de-novo lipogenesis pathway…” — and it spreads very fast.

Only a few adenovirus subgroups have been examined relative to adiposity. “Adipogenic potential of remaining the 45 known human adenoviruses has not been tested.” Of course, that was in 2009, so additional research has surely changed the statistic. Still, a search for several keywords reveals that since then, not much seems to have been done toward finding out about the adipogenic potential of the remaining almost four dozen varieties.

A federal government page says,

Sometimes the virus can be shed (released from the body) for a long time after a person recovers from an adenovirus infection, especially among people who have weakened immune systems. This “virus shedding” usually occurs without any symptoms, even though the person can still spread adenovirus to other people.

Just a few more words about human adenoviruses, or HAdVs, which are associated with “an array of diseases”:

HAdV is classified into seven groups (A-F). There are more than 100 serotypes, and approximately 67 serotypes (1-67) are known to be pathogenic in humans… HAdV can evade the immune response and produce persistent or latent infections.

Your responses and feedback are welcome!

Source: “Ten putative contributors to the obesity epidemic,” ncbi.nlm.nih.gov, November 2009
Source: “Transmission, CDC.gov, undated
Source: “Perspective on Adenoviruses: Epidemiology, Pathogenicity, and Gene Therapy,” NIH.gov, August 2019
Image by Dr. Yale Rosen Atlas of Pulmonary Pathology/CC BY-SA 2.0 DEED