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

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

Obesity Villains Exonerated

This is an extension of the recent post, “Obesity Villains Reconsidered,” which discusses an interesting 2009 paper in which multiple authors looked closely at many accepted or alleged causes of obesity. One of their reactions was to divide pretty much all those possible causes into two subheadings: “food marketing practices” and “institutionally-driven reductions in physical activity” — which for convenience, they called the “big two.” But they also went on to propose quite a number of other causes, in a “more thorough discussion of factors that may be contributing to the obesity epidemic.”

Myopic emphasis

They proposed that there has been a narrowly focused concentration on two very big concepts, both having to do with energy: how to get it, and how to spend it. At the same time, the characterization of those categories has grown ever more broad. Human nature is such that, in many departments of life, we seem unable to count higher than two. A thing is either this or that. It is either intake or output — but that insistence on duality is a sticking point.

The paper titled “Ten putative contributors to the obesity epidemic” spells out that while each unit of the “big two” contains many problematic elements, there are also quite a number of other potential hazards to worry about. They fall outside the purview of either intake or expenditure, yet still need to be accounted for. This paragraph encapsulates the crux of the problem:

[E]ven though some elements of the big two do very likely play some role in influencing obesity levels, we believe that an unquestioned assumption of their preeminence has led to the possibly ill-advised expenditure of public effort and funds on programs aimed at reducing population levels of obesity and has also reduced the exploration of other potential causes and the alternative obesity reduction programs that might stem from their identification.

Consequently, these authors point the finger at some hitherto blameless suspects. More intriguingly, after examining the cases against a few traditionally acknowledged obesity villains, those factors are let off the hook. Take fast-food establishments. A 2008 study showed that although people might consume a boatload of calories at a restaurant, “they largely compensated by eating less at other occasions…”

Of course, that all transpired some years back. Since then, the evidence against fast food has mounted and multiplied. There are indications that people who eat home cooking absorb less sugar and fat, and have lower cholesterol levels. Also, at home, there is more opportunity for portion control, although that could backfire. (“It’s my kitchen, I paid for the food, and by golly, I’ll eat as much of it as I please.”) Another element of domestic culinary art is that, of course, the (traditionally female) cook has more control over what ingredients go into a meal in the first place.

PE still counts

A 2012 meta-study looked at data from “observational studies, 20 cross-sectional studies, and 8 prospective cohort studies.” However, there were methodological differences between those studies, and the conclusions drawn turned out to be “far from conclusive.” A 2018 paper said it all in the title: “Frequency of Eating Out at Both Fast-Food and Sit-Down Restaurants Was Associated With High Body Mass Index in Non-Large Metropolitan Communities in Midwest.” No doubt, plenty of evidence for either claim could be found by a motivated seeker.

As for Physical Education in schools, the evidence that it has decreased is not convincing, and furthermore, “much evidence suggests that standard PE classes have no appreciable impact on obesity levels.” Again, this was stated in 2008, so it is appropriate to look for something fresher — like two reports from 2023. The first, from the University of Texas at Austin, bluntly states in its title, “Physical Education Policies in Schools Have Not Curbed Childhood Obesity.”

Over the past few years, many states have supposedly adopted the 150-minutes-per-week standard. But…

Researchers found that schools largely disregarded state laws and did not increase the time that elementary students actually spent in PE or recess. Relative to states that did not change their laws, states that passed increases did not see a decline in children’s body mass index, overweight prevalence or obesity prevalence.

“Closer oversight of schools would be needed to improve compliance with state PE laws,” said Paul von Hippel […] who co-authored the study. “Yet, even with better compliance, we estimate PE classes just don’t burn enough calories to make a noticeable impact on obesity. At least not as they’re currently conducted.”

But to balance the scales, another fairly contemporary article is titled, “PE classes vital to children’s physical and mental health.” It quotes pediatrician Dr. Rebecca N. Dudovitz affirming that PE classes are definitely helpful, especially post-pandemic, for both the physical and mental health of children. And as always, there are obstacles to the achievement of necessary goals. In far too many cases…

PE class is the only time exclusively set aside for exercise. That’s particularly true for children who do not have access to safe places to play outside of school. Families of students in underserved communities may not have the same resources or privileges of a safe environment for exercise in their neighborhood.

Do parents need to play a role in ensuring that kids move enough? Absolutely. Dr. Dudovitz makes five recommendations:

1. Carve out daily time for physical activity
2. Use fun competition as a motivator
3. Incorporate nutrition (a healthy diet reinforces performance and ambition to stay fit)
4. Encourage your child to join a sports program or organized after-school fitness activity
5. Limit time on video games and cell phones

Your responses and feedback are welcome!

Source: “Ten putative contributors to the obesity epidemic,” ncbi.nlm.nih.gov, November 2009
Source: “Association between eating out of home and body weight,” ncbi.nlm.nih.gov, February 2012
Source: “Frequency of Eating Out at Both Fast-Food and Sit-Down Restaurants Was Associated With High Body Mass Index in Non-Large Metropolitan Communities in Midwest,” ncbi.nlm.nih.gov, Jan 2018
Source: “Physical Education Policies in Schools Have Not Curbed Childhood Obesity,” UTexas.edu, 03/21/23
Source: “PE classes vital to children’s physical and mental health,” UCLAHealth.org/ 04/08/22
Image by Jaguar MENA/CC BY 2.0 DEED