The Support Matrix for Mental Health Diagnostics

The world has a lot to say about binge eating. Sometimes the search for a more precise definition leads off into fascinating side roads.

In its 5th edition, the Diagnostic and Statistical Manual of Mental Disorders decided to file BED, or Binge Eating Disorder, under OSFED, or “Other Specified Feeding or Eating Disorder.” Additionally, BED itself has been broken down into “low frequency and/or limited duration” and “higher frequency and duration;” and then it might be further categorized as mild, moderate, or severe.

Within those parameters, it is still important to understand that not all obese people suffer from BED, nor are all people with BED obese. But they do mostly tend to be moody and anxious.

Classification problems have haunted the field for a long time — not just in the realm of eating disorders, but in everything connected with mental health. To get a grip on this topic, it is apparently necessary to keep track of a lot of initials. For instance, the cluster of letters DSM-ICD. Spelled out, that stands for “Diagnostic and Statistical Manual of Mental Disorders and International Classification of Diseases.”

A 2016 paper explicated the basis of that school of thought, classified as “an Aristotelian view.” From this angle, mental disorders are seen as “largely discrete entities that are characterized by distinctive signs, symptoms, and natural histories.”

And, as far back as 1989, there had been mumbles and grumbles, an example of which came from psychiatrist R. E. Kendell:

One important possibility is that the discrete clusters of psychiatric symptoms we are trying to delineate do not actually exist.

Then, along came a contrary modality, in fact, a paradigm shift, described as “a Galilean view of psychopathology as the product of dysfunctions in neural circuitry.” This is the RDoC (Research Domain Criteria) initiative, which strives to make sense of what were called the “accumulating anomalies” that troubled professionals when contemplating the older system. Many factors contributed to the restlessness that inspired leaders in the field to call for change.

Remedies made to order

For instance, the authors cited “precision medicine” or “personalized medicine” which translates lab results directly into an individually tailored plan of action. As an example, they mentioned a targeted drug treatment that works for 4% of cystic fibrosis patients, and went on to describe another advance that has “stirred hopes for a similar revolution in psychiatry and clinical psychology.”

Also in the conversation is Oncotype testing, which has revolutionized the treatment of breast cancer by “permitting physicians to move from a ‘one size fits all’ intervention approach to treatment geared to specific genetic profiles.”

They go on to explain the analogy to the Research Domain Criteria:

Rather than base psychiatric diagnosis on presenting signs and symptoms […] RDoC strives to anchor psychiatric classification and diagnosis in a scientifically supported model of neural circuitry. RDoC conceptualizes mental disorders as dysfunctions in brain systems that bear important adaptive implications, such as systems linked to reward responsiveness and threat sensitivity.

Of course, this fundamental declaration branches out into several “crucial assumptions,” some of which are explained in detail. Other experts added depth and breadth to the many dimensions of this expanded worldview.

One was neuroscientist and psychiatrist Thomas R. Insel, who was for more than a decade in charge of the National Institute of Mental Health. Even though in most areas of medicine the public has come to expect a high degree of specificity, he warned, we might as well not anticipate anything of the sort in the field of psychiatric diagnostics.

Because behavioral symptoms are multidetermined (our old friend “multifactorial“), he wrote, “[…] diagnoses based only on presenting complaints are unavoidably heterogeneous in terms of pathophysiology.” Along with this unavoidable truth comes a danger:

[W]hen diagnosis is limited to symptoms, treatments may be limited to symptom relief, precluding cures or preventive interventions.

Your responses and feedback are welcome!

Source: “Clashing Diagnostic Approaches: DSM-ICD versus RDoC,” NIH.gov, 02/03/16
Source: “The NIMH Research Domain Criteria (RDoC) Project: Precision Medicine for Psychiatry,” PsychiatryOnline.org, 04/01/14
Image by Tatinauk/CC BY-ND 2.0 DEED

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