Disease is Defined

Many diseases require lifestyle adaptations, but it is impossible to know what changes will contribute to optimum health until the disease is defined. Unfortunately, that doesn’t keep us from throwing a lot of treatment plan spaghetti at the wall, especially when there’s money to be made from pharmaceuticals.

I read two New York Times articles last week on obesity. The subject has consumed copious column inches for years, but the emphasis has changed with the availability of Ozempic®, Mounjaro® and similar drugs. These drugs may have entered the market as treatments for diabetes, but they quickly morphed into popular weight loss drugs.

tape measure belly

Some doctors prescribe these drugs for weight loss in obese patients, with or without diabetes, as defined by a body mass index (BMI) of 30 or greater. BMI is a simple medical screening tool that measures the ratio of height to weight to give a rough calculation of  body fat. While it may be roughly correct, BMI can’t actually determine disease. What it can do, and does, is create faux legitimacy for fat bias.

Experience with the painful reality of fat bias has created masses who are desperate to lose weight. Promise them 15% weight loss and they won’t care a flip about the dangers or consequences. In other words, they’re not as concerned about health as they are about acceptance.

And to make them acceptable (or fit their own idea of ideal), doctors by the droves are willing to write prescriptions. This is how things work in a system that’s out of control. And it’s how things currently work in the US healthcare system.

Obesity, like any disease, can be most effectively prevented, and treated when we agree on exactly what it is. The NYTs quotes Dr. Beverly Tchang, assistant professor of clinical medicine at Weill Cornell as saying: “The problem is that we’ve allowed society, insurance companies and everyone else to decide that obesity is just too much fat, which is an oversimplification.”

And it was clear from reading the comments on this article that a majority of those led to post believe obesity both correlates with fat and is an impulse control issue. Even those who allowed a caveat here and there often tacked on a statement to remind us it’s as simple as calories in calories out and you’re the one choosing how many calories go in.

According to the article, “…B.M.I. helped create an equivalency between a disease and body size, but that’s not how researchers understand obesity today. A person can be fat without illness or “thin fat” and sick. Fat can cause mechanical problems in the body — sore knees, difficulty breathing. It can also be a symptom, rather than the causeof illness, like weight gain associated with a thyroid problem.”

My mother suffered some complications associated with obesity, but she was always thin. Always. I can’t think of any time she would have tipped the scales at overweight. The pinky ring she wore in her 20s is too small for my 6-year-old granddaughter’s pinky. But she very well may have suffered from inflammation. She was riddled with allergies.

So was she really obese, but not fat? Was she not obese, but had some linked conditions because inflammation is the real basis of her (and other’s) disease? Hard to know because we have no agreed upon definition of obesity in the US.

The good news is that there is now a Lancet Commission to bring together health experts from around the world together to define the illness of obesity, not just how it looks. “One of several efforts to push the medical community beyond size metrics like B.M.I., the commission’s report, coming this fall, will for the first time describe what it is calling “clinical obesity,” naming signs and symptoms of sickness, organ by organ, tissue by tissue with plausible mechanisms for each one.”1

Having a document in which the disease is defined will give doctors much needed guidance to refine and standardize best practices. It will provide support for treatments that improve symptoms or disease process and (hopefully) eliminate prescriptions of unnecessary medication. One report will not remove bias entirely, but it will allow patients a stronger position from which to review treatment plans to see if they are in line with current science.

This, as they say, is progress.

Disclosure of Material Connection: I have not received any compensation for writing this post. I have no material connection to the brands, products, or services that I have mentioned. I am disclosing this in accordance with the Federal Trade Commission’s 16 CFR, Part 255: “Guides Concerning the Use of Endorsements and Testimonials in Advertising.”

1) https://www.nytimes.com/2024/09/19/opinion/obesity-disease-ozempic-weight-loss.html

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Could Ghrelin be my Hunger Gremlin?

Could ghrelin be my hunger gremlin? For years I’ve been wondering whether my hunger sensor is broken. I can end up with all the symptoms of low blood sugar before I ever feel hungry. On the flip side, I can eat and eat and never feel full. Most likely, there’s a communication problem between my celiac damaged gut and my brain. The question is, what’s the problem and can it be fixed?
gremlin
Asking this question led me to some reading on the hormone ghrelin. I’ll keep the information here simple, but have placed some links below if you’d like to read about the function of this multifaceted hormone in greater detail.

Initially, I ran across information that indicated ghrelin is known as the hunger hormone. It activates its receptor, growth hormone secretagogue receptor (GHS-R), to regulate nutrient sensing, meal initiation, appetite, fat deposition, and growth hormone release. This sounds related to my hunger sensor concern. Perhaps ghrelin is my hunger gremlin. In order to find out, I had to keep reading.

Scientific literature now suggests its functions go well beyond those related to simple appetite stimulation. Ghrelin has been increasingly recognized as having a role in regulating many organs and systems such the process of creating glucose from non-carbohydrate sources (gluconeogenesis) by inhibiting insulin secretion. It can also regulate energy expenditure by signaling a decrease in heat in the body.

This hormone provides a measure of cardioprotection by reducing sympathetic nerve activity which increases the survival prognosis after a heart attack. That doesn’t sound like gremlin activity. That sounds helpful. It prevents muscle atrophy — also helpful. In spite of all these helpful functions, Ghrelin has a gremliny side. It may promote cancer development and metastasis.

And it seems that ghrelin prevents excessive anxiety under conditions of chronic stress. Now we could be getting somewhere. My early years were filled with enough chronic stress to wear out whatever mechanisms were regulating my stress levels. Still, I don’t have enough information to quite put the pieces together to figure out why my hunger sensor is off.

It’s possible that in the future, ghrelin-related drugs will be produced to help with my problem and many others. The wide-ranging roles of ghrelin and GHS-R make them likely targets for drug development.

A paper has already been published showing that in rats ghrelin can alleviate disturbance of glucose and lipids caused by consumption of the party drug ecstasy (MDMA). Sounds like this could lead to a drug to fight the detrimental effects of a drug. That can either be good or bad, depends on how you look at it.

With all my reading I learned a lot, but I did not find a definitive answer. I don’t know if the problem with my hunger signals is primarily in my brain, my gut, my adrenal glands or somewhere else. I still don’t know whether ghrelin is my hunger gremlin.

http://theconversation.com/chemical-messengers-how-hormones-make-us-feel-hungry-and-full-35545

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4049314/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3273630/

https://www.ncbi.nlm.nih.gov/pubmed/22535766

http://acta.tums.ac.ir/index.php/acta/article/viewFile/6420/5025

https://www.ncbi.nlm.nih.gov/pubmed/22521145