Winter 2024
The Changing Winds of Weight Management
Sometime over the past 30+ years, many in the medical and fitness world came to a difficult and exasperating conclusion: weight loss is not so simple as eat less, move more. This is a topic we have discussed previously here, here, and here but it’s not the thrust of this blog. It’s what’s new that we’re addressing here.
For the past 50 years or so the estimated calculus of 3,500 calories = a pound of fat. So if you ate 500 calories more per day for a week, like on a cruise ship, you’d gain one pound of fat. Similarly, if burn off 500 calories more than you consume while hiking the national parks for a week, you’d lose a pound of fat.
We’ve since learned that an old concept negated the effectiveness of that simple math.
That concept, popularized by a former Vanderbilt psychology professor, Dr. Martin Katahn, was the ‘set point’ theory and here. This posited that our body’s weight was regulated, like a thermostat, to remain close to where it had settled in. Thus, as you gain and hold extra weight, the body acclimates to its ‘new’ size and shape and resists changes brought about by dietary or activity adjustments. (As you can ascertain, this should hold true for those who are naturally lean, but other variables factor into leanness that don’t seem to hold as true as fatness. Hence all the “used-to’s” we hear in the gym.)
This resistance to change is referred to as homeostasis: “any self-regulating process by which biological systems tend to maintain stability while adjusting to conditions that are optimal for survival.”
Today, we now know that there are gut and brain hormones that react and respond to how much and even what we’ve eaten by sending signals to stop eating, eat more, or eat differently. The primary hormones – ghrelin, leptin, GLP-1, PYY, insulin, and others – provide our neurogastric – nerves and stomach – feedback system with information as to whether we’re hungry, should be hungry, or should be sated.
What we’ve since learned is that these hormones, which signal other cells what and how to perform, sometimes lose effectiveness. Like those with type 2 diabetes, with chronic high blood sugar and excessively high insulin output from the pancreas, the cells’ receptors that receive insulin are now clogged up. So now the cells are less able to do their jobs.
The feedback loop is now disrupted: if the hormone is rendered ineffectual due to cellular resistance, it takes more stimulus to increase its output. In the case of the gut and brain hormones, stop-eating signals don’t get heeded, and you consume more calories as a result. And store more fat!
It is this biochemistry that calls for attention to a more recent perspective of how we view overweight-ness and obesity: it’s a disease, not a moral or motivational failing on the part of the person. This philosophical approach is similar to how the healthcare community is changing concerning other diseases. For example, it is no longer appropriate to refer to someone with diabetes as diabetic any more than we should refer to someone with cancer as cancerous.
The disease is not the person any more than the person is the disease.
Taken too far in other aspects of life, this shift might appear to be political correctness. But, in medicine, this shift allows doctors to treat the disease independently of the person…without losing sight of the person suffering from the disease. This paradigm shift is crucial to understanding the introduction of some of the new weight loss medications.
Along came semaglutide, a man-made drug; it is a GLP-1 agonist and helps boost insulin output. This was initially found to help those with type 2 diabetes. Like many drugs, however, it had a remarkable set of side effects: less hunger (slows the emptying of food from the stomach making you feel fuller longer), less food-thoughts (decreases obsessions with eating), less addiction to other substances (like alcohol, tobacco, even gambling and sex in some cases), and decreased weight. By a lot! And faster than you could accomplish with diet and/or exercise.
Sold under various names that have become synonymous with weight loss, such as Wegovy, Rybelsus, and Ozempic, this fantastic drug is new enough for weight management yet we don’t even know certain basic things about it. For example, how long does one have to take it? What are the long-range negative effects of taking it? And is it safe or dangerous for those with comorbidities related to or unrelated to obesity?
The obvious medico-ethical and medico-legal answers to the above are an emphatic ‘we don’t know’. But that won’t stop some purveyors of these kinds of drugs from fulfilling clients’ and/or patients’ requests. Nor will it stop many of those who are, for good reasons or wrong reasons, desirous to lose body weight even if not medically warranted.
For a more in-depth look at this new drug and the issues surrounding it, see the STEPS Fitness blog post “Weight Management’s New Look”. Also, check out the following links:
Semaglutide & childhood obesity
Ozempic and its contemporaries
Semaglutide & heart event risk reduction
To Pre or Not to Pre?
Perhaps it’s because I’ve had a few too many but people often contact STEPS for prehab training in anticipation of an upcoming joint replacement. Whether it’s a knee or hip, though occasionally a shoulder, prehab, which is the common lingo for training that occurs prior to surgery, rest mostly on anecdote not data. The reasons are many not the least of which is that there are so many different protocols for a specific joint replacement. Every study must compare a particular supervised or unsupervised protocol to a ‘control’ protocol such as an assignment of exercises to be done at home without supervision.
But real-world prehab as might be found in a fitness center is less regulated, less specific, and more comprehensive than physical therapy programs. We can take into account multiple lifestyle considerations beyond the specific joint.
An article in the American Journal of Physical Medicine and Rehabilitation (Jan. 2023) reports on a comprehensive analysis of other studies on “performance-based, patient-reported, or healthcare utilization outcomes.” They concluded that knee prehab “may [my emphasis] result in increased strength and reduced length of stay and may not lead to increased harms but may be comparable in terms of pain, range of motion, and activities of daily living (all low strength of evidence).” And, although there were only 6 hip prehab studies, all they could conclude was that there was “no evidence or insufficient evidence for all total hip arthroplasty outcomes.”
The ‘may’ results and the ‘no evidence or insufficient evidence’ appear to negate or minimize the value of prehab. However, it should be understood that many of these programs are low in intensity and variety of exercises, accounting for the complexities of insurance-based physical therapy and the protocol-restrained exercise programs therapists are confined to.
Does this mean prehab is insufficient to benefit someone preparing for a joint replacement? No. It merely means that most prehab programs are probably insufficient to yield the kinds of results the study itself was limited to finding. For the rest of us joint replacement patients, it’s clearly a benefit if done under the right circumstances with the right professionals….at STEPS.
