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internal bathroom scales.
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https://www.sciencedaily.com/releas...71227150442.htm Quote:
It's an interesting idea, but where does it properly belong? There are studies with rodents on vibrating pads, these have the effect of directing certain stem cells away from differentiation into fat cells. One of the vibration studies; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2689082/ Quote:
Some studies on obesity in rodents and appetite look at what the animals are willing to do to get food. Put food at the top of a slope, the steeper the slope, the less the animals will bother. The less interesting the food, the less the animals will bother. They'll work harder for more interesting food, in other words. This goes as far as the animals losing weight if the effort doesn't seem worth the reward. Adding weight to an already overweight animal seems strongly similar to increasing that slope. Maybe they'd eat more when they got to the food, but constantly running up to the dish for little snacks might decrease. Some sort of feedback to prevent a bodyweight that puts excess strain on the skeletal system does make sense. The full text is free, this bit shows what they've done to substantiate their proposed mechanism; Quote:
https://www.researchgate.net/public...nd_adult_humans Regulation of fat mass independent of leptin levels gets mentioned a few times. Leptin, the skeletal system and the central nervous system sort of come hand in hand. Quote:
You can make mice lose most of their body fat by injecting leptin into their brains--but they suffer a loss of bone mass. Maybe a result of the loss of peripheral leptin rather than a direct effect of central leptin? This is one of the problems with making body weight regulation entirely a central thing. Insulin is anti-obesogenic, because it reduces bodyweight when injected into the hypothalamus? What happens to the rest of the body? Circumventing peripheral signals might be okay, as long as those peripheral signals don't actually serve a purpose. What are the odds of that? |
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I wrote something smarty, changed my mind. That quote illustrates everything wrong about the experiment result interpretation - assumed premise is biased, i.e. sitting is the cause, obesity and bad health is the effect. |
We hypothesized that there is a second homeostat regulating body weight with an impact on fat mass. In this study we have added and removed weight loads from experimental animals and measured the effects on the biological body weight. The results demonstrate that there is a body weight homeostat that regulates fat mass independently of leptin.
I'm not dismissing their hypothesis, but could we also assume a simpler hypothesis that carrying extra weight make us burn more calories? |
I don't want to jump to the conclusion that they're wrong though, either.
One thing the study doesn't really look at is time spent on the animal's feet. If you look at another area where standing vs. not standing definitely makes a difference, in lean mass, the actual amount of time that needs to be spent weight-loaded vs. not to increase lean mass/prevent loss is fairly short. The mice were loaded with 15 percent of their bodyweight. One thing here, weight loading isn't much of a thing with mice. For me 15 percent is like 24 pounds, it's a rare day where I wouldn't be loaded at some point with a lot more weight than that. Even if this applies to both mice and humans, a lot of us might already be bearing enough weight on a regular basis that any benefit to be had by weight bearing has already been had. If you look at the vibrating platform study I posted Quote:
These mice were also used for the added weight study, and it only took 15 minutes of stimulus a day, cute little weighted vests for short periods of time daily might have been just as effective as the permanently implanted weight pellets. |
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They produced mice with compromised osteocytes/weight sensing to rule this out. Also--burning more calories isn't what happened, because the mice ate considerably less calories. Pair fed mice had similar results. Nobody asked if any of the mice were happy about the whole situation. |
I tend to buy into the weight set point theory because that's what I've observed happen in myself and others, that the body "defends" a certain weight (whether it's higher than the amount we'd ideally like or not) despite varying amounts of daily food, activity, etc. So the discovery of yet another method the body uses to monitor its own parameters in regard to weight makes sense to me. The trick seems to be to find ways to tell the body it's okay to lower its defended set point so that it will automatically work to maintain the new weight. I lost a bunch of weight and was maintaining extremely well until I thought it was alright to add back a bit more carbs from healthy things like low-carb vegetables and nuts. For my body, not a good plan. My weight started climbing and now having a lot of trouble trying to control it. I think the increase in carbs, while still pretty low, was too much for my body and triggered metabolic changes that raised my weight set point. So yeah, it's an interesting idea that in addition to hormones, the body may also use its own bones to sense how much weight its carrying so it can make needed adjustments to meet its perceived set point. You know there are some kind of mechanisms going on in there sensing and regulating things where you can pay no attention to energy intake/output and still weigh the same amount for long periods of time.
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