Excellent points on the weights of various body parts.
I don’t disagree on the absolute numbers, I don’t pay a lot of attention to those other than the body weight as that one is pretty accurate. I do pay more attention to trends and how I look, which is pretty spectacular LoL!
Animal dressing weight… the hide is quite heavy. We used to kill for the hide and store them until the hide market was high, then cash out.
I’ve killed thousands of cattle, pigs and lambs and have dressed hundreds of deer, moose and bear. But that was a long time ago Also dead weight is quite different from live weight, the blood drained out during the sticking process is quite heavy.
And then in humans there is the interstitial organ. Only discovered in 2017 or 18? It collapses and basically disappears at the time of death. I’m guessing it does not make much difference between live and dead weight though.
I did a poor job of communicating agreement with @Davin8r . I was trying to say that I see more mass as a prerequisite for getting stronger once you get to a certain level of training. So that’s one reason why I’m training for hypertrophy now. I also like looking good at the pool/beach and it’s important in my work environment. Too much strength training and I get pretty beat up.
Re: body comp, it looks like my Hologic DEXA results put my bone mineral content at 6.43 lbs, then there’s fat mass and lean. I guess bones don’t amount to much. We won’t get reliable estimates of skeletal muscle mass without CT or MRI, but if these data from 2000 are still relevant (but for fluffy people), we can get a rough idea of the ratio of SMM to total lean mass. The mean values are pretty much what @RapMet quoted (70 lbs).
Leaner people have less SMM, of course.
I’m fine with just tracking lean mass deltas, and I prefer the DEXA total LM to appendicular b/c appendicular doesn’t say anything about chest and back.
Here’s a rather interesting article about ancient Japanese ancestry. When looking at extremely ancient genes, so ancient that humans got them from Denisovans and other hominids, we see that they can contribute to very different reactions to modern medications:
" For instance, other researchers have shown that people in Tibet have Denisovan-derived DNA within a gene called EPAS1, which is believed to have aided their colonization of high-altitude environments.[3] More recently, scientists discovered that a cluster of Neanderthal-inherited genes on chromosome 3—a trait that is present in roughly half of all south Asians—is linked to a higher risk of respiratory failure and other severe symptoms of Covid-19.[4]
The analysis by Terao’s team shed light on 44 ancient DNA regions present in Japanese people today, most of which are unique to East Asians. These include a Denisovan-derived one, located within the NKX6-1 gene, known to be associated with type 2 diabetes, which the researchers say could affect a person’s sensitivity to semaglutide, an oral medication used to treat the disease. They also identified 11 Neanderthal-derived segments linked to coronary artery disease, prostate cancer, rheumatoid arthritis, and four other conditions."
Readily available nutrient-rich foods exploit our inherent drive to overconsume, creating an environment of overnutrition. This transformative setting has led to persistent health issues, such as obesity and metabolic syndrome. The development of glucagon-like peptide-1 receptor (GLP-1R) agonists reveals our ability to pharmacologically manage weight and address metabolic conditions. Obesity is directly linked to chronic low-grade inflammation, connecting our metabolic environment to neurodegenerative diseases. GLP-1R agonism in curbing obesity, achieved by impacting appetite and addressing associated metabolic defects, is revealing additional benefits extending beyond weight loss. Whether GLP-1R agonism directly impacts brain health or does so indirectly through improved metabolic health remains to be elucidated. In exploring the intricate connection between obesity and neurological conditions, recent literature suggests that GLP-1R agonism may have the capacity to shape the neurovascular landscape. Thus, GLP-1R agonism emerges as a promising strategy for addressing the complex interplay between metabolic health and cognitive well-being.
This is the key sentence as I see it. Elsewhere I asked what do GLP-1 agonists bring to the table above and beyond SGLT2i for a specific kind of presentation: the subject (in this case myself) who never struggles with appetite or weight. I appreciate that for many curbing appetite is key, as is weight loss, and so GLP-1 agonists are vital.
But these are not my problems. I did eight years of pretty robust CR, with zero issues as far as appetite and hunger. Now I am on a set diet, eat my portions and don’t snack, so there isn’t even an opportunity to overeat. I’d have to go out of my way to take extra portions, which simply doesn’t happen. My bowl is of a certain size, and that’s it, there are no seconds; f.ex. I have a small cup I fill with a few peanuts, some walnuts and a fistful of almonds - I consume it daily, but that’s it, I don’t understand this concept of “can’t stop eating nuts”, the cup has a bottom and that’s it for the day. In other words, overeating and weight control does not apply to my situation.
Therefore if the sole benefit of suppressing GLP-1 is that appetite is suppressed and downstream of that weight is controlled, I need it as a fish needs a bicycle as a sage once said.
On the other hand if GLP-1 suppression provides other benefits than those mediated by appetite suppression and weight control, I’m all ears.
I’m looking to take SGLT2i (empa) soon, because my blood glucose is high despite a good diet and exercise, and metformin at 500mg doesn’t do jack for me and I’m unwilling to go higher. So if empa can dump excess blood sugar, that’s great, plus apparently it can provide benefits above and beyond just getting rid of excess serum glucose. All with an apparently good risk profile. That’s a win. What does a GLP-1 agonist do for me beyond what empa can?
I was very eager to read about the remodeling of the “neurovascular landscape”, but it all came to a screeching halt with that sentence, which in my mind is nothing more than taping your mouth shut so you don’t overeat and gain weight. If that’s all a GLP-1 agonist does, I’ll pass.
Again: many GLP-1RAs barely suppress appetite (albiglutide, exenatide, dulaglutide?). That’s why it took so long to repurpose GLP-1RAs from diabetes to weight loss. On top of that, people with T2D lose way less weight on GLP-1RAs compared to overweight people without diabetes. In the PD trial of lixisenatide, patients didn’t lose weight. Obesity is protective against PD, and yet GLP-1RAs seem protective against PD.
“Whether GLP-1R agonism directly impacts brain health or does so indirectly through improved metabolic health remains to be elucidated.”: they say “metabolic health” and not “appetite suppression” or “weight loss”. Metabolic health is broader: BP, glycemic control, lipids, inflammation, liver enzymes, etc. See, for instance: Intermittent (oral) Rybelsus / Semaglutide use in healthy individuals? - #382 by adssx . For sure, the effect of GLP-1RAs goes beyond weight loss. But does it go beyond optimizing “everything”? Does it do something additional in the brain?
Pendulum is one of the few probiotics manufacturers that use a process that preserves live gut bacteria (primarily acarmancia) that can survive stomach acid. They seem legit with clinical trials to back up their claims. Attia has an informative interview with their CEO. Anyway, they have both a glucose control product and a GLP-1 product. I’m going to try the GLP-1.
and store them until the hide market was high, then cash out.
