I'm thinking about starting a very low dose when the pills come out in Europe. That gives an extra year for more data.

For me it's purely about health (well, about 90% about healthj). I'm a marginal case weight-wise, but the overall health impact profile looks spectacular. If a pill seems likely to add a number of healthy years to my lifespan, yes please. But the more data the better.

One thing that held me back was, I'm very averse to addiction, to anything that might have withdrawal symptoms. People report being ravenous and needing to eat all the time when they quit. BUT - the data shows that after one year, people still retain about 25% of their weight loss, and at two years they're about baseline (some above baseline, some below - the "above" people may be due to sarcopenic obesity, in that you put fat back on faster than muscle, and so your metabolism is lower until the muscle comes back). This is very different from when you diet to lose weight and then stop dieting - you're not ravenous at all, you finally have satiation.

But given the weight regain stats, and the general way these work, what I think is going on is: when you lose weight, you've been training yourself for months on how to ignore or alleve your hunger pangs, so when you stop, you're well trained to it. Whereas GLP-1 agonists are just the opposite: you don't even need to think about resisting the temptation to eat, it just comes naturally; you can get pleasure from something, such as a tasty dessert, without feeling the need to eat everything on your plate; pleasure and craving get separated. So people who just suddenly cut off from GLP-1 agonists are "mentally unarmed" for the reversal. The weight-regain stats however suggest that it doesn't leave you long-term disabled in this regard; that you're just back to your old self once you readjust, whatever that old self may have been.

I haven't read these particular studies, but a lot of the fascinating impacts of GLP-1 agonists occur whether the person loses weight or not. For example, the cardiac benefits are massive, like 2/3rds of the scale of benefits of being on statins, and it apparently occurs independent of weight loss.

One of the annoying things about our wetware is that systems aren't isolated; a "part" that gets used for one thing might also be used for half a dozen unrelated things.

Please understand that there is a balance. Taking things to "reduce inflammation" or to "boost the immune system" run counter to each other. Inflammation *is* the reaction of the innate immune system. The immune system defends not just against pathogens, but also cancer. If you shut down the immune system too much, you can shut down cancer surveillance, which I don't need to stress, is a bad thing.

The downside to inflammation is that, yes, it is damaging. Needless inflammation is bad. And, as an added twist, from a personal example: my mother has Sjögren's and MALT lymphoma in the salivary glands. Sjögren's is an autoimmune condition that attacks exocrine glands. In doing so, it triggers a nonstop immune reaction in the salivary glands and the development of lymphoid tissue, with lymphocytes constantly proliferating. This nonstop proliferation runs the risk of - as in my mother's case - developing mutations that lead to lymphoma. So too much of a needless immune reaction can also cause cancer.

The immune system is an extremely complex, with hundreds of known cytokines, each causing various activation / suppression effects in others and having various other interactions with the body. So it's extremely hard to say, if you tweak this one thing, what will be the overall impact in the long term?

These GLP-1 agonists inhibit the NF-kB pathway and downregulate pro-inflammatory cytokines like TNF-a, IL-6, and IL-1. We think that this sort of downregulation is probably in general beneficial, in that in most cases it should not weaken cancer surveilance, and actually can help with certain types of cancers (but still can be harmful to some). Everything is situation dependent, and there's a lot we don't know.

I decided to randomly pick one of your claims to fact check - that beans are "less than 300 calories a pound!" Here's the info I find:

Cooked Bean Variety Calories per 100g Calories per Pound (approx.)
Red Kidney Beans 127 kcal ~576 calories
Black Beans 132 kcal ~600 calories
Navy Beans 140 kcal ~635 calories
Pinto Beans 143 kcal ~649 calories
Chickpeas (Garbanzo) 164 kcal ~744 calories
Great Northern Beans 139 kcal ~630 calories
Lentils (Cooked) 116 kcal ~526 calories

According to FAO, the average person eats 1,88kg (4,1 pounds) of food (wet mass) per day. Thus beans, with an *average* dietary wet mass (not that one can't readily just eat more!) corresponds to 2157-3050 calories per day.

Globally, most hunter-gather tribes get most of their calories from plants, not animals. Meat commonly acts like a multivitamin - while not that much is eaten compared to plant matter, it provides nutrients that are hard to get (or impossible) from plants. My favorite example is that there are tribes that get the vast majority of their calories from sago, with the Yimar/Yimas getting 93% of calories purely from sago alone. BUT they also eat the sago grubs they find while pounding sago. Sago provides the energy, and the other 7% (commonly shrimp and small fish) provide critical protein and nutrients that aren't present in the starchy sago.

GLP-1 isn't a drug at all...

You know what else distributes spike proteins throughout the body in orders of magnitude greater quantities (rather than the barely-measurable quantities you're referring to)? *Getting infected*. And the lower your antibody titres, the more the spike proteins. Also, vaccine spike proteins are mostly disabled. They're double-proline stabilized; while they can still bind with ACE2, they can't retract the way the virus does for cell entry.

You know what causes far more significant long-term antigen persistence? *Infection, particularly without preexisting immunity, such as from vaccination*.

You know what also causes cardiovascular distribution, prolonged antigen production, and immune-mediated injury vastly more often and more seriously than vaccination* *Infection, particularly without preexisting immunity, such as from vaccination*.

Modern diets barely resemble early diets. While hunter-gatherer diets have varied greatly (paleoarctic people eating significantly more meat than average, for example), modern diets compared to the average paleodiet are high meat, high protein, and very low fibre.

If you want an "average caveman diet", you'd be swapping out a lot of the red meat for plant fibre.

If you hear "Israeli" and immediately translate it to "ALL JEWS IN ALL THE WORLD", the problem is you.

That Wix is Israeli.

Other related terms:

  * Pseudo-quotation: Putting a paraphrase or the general "gist" of someone’s argument inside quotation marks, rather than their literal verbatim words. Acts structurally like a quote, but semantically is a summary.
  * 'Fictive Direct Speech (Esther Pascual): The structure of direct speech used to express a non-conversational concept, such as a belief, attitude, or general stance.
  * Constructed Dialogue (Deborah Tannen): Used for "reported speech" - when people "quote" others in conversation, they are rarely reciting a literal transcript. Instead, they construct dialogue to dramatize a stance, represent a general attitude, or summarize a complex argument in a digestible way.

Sneer quotes (also called scare quotes) are similar, in that they summarize a person's stance, but have the distinction of also being dismissive of the person / stance as well.

That's not what "sneer quotes" do.

(And the quotes in the above are neither direct quotation nor sneer quotes, but use-mention distinction quotes, which let the sentence "know" that the thing in the quotes is the word/phrase itself, not what it refers to)

(And the quotes in the above are signaling quotes, to convey that a word is being used in an unconventional manner; it's a "clever" way to distance yourself from the word)

(And the quotes in the above are irony quotes....)

Yeah, I've been using canisters, and they're expensive and a chore (and because of that, it encourages me to give the plants much less than would be ideal).

The basic process is potassium carbonate/bicarbonate swing absorption. Potassium carbonate absorbs CO2 (and H2O) from the air at low temperatures , forming bicarbonate, but the bicarbonate emits CO2 (and H2O) at high temperatures. So the system has two modes: one, a powerful radial blower blows air through a pumice bed packed with potassium carbonate so that it absorbs CO2 (more specifically, it first absorbs H2O, and then CO2); and in the other, the fan is shut off and a PTC heater turns on to heat the pumice bed.

I'm trying to make the whole system as passive as possible. Since the fan is so powerful (you have to move a LOT of air to capture CO2), it's designed to blow dampers shut or open that control its path, while a different path opens up when the fan is not on. The PTC heater being on will automatically force the fan off. I've also set up (cross my fingers whether it works...) a weight-based system to control fan/heater switching. The core is PPS-CF (super heat tolerant) and mounted on springs, so it should move downward as it absorbs more moisture and CO2, and when it's full, it should force the fan off (even if my greenhouse controller hasn't requested CO2, aka triggered the PTC heater). And when the PTC heater is on, it rises from losing H2O and CO2 mass, and if it rises too much, that triggers a switch to force the fan off.

I'm also perhaps overcomplicating it and making a rod for my own back, in that I've designed it so that both modes have the air travel through a system of (also 3d printed) heat exchangers (in general, heat exchangers working with air have no issue with being made of plastic, because the heat flow from the air to the wall is slower than heat transfer across the wall). So these are big and made of multiple parts, in order to not slow down the airflow from the blower too much. But the idea is that the CO2+H2O flowing outwards cools and deposits H2O in the exchanger (then a secondary heat exchanger re-heats it to drive the convection force), while in capture mode, the incoming air can use that H2O instead of having to rely just on atmospheric H2O (which is viable, but does impose a capture delay). And of course, it helps maintain a warmer temperature inside the core on very cold days that might slow down the reaction (it's designed to be able to be mounted outside; the bulk of it will be printed in ASA).

Right now I'm in that annoying phase of prototyping where you print chunks of parts out, see if they actually print right ("whoops, there are supports in this area, but I CAN'T REACH THAT!"), actually fit together right (for example, dampers not jamming in their paths), the non-printed parts actually fit (I keep screwing up the mount for the blower, lol), that sort of stuff.

Dunno, but it's a fun project, and hopefully it will work :) Then the question for me (if it actually works well) will be, just release the plans open source, or actually manufacture them (and if so, continue 3d printing, or switch to injection moulding - though that would take redesign!). Because I've not found anything else like it on the market. There are some greenhouse CO2 capture systems out there, but they're gigantic and super-expensive, with even the monthly service contracts being in the hundreds of dollars. This - because it relies on the super stable potassium carbonate/bicarbonate swing absorption cycle (even though it's not the most efficient) - should last basically forever with minimal maintenance (though it is designed for maintenance - for example, I've designed it so that the switch set points that determine when the core is fully saturated vs. fully unsaturated, can be adjusted with a screwdriver)

I do think your "you can't print horizontal holes" in PETG thing is pretty hilarious, BTW, because it's an open admission that you're terrible at understanding how to set print parameters ;)

I don't plan to link anything with my name to you, so you can believe whatever you want, though if you'd like I'll 3d print something with your name on it, with horizontal holes, in PETG and post it online for you. And yes, I have a BA in Horticulture (subfield: greenhouse cultivation) from Fjölbrautaskóli Su[th]urlands (originally Landbúna[th]arháskólinn, in Hveragerði), along with a BS in CS - again, I don't plan to link anything with my name on it, so you're free to believe whatever you want, if it shocks you that people have more than one field. Just like you're free to believe whatever nonsense you want about forests.

https://carbonneutral.com.au/carbon-jargon-how-trees-capture-and-store-carbon/

Age also has an influence when thinking about collective communities of trees rather than individuals. Younger forests typically grow faster and absorb more carbon overall because trees can be crowded together when they’re small.

When forests consist of middle-aged trees, they also capture and store relatively high amounts of carbon, because middle-aged trees sequester more carbon than younger trees, and if any trees die, they are replaced by younger trees that grow more quickly.

Old-growth forests have a less fluctuating carbon cycle. There are usually fewer trees in an old-growth forest, and the large old trees dominate by blocking out light for younger trees.

https://www.stateforesters.org/wp-content/uploads/2022/03/NCASI22_Forest_Carbon_YoungVsOld_print.pdf

Forests of different ages play different roles in removing carbon from the atmosphere and storing it in wood. Old forests
have accumulated more carbon than younger forests; however, young forests grow rapidly, removing much more CO2
each year from the atmosphere than an older forest covering the same area. Managing forests to avoid large emissions
from the loss of old trees while rapidly removing CO2 from the atmosphere through young forest growth can provide both
storage and sequestration benefi ts

https://www.frontiersin.org/journals/forests-and-global-change/articles/10.3389/ffgc.2025.1702442/full

During the initial years of stand development, either after a new establishment or a stand from regeneration after disturbance, the losses due to RA (autotrophic root respiration) and RH (soil organic matter decomposition) exceed the carbon sequestration resulting in forest ecosystems typically functioning as net carbon emission sources. The duration of this phase varies based on growth rates, site conditions, climate variables, and post-disturbance effects. Rapidly growing forests then transition to carbon sinks within approximately 10-20 years as increasing leaf area and biomass accumulation enhance carbon uptake and eventually surpasses carbon losses from respiration and decomposition. NEP reaches its maximum at an intermediate stand age, after which age-related declines in net primary production (NPP) occur due to reduced nutrient availability, increased mortality (Ryan, 1991; Hartmann and Trumbore, 2016), changes in stomatal conductance, and decreases in photosynthetic efficiency, which shift the balance between carbon uptake and respiratory losses (Bond-Lamberty et al., 2004; Gower et al., 1996; Tang et al., 2014), so that old-growth forests frequently function as a minor carbon sink, or remain carbon neutral, or even become a net emissions source, depending on various factors such as climate, disturbance history, and species composition (Chang et al., 2020; He et al., 2012).

The traditional view is that old-growth forests are roughly carbon neutral - that new growth happens roughly at the same rate as decay. This is not entirely accurate (esp. e.g. in boggy areas or other long-term-accumulation-prone habitats), but by and large, yes, old-growth forests are primarily neutral. Carbon-bearing matter grows, dies, and decays. Certain types of compounds decay faster than others - for example, lignin is humus-forming, and humus is very decay resistant, but is not immune to decay, and is lost over time from the soil. It requires anoxia or mineral binding to protect over geological timeframes. In general, the rates of this, if present at all, are orders of magnitude lower than than the influxes from photosynthesis and loss to decay.

To be clear, this is not that individual trees store less carbon as they age - just the opposite, rates continue to grow as a trees get older. But every tree is fated to die, and when it does, it overwhelmingly rots. Mature forests are in balance. It is forests that are not in balance - e.g. young forests, say 20-40 years old - that are massive at net removing CO2 from the atmosphere, because growth is fast but decay is slow (because not much has yet died).

TL/DR:
* Clearcut forest: terrible emission source. Lots of decay going on / soil carbon loss, even if immediately replanted. Takes a decade or more to go back to net sequestration
* Young growing forest: peaking at 20-40 years, massively net sequestering. Lots of new growth, comparatively little decay.
* Old growth forest: roughly in balance between growth and decay. Stores lots of carbon, but does not net sequester much, if any, carbon.

I hope that helps.

Literally just look at the spec sheets from Bambu above you:

Max bridging length: 30mm vs. 30mm (tie)