I agree with your comment regarding fairer distribution, but I think when we look at globalisation's impact on war, I'm not sure this is really playing out.
Iran has not benefitted hugely from globalisation (unless I'm missing something), however because of globalisation and their ability to impact the global economy, they have an outsized hand to play relative to their GDP.
The "perscription system" used to be that you'd have to go see a doctor, the doctor knew who you were, and would make decisions on what prescriptions/medications you should be given.
Due to drug advertising rules, the prescription system has been turned on its head, and the patient now goes to their doctor asking for a specific prescription.
Telemedicine took advantage of this and has effectively removed the middleman (the doctor) in many cases and you just sign-up look at a person on a camera, and get your drugs sent to you.
> Telemedicine took advantage of this and has effectively removed the middleman (the doctor) in many cases and you just sign-up look at a person on a camera, and get your drugs sent to you.
This is only true for a handful of drugs that are basically OTC already (or that have OTC formulations). Additionally, telemedicine didn’t take advantage of drug advertising- that’s an odd assertion.
The system changed from the doctor deciding what drugs you should take to the patient asking for the drug by name from the doctor.
I think this enabled telemedicine to work in the way it does not. The patient says "I want wegovy" and the telemedicine platform says "ok, here you go".
Would telehealth pill-pushers exist without this mentality?
The intricate and what looks like soft handling of closing the boxes, using the 2nd finger gently, as well as turning the washer to fit in the slot stood out to me.
Though I was curious about fitting the belt into the square slot. Did it have a map of where the belt was supposed to go? Or was it able to figure out itself that it would bend to fit in that slot?
I actually just responded with almost the exact opposite, but maybe I'm the "lipid hypothesis skeptic".
Seeing as the threat is calcium build-up in the arteries, and because cholesterol is a vital component of health, I believe that if you are in good health, and don't have a history of heart-disease, or have diabetes or other auto-immune disease which increases risk of atherosclerosis, lowering cholesterols is an in direct measure.
It's about understanding your personal risk and making decisions based on that.
I actually don't think your response is the exact opposite, but you touch on some of the skeptic stuff, so I'll respond to here:
First of all, I agree with your points that you should consider the individual. My long term interest in this is also from being a very fit, low blood pressure, metabolically healthy person who always had at least somewhat elevated LDL (sometimes very elevated) that doctors would flag.
PCSK9 people are as close to a natural experiment on the effects of life time low LDL as you will get and they get near total protection, even when they have no other risk factors. People like smokers, hypertensives and diabetes have ~90% less than other high risk people, but people without any of those factors also have significantly less heart disease. People with two broken PCSK9 genes have close to zero LDL and have noticeably completely plaque free arteries as adults. I do think this does pretty fatal damage to the theory that you must have some other health issue for LDL to be bad.
It's very likely that "LDL-C" the lab measurement isn't as good as measuring ApoB, but for most people, they are concordant. And ApoB is a different way of looking at low density lipids, by particle count instead of weight. Dietary stuff like the fats in the article that lowers LDL measurements typically also lowers ApoB in most people.
So, in part, I agree that more precise biomarkers can help adjust individual risk. But most people are concordant. And the evidence that the underlying "low density lipids", no matter how you measure them, are causally part of the disease process is very strong.
> People with two broken PCSK9 genes have close to zero LDL and have noticeably completely plaque free arteries as adults. I do think this does pretty fatal damage to the theory that you must have some other health issue for LDL to be bad.
i'm not sure i follow this extrapolation from low-ldl individuals to any direct statement about causes and effects at higher ldl levels.
if there was, for instance, some thought-harmless virus endemic to a large portion of the population which somehow caused plaque buildup but only at sufficiently high ldl levels, people with naturally low levels their entire lives would still have plaque free arteries and we would still, as we do, see a broader range of plaque buildup among people with high levels. how do you propose to distinguish this hypothetical (and admittedly most likely biologically incoherent) explanation from yours by only looking at people with naturally low levels?
your assertion that such individuals are an excellent approximation to an experiment on the arterial health effects of lifetime low ldl seems reasonable enough, but you then appear to draw unfounded conclusions about the nature of potential inverse effects at higher ldl levels.
The point I was making re double variants having even more apparent protection is simply that these people continue the dose response curve you expect to see all the way to the extreme low end. Single variant people have massive protection, double variant people have essentially 100%.
You are correct that it doesn't rule out lipids + unknown additional factor(s). However: If there is a mystery factor, it must be close to universal. We know from autopsy studies of non-cardiac deaths that fatty streaks are present in virtually all children and that by 30 most people have advanced fibrous plaques (including soft plaque invisible to calcium score tests). The double variant people don't. So LDL is at minimum a necessary, limiting factor.
It also doesn't exclude that there is some more specific subset of the low density lipids that cause problems (this is what switching to ApoB testing is supposed to get at). Which is actually where we are at in the first place with LDL-C measurement being a refinement over previously looking at total cholesterol.
There is push back on the high LDL leads to cacium build-up in arteries (being specific instead of just "longevity").
The challenge is that some people, like myself, have outrageously high LDL, yet no calcium build-up in arteries via calcium score testing.
This is why ApoB is the newer more common test. Molecules containing ApoB can stick to the walls of arteries, and the theory is that the more ApoB molecules in the blood, the more likelihood of a molecule sticking and then becoming calcified.
If you have an auto-immune disease or diabetes, which increases the amount of time it takes for tears in the arteries to repair, you have a longer exposure time of fats sticking to the arterial walls which increases the likleihood of calcifying.
However, that doesn't mean that everyone with high LDL and high ApoB are at higher risk.
This is why I went for the calcium score. Don't show me the things that might lead to calcium build up later, just measure my calcium levels and let's see if I am currently at risk, and we can keep monitoring this.
Doctors are still trying to push me on to statins, but without a history of heart-disease and every other biomarker being off the charts high, I am taking that risk myself, knowing that calcium score is 0, so my suspected risk is actually very low.
Long answer, but hopefully that clarifies the understanding.
I'm not a doctor, I work in neurotech so am around health and have gone through this process myself.
I'm with the sceptics, but also they don't show it in use. But from the product screenshot of the person hitting the button, it seems not to be wearable, so.....when would I use this? When I'm in a room that has a smart-speaker? So I go to a friends place for dinner and I put this device on the table so that my friends Alexa can't hear me.
Good thing I wore my tin-foil hat to dinner, but sadly, my friend didn't wear one, and now they can't get a timer for their cooking and the meal is ruined. Brilliant.
Of all the things wrong with windows, I don't feel that having a Microsoft account is the worst of them, or the one that needs the most attention.
Is the reasoning that if you don't have a Microsoft account, they'll do less of the ads nonsense which is baked into the OS? Maybe I don't get what the issue is.
I've tried linux, but haven't converted (though I'm tempted), but my mac has a mac account and nobody seems to complain about that, my android has a google account, why is a Microsoft account so much worse.
The things I feel it is more important for Microsoft to get rid of
1) the push for OneDrive everywhere - Mac is as bad if you don't have iCloud
2) updates requiring "set-up" and trying to trick you into adding services in the process
3) Windows Hello moving the "sign in" button down 10px once it recognizes you....WTF!!
4) ads, ads, ads (though if you don't use start button much or Edge, I think this is mostly avoided
5) letting apps add shortcuts to your desktop on an update.
"Requiring an account" means leaning in the Apple/Disney direction - upselling, walled gardens and milking captive customers. Dropping the account requirement is a symbolic (and practical!) step in the other direction, towards using the product as a tool.
That's fair, so is the outrage focused on Microsoft because they are a "more" open system without the app store being the default method of installing apps?
I guess I'm wondering why Apple and Google don't get the same pushback?
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