What do you tell your Doctor

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lessthanhalf said:
no one should be stopping statins used for high cardiovascular risk or known heart disease because GLP's also can lower lipid levels .
Ironically, you bolded and most confidently stated the one claim in your post that has never been studied clinically. I agree that someone in the situation you're describing (who has already narrowed their treatment lane to statins, progressed to that point, and been on them for years) would likely do poorly to abandon statins at that point from a purely cardiovascular point of view.

Still, "no one" is a pretty broad qualifier. Statins are not the one true drug that all must believe in and proclaim their deference to from the rooftops. They're just another class of drugs with their own mix of pros and cons, like every other class of drug.

As a simple exception to "no one," it's easy to posit someone who is experiencing dementia, finds that symptoms reduce when statins are discontinued, and has decided they would prefer to be able to think more clearly in their final years over letting their cognitive faculties slip away from them just to get an extra year of life in a memory care unit. As arrogant as your typical cardiologist can be, I suspect that even in that case you'd find agreement from them if the family pushed for such a trade off.
 
It is pretty close to impossible to find a decent PCP where I live, unless you have the money to be self pay and/or a concierge service. My PCP is meh at best and didn’t tell me that my Testosterone was really low because it was at a 6 when the bottom limit of acceptable for a woman is a 4. So I walked around with horrible brain fog, inability to gain muscle, and zero libido for an extra year until I started on TRT through a private clinic.

All this to say, I go for a yearly check up and blood work just to keep a general eye on things, but I don’t tell him anything because he’s lost his entitlement to a medical opinion as far as I’m concerned.
 
Nopenada said:
It is pretty close to impossible to find a decent PCP where I live, unless you have the money to be self pay and/or a concierge service. My PCP is meh at best and didn’t tell me that my Testosterone was really low because it was at a 6 when the bottom limit of acceptable for a woman is a 4. So I walked around with horrible brain fog, inability to gain muscle, and zero libido for an extra year until I started on TRT through a private clinic.

All this to say, I go for a yearly check up and blood work just to keep a general eye on things, but I don’t tell him anything because he’s lost his entitlement to a medical opinion as far as I’m concerned.
Sadly, I think concierge care will be the only path forward there and like you I'm also in an area where nobody is doing it so I too am stuck doing extended research. Part of that is that medical school doesn't really select for good critical thinking skills so only a minority of doctors are effective in that regard, so finding a capable doctor is already a challenge. Then add in that there are so many guardrails in place (standard of care, guidelines and policies set by the clinic they're working at, medical liability quirks, etc.) that even if you find a sharp doctor they'll be pretty limited in their ability to properly personalize your care. At this point you're basically engaging in the medical equivalent of going from McDonald's to McDonald's location trying to find one that sells real ice cream instead of soft serve.
 
esdsafepoet said:
Luckily my doctor is so swamped with patients he's never bothered to inquire why I haven't asked for a tirz refill in 6 months. In fact, if it wasn't for having my chart on his computer, he'd probably think I'm a new patient at every visit.
Kinda where I am at. My actual Dr I see once a year, and for any other visit I get a random nurse practicioner. At my last weight loss appt I said I got my perscription online. They see the same commercials we all do.
 
tubby said:
At this point you're basically engaging in the medical equivalent of going from McDonald's to McDonald's location trying to find one that sells real ice cream instead of soft serve.

I respect and agree with your take on doctors, but I cannot get behind your unflattering likening to McD’s soft serve. Those hot fudge sundaes, when made right, are pure heaven.

…Except I don’t want one right now because my Reta dose for the week appears to have kicked in.
 
I've told my PCP a couple of times I'm taking "Chinese Research Chemicals I bought from strangers on the Internet." I'm a funny guy, so he always thinks I'm joking.
 
I'm not telling mine unless for some serious reason I have to tell.
 
I'm honest with my VA doc. She's a NP at a local clinic in a small town, so not VA proper. The VA makes you jump through flaming hoops to get prescribed a GLP1, and I know those hoops would make me punch someone in the face and quit. So I went with a compounding pharmacy out of pocket for Tirz. Tirz started out amazing, but then it went bad fast with side effects that wouldn't go away. I told them I was going to take dosing and medication into my own hands so I knew what was going on. They know I'm smart enough to educate myself on the science and if I have questions, I'll go to them! I'm not a medical professional, but I studied/tutored with half of them in college classes. I helped the head nurse get through bio-chem.

But after years of struggling with depression, statin, and thyroid meds because they make me feel weird, as well as constant debilitating pain, my doc is honestly happy I'm making life changes.

I don't keep a scale at home. I make myself go to the clinic to weigh in every few weeks and get a blood pressure check. The weight loss is a side effect to feeling better for me. I want them to watch the biological changes in real time along with me. I want them to see the ups and downs so they can use that knowledge when dealing with other patients. I want them to see what kinds of crazy changes this stuff can manage so that in the future, they'll help other people fight to get meds that might help them.
 
rGrain said:
I told her I was on compounded Zepbound and she got me on actual Zepbound through the VA she was like "you guys shouldn't be on compounded it's not safe but your numbers are really good finally
Did you have to go through the MOVE program and did they limit your maximum dose? That's what my doc told me I would have to do.
 
tubby said:
Ironically, you bolded and most confidently stated the one claim in your post that has never been studied clinically. I agree that someone in the situation you're describing (who has already narrowed their treatment lane to statins, progressed to that point, and been on them for years) would likely do poorly to abandon statins at that point from a purely cardiovascular point of view.

Still, "no one" is a pretty broad qualifier. Statins are not the one true drug that all must believe in and proclaim their deference to from the rooftops. They're just another class of drugs with their own mix of pros and cons, like every other class of drug.

As a simple exception to "no one," it's easy to posit someone who is experiencing dementia, finds that symptoms reduce when statins are discontinued, and has decided they would prefer to be able to think more clearly in their final years over letting their cognitive faculties slip away from them just to get an extra year of life in a memory care unit. As arrogant as your typical cardiologist can be, I suspect that even in that case you'd find agreement from them if the family pushed for such a trade off.
It is great to see a lot of people making great progress in improving their health and wellbeing by weight loss, often after lifelong severe obesity. It concerns me that after doing this useful thing , many are making changes to treatment without medical advice that could put them at more risk than they were before they lost the weight, such as ceasing lipid lowering therapy. I realise that I am mostly saying the same thing in these responses, but if explaining it differently makes one more person understand what I am trying to say then it is worthwhile, and I get to vent in the process.

While technically no one has ever done a prospective study directly comparing the effectiveness of GLP medications vs statins for cardiovascular disease prevention, the information required to compare their effectiveness already exists. Without trying to make this into a scientifically correct response with accurate numbers and references as that would take 50 times as long to write, statins, and other lipid lowering therapies are much more effective, and the weight of that evidence is much stronger. No clinician or scientist would dispute that statement.

And it really misses the point of what I am trying to say. I do understand why so many people are disappointed or discouraged by conventional medicines' treatment of obesity, the bigotry shown by many doctors towards the obese, which I have seen first hand from both sides of the aisle, the near total lack of any actually useful treatments until GLP's arrived, given that advice to eat less and exercise more is not wrong but it just does not really work very well and is mostly not actually helpful. And in the US especially lack of access to good quality basic primary care doctors. And worldwide, there are finally , for many , after decades of waiting, there are treatments that actually help -- but you cannot have them as they are too expensive. This last bit probably applies to nearly everyone on this forum. And it certainly pissed me off.

So as a not surprising result people have turned in large numbers to a new black ( or grey ) market for GLP medications, and I am fine with that. But it risks throwing the baby out with the bathwater to reject or ignore the advantages that standard medical treatment offers, such as lipid lowering therapies and hypertension treatment that are some of the most proven treatments to have ever existed, in exchange for a peptide for everything type of treatment that sadly is mostly not backed by scientific evidence.

The purpose of lipid lowering therapy is to prevent cardiovascular disease or to prevent it from getting worse. Preventing heart attacks , strokes, vascular dementia, peripheral vascular disease, heart failure and more.

There are reasons for the existence of prescription drugs, the vast majority of the population do not have the scientific background to read , analyse and critique the science behind most medical treatments. Doctors may not be great at this, but learn a lot of the science and a lot of rules over a long time from other doctors in training to make safe decisions ( nearly all the time ) and specialists definitely need to know the science. Over the past couple of years I have read a lot more medical papers than ever before, hundreds at least in full and many more abstracts, and I found that my previous understanding was really quite limited, despite having a degree in that area and having mostly kept up with developments, to the point that I realise many of my understandings of research from the past were wrong and based on an inadequate understanding of the science. And this is a good thing , realising how little you know of complex fields is how you start to learn more. Now I think I am starting to get to a point where I can have a reasonable understanding of some of the research. But hardly anyone is going to spend anywhere near that much time reading and learning to get to a point where decisions about safety or effectiveness about self treatment can be made. Most people using peptides are making their decisions based on anecdotes from other people online, which is very different to reading the underlying scientific studies, and usually they say different things.

I see a lot of people on this forum rejecting medical therapies, or deciding they are no longer needed due to weight loss, and in many cases this may be correct, but not always, and it would almost always be better to have a medical opinion on whether stopping antihypertensive medication or lipid lowering therapy is a good idea.

For blood pressure, it is easy to measure and if it is consistently less than 120/80, there is no evidence that getting it lower than that helps, so ,,, so long as you do not have known cardiovascular disease or kidney disease then stopping it is probably safe, but getting a medical opinion is still a good idea as they can be used for other reasons like preventing heart failure or kidney failure progression.

Lipids are not as simple, lowering LDL more lowers risk more, and targets are different depending on degree of cardiovascular risk. Generally the lower the better for LDL if absolute risk is high. Target level might be as low as 0.5 to 1 mmol/l or 19 - 38 mg/dl ( US units ) in very high risk persons.

If you have known cardiovascular disease ( by symptoms , history of heart attack, angina, stroke, tia, heart failure, peripheral vascular disease or by testing - calcium score, stress test, ECG, angiography or echocardiography ) then ceasing lipid lowering therapy like statins, because GLP medications can also lower lipids, is a really bad idea, unless an expert has assessed the numbers and agrees, which is unlikely, doing this exposes you to a percentage point or more of extra risk for every year going forwards, and is literally risking your life. Adding GLP medications to usual treatment reduces cardiovascular disease progession more than just usual treatment. So both statins and GLP's are a good idea.

Many people who have, or have had, severe long term obesity that has been improved by GLP medications, are in a very high cardiovascular risk category, with risks as bad as those with known cardiovascular disease. And there are a lot of people on this forum in this position. Obesity even if reversed will most likely have caused damage over time, this cannot usually be fixed but you can stop it from getting worse or from causing illness. Ceasing lipid lowering therapy in this group is just as dangerous as in the group with known cardiovascular disease.

Most people are not going to have any idea what risk group they are in, if you do not know for sure then stopping prescribed statins does not sound like a good idea. Doctors make these assessments all the time and use that to decide if lipid lowering therapy is needed, not just based on lipid numbers, as all the other risk factors like family history, smoking, high blood pressure , diabetes, metabolic syndrome, impaired glucose tolerance, proteinuria, NAFLD/NASH, renal function and age all factor into determining risk. There are online calculators that can give you a pretty good idea.

Self treatment without adequate scientific knowledge is dangerous ( and even with good knowledge ) and in the end people will be harmed by it, there will also be some benefits , but mostly from the GLP medications as they are proven to work. Getting a medical opinion on potentially life risking medical decisions like stopping statin or other lipid lowering therapy, is a good idea. It seems ridiculous to be saying this, but unless you know what your 10 year cardiovascular risk is you should be getting expert advice before making those decisions, otherwise you could be risking your life and health to stop a treatment that for most people has no side effects.
 
lessthanhalf said:
It is great to see a lot of people making great progress in improving their health and wellbeing by weight loss, often after lifelong severe obesity. It concerns me that after doing this useful thing , many are making changes to treatment without medical advice that could put them at more risk than they were before they lost the weight, such as ceasing lipid lowering therapy. I realise that I am mostly saying the same thing in these responses, but if explaining it differently makes one more person understand what I am trying to say then it is worthwhile, and I get to vent in the process.

While technically no one has ever done a prospective study directly comparing the effectiveness of GLP medications vs statins for cardiovascular disease prevention, the information required to compare their effectiveness already exists. Without trying to make this into a scientifically correct response with accurate numbers and references as that would take 50 times as long to write, statins, and other lipid lowering therapies are much more effective, and the weight of that evidence is much stronger. No clinician or scientist would dispute that statement.

And it really misses the point of what I am trying to say. I do understand why so many people are disappointed or discouraged by conventional medicines' treatment of obesity, the bigotry shown by many doctors towards the obese, which I have seen first hand from both sides of the aisle, the near total lack of any actually useful treatments until GLP's arrived, given that advice to eat less and exercise more is not wrong but it just does not really work very well and is mostly not actually helpful. And in the US especially lack of access to good quality basic primary care doctors. And worldwide, there are finally , for many , after decades of waiting, there are treatments that actually help -- but you cannot have them as they are too expensive. This last bit probably applies to nearly everyone on this forum. And it certainly pissed me off.

So as a not surprising result people have turned in large numbers to a new black ( or grey ) market for GLP medications, and I am fine with that. But it risks throwing the baby out with the bathwater to reject or ignore the advantages that standard medical treatment offers, such as lipid lowering therapies and hypertension treatment that are some of the most proven treatments to have ever existed, in exchange for a peptide for everything type of treatment that sadly is mostly not backed by scientific evidence.

The purpose of lipid lowering therapy is to prevent cardiovascular disease or to prevent it from getting worse. Preventing heart attacks , strokes, vascular dementia, peripheral vascular disease, heart failure and more.

There are reasons for the existence of prescription drugs, the vast majority of the population do not have the scientific background to read , analyse and critique the science behind most medical treatments. Doctors may not be great at this, but learn a lot of the science and a lot of rules over a long time from other doctors in training to make safe decisions ( nearly all the time ) and specialists definitely need to know the science. Over the past couple of years I have read a lot more medical papers than ever before, hundreds at least in full and many more abstracts, and I found that my previous understanding was really quite limited, despite having a degree in that area and having mostly kept up with developments, to the point that I realise many of my understandings of research from the past were wrong and based on an inadequate understanding of the science. And this is a good thing , realising how little you know of complex fields is how you start to learn more. Now I think I am starting to get to a point where I can have a reasonable understanding of some of the research. But hardly anyone is going to spend anywhere near that much time reading and learning to get to a point where decisions about safety or effectiveness about self treatment can be made. Most people using peptides are making their decisions based on anecdotes from other people online, which is very different to reading the underlying scientific studies, and usually they say different things.

I see a lot of people on this forum rejecting medical therapies, or deciding they are no longer needed due to weight loss, and in many cases this may be correct, but not always, and it would almost always be better to have a medical opinion on whether stopping antihypertensive medication or lipid lowering therapy is a good idea.

For blood pressure, it is easy to measure and if it is consistently less than 120/80, there is no evidence that getting it lower than that helps, so ,,, so long as you do not have known cardiovascular disease or kidney disease then stopping it is probably safe, but getting a medical opinion is still a good idea as they can be used for other reasons like preventing heart failure or kidney failure progression.

Lipids are not as simple, lowering LDL more lowers risk more, and targets are different depending on degree of cardiovascular risk. Generally the lower the better for LDL if absolute risk is high. Target level might be as low as 0.5 to 1 mmol/l or 19 - 38 mg/dl ( US units ) in very high risk persons.

If you have known cardiovascular disease ( by symptoms , history of heart attack, angina, stroke, tia, heart failure, peripheral vascular disease or by testing - calcium score, stress test, ECG, angiography or echocardiography ) then ceasing lipid lowering therapy like statins, because GLP medications can also lower lipids, is a really bad idea, unless an expert has assessed the numbers and agrees, which is unlikely, doing this exposes you to a percentage point or more of extra risk for every year going forwards, and is literally risking your life. Adding GLP medications to usual treatment reduces cardiovascular disease progession more than just usual treatment. So both statins and GLP's are a good idea.

Many people who have, or have had, severe long term obesity that has been improved by GLP medications, are in a very high cardiovascular risk category, with risks as bad as those with known cardiovascular disease. And there are a lot of people on this forum in this position. Obesity even if reversed will most likely have caused damage over time, this cannot usually be fixed but you can stop it from getting worse or from causing illness. Ceasing lipid lowering therapy in this group is just as dangerous as in the group with known cardiovascular disease.

Most people are not going to have any idea what risk group they are in, if you do not know for sure then stopping prescribed statins does not sound like a good idea. Doctors make these assessments all the time and use that to decide if lipid lowering therapy is needed, not just based on lipid numbers, as all the other risk factors like family history, smoking, high blood pressure , diabetes, metabolic syndrome, impaired glucose tolerance, proteinuria, NAFLD/NASH, renal function and age all factor into determining risk. There are online calculators that can give you a pretty good idea.

Self treatment without adequate scientific knowledge is dangerous ( and even with good knowledge ) and in the end people will be harmed by it, there will also be some benefits , but mostly from the GLP medications as they are proven to work. Getting a medical opinion on potentially life risking medical decisions like stopping statin or other lipid lowering therapy, is a good idea. It seems ridiculous to be saying this, but unless you know what your 10 year cardiovascular risk is you should be getting expert advice before making those decisions, otherwise you could be risking your life and health to stop a treatment that for most people has no side effects.

Words to take to heart, thank you.
 
I agree with your sentiment and I can tell you've put some real time into reading up on the topic of cardiovascular health, but one of the challenges inherent in this endeavor is that we don't know what we don't know. Given your stated philosophy I would have expected your attitude to be more along the lines of "are there additional factors or angles I might be missing here?" rather than "let me tell you why I'm certain than I'm right using forceful language." I kind of get it. You've invested a lot of time into reading scholarly articles and papers on the subject and in doing so believe that you now know more than 90% of laypeople when it comes to the topic. Not an unreasonable conclusion to reach.

With that said, here is what you could be missing. I'm going to purposely keep the language as simple as possible so everyone else here can easily follow too.

The current modeling of cardiovascular disease progression is incomplete in one very significant way. It doesn't do a very good job of accounting for why some LDL particles will attach themselves to arterial walls and go on to become plaque, while others will not. It has been observed that higher circulating LDL levels correlate to greater plaque buildup. This led scientists to conclude that it was probably some sort of statistical process. If you imagined LDL particles to be analogous to ping pong balls bouncing around and with each bounce there was a very small chance one might stick, it would stand to reason that if you have less ping pong balls bouncing around in a room, you'd end up with less stuck to the walls after an hour. That's the rationale behind LDL lowering therapies like statins.

If it is in fact a random process and any LDL is just as likely as any other LDL to be captured into an arterial wall then their logic would be sound. If it turns out that there are only certain types of LDL that are more susceptible to being captured then lipid lowering could turn out to be short-sighted, unless it proves to be good at lowering that particular type of LDL. This would be analogous to throwing more people in prison in an attempt to reduce crime. It's only going to work if the additional people you throw in prison were/are criminals. Throwing non-criminals in prison would reduce the number of potential victims walking around free, but other than that wouldn't likely lead to a reduction in crime. And that's why instead of randomly keeping a set percentage of people in prison we specifically target keeping criminals there.

So this leads to the open question: Are all LDL particles created equal and is lowering LDL across the board the best approach? We do know that small dense LDL particles are much more likely to lead to plaque build-up than large fluffy LDL particles, but what is the difference between the two? It could just be that small dense LDL particles are simply LDL particles that have already delivered most of their lipid load to the rest of your body and are just waiting around to be reabsorbed by the liver. To the extent that is true, we'd expect broad lipid-lowering therapy to be effective. It's also possible that small dense LDL represent those where oxidative damage has occurred, changing them to a state where the liver doesn't reabsorb them as easily and their natural exit from the bloodstream is to stick to arterial walls. To the extent that is true, it would be much more productive to try to stop that damage from occurring to the LDL in the first place. Ambiguity sucks when it comes to life or death issues, but let's hold our emotions and reflexive instincts in check here and see what the data says...

When it comes to studying cardiovascular disease, we do have good data on what the biggest risk factors for it are. If all LDL particles are created equal, this is a statistical process, and it's just a matter of getting the LDL down, we'd expect LDL to be near the top of that list. We'd also expect LDL lowering therapies to drastically reduce plaque progression and all cause mortality in high risk individuals. If it turns out that damage to LDL particles and/or arterial walls are the key driver in plaque build up then we'd expect other risk factors to be at the top of the list with LDL being closer to the bottom of the list.

In comparing risk factors the most productive way to do it is to compare what are called hazard ratios, which is represent how much risk increases on average for each risk factor. Hazard ratios close to 1 are low-risk, higher hazard ratios are high risk, and those below 1 would be protective factors. Click on the following link and scroll down to Figure 1:

https://jamanetwork.com/journals/jamacardiology/fullarticle/2775559

You'll be surprised to see that the hazard ratio associated with LDL is actually quite low. It turns out obesity, smoking, diabetes, metabolic syndrome, and hypertension all matter way more than LDL does when it comes to heart disease. This is quite shocking the first time you see it, but the reason we focus so strongly on LDL is because (up until recently) LDL and hypertension were the only two things doctors could prescribe pills for. Now that GLP1 meds are available, doctors can use them to tackle obesity, diabetes, and metabolic syndrome.

So that was a really long path to demonstrate that, no, statins would actually be expected to be LESS effective than GLP1s when it comes to reducing cardiovascular risk. If a rational person had to choose between statins and GLP1s, the latter would be expected to offer better protection (to the extent they suffer from the risk factors I mentioned). Of course, this doesn't have to be an either/or. You can take both statins and GLP1s at the same time. Also, it's worth noting that if you've had previous cardiac events or already have significant plaque accumulation, the analysis is more complicated. But I think this answers the thought problem of if a crazed pharmacist holds a gun to your head and forced you to choose between a GLP1 and a statin that most would be better off opting for the GLP1, contrary to popular perception.

Hopefully you don't take this as an attack on you, since I'm only trying to inform here and I believe that your position is a perfectly reasonable conclusions to have reached if you limit yourself to consuming AHA/cardiologist/myopic literature on the subject. You seemed like a thoughtful person so I thought you might appreciate having the full logical progression laid out.
 
tubby said:
I agree with your sentiment and I can tell you've put some real time into reading up on the topic of cardiovascular health, but one of the challenges inherent in this endeavor is that we don't know what we don't know.

Not to mention the studies that show that lifespan increases from statins can be surprisingly low or non-existent. So still a lot a room for debate and "further research" for Joe Blow being on statins vs. other interventions (not that they are mutually exclusive):

quoted said:
The effect of statins on average survival in randomised trials, an analysis of end point postponement

Death was postponed between −5 and 19 days in primary prevention trials and between −10 and 27 days in secondary prevention trials.

The median increase in lifespan was 3.2 days for primary prevention and 4.1 days for secondary prevention. OTOH, preventing even one person from getting a major event (using statins, BP meds, smoking cessation, and/or lifestyle interventions) can be a big deal:

quoted said:
Distribution of lifespan gain from primary prevention intervention

93% of these identical individuals gain no lifespan, while the remaining 7% gain a mean of 99 months [8.25 years].

As mostly a vegetarian (pescatarian), I am a big fan of plant-based diets and somewhat a fan of the late Dr. John McDougal ("Dr. Potato"). Like the peptide pusher Dr. Seeds, the potato pusher Dr. McDougall had a great personality for Youtube. But even with his strict vegan diet, McDougall may have lived longer if he didn't dismiss statins or big-time exercise, especially since he had genetic factors (having had a massive stroke at age 18). We'll never know. His numbers were good without statins, but his LDL was not aggressively low like under 55 (or even sub-40):

Gemini said:
Dr. John McDougall’s Lipid Profile

Marker His Personal Levels The "McDougall Grade" (Goal) Standard Medical Ref Total Cholesterol 140–150 mg/dL 40 mg/dL (Men) Triglycerides Variable

McDougall lived to age 77, which was 59 years after the stroke that gave him a permanent limp. For his patients, McDougall was unfortunately against GLPs, did not give enough attention to exercise, and his starch-based vegan diet didn't allow for healthy fats (which the American Heart Association didn't like, favoring instead a Mediterranean-style, plant-based diet). He was also against the use of supplements. But I don't see the harm in taking collagen on a mostly vegetarian diet.

Dr. Seeds would say injectable peptides are better than oral supplements, as peptides are corrective (give instructions/signals rather than just building blocks). But high-potency natto seems better for removal of existing plaque (up to 36 percent reduction in 26 weeks, with some blood thinning, for better or worse). Natto also has synergistic effects with vit K2 (MK7). Peptides like SS-31 and hexarelin may be better for prevention for some cardiovascular factors, though not as much as GLPs.
 
I initially told my doctor that I was interested in Zepbound, and she gave me a brochure for it. They have a weight loss management program. She told me to come back for my physical, and she would run blood tests to make sure I am good.

I went to my physical, and she gave me an order for labs and told me about the pills, which are cheaper now. I said thanks. I will get my labs done, then I will continue what I have been doing. I also asked her about peptides for energy. She told me to take B12 and ashwagandha pills.
 
Gt3294a said:
This is all making me feel better about some times ducking blood work for a few months to avoid saying “well, given I’m blasting on some UGL test, the Reta really is keeping that lipid profile in pretty good check, not to mention the liver markers, so the slight variance is actually better than one should expect”. Now my online doctor wouldn’t take such notes and even says stuff like get your bloods right before you pin to even make the lab tests look as good as possible. Crappy issue we got to deal with when in reality, me finding Reta, as well as some other items, has been great for me. I mean my regular doctor is too busy to even flag the obvious supplements and diet changes one can make and rather just throw a statin at people (like he did my mom, and she just changed her diet and fixed it herself).
Ain't that the truth 90% of the time the modern medical community just writes the preordained prescription for a condition. Never looks at what's really there at all or considers who their patient is at all.
 
Calm Logic said:
McDougall lived to age 77, which was 59 years after the stroke that gave him a permanent limp.

He has a stroke when he was 18 yrs old? Yikes.
 
My doctor is the one who steered me to a local compounding pharm. He even called one of the pharmacies during my office visit, found they were backing out due to newer FDA crackdowns and got a suggestion from that pharm for another that was still going to compound. He wrote me monthly scripts until the medical group he's with said they weren't allowing their MDs to prescribe compounded GLP1s. Luckily, when we were in that initial office visit discussing GLP1s, he mentioned he had other patients using grey market products ("stuff from China") with great success. His comment was something like "I don't have a problem with undercutting companies like EL who are making ridiculous profits already."

So I'd obviously have no issue telling him what I'm doing now.
 
Hopefully the entire field is going to be completely exploded in the next 5 to 10 years, with radically new therapies based on new understandings of what is occurring where plaques are forming and rupturing. None of it will invalidate the previous research but will hopefully produce new and more effective treatments. Both from 2025. So there is always more research.

This article was interesting "Imidazole propionate is a driver and therapeutic target in atherosclerosis" https://www.nature.com/articles/s41586-025-09263-w

A chemical produced by common gut bacteria Imidazole propionate directly causes atherosclerosis independently of blood lipids, in rodent studies, and blocking the action of that chemical on imidazole 1 receptors prevents the development of atherosclerosis, independently of lipids. There are several other pieces of research on this chemical showing associations with human disease, but this very clearly demonstrates the mechanism involved. Obviously it will need human testing and drug development, but I would expect to see a lot more about it in the future.

The other piece of research I found was the study of autopsy specimens from humans who died from myocardial infarctions, all of the plaques that had ruptured causing the heart attacks had live bacteria in the plaques and inflammation associated with it. Various studies have found bacteria in odd or unexpected places before but this was interesting because their presence was clearly demonstrated in all of the lesions and those plaques rupturing was the cause of death in all of the patients studied. "In all 24 cases of MI due to complicated coronary plaques with a rupture or thrombosis/hemorrhage (AHA type VI), the plaques were infiltrated by immunopositive viridans streptococci, localizing inside macrophages or freely at the rupture site "

The study did test other things but this was the most interesting part as far as I was concerned.

title and link

Viridans Streptococcal Biofilm Evades Immune Detection and Contributes to Inflammation and Rupture of Atherosclerotic Plaques https://www.ahajournals.org/doi/full/10.1161/JAHA.125.041521

There are almost certainly no simple methods of killing these bacteria, in general antibiotics will not work in mostly metabolically inactive organisms protected by biofilms in inaccessible locations, but it is still interesting.
 
tubby said:
I agree with your sentiment and I can tell you've put some real time into reading up on the topic of cardiovascular health, but one of the challenges inherent in this endeavor is that we don't know what we don't know. Given your stated philosophy I would have expected your attitude to be more along the lines of "are there additional factors or angles I might be missing here?" rather than "let me tell you why I'm certain than I'm right using forceful language." I kind of get it. You've invested a lot of time into reading scholarly articles and papers on the subject and in doing so believe that you now know more than 90% of laypeople when it comes to the topic. Not an unreasonable conclusion to reach.

With that said, here is what you could be missing. I'm going to purposely keep the language as simple as possible so everyone else here can easily follow too.

The current modeling of cardiovascular disease progression is incomplete in one very significant way. It doesn't do a very good job of accounting for why some LDL particles will attach themselves to arterial walls and go on to become plaque, while others will not. It has been observed that higher circulating LDL levels correlate to greater plaque buildup. This led scientists to conclude that it was probably some sort of statistical process. If you imagined LDL particles to be analogous to ping pong balls bouncing around and with each bounce there was a very small chance one might stick, it would stand to reason that if you have less ping pong balls bouncing around in a room, you'd end up with less stuck to the walls after an hour. That's the rationale behind LDL lowering therapies like statins.

If it is in fact a random process and any LDL is just as likely as any other LDL to be captured into an arterial wall then their logic would be sound. If it turns out that there are only certain types of LDL that are more susceptible to being captured then lipid lowering could turn out to be short-sighted, unless it proves to be good at lowering that particular type of LDL. This would be analogous to throwing more people in prison in an attempt to reduce crime. It's only going to work if the additional people you throw in prison were/are criminals. Throwing non-criminals in prison would reduce the number of potential victims walking around free, but other than that wouldn't likely lead to a reduction in crime. And that's why instead of randomly keeping a set percentage of people in prison we specifically target keeping criminals there.

So this leads to the open question: Are all LDL particles created equal and is lowering LDL across the board the best approach? We do know that small dense LDL particles are much more likely to lead to plaque build-up than large fluffy LDL particles, but what is the difference between the two? It could just be that small dense LDL particles are simply LDL particles that have already delivered most of their lipid load to the rest of your body and are just waiting around to be reabsorbed by the liver. To the extent that is true, we'd expect broad lipid-lowering therapy to be effective. It's also possible that small dense LDL represent those where oxidative damage has occurred, changing them to a state where the liver doesn't reabsorb them as easily and their natural exit from the bloodstream is to stick to arterial walls. To the extent that is true, it would be much more productive to try to stop that damage from occurring to the LDL in the first place. Ambiguity sucks when it comes to life or death issues, but let's hold our emotions and reflexive instincts in check here and see what the data says...

When it comes to studying cardiovascular disease, we do have good data on what the biggest risk factors for it are. If all LDL particles are created equal, this is a statistical process, and it's just a matter of getting the LDL down, we'd expect LDL to be near the top of that list. We'd also expect LDL lowering therapies to drastically reduce plaque progression and all cause mortality in high risk individuals. If it turns out that damage to LDL particles and/or arterial walls are the key driver in plaque build up then we'd expect other risk factors to be at the top of the list with LDL being closer to the bottom of the list.

In comparing risk factors the most productive way to do it is to compare what are called hazard ratios, which is represent how much risk increases on average for each risk factor. Hazard ratios close to 1 are low-risk, higher hazard ratios are high risk, and those below 1 would be protective factors. Click on the following link and scroll down to Figure 1:

https://jamanetwork.com/journals/jamacardiology/fullarticle/2775559

You'll be surprised to see that the hazard ratio associated with LDL is actually quite low. It turns out obesity, smoking, diabetes, metabolic syndrome, and hypertension all matter way more than LDL does when it comes to heart disease. This is quite shocking the first time you see it, but the reason we focus so strongly on LDL is because (up until recently) LDL and hypertension were the only two things doctors could prescribe pills for. Now that GLP1 meds are available, doctors can use them to tackle obesity, diabetes, and metabolic syndrome.

So that was a really long path to demonstrate that, no, statins would actually be expected to be LESS effective than GLP1s when it comes to reducing cardiovascular risk. If a rational person had to choose between statins and GLP1s, the latter would be expected to offer better protection (to the extent they suffer from the risk factors I mentioned). Of course, this doesn't have to be an either/or. You can take both statins and GLP1s at the same time. Also, it's worth noting that if you've had previous cardiac events or already have significant plaque accumulation, the analysis is more complicated. But I think this answers the thought problem of if a crazed pharmacist holds a gun to your head and forced you to choose between a GLP1 and a statin that most would be better off opting for the GLP1, contrary to popular perception.

Hopefully you don't take this as an attack on you, since I'm only trying to inform here and I believe that your position is a perfectly reasonable conclusions to have reached if you limit yourself to consuming AHA/cardiologist/myopic literature on the subject. You seemed like a thoughtful person so I thought you might appreciate having the full logical progression laid out.
I do not take any of this personally , I am only trying to say these things as I believe they are important and a rising tide of anti medicalism carries serious risks to peoples health, which is extra ironic and tragic in that it is partly a result of doing something that massively improves long term health outcomes, which is using GLP peptides to treat obesity.

I have not worked as a doctor for 25 years or so, but I have seen enough truly idiotic and offensive behaviour from doctors, that peoples lack of trust is not that surprising. Treatment for these issues like lipids or blood pressure is not even close to a contentious issue, and it is an area of medicine with a very solid scientific grounding, even if some aspects do change a bit over time as research progresses.

You are clearly a better persuasive writer than I am ( according to chatgpt ) , this is not news since I nearly failed to get into medical school based on poor high school english results, but in the end the problem with any non mainstream perspectives on medical issues is that the mainstream views are the ones best supported by the evidence, and especially with respect to cardiology, which from what I have seen is much more dominated by research than the average medical specialty. A lot of cardiovascular treatments are in people who are not especially unwell at the time and are aimed at preventing or reducing long term outcomes, these long term real outcome based studies are critical to deciding what therapies are or are not a good idea.

I copied and pasted my more recent post and your response to it into chatgpt. I have a long and complex pre prompt first to stop it agreeing with me if I am wrong, which given it's tendency to agree with people is critical, and to minimise hallucinations and focus it's answers on research in humans, and to provide evidence where possible for it's statements. I genuinely want to know if I have something wrong.

Going through every statement of fact in your post would take a lot of work, and chatgpt is excellent at looking at a lot of stuff quickly , even if it is not perfectly accurate. Thankfully it did not find much in the way of errors of fact or opinion in my post, but although it thought your rhetorical framing was better it did disagree with many of your statements as being inconsistent with known research . If you really want I can post the whole thing, but it is pretty long. And this is about 1/10th of it and does not include most of the criticisms.

In terms of the issue I was concerned about which was people , who may be at high or extreme cardiovascular risk due to past or current obesity, should not be stopping lipid lowering / statin therapy prescribed for cardiovascular protection, without expert advice.

I managed to exceed the character limit so to be continued...
 
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