Liter O' Test
Member
this female dog , dei degree, should be doing tupperware parties instead of fearmongering facebook tier health theories on youtube to gulliable middle aged people
MESO-Rx
Anabolic Steroids
Pitavastatin
- Thread starter keengkong
- Start date
this female dog , dei degree, should be doing tupperware parties instead of fearmongering facebook tier health theories on youtube to gulliable middle aged people
Ghoul
Member
The man's a certified liar, though a genius at self promotion. Confirm the long standing statin-phobia by telling people what they want to hear, and you'll find a huge built in audience. That the pseudoscientific advice of this media savvy, but otherwise mediocre physician, has certainly led to necessary death in his quest for fame has been noted by nearly every major medical organization in the UK.
In medical science, the absolute highest standard of evidence, rarely achieved, is establishing a "Causal" link. That has been achieved between LDL and #1 cause of death, arteriosclerosis induced heart attacks, strokes, and death.
There's quite literally no other root cause - effect of health harm that's been more thoroughly proven.
Butter nonsense: the rise of the cholesterol deniers
A group of scientists has been challenging everything we know about cholesterol, saying we should eat fat and stop taking statins. This is not just bad science – it will cost lives, say experts
I think this guy is actually saying that opposite of the other two videos.
Ghoul
Member
I'll tell you the same thing I tell other statin conspiracy theorists who believe these meds, along with ezetimibe and bempodoic acids, all cheap generics with an average wholesale price less than 5¢ / pill. (except pitavastatin, but it will get there in a few years) are fueling the "Big Cholesterol Lie".
Don't take them. Tell your entire family and friends not to take them (you'll find a receptive audience, I guarantee).
This will be the best way to either a) Increase the living examples who can attest how it was all a big pharma scam made possible by millions of corrupt cardiologists and scientists in cahoots to deceive people, or b) the problem of those spreading this nonsensical view will resolve itself via darwinism.
Do you not believe there is corruption and the manipulation of studies in general that benefit the pharmaceutical industry?
explodingHeart
Member
How much raw milk drinking and raw meat do I need to consume to achieve self-actualization?
By the way, I've always been rather pro-statin. Yet I'm the one whose liver can't handle atorvastatin. Although I'm temporarily off a statin, seeing how my LDL is going up although my liver enzymes are going down, I realize the odds of me living a long life go up if I'm taking one. I'm inclined to go with pitavastatin, although I'm worried that my cardiologist will push rosuvastatin.The man's a certified liar, though a genius at self promotion. Confirm the long standing statin-phobia by telling people what they want to hear, and you'll find a huge built in audience. That the pseudoscientific advice of this media savvy, but otherwise mediocre physician, has certainly led to necessary death in his quest for fame has been noted by nearly every major medical organization in the UK.
In medical science, the absolute highest standard of evidence, rarely achieved, is establishing a "Causal" link. That has been achieved between LDL and #1 cause of death, arteriosclerosis induced heart attacks, strokes, and death.
There's quite literally no other root cause - effect of health harm that's been more thoroughly proven.
Butter nonsense: the rise of the cholesterol deniers
A group of scientists has been challenging everything we know about cholesterol, saying we should eat fat and stop taking statins. This is not just bad science – it will cost lives, say expertswww.theguardian.com
Yes, and there are plenty of folks dying every day because they are not willing to believe that their doctor is actually trying to look out for their health.
anon55
Member
What's are your opinion on taking 8mg of pitavastatin? It doesn't seem to lower LDL-C much but the HDL-C increase is pretty interesting
Wizbang
Member
How long should i wait to take a new blood draw now that i've added pita to the mix? 30days? 90?
Sure, many of them uninformed just pushing the same old stuff trying to keep insurance happy.
Photon
Member
Looks like 4% regardless of dose from 1-16mg
Pitavastatin for lowering lipids - PubMed
Pitavastatin lowers blood total cholesterol, LDL cholesterol and triglyceride in a dose-dependent linear fashion. Based on the effect on LDL cholesterol, pitavastatin is about 6-fold more potent than atorvastatin, 1.7-fold more potent than rosuvastatin, 77-fold more potent than fluvastatin and...
pubmed.ncbi.nlm.nih.gov
Laxman3221
Member
Food for thought
Doubt cast on wisdom of targeting ‘bad’ cholesterol to curb heart disease risk
Each of the 35 included trials was categorised according to whether it met the LDL cholesterol reduction target outlined in the 2018 American Heart Association/American College of Cardiology guidelines.
The researchers then calculated the number of people who would need to be treated in order to prevent one ‘event’, such as a heart attack/stroke, or death, and the reduction in absolute risk in each study that reported significantly positive results.
Their analysis showed that over three quarters of all the trials reported no positive impact on risk of death and nearly half reported no positive impact on risk of future cardiovascular disease.
LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature
The idea that high cholesterol levels in the blood are the main cause of CVD is impossible because people with low levels become just as atherosclerotic as people with high levels and their risk of suffering from CVD is the same or higher. The cholesterol hypothesis has been kept alive for decades by reviewers who have used misleading statistics, excluded the results from unsuccessful trials and ignored numerous contradictory observations.
Most heart attack patients' cholesterol levels did not indicate cardiac risk
Older article from 2009
A new national study has shown that nearly 75 percent of patients hospitalized for a heart attack had cholesterol levels that would indicate they were not at high risk for a cardiovascular event, based on current national cholesterol guidelines.
Specifically, these patients had low-density lipoprotein (LDL) cholesterol levels that met current guidelines, and close to half had LDL levels classified in guidelines as optimal (less than 100 mg/dL).
"Almost 75 percent of heart attack patients fell within recommended targets for LDL cholesterol, demonstrating that the current guidelines may not be low enough to cut heart attack risk in most who could benefit," said Dr. Gregg C. Fonarow, Eliot Corday Professor of Cardiovascular Medicine and Science at the David Geffen School of Medicine at UCLA and the study's principal investigator.
Doubt cast on wisdom of targeting ‘bad’ cholesterol to curb heart disease risk
Each of the 35 included trials was categorised according to whether it met the LDL cholesterol reduction target outlined in the 2018 American Heart Association/American College of Cardiology guidelines.
The researchers then calculated the number of people who would need to be treated in order to prevent one ‘event’, such as a heart attack/stroke, or death, and the reduction in absolute risk in each study that reported significantly positive results.
Their analysis showed that over three quarters of all the trials reported no positive impact on risk of death and nearly half reported no positive impact on risk of future cardiovascular disease.
LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature
The idea that high cholesterol levels in the blood are the main cause of CVD is impossible because people with low levels become just as atherosclerotic as people with high levels and their risk of suffering from CVD is the same or higher. The cholesterol hypothesis has been kept alive for decades by reviewers who have used misleading statistics, excluded the results from unsuccessful trials and ignored numerous contradictory observations.
Most heart attack patients' cholesterol levels did not indicate cardiac risk
Older article from 2009
A new national study has shown that nearly 75 percent of patients hospitalized for a heart attack had cholesterol levels that would indicate they were not at high risk for a cardiovascular event, based on current national cholesterol guidelines.
Specifically, these patients had low-density lipoprotein (LDL) cholesterol levels that met current guidelines, and close to half had LDL levels classified in guidelines as optimal (less than 100 mg/dL).
"Almost 75 percent of heart attack patients fell within recommended targets for LDL cholesterol, demonstrating that the current guidelines may not be low enough to cut heart attack risk in most who could benefit," said Dr. Gregg C. Fonarow, Eliot Corday Professor of Cardiovascular Medicine and Science at the David Geffen School of Medicine at UCLA and the study's principal investigator.
explodingHeart
Member
Cholesterol and LDL drops after a heart attack.
Lifelong exposure to high LDL / apoB is what matters.
That's like saying high BP doesn't cause strokes because they measured the BP of the bedridden stroke patients a week after and found they had low BP.
Lifelong exposure to high LDL / apoB is what matters.
That's like saying high BP doesn't cause strokes because they measured the BP of the bedridden stroke patients a week after and found they had low BP.
Laxman3221
Member
Statins lower glp1 levels up to 50%
Don’t worry though, they have a super expensive drug to correct that side effect.
Don’t worry though, they have a super expensive drug to correct that side effect.
The manufacturer says the maximum dose if four milligrams.Looks like 4% regardless of dose from 1-16mg
View attachment 354270Pitavastatin for lowering lipids - PubMed
Pitavastatin lowers blood total cholesterol, LDL cholesterol and triglyceride in a dose-dependent linear fashion. Based on the effect on LDL cholesterol, pitavastatin is about 6-fold more potent than atorvastatin, 1.7-fold more potent than rosuvastatin, 77-fold more potent than fluvastatin and...
"The maximum recommended dosage is LIVALO 4 mg once daily."
Looks like 4% regardless of dose from 1-16mg
View attachment 354270Pitavastatin for lowering lipids - PubMed
Pitavastatin lowers blood total cholesterol, LDL cholesterol and triglyceride in a dose-dependent linear fashion. Based on the effect on LDL cholesterol, pitavastatin is about 6-fold more potent than atorvastatin, 1.7-fold more potent than rosuvastatin, 77-fold more potent than fluvastatin and...
Whew, this thread had a good run before the anti-science brigade showed up. No, grifters on Joe Rogan are not a better source of information than mountains of RCTs.
The results do not match other meta-analysis on statins, e.g.
Or the results we see on PCSK9 inhibitors, e.g.
pubmed.ncbi.nlm.nih.gov
Or the fact that people with genetically low LDL just do not die of ASCVD like others do.
And as others have pointed out, LDL at point of admission mean basically nothing. It's not a binary switch - you are at risk of a heart attack when your LDL is high, not at risk when it's low. It's your lifetime accumulation of plaque.
People with ASCVD are more likely to have heart attacks. People with ASCVD are more likely to be on medication for their ASCVD. This medication reduces their LDL, but it is often started too late and treatment targets not aggressive enough even if it had been started earlier to cause regression.
----
We've got people posting that they believe statins are bunk because of some nebulous association between doctors, researchers, insurance companies, and pharma companies over dirt cheap generics that anyone can produce while posting "refutations" by people who have direct financial incentive to sell books they wrote arguing for alternative treatment methods.
Who do you think is making more money off of their claims? Someone with a book to sell? Or someone suggesting you take basically any one generic medication from a whole class that can be made by any licensed drug producer?
A single study shows that a single statin reduced glp1 levels. Definitively stating that this is a universal effect to statins without evidence of that being the case is irresponsible when we know that many statins have different effects on a variety of systems - including those which do not decrease insulin sensitivity, which from the paper, seems to be intrinsically linked to the GLP-1 reduction.
As for needing a super expensive drug, the study itself points out that just supplementing UDCA seems to resolve it.
Why do you think your doctor is trying to keep insurance happy? Every doctor I've had I could describe their relationship with insurance as closer to being adversarial than friendly. Their administrative staff all fucking hate working with insurance. The doctors hate dealing with prior auths being sent back and having to be reworked over and over again. They had bargaining with insurance to keep them in network.
Fulltext is paywalled, my usual source for paywalled studies doesn't have it, and the abstract is pitiful so this is basically impossible to discuss in a meaningful manner. One of the authors has direct financial interest in selling a book that preaches an alternative method to fighting ASCVD.
The results do not match other meta-analysis on statins, e.g.
Or the results we see on PCSK9 inhibitors, e.g.
Association Between Achieved Low-Density Lipoprotein Cholesterol Levels and Long-Term Cardiovascular and Safety Outcomes: An Analysis of FOURIER-OLE - PubMed
gov; Unique identifier: NCT01764633.
pubmed.ncbi.nlm.nih.gov
Or the fact that people with genetically low LDL just do not die of ASCVD like others do.
Ravnskov is well known in this space. He has spent decades making money as a contrarian grifter selling books, getting media spots, etc. As he realized the data around statins improving health outcomes was getting more and more impossible for him to refute, he pivoted to claiming it was some other mechanism responsible for all of their success in lowering ASCVD events (but even he still admits that statins lower ASVD events.) Look into the studies he references to back up his points, and you'll find that most of them can't be called RCTs (which are universally considered to be the gold standard of study for a reason) because they lack control groups altogether. Others he'll argue that since the results aren't always linear they somehow can't be a result of the LDL lowering.
Your third link is pretty explicit in that they believe the issue is the guidelines are too permissive - which is also the stance of the discussion in here. You are almost certainly still causing plaque buildup at levels significantly below 100mg/dl. Studies start to consistently show regression below 50, and some a bit higher at below 70, but 80? You're still gunking up your arteries, just at a slower rate.
And as others have pointed out, LDL at point of admission mean basically nothing. It's not a binary switch - you are at risk of a heart attack when your LDL is high, not at risk when it's low. It's your lifetime accumulation of plaque.
People with ASCVD are more likely to have heart attacks. People with ASCVD are more likely to be on medication for their ASCVD. This medication reduces their LDL, but it is often started too late and treatment targets not aggressive enough even if it had been started earlier to cause regression.
----
We've got people posting that they believe statins are bunk because of some nebulous association between doctors, researchers, insurance companies, and pharma companies over dirt cheap generics that anyone can produce while posting "refutations" by people who have direct financial incentive to sell books they wrote arguing for alternative treatment methods.
Who do you think is making more money off of their claims? Someone with a book to sell? Or someone suggesting you take basically any one generic medication from a whole class that can be made by any licensed drug producer?
A single study shows that a single statin reduced glp1 levels. Definitively stating that this is a universal effect to statins without evidence of that being the case is irresponsible when we know that many statins have different effects on a variety of systems - including those which do not decrease insulin sensitivity, which from the paper, seems to be intrinsically linked to the GLP-1 reduction.
As for needing a super expensive drug, the study itself points out that just supplementing UDCA seems to resolve it.
I'll just stick with keeping my four humors in balance, generously using leeches when necessary.Whew, this thread had a good run before the anti-science brigade showed up. No, grifters on Joe Rogan are not a better source of information than mountains of RCTs.
Why do you think your doctor is trying to keep insurance happy? Every doctor I've had I could describe their relationship with insurance as closer to being adversarial than friendly. Their administrative staff all fucking hate working with insurance. The doctors hate dealing with prior auths being sent back and having to be reworked over and over again. They had bargaining with insurance to keep them in network.
Fulltext is paywalled, my usual source for paywalled studies doesn't have it, and the abstract is pitiful so this is basically impossible to discuss in a meaningful manner. One of the authors has direct financial interest in selling a book that preaches an alternative method to fighting ASCVD.
The results do not match other meta-analysis on statins, e.g.
Or the results we see on PCSK9 inhibitors, e.g.
Association Between Achieved Low-Density Lipoprotein Cholesterol Levels and Long-Term Cardiovascular and Safety Outcomes: An Analysis of FOURIER-OLE - PubMed
gov; Unique identifier: NCT01764633.
Or the fact that people with genetically low LDL just do not die of ASCVD like others do.
Ravnskov is well known in this space. He has spent decades making money as a contrarian grifter selling books, getting media spots, etc. As he realized the data around statins improving health outcomes was getting more and more impossible for him to refute, he pivoted to claiming it was some other mechanism responsible for all of their success in lowering ASCVD events (but even he still admits that statins lower ASVD events.) Look into the studies he references to back up his points, and you'll find that most of them can't be called RCTs (which are universally considered to be the gold standard of study for a reason) because they lack control groups altogether. Others he'll argue that since the results aren't always linear they somehow can't be a result of the LDL lowering.
Your third link is pretty explicit in that they believe the issue is the guidelines are too permissive - which is also the stance of the discussion in here. You are almost certainly still causing plaque buildup at levels significantly below 100mg/dl. Studies start to consistently show regression below 50, and some a bit higher at below 70, but 80? You're still gunking up your arteries, just at a slower rate.
And as others have pointed out, LDL at point of admission mean basically nothing. It's not a binary switch - you are at risk of a heart attack when your LDL is high, not at risk when it's low. It's your lifetime accumulation of plaque.
People with ASCVD are more likely to have heart attacks. People with ASCVD are more likely to be on medication for their ASCVD. This medication reduces their LDL, but it is often started too late and treatment targets not aggressive enough even if it had been started earlier to cause regression.
----
We've got people posting that they believe statins are bunk because of some nebulous association between doctors, researchers, insurance companies, and pharma companies over dirt cheap generics that anyone can produce while posting "refutations" by people who have direct financial incentive to sell books they wrote arguing for alternative treatment methods.
Who do you think is making more money off of their claims? Someone with a book to sell? Or someone suggesting you take basically any one generic medication from a whole class that can be made by any licensed drug producer?
A single study shows that a single statin reduced glp1 levels. Definitively stating that this is a universal effect to statins without evidence of that being the case is irresponsible when we know that many statins have different effects on a variety of systems - including those which do not decrease insulin sensitivity, which from the paper, seems to be intrinsically linked to the GLP-1 reduction.
As for needing a super expensive drug, the study itself points out that just supplementing UDCA seems to resolve it.
Photon
Member
lol my post was about HDL
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