Nowhere in this discussion, as interesting as it is, are genetics brought up. In my family there have been no cardiac events of any kind going back to at least my grandfather and including all my uncles, yet we all have or had high cholesterol. My poor father was talked into statins in his 80s and he would tell you that the discussion of side effects was very dismissive--he had terrible muscle cramps until he stopped taking the statins. And, oh, he died recently at 92. I think I'll take my chances and skip the statins my GP keeps trying to sell me.
Nowhere here is the substantial lowering of coenzymeq10 mentioned. Many call it the most important enzyme in your body. It helps the mitochondria in every cell make energy. So your heart needs it more than any muscle. The first statin maker knew this was bad and put it in their formula and then took it out when none of the competitors did. Many say that with it lowered your heart just suffers a slow steady decline that no one attributes to anything. The author just needs to mention NNT too - number needed to treat - with all the horrible side effects the NNT needs to be WAY WAY lower that it is in the studies. Any my last VERY telling question is - uh duh, I guess you could say that Big Pharma likes to use media to push their drugs? At least one out of every three ads now. Where are the screaming headlines and posts everywhere about all the HEART EVENTS BEING AVOIDED? WHERE? They lie in their studies and I am amazed they havent lied in their headlines and stories.
Sirs. I finally agreed to take a Statin a few years ago for high cholesterol I'd had all my life. I was 70, and in reasonably good shape - 6'1", 190 with a low BMI, no high blood pressure. The Statin first attacked my teeth then gave me Gout. I stopped it; Gout went away. Started it again - Gout came back. I will not take it again. This may be a rare side effect but it was very real and my heart doctor was a witness. There are side-effects to any medicine unfortunately.
Reduces cholesterol, doesn't reduce deaths by cardiac arrest: Cholesterol is the wrong marker. Magnesium is much more effective but doesn't do much for the pharma shareholders..
On August 23rd, 2022, I was taken to the emergency room of my local hospital. I believed myself about to have a heart attack. Fatigue, lack of any body strength, body aches, mental confusion, depression, and a myriad of other symptoms had been torturing me for months, and were steadily getting worse. Frankly, I thought I was aproaching my death. I needed a wheelchair by the time I got to the hospital.
Three days, a cardiac catheterization, and $42,000.00 later, the hospital sent me home with absolutely no idea what was wrong with me. I took a guess and stopped taking my cardiologist-prescribed rosuvastin. After a couple of weeks, I had no ill symptoms and felt normal.
Interesting that lovastatin was listed on my allergy list and my cardiologist knew it.
Men are the most likely candidates to benefit from statins. Before you go negating potentially live extending treatments for men, address what you intend to do to improve men’s excess mortality compared to women.
This is thoughtful and well written article on statins. I am a recently retired MD who has had a crappy lipid profile for 45 yrs and I started myself on low dose 5mg simvistatin in the ‘70s. So far, so good with no MI, CVA or angina. I wonder if there are enough of us to comprise a statistical analysis?
- On a separate note, one of my professors at Albany Med Ctr was Dr. Dan “Hollander,” Gastroenterologist, who I believe ended up at UCLA?
I appreciate any doctor who takes the time to ponder the pharmacological status quo which has created multi billion dollar profits and still skews statistics in their favor.
Circulating cholesterol appears to be an entirely different beast than a vascular plague. The heart is an important muscle that doesn't seem to have any opportunity for rest. Until or unless a plaque blocks a vessel or breaks away from the vessel our bodies seem to tolerate such plaques. At what point do we continue to accept that circulating cholesterol levels are proportional to the risk of death as a result of a blockage, heart disease or stroke? To me that seems more like sticky statistical analysis.
As a dental hygienist I daily saw thin, fit, well nurished, low cholesterol patients whose chests had been ripped open via cardiac intervention. I saw others that fit the profile of the overweight, unfit, high cholesterol heart attack in-waiting patients who had no openly expressed issues with their cardiovascular system. The difference? Their mouths.
The fit, low cholesterol patient's mouths were high in tooth decay rates, poor oral hygiene, and generally suffering from moderate to severe periodontal disease. That included heavy plaque, tartar aka calculus, and breath that could knock you down if you weren't wearing a mask.
Our bodies are riddled with bacteria, some good, some not so good.
The mouth is a window to the body in more ways than one. The bacteria in our mouths, particularly anaerobic bacteria enters our blood stream by way of their close proximity to the cardiovascular system, capillary beds in the gingiva. They travel to every organ in our bodies through our cardiovascular system. We absorb them when we breath, eat, swallow and yes when we brush and floss.
Think about the use of prophylactic antibiotics for transplant patients, or joint replacements. Prior to the discovery of antibiotics oral infection was in the top 5 causes of death. Ancient humans knew that an oral infection could kill them. They became adept at tooth extraction, even if it meant a rock to the jaw.
I look forward to the day when genetics, and so called lifestyle diseases will tell us more about our ultimate existence.
Statistics can only go so far. Math is valuable in medicine, but it cannot prolong our lives nor can it predict our ultimate demise or the exact reasons of our death because of our genetic history or our lifestyle.
I do value studies regarding the human condition, but not to the degree that it simply pads the pockets of the pharmaceutical industry.
This makes the issue of biochemistry more important than ever. I look forward to the day when there is no risk versus benefit ratio, only benefits.
Inflammation is a fact of life. Death is a fact of life. Living a disease free life to its fullest doesn't have to be a pipe dream. I'm not sure that the whole of humanity, statins or pretty blue pills are equipped to make that reality possible. Let's take a better look at our microbiomes, the toxic environment in which we must survive and our ultimate fate.
I’m actually impressed that this study suggested a greater risk reduction (nearly 40%) for MI than I have been quoting patients (generally 30-35%). If anything, this paper makes the statin argument stronger.
I will have to take a closer look at the study, as the low ARR of only 0.7%, suggests to me that the duration of 2-6 years was simply too short to show much benefit. I’m generally quoting a patient with a 15% risk of cardiovascular events a 30-35% risk reduction which should translate to an ARR of around 5% over 10 years. Obviously unlike relative risk reduction, ARR is heavily influenced by study duration and so it’s a mistake to quote a 0.7 % ARR if your patients actually plan to take the medication for over 10 years. Perhaps this is what Peter Attia is getting at.
I would also suggest an element of caution with that BMJ open paper. It’s written by the statin skeptics. It was actually their shoddy and often erroneous criticisms of statin studies that convinced me to read into the data more deeply and develop a greater appreciation for the value of this medication class. I can’t say that all of their work is flawed, but I have found frequent errors in their review papers, including dubious actions like counting all adverse events that occur in a study of 2 statin dosages (with no placebo comparator group) as “side effects” of the medication, including death due to MI. Sometimes I wonder if they even read the studies that they cite in their reviews.
This doesn’t change the need to use data to inform patient decisions, and of course if patients balk at a small ARR, they are quite right to decline statin treatment. I wouldn’t take one of these meds for a decade, if it only dropped my absolute risk by 1 or 2%, either.
Have you considered the possibility that statins lower cardiovascular events for reasons that have nothing to do with their cholesterol lowering impact? I believe there are studies that show statins lower the risk of CVD events in patients whose cholesterol did not decline after statin therapy as well as in patients whose cholesterol did decline following statin therapy. Statins may work because they exert a general anti-inflammatory effect and not because they lower cholesterol. Thoughts?
We are starting to see similar types of studies with Diabetes meds like the SGLT inhibitors and GLP-RAs and a decrease in RRR for MI, Stroke and CV Death. Also, seeing the effect in diabetics that are controlled and also for heart failure without diabetes.
I agree the old guidelines (ie push average risk people to ldl <130) were too aggressive for most folks. I don't see how the current guidelines to calculate a 10 year CV risk dont address your concerns.
I know this isn’t the point of the article, but I got my Dr to let me go to a half dose )of my very low dose statin anyway). My numbers are still in range. Doc. Is cool with it.
Nowhere in this discussion, as interesting as it is, are genetics brought up. In my family there have been no cardiac events of any kind going back to at least my grandfather and including all my uncles, yet we all have or had high cholesterol. My poor father was talked into statins in his 80s and he would tell you that the discussion of side effects was very dismissive--he had terrible muscle cramps until he stopped taking the statins. And, oh, he died recently at 92. I think I'll take my chances and skip the statins my GP keeps trying to sell me.
Nowhere here is the substantial lowering of coenzymeq10 mentioned. Many call it the most important enzyme in your body. It helps the mitochondria in every cell make energy. So your heart needs it more than any muscle. The first statin maker knew this was bad and put it in their formula and then took it out when none of the competitors did. Many say that with it lowered your heart just suffers a slow steady decline that no one attributes to anything. The author just needs to mention NNT too - number needed to treat - with all the horrible side effects the NNT needs to be WAY WAY lower that it is in the studies. Any my last VERY telling question is - uh duh, I guess you could say that Big Pharma likes to use media to push their drugs? At least one out of every three ads now. Where are the screaming headlines and posts everywhere about all the HEART EVENTS BEING AVOIDED? WHERE? They lie in their studies and I am amazed they havent lied in their headlines and stories.
Sirs. I finally agreed to take a Statin a few years ago for high cholesterol I'd had all my life. I was 70, and in reasonably good shape - 6'1", 190 with a low BMI, no high blood pressure. The Statin first attacked my teeth then gave me Gout. I stopped it; Gout went away. Started it again - Gout came back. I will not take it again. This may be a rare side effect but it was very real and my heart doctor was a witness. There are side-effects to any medicine unfortunately.
Should definitely stop pushing Stalinism.
Reduces cholesterol, doesn't reduce deaths by cardiac arrest: Cholesterol is the wrong marker. Magnesium is much more effective but doesn't do much for the pharma shareholders..
On August 23rd, 2022, I was taken to the emergency room of my local hospital. I believed myself about to have a heart attack. Fatigue, lack of any body strength, body aches, mental confusion, depression, and a myriad of other symptoms had been torturing me for months, and were steadily getting worse. Frankly, I thought I was aproaching my death. I needed a wheelchair by the time I got to the hospital.
Three days, a cardiac catheterization, and $42,000.00 later, the hospital sent me home with absolutely no idea what was wrong with me. I took a guess and stopped taking my cardiologist-prescribed rosuvastin. After a couple of weeks, I had no ill symptoms and felt normal.
Interesting that lovastatin was listed on my allergy list and my cardiologist knew it.
Men are the most likely candidates to benefit from statins. Before you go negating potentially live extending treatments for men, address what you intend to do to improve men’s excess mortality compared to women.
This is thoughtful and well written article on statins. I am a recently retired MD who has had a crappy lipid profile for 45 yrs and I started myself on low dose 5mg simvistatin in the ‘70s. So far, so good with no MI, CVA or angina. I wonder if there are enough of us to comprise a statistical analysis?
- On a separate note, one of my professors at Albany Med Ctr was Dr. Dan “Hollander,” Gastroenterologist, who I believe ended up at UCLA?
I appreciate any doctor who takes the time to ponder the pharmacological status quo which has created multi billion dollar profits and still skews statistics in their favor.
Circulating cholesterol appears to be an entirely different beast than a vascular plague. The heart is an important muscle that doesn't seem to have any opportunity for rest. Until or unless a plaque blocks a vessel or breaks away from the vessel our bodies seem to tolerate such plaques. At what point do we continue to accept that circulating cholesterol levels are proportional to the risk of death as a result of a blockage, heart disease or stroke? To me that seems more like sticky statistical analysis.
As a dental hygienist I daily saw thin, fit, well nurished, low cholesterol patients whose chests had been ripped open via cardiac intervention. I saw others that fit the profile of the overweight, unfit, high cholesterol heart attack in-waiting patients who had no openly expressed issues with their cardiovascular system. The difference? Their mouths.
The fit, low cholesterol patient's mouths were high in tooth decay rates, poor oral hygiene, and generally suffering from moderate to severe periodontal disease. That included heavy plaque, tartar aka calculus, and breath that could knock you down if you weren't wearing a mask.
Our bodies are riddled with bacteria, some good, some not so good.
The mouth is a window to the body in more ways than one. The bacteria in our mouths, particularly anaerobic bacteria enters our blood stream by way of their close proximity to the cardiovascular system, capillary beds in the gingiva. They travel to every organ in our bodies through our cardiovascular system. We absorb them when we breath, eat, swallow and yes when we brush and floss.
Think about the use of prophylactic antibiotics for transplant patients, or joint replacements. Prior to the discovery of antibiotics oral infection was in the top 5 causes of death. Ancient humans knew that an oral infection could kill them. They became adept at tooth extraction, even if it meant a rock to the jaw.
I look forward to the day when genetics, and so called lifestyle diseases will tell us more about our ultimate existence.
Statistics can only go so far. Math is valuable in medicine, but it cannot prolong our lives nor can it predict our ultimate demise or the exact reasons of our death because of our genetic history or our lifestyle.
I do value studies regarding the human condition, but not to the degree that it simply pads the pockets of the pharmaceutical industry.
This makes the issue of biochemistry more important than ever. I look forward to the day when there is no risk versus benefit ratio, only benefits.
Inflammation is a fact of life. Death is a fact of life. Living a disease free life to its fullest doesn't have to be a pipe dream. I'm not sure that the whole of humanity, statins or pretty blue pills are equipped to make that reality possible. Let's take a better look at our microbiomes, the toxic environment in which we must survive and our ultimate fate.
What about lowering the dosage to an absolute minimum, rather than standardized dosages?
Thanks for the write up Buzz.
I’m actually impressed that this study suggested a greater risk reduction (nearly 40%) for MI than I have been quoting patients (generally 30-35%). If anything, this paper makes the statin argument stronger.
I will have to take a closer look at the study, as the low ARR of only 0.7%, suggests to me that the duration of 2-6 years was simply too short to show much benefit. I’m generally quoting a patient with a 15% risk of cardiovascular events a 30-35% risk reduction which should translate to an ARR of around 5% over 10 years. Obviously unlike relative risk reduction, ARR is heavily influenced by study duration and so it’s a mistake to quote a 0.7 % ARR if your patients actually plan to take the medication for over 10 years. Perhaps this is what Peter Attia is getting at.
I would also suggest an element of caution with that BMJ open paper. It’s written by the statin skeptics. It was actually their shoddy and often erroneous criticisms of statin studies that convinced me to read into the data more deeply and develop a greater appreciation for the value of this medication class. I can’t say that all of their work is flawed, but I have found frequent errors in their review papers, including dubious actions like counting all adverse events that occur in a study of 2 statin dosages (with no placebo comparator group) as “side effects” of the medication, including death due to MI. Sometimes I wonder if they even read the studies that they cite in their reviews.
This doesn’t change the need to use data to inform patient decisions, and of course if patients balk at a small ARR, they are quite right to decline statin treatment. I wouldn’t take one of these meds for a decade, if it only dropped my absolute risk by 1 or 2%, either.
I challenge all, including Buzz Hollander MD, who have interests concerning statins, cholesterol, and heart disease to read Dr. Kendrick Malcom's book, The Clot Thickens. https://www.amazon.com/Clot-Thickens-enduring-mystery-disease/dp/1907797769
Have you considered the possibility that statins lower cardiovascular events for reasons that have nothing to do with their cholesterol lowering impact? I believe there are studies that show statins lower the risk of CVD events in patients whose cholesterol did not decline after statin therapy as well as in patients whose cholesterol did decline following statin therapy. Statins may work because they exert a general anti-inflammatory effect and not because they lower cholesterol. Thoughts?
We are starting to see similar types of studies with Diabetes meds like the SGLT inhibitors and GLP-RAs and a decrease in RRR for MI, Stroke and CV Death. Also, seeing the effect in diabetics that are controlled and also for heart failure without diabetes.
I agree the old guidelines (ie push average risk people to ldl <130) were too aggressive for most folks. I don't see how the current guidelines to calculate a 10 year CV risk dont address your concerns.
I know this isn’t the point of the article, but I got my Dr to let me go to a half dose )of my very low dose statin anyway). My numbers are still in range. Doc. Is cool with it.