The Dark Side of Statins (2017), Duane Graveline, MD, MPH
(Also included is The Wonder of Cholesterol by Glyn Wainwright)
The author, Dr Duane Graveline was a former US Air Force and US Army Flight Surgeon, NASA Astronaut, and Family Doctor. In this book he relates his own statin story and his research into the side effects of statins over a 15 year period. His own statin-related issues began in 1999 and he died (the given causes: cardiorespiratory arrest, acute myocardial infarction, cardiac dysrhythmia, and peripheral neuropathy) in 2016 at the age of 85 as a result of his history of statin use.
The book provides a powerful mix of descriptive explanations, case reports, and scientific research references to inform readers – from lay people to expert. Whilst for the avid researcher of this topic, there is nothing spectacularly new, the information is all in one place, and there is more knowledge given on the effects on peripheral neuropathy – and much of that damage is below the threshold of clinical awareness – i.e. silently damaging the unsuspecting.
The book is suitable for those who have experienced adverse reactions to statin drugs and those who are family, friends, or caregivers of statin users, as well as for those facing the use of statins. As well as the technical aspects, there is discussion and guidance on dietary changes and supplements which may help in mitigating the more extreme damage done by statins to mitrochondria, CoQ10, dolichols, and the protective role of antioxidents.
However, whilst the book deals with problems, as far as diet is concerned, the author was a big fan of the Paleo diet, and states how ingrained in our physiology is the thoroughly tested construct pattern from our ancestors – that of a hunter-gather lifestyle.
{My experience as a reviewer: I had a heart attack 18 months ago, was immediately operated upon and received 3 stents. After initially taking statin drugs I weaned off them. Nine months ago, I had 3 more operations that placed 2 more stents around my heart. As a precaution against further problems (I had elevated levels of C-Reactive Protein), I was advised to resume statin use, although at a lower dose than that prescribed (see later bullet point) by the hospital cardiologist.}
Each chapter in the book includes a summary that covers the main points in easy to understand bullet points. These are given below (with my own paraphrasing, omissions and additions (as to what seemed important) to those given in the book text – you will have to read the book yourself to get to the details behind these main points).
The Wonder of Cholesterol is that our cells need cholesterol to function properly.
High cholesterol is more often associated with good health and longevity.
The rising obesity rates observed by the 1980s coincided with the widespread adoption of high-sugar, and low-fat formulations in processed foods.
Fat does not cause obesity or disease. It is excess sugars which create abdominal obesity.
Cholesterol levels are not measured, merely estimated from the quantity of very useful ‘lipid droplets’ circulating in our blood.
LDL cholesterol does many jobs, like transporting vital fat soluble vitamins, lipids, and proteins. Sugar-damaged LDL is not recognised by the organs that need these essential nutrients.
It doesn’t matter how high your total blood serum cholesterol is. What really counts is the damaged conditions of the LDL lipids.
As we age excessive amounts of free sugars in the blood may eventually cause damage quicker than the body can repair it. {in my case, as one example, degeneration is evident in the production of new skin cells which are ‘plastic’ (full of cellulite), instead of the ‘bright new unblemished skin of youth, to replace dead skin cells.}
HbA1c is a widely available blood test to check for sugar damage.
Cholesterol-lowering drugs can cause diabetes {when I was in a rehabilitation clinic for patients who had undergone heart surgery and/or angioplasty, I was struck by how many were also diabetics, and, of their relative youth}
Cholesterol is vital for brain and nervous system functions.
Behavioural changes, personality changes and dementias have all been associated with low levels of cholesterol.
Cholesterol lowering drugs known to cause adverse effects in anywhere from 10% to 30% of patients.
Cholesterol does not cause heart disease.
What has been taught since 1955 about the cause of atherosclerosis has been dead wrong.
New guidelines for LDL cholesterol are artificially low (individuals at high cardiovascular disease risk to attain <100mg/dL, and individuals at very high risk to attain <70mg/dL) and grossly unnatural for the human body.
There is no credible science that offers proof that lowering cholesterol levels to physiologically normal levels reduces cardiovascular risk.
Clinical trials challenge cholesterol causation, cholesterol lowering does not appear to have a significant role in cardiovascular disease control.
LDL cholesterol lowering is not the key in atherosclerosis treatment or prevention.
Cholesterol is nothing but an innocent bystander drawn into the plaques as part of a natural healing process.
We have learned in the past decade that statins are also powerful anti-inflammatory agents. Many now believe that it is the anti-inflammatory effect of statins that is beneficial in atherosclerosis control.
Forward thinking doctors are cutting statin doses in an effort to get the described anti-inflammatory effects without seriously interfering with mavolonate pathway function, the cause of many adverse reactions.
The JUPITER findings demonstrated for the first time cardiovascular benefit from statin therapy on the basis of an elevated hs-CRP (high sensitivity CRP – a measure of inflammation level) level, independent of cholesterol.
Lower LDL and higher HDL have been of no benefit to the patients in clinical trials.
Mechanism of statin drug benefit.
The idea of statin use for high risk people, but at non-cholesterol lowering doses (low level). Even at a relatively low dose of a statin, inflammation is suppressed substantially (a study, and repeated several times, confirmed that 10mg versus 80mg Lipitor on hs-CRP levels reported that the lower dose (10mg) gave 70% of the value of the higher dose). {the hospital cardiologist has me on a high dose combined, or enhanced, statin of the second highest potency – however, I’m taking a single statin at a reduced dosage, and of a lower potency on medical advice}
Any cardiovascular risk benefits from statins has no relationship to cholesterol reduction.
In addition to blockading cholesterol production, dolichols, CoQ10, selenoproteins and rho are equally diminished by the effects of statins.
Like aspirin, statins reduce the production of the blood clotting agent thromboxane, also, aspirin has shown benefits in both primary and secondary prevention of heart attacks and strokes.
Ora Shovman in 2012 published report concluded that inflammation was the cause of atherosclerosis. (He first introduced the concept in 2002.)
Studies are needed to see whether statin sensitive people can tolerate low dose statins without the often debilitating side effects from higher doses (as low as 2-3mg of the stronger statins).
To be continued …
(Also included is The Wonder of Cholesterol by Glyn Wainwright)
The author, Dr Duane Graveline was a former US Air Force and US Army Flight Surgeon, NASA Astronaut, and Family Doctor. In this book he relates his own statin story and his research into the side effects of statins over a 15 year period. His own statin-related issues began in 1999 and he died (the given causes: cardiorespiratory arrest, acute myocardial infarction, cardiac dysrhythmia, and peripheral neuropathy) in 2016 at the age of 85 as a result of his history of statin use.
The book provides a powerful mix of descriptive explanations, case reports, and scientific research references to inform readers – from lay people to expert. Whilst for the avid researcher of this topic, there is nothing spectacularly new, the information is all in one place, and there is more knowledge given on the effects on peripheral neuropathy – and much of that damage is below the threshold of clinical awareness – i.e. silently damaging the unsuspecting.
The book is suitable for those who have experienced adverse reactions to statin drugs and those who are family, friends, or caregivers of statin users, as well as for those facing the use of statins. As well as the technical aspects, there is discussion and guidance on dietary changes and supplements which may help in mitigating the more extreme damage done by statins to mitrochondria, CoQ10, dolichols, and the protective role of antioxidents.
However, whilst the book deals with problems, as far as diet is concerned, the author was a big fan of the Paleo diet, and states how ingrained in our physiology is the thoroughly tested construct pattern from our ancestors – that of a hunter-gather lifestyle.
{My experience as a reviewer: I had a heart attack 18 months ago, was immediately operated upon and received 3 stents. After initially taking statin drugs I weaned off them. Nine months ago, I had 3 more operations that placed 2 more stents around my heart. As a precaution against further problems (I had elevated levels of C-Reactive Protein), I was advised to resume statin use, although at a lower dose than that prescribed (see later bullet point) by the hospital cardiologist.}
Each chapter in the book includes a summary that covers the main points in easy to understand bullet points. These are given below (with my own paraphrasing, omissions and additions (as to what seemed important) to those given in the book text – you will have to read the book yourself to get to the details behind these main points).
The Wonder of Cholesterol is that our cells need cholesterol to function properly.
High cholesterol is more often associated with good health and longevity.
The rising obesity rates observed by the 1980s coincided with the widespread adoption of high-sugar, and low-fat formulations in processed foods.
Fat does not cause obesity or disease. It is excess sugars which create abdominal obesity.
Cholesterol levels are not measured, merely estimated from the quantity of very useful ‘lipid droplets’ circulating in our blood.
LDL cholesterol does many jobs, like transporting vital fat soluble vitamins, lipids, and proteins. Sugar-damaged LDL is not recognised by the organs that need these essential nutrients.
It doesn’t matter how high your total blood serum cholesterol is. What really counts is the damaged conditions of the LDL lipids.
As we age excessive amounts of free sugars in the blood may eventually cause damage quicker than the body can repair it. {in my case, as one example, degeneration is evident in the production of new skin cells which are ‘plastic’ (full of cellulite), instead of the ‘bright new unblemished skin of youth, to replace dead skin cells.}
HbA1c is a widely available blood test to check for sugar damage.
Cholesterol-lowering drugs can cause diabetes {when I was in a rehabilitation clinic for patients who had undergone heart surgery and/or angioplasty, I was struck by how many were also diabetics, and, of their relative youth}
Cholesterol is vital for brain and nervous system functions.
Behavioural changes, personality changes and dementias have all been associated with low levels of cholesterol.
Cholesterol lowering drugs known to cause adverse effects in anywhere from 10% to 30% of patients.
Cholesterol does not cause heart disease.
What has been taught since 1955 about the cause of atherosclerosis has been dead wrong.
New guidelines for LDL cholesterol are artificially low (individuals at high cardiovascular disease risk to attain <100mg/dL, and individuals at very high risk to attain <70mg/dL) and grossly unnatural for the human body.
There is no credible science that offers proof that lowering cholesterol levels to physiologically normal levels reduces cardiovascular risk.
Clinical trials challenge cholesterol causation, cholesterol lowering does not appear to have a significant role in cardiovascular disease control.
LDL cholesterol lowering is not the key in atherosclerosis treatment or prevention.
Cholesterol is nothing but an innocent bystander drawn into the plaques as part of a natural healing process.
We have learned in the past decade that statins are also powerful anti-inflammatory agents. Many now believe that it is the anti-inflammatory effect of statins that is beneficial in atherosclerosis control.
Forward thinking doctors are cutting statin doses in an effort to get the described anti-inflammatory effects without seriously interfering with mavolonate pathway function, the cause of many adverse reactions.
The JUPITER findings demonstrated for the first time cardiovascular benefit from statin therapy on the basis of an elevated hs-CRP (high sensitivity CRP – a measure of inflammation level) level, independent of cholesterol.
Lower LDL and higher HDL have been of no benefit to the patients in clinical trials.
Mechanism of statin drug benefit.
The idea of statin use for high risk people, but at non-cholesterol lowering doses (low level). Even at a relatively low dose of a statin, inflammation is suppressed substantially (a study, and repeated several times, confirmed that 10mg versus 80mg Lipitor on hs-CRP levels reported that the lower dose (10mg) gave 70% of the value of the higher dose). {the hospital cardiologist has me on a high dose combined, or enhanced, statin of the second highest potency – however, I’m taking a single statin at a reduced dosage, and of a lower potency on medical advice}
Any cardiovascular risk benefits from statins has no relationship to cholesterol reduction.
In addition to blockading cholesterol production, dolichols, CoQ10, selenoproteins and rho are equally diminished by the effects of statins.
Like aspirin, statins reduce the production of the blood clotting agent thromboxane, also, aspirin has shown benefits in both primary and secondary prevention of heart attacks and strokes.
Ora Shovman in 2012 published report concluded that inflammation was the cause of atherosclerosis. (He first introduced the concept in 2002.)
Studies are needed to see whether statin sensitive people can tolerate low dose statins without the often debilitating side effects from higher doses (as low as 2-3mg of the stronger statins).
To be continued …
