by Jeffrey Dach MD
If you are concerned about your cholesterol, you need to watch this two part video on Australian TV by Maryanne Demasi (upper left image).. Each segment is 30 minutes.
Click Here for Part One Video…and Click Here for Part Two of the Video
Our routine lab sheet includes a cholesterol panel which we review with every patient.
Here are a few questions I hear every day:
“I am worried about my cholesterol. What is it ? Is my cholesterol too high?” ,
“My cholesterol is higher than the lab range? Should I be worried?”
“My other doctor says my cholesterol is too high and I need a statin drug. What should I do?.
“How can I lower my cholesterol ?”
Above left image courtesy of Maryanne Demasi.Australian Journalist and Celebrity who produced a new video on Cholesterol..
The Cholesterol Myth
We live in a society which has an obsession with cholesterol levels. The reality is that our cholesterol level correlates very poorly (if at all) with risk for heart disease.
Some people have a low serum cholesterol, yet are not protected from heart disease. In spite of the low cholesterol, they have repeated heart attacks. Others have high cholesterol, yet seem to be protected, with no heart disease. Finally there are the genetic familial hypercholesterolmeia patients. Some of these people live into their 60’s in perfect health, without the slightest hint of heart disease, yet have very high cholesterol above 300 their entire lives..
Proof The Cholesterol Theory is a Myth
What is Familial Hypercholesterolemia ?
These are the people who have very high cholesterol levels, in the 300-350 range their entire lives, from a genetic mutation in the LDL receptor.
The Simon Broome Familial Hypercholesterolemia Registry
The Simon Broome Familial Hypercholesterolemia Registry reports their experience treating Familial Hypercholesterolemia with statin drugs to lower cholesterol. Yet, hidden in the report is a nugget of information about a sub-group over the age of 60 with high cholesterol (over 300-350) their entire lives. They go on to say that their data shows these people are a “highly selected group with no increased risk of coronary artery disease“ !!! (3,4) This is astounding ! They report life long high cholesterol of 350, yet no heart disease in this group.!! The existence of this group proves that the Cholesterol Theory is a Myth, and cholesterol is NOT the culprit which causes heart disease.
Watch the Video by Maryanne Demasi
Maryanne Demasi, an Australian journalist and TV Producer, has compiled a two part video with interviews of cardiologists, lipidologists and other experts on the question of cholesterol and heart disease. Part one discusses the Cholesterol Theory .and Part Two the Statin anti-cholesterol drugs. She interviews Rita Redberg MD, Beatrice Golomb MD, Jon Abramson MD and Stephen SInatra MD in part two.
Part One of Heart of the Matter, Dietary Villains.
Part Two of Heart of the Matter , Cholesterol Drug War.
Thanks to Uffe Ravnskov MD PhD of Thincs for bringing this to my attention.
Articles with Related Interest
Atherosclerotic Plaque As Infected Bio-Film
Choirboy Turns Disbeliever on Cholesterol Drugs
Healthy Men Should Not Take Statin Drugs
Heart Disease Vitamin C and Linus Pauling
Getting Off Statin Drug Stories
How to Reverse Heart Disease with the Coronary Calcium Score (part one)
Reversing Heart Disease Part Three
Cholesterol Lowering Drugs for the Elderly, Bad Idea
Cholesterol Lowering Statin Drugs for Women Just Say No
Jeffrey Dach MD
7450 Griffin Road, Suite 190
Davie, Fl 33314
Heart of the Matter. Does high cholesterol really increase your risk of heart attacks? Thursday 24 October 8pm on ABC 1
Is the role of cholesterol in heart disease really one of the biggest myths in the history of medicine? For the last four decades we’ve been told that saturated fat clogs our arteries and high cholesterol causes heart disease. It has spawned a multi-billion dollar drug and food industry of “cholesterol free” products promising to lower our cholesterol and decrease our risk of heart disease. But what if it all isn’t true? What if it’s never been proven that saturated fat causes heart disease? In a special two part edition of Catalyst, Dr Maryanne Demasi investigates the science behind the claims that saturated fat causes heart disease by raising cholesterol.
Simon Broome Familial Hyperlipidaemia Register Group 2008
Reductions in all-cause, cancer, and coronary mortality in statin-treated patients with heterozygous familial hypercholesterolaemia: a prospective registry study.
Neil A, Cooper J, Betteridge J, Capps N, McDowell I, Durrington P, Seed M, Humphries SE.Source NIHR School of Primary Care Research, Division Public Health and Primary Health Care, University of Oxford, Old Road Headington, Oxford, UK.
Methods and results A total of 3382 patients (1650 men) aged <80 years were recruited from 21 lipid clinics in the United Kingdom and followed prospectively between 1980 and 2006 for 46 580 person-years. There were 370 deaths, including 190 from coronary heart disease (CHD) and 90 from cancer. The standardized mortality ratio (compared with the population in England and Wales) was calculated before and from 1 January 1992. In patients aged 20–79 years, CHD mortality fell significantly by 37% (95% CI = 7–56) from 3.4- to 2.1-fold excess. Primary prevention resulted in a 48% reduction in CHD mortality from 2.0-fold excess to none, with a smaller reduction of nearly 25% in patients with established disease. Coronary mortality was reduced more in women than in men. In patients without known CHD at registration, all-cause mortality from 1992 was 33% (21–43), lower than in the general population, mainly due to a 37% (21–50) lower risk of fatal cancer.Introduction
Familial hypercholesterolaemia (FH) is an autosomal co-dominant disorder.1 Defects in at least three different genes that code for proteins involved in hepatic clearance of low-density lipoprotein-cholesterol (LDL-C) can cause FH. These include, most commonly, mutations in the gene coding for the LDL-receptor that removes LDL,2 much less commonly in the gene for Apolipoprotein B which is the major protein of the LDL particle, and rarely in the gene coding for an enzyme called PCSK9 involved in degrading the LDL receptor.3 In all cases, this results in an accumulation of LDL in the plasma from birth, and to subsequent development of tendon xanthomas, xanthelasmas, and atheroma.1
In the heterozygous condition, the cumulative risk of a coronary event by the age of 60 years without effective treatment is at least 50% in men and ∼30% in women. Coronary disease occurs ∼10 years earlier in men than in women, with a marked increase in women post-menopausally.4–6
The aim of this paper was to extend our previous reports7,10–13 by studying an enlarged cohort of 3382 heterozygous patients followed for up to 26 years until the end of 2006, by when the exposure had more than doubled to 46 580 person-years. This has allowed us to examine more informatively the changes in mortality compared with the general population both before and after the routine use of statins.Principal findings : This large long-term prospective registry study of 3382 patients with heterozygous familial hypercholesterolaemia demonstrates a statistically significant reduction in coronary mortality of about one-third since the widespread use of statins.
Coronary mortality: We found that, before and after statins became widely available, there was no excess coronary mortality in patients aged >60 years without known coronary disease at registrationPatients surviving into older age before statins became available were therefore likely to be a highly selected group at lower risk of coronary disease.
BMJ. 1991 October 12; 303(6807): 893–896.
Risk of fatal coronary heart disease in familial hypercholesterolaemia. Scientific Steering Committee on behalf of the Simon Broome Register Group.
OBJECTIVES–(a) To determine the excess mortality from all causes and from coronary heart disease in patients with familial hypercholesterolaemia; (b) to examine how useful various criteria for selective measurement of cholesterol concentration in cardiovascular screening programmes are in identifying these patients. DESIGN–Prospective cohort study. SETTING–Eleven hospital outpatient lipid clinics in the United Kingdom. PATIENTS–282 men and 244 women aged 20-74 with heterozygous familial hypercholesterolaemia. MAIN OUTCOME MEASURE–Standardised mortality ratio, all adults in England and Wales being taken as standard (standardised mortality ratio = 100 for standard population). RESULTS–The cohort was followed up for 2234 person years during 1980-9. Fifteen of the 24 deaths were due to coronary heart disease, giving a standardised mortality ratio of 386 (95% confidence interval 210 to 639). The excess mortality from this cause was highest at age 20-39 (standardised mortality ratio 9686; 3670 to 21,800) and decreased significantly with age. The standardised mortality ratio for all causes was 183 (117 to 273) and also was highest at age 20-39 (standardised mortality ratio 902; 329 to 1950). There was no significant difference between men and women. Criteria for measurement of cholesterol concentration in cardiovascular screening programmes (family history, presence of myocardial infarction, angina, stroke, corneal arcus, xanthelasma, obesity, hypertension, diabetes, or any of these) were present in 78% of patients. CONCLUSIONS–Familial hypercholesterolaemia is associated with a substantial excess mortality from coronary heart disease in young adults but may not be associated with a substantial excess mortality in older patients. Criteria for selective measurement of cholesterol concentration in cardiovascular screening programmes identify about three quarters of patients with the clinically overt condition.
5) Ravnskov, Uffe, et al. “LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature.” Expert review of clinical pharmacology 11.10 (2018): 959-970. LDL-C does not cause cardiovascular disease Ravnskov Uffe Expert rev clin pharm 2018
6) The Cholesterol Drug War: ABC Australia Bans Documentary Exposing Statin Drug Scandal
Jeffrey Dach MD
7450 Griffin Road, Suite 190
Davie, Fl 33314
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“Adverse reactions involved far more than impaired cognition, including personality change, myopathy, myopathy and a chronic neuromuscular degeneration similar to ALS and all statins were contributing to these adverse reactions, not just Lipitor.” – http://www.spacedoc.com/
In a nutshell, inflammation is the real enemy – GlyCop
I remember reading an article before from a doctor that said if his cholesterol wasn’t around 300 he would panic. So I agree with you, that this whole thing is being pushed, where maybe it shouldn’t be……. ??
Check out Denise Minger’s website for her formidable critiques of Keys and Campbell. http://rawfoodsos.com
Her new book, “Death by Food Pyramid: How Shoddy Science, Sketchy Politics and Shady Special Interests Have Conspired to Ruin the Health of America w book, ” is due out in January, 2014.
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default Cholesterol readings are given below
On sim a statin and Ezetimibe (10 mg +10 mg) since 2006
Sugar increased from 85 to 125 fasting
Pp is normal 119
Hb1ac increased from 6 to 8.2
I am amlodipine 5mg once morning
losar25mg one morning and one evening
simva statin 10 mg one evening
ezetimibe 10 mg one eveng
ecosprin 150 mg one after lunch
clopid 75 mg one after lunch
Feeling dizzy many a times since 2010 MRI IS NORMAL
CT SCAN IS NORMAL
IS IT NEUROPATHY DUE TO STATIN
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