Has the LCHF diet been accused of a crime that never happened? Yes, argues the Icelandic cardiologist Dr Sigurdsson, and it’s a good read:
Doc’s Opinion: Accused of a crime that never happened – LCHF on trial in Sweden
I think LCHF must really be striking fear into the hearts (and wallets) of those with a vested interest in maintaining the "conventional wisdom". The internet is being instrumental in facilitating those who have the will to stop and ask questions, rather than blindly accepting the authority of "experts".
A fascinating story that I think would play well to audiences with someone like Meryl Streep as Dr. Dahlquist!
Sweden has not been consuming a LCHF diet for long enough to contribute significantly to an increased risk of cvd (ie. time lag hypothesis), especially considering the apparently high quality cardiovascular care in Sweden. Moreover, LCHF-diet has been popular among the young and people in their pre-midlife. Those at the highest risk of dying with previous heart events are usually in the typical "low cholesterol, low saturated fat" -diets and are in the age where they are less keen on following popular trends.
In some countries the rates of lung cancer kept on climbing for two decades after smoking prevalence declined before the rates of lung cancer finally declined.
http://en.m.wikipedia.org/wiki/Smoking
Anyways, what we know for a fact is that younger women in Northern Sweden were amongst the first portion of the population to change their diet to one lower in carbohydrates and higher in fat, especially for butter used in cooking.
http://www.nutritionj.com/content/11/1/40
We also know that about 40% of the large decrease in chd mortality in Sweden Bettendorf 1986 and 2002 has been explained by a large decrease in serum cholesterol, which was largely explained by a decrease in saturated fat.
http://m.eurheartj.oxfordjournals.org/content/30/9/1046.long?view=lon...
http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed�...
I am curious about is to whether young women are least likely to be prescribed cholesterol lowering medication (in amounts sufficient to significantly lower cholesterol) compared to the rest of the population. These factors may explain why younger women were among the first to show increases in stroke and heart attacks. Any ideas Doc?
It has been demonstrated that elevated serum cholesterol and the feeding of dietary cholesterol and saturated fat accelerates the development of atherosclerosis in virtually all vertebrates (including nonhuman primates) that have been sufficiently challenged (so long as a way is found to raise serum cholesterol high enough for a sufficient period of time), very compelling evidence is required in order to safely say that this does not apply to humans. Therefore, based on the Darwinian foundation of our biomedical research paradigm, it's extremely likely that LCHF induced elevation of LDL cholesterol will result in increased rates of heart events among Swedes in the future.
This kind of disingenuous reasoning may seem superficially sound but it is nothing but an house of cards.
"DESIGN AND SETTING:
The Pathobiological Determinants of Atherosclerosis in Youth Study, a multi-institutional autopsy study conducted in US medical centers. Subjects A total of 2876 study subjects, between 15 and 34 years old, black and white, men and women, who died of external causes and underwent autopsy between June 1, 1987, and August 31, 1994.
MAIN OUTCOME MEASURES:
Extent, prevalence, and topography of atherosclerotic lesions.
RESULTS:
Intimal lesions appeared in all the aortas and more than half of the right coronary arteries of the youngest age group (15-19 years) and increased in prevalence and extent with age through the oldest age group (30-34 years). Fatty streaks were more extensive in black subjects than in white subjects, but raised lesions did not differ between blacks and whites. Raised lesions in the aortas of women and men were similar, but raised lesions in the right coronary arteries of women were less than those of men. The prevalence of total lesions was lower in the right coronary artery than in the aorta, but the proportion of raised lesions among total lesions was higher in the right coronary artery than in the aorta."
JAMA. 1999 Feb 24;281(8):727-35.
Prevalence and extent of atherosclerosis in adolescents and young adults: implications for prevention from the Pathobiological Determinants of Atherosclerosis in Youth Study.
http://www.ncbi.nlm.nih.gov/pubmed/10052443
I recall hearing the same during combat medicine training when I was a Medic in the British Royal Navy.. that the USA surgeons in Vietnam where surprised to find atherosclerosis in many of the otherwise fit and healthy young men (boys) who they operated on in field hospitals.
So once again "A leads to B" and "B leads to C" but it does NOT follow that "A leads to C".
"Anyways, what we know for a fact is that younger women in Northern Sweden were amongst the first portion of the population to change their diet to one lower in carbohydrates and higher in fat"
No, you don´t know that for a fact! This opinion poll on LCHF indicates that LCHF complience is lower than average in Nothern Sweden and it indicates that the it is lower among the people with low education and low income - the group we are speaking of. You might also note that +65 year olds has a higher complience with the LCHF diet than the average Swede. This is the group that suffers a lot more heart attacks and strokes than people aged 34-44 years. Why has not the older population that stick more to LCHF showed an trend of more infarctions and strokes?
The full opinion poll in Swedish: http://www.kostdoktorn.se/wp-content/2011/03/demoskop_mars_2011.pdf
Parts of the opinion poll translated to English: http://www.dietdoctor.com/the-swedish-low-carb-revolution
Occhams razor: The most uncomplicated explanation is to be preferred. That is that people with low education have more social stress (well known risk factor), smoke more, exercize less and eat more sugary junk food. Period.
Anyways, a survey suggests LCHF more popular in Sweden among the unemployed, people with low income and in women.
http://www.kostdoktorn.se/wp-content/2011/03/demoskop_mars_2011.pdf
FrankG,
high cholesterol correlates staggeringly well with hardening of arteries among infants. See Michaels Gregers video for information. He covers the same studies that you did + plenty of others. Diet low in saturated fat and cholesterol has favorable effect on the arteries of child.
Heart disease starts in childhood.
https://www.youtube.com/watch?v=vlubvTMLrLM
Anyways, make sure to watch Greger's video. Excellent insight into to atherosclerosis and serum cholesterol in infants.
Pathobiological determinants of atherosclerosis in youth risk scores are associated with early and advanced atherosclerosis.
http://www.ncbi.nlm.nih.gov/pubmed/17015535
http://en.wikipedia.org/wiki/Michael_Greger
Interesting that I DON'T refer to myself as an "LCHF".
Funny how the facts take second place when vegan ideologies come into the picture. And you must be even barmier than I thought if you seriously expect me to take any of your recommendations Pee Pee.
Exactly, good that you corrected this. This highlight how important cholesterol is (a master switch) in initiating the atherosclerotic process in young people. All this supports the stance made by the "formidable five". LCHF advocates are the merchants of death & confusion!
What part of the video made by Greger you did not like?
One might put it this way.
Suppose,
A(1) => B
A(2) => B + D
D => C
In a population study where more people eat high glycemic diet, this will give the false impression that B causes C and that A(1) causes C.
Let A(1) = dietary saturated fats
A(2) = continual high blood sugar
B= higher cholesterol
D = endothelial glycation and higher inflammation
C = vascular disease
in both cases we are being fed what looks superficially like science, while underlying it all is simply a blind, closed-minded, faith-based ideology.
Terms like "irreducible complexity" in one case and the ohh so scary inferences that eating saturated animal fat will somehow kill us all...despite the evidence of our own experience to the contrary.
Despite their efforts, the agenda in both cases is quite transparent but the way that both try to deceive their true intent, does nothing except underline for me what a bunch of lying hypocrites they are. It is a game, nothing more, there is no desire to genuinely help anyone... except themselves.
Despite Pee Pee's protestation that he means no inference, it is quite clear that by repeatedly drawing a line from saturated fat to atherosclerosis he expects us to automatically continue that line (or "lie" as I originally typo'd) to CVD. Unfortunately for him, he has come across a group of folks who are not as gullible (or malnourished) as his usual vegan drones. Not that all vegans fall into this category but he clearly relies on many doing so.
Even if it were true that all (or even most) cases of CVD show signs of atherosclerosis -- and I am pretty sure it is NOT true -- it STILL does not follow that atherosclerosis inevitably leads to CVD. The observations (as cited above) that "Intimal lesions appeared in all the aortas and more than half of the right coronary arteries of the youngest age group (15-19 years)", offers the possible interpretation that atherosclerosis is not some big scary modern thing that we need run for in fear OR perhaps it is? But so long as there is a question mark over this it would be wrong to assume the worst as he cautions... especially as so many of us already and definitely know the actual harm which would come from following his dietary advice. These people did NOT die of CVD nor did a great many of the young soldiers who fought in Vietnam. Nor does the great majority of the population BUT this study suggests that atherosclerosis may be highly prevalent in many, if not most of us. It's hard to see, except for those folks who die young (and are autopsied) or who develop symptoms.
The approach being offered by Pee Pee is NOT scientific even though it is dressed up in "sciency" words. Again we are not so easily led here Pee Pee.
His whole line of reasoning relies on spreading fear of heart disease or cancer... what "might" happen if you don't heed his words. Much like a discussion with a religious fundamentalist -- fear is also a popular weapon in their arsenal as well. It is getting very tiresome and boring But I am not done yet.
Lipid levels in patients hospitalized with coronary artery disease: An analysis of 136,905 hospitalizations in Get With The Guidelines
http://download.journals.elsevierhealth.com/pdfs/journals/0002-8703/P...
Of note...
The patient population included patients hospitalized with confirmed clinical diagnoses of CAD, including patients with acute coronary syndromes, stable CAD hospitalized for revascularization, and patients with documented CAD hospitalized for reasons other than heart failure.
"Whole-body computed tomography (CT) scans of mummies from four geographical regions across a period of 4000 years suggest that atherosclerosis was more common in ancient populations than previously believed [1] Studying individuals from ancient Egypt, ancient Peru, ancestral Puebloans of southwestern America, and hunter-gatherers from the Aleutian Islands, researchers were able to identify atherosclerosis in more than one-third of the mummified specimens, raising the possibility that humans have a natural predisposition to the disease.
Our findings greatly increase the number of ancient people known to have atherosclerosis and show for the first time that the disease was common in several ancient cultures with varying lifestyles, diets, and genetics, across a wide geographical distance and over a very long span of human history,
These findings suggest that our understanding of the causative factors of atherosclerosis is incomplete and that atherosclerosis could be inherent to the process of human aging."
Please note that "mummies" does not always mean Egyptian Pharaohs who lived high on the "fat of the land" :-P
I'd suggest that the comments following this article are worth reading also.
1) Control your variables. If there are multiple factors changing you cannot know which variable is responsible for the results or to what extent each variable is involved in the result.
2) Correlation does not imply causation. Contrary to what vegans may say, this principle is not something made up by low carbers or Paleo followers but rather a principle that is seen in just about every statistical text. It simply means that the conjunction (correlation and non-causation) is possible.
3) Multivariable analyses are not replacements for randomized controlled trials. Statistical models are not sufficient and cannot establish causation. A meta-regression analysis is observational in nature. Yep, all these fancy words refer to things that assess associations, not causal relationships.
4) Logical fallacies are not cool. Some common vegan ones are appeals to fear, guilt by association, false dichotomies, non sequiturs, faulty analogies and appeals to authority.
5) Non-causation is assumed until proven otherwise. Until you actually provide positive evidence against e.g. saturated fat, talking about regression dilution, inter/intra individual variability, measurement error or whatever does nothing to advance the vegan cause i.e. complaining about the problems of studies is not evidence against anything.
Statins are useless in primary prevention in all women. And in men less than 50 or more than 65. And especially in children... You may decrease by a small margin the number of cardiovascular events in a high risk population, but NO STUDY showed any increase in days lived. In other words, with statins, you may change the diagnosis on the death certificate, not the date.
And as far as the extraordinary decreases in cardiovascular disease with statins, those extraordinary numbers are RELATIVE risks. Look at the Jupiter study. A 54% reduction in cardiac events, a 27% reduction in strokes... Why on earth do we not put statins in drinking water? Simply because those numbers are relative. The true numbers are far, far less impressive. In the placebo group, 0,76% of people had an MI. In the treated group, it was 0,35%. So in absolute numbers, the true difference is 0,75% - 0,35% = 0,41%, thus less than half of one percent of people. Not glorious. But wait! Let's change this into a relative risk! 0,35/0,76 is 0,46. 1 - 0,46 is 0,54 and voilà! You can now state that the medication in primary prevention decreased the risk of heart disease by 54%. People's brains think in absolute numbers and thus conclude that more than half of people were saved from heart disease. But this is not true! Less than one half of one percent were saved. Also think that in absolute numbers, around 20% of people (highly under-reported by physicians) suffer important side effects of statins. I hope no one ever puts it in the drinking water.
May I finally refer you to the following article?
Sachdeva A, Cannon CP, Deedwania PC, Labresh KA, Smith SC Jr, Dai D, Hernandez A, Fonarow GC. Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines. Am Heart J. 2009 Jan;157(1):111-117.e2. doi: 10.1016/j.ahj.2008.08.010. Epub 2008 Oct 22.
It was found that cardiac patients had lower LDL (2,7mmol/L) than the normal population (3,2mmol/L). The authors simply did not discuss this rather "paradoxical" finding. They simply stated that since a fair number of heart patients had a rathr low cholesterol, this added weight to the new recommendations to lower cholesterol levels even more (thus selling a lot more statins ).
Cholesterol does not cause heart disease. Inflammation does. The body uses cholesterol to repair endovascular lesions. Caused by inflammation. Dropping cholesterol is like getting rid of firefighters to stop house hires.
And by the way, feeding cholesterol to a herbivore is a pretty stupid thing to do: they cannot metabolize it. Professor Ashnikov did this with rabbits in 1913 (guess what, they got massive atherosclerosis). More recently, industry fed animal by products to cows, and we now have mad cow's disease. Any stupid diet not meant for a species will bring problems (think Standard American Diet in humans). I'll stick to my species diet: LCHF.
there's not a single RCT trial that has managed to show an effect with smoking cessation. At least 3 have tried (Whitehall Study, the Lung Health Study, and MRFIT). As Katan (2011) wrote: "evidence from epidemiologic, metabolic, and laboratory studies confirms that high intakes of saturated fat do cause heart disease. Ignoring this evidence leads to absurd consequences. For instance, our knowledge of the ill effects of cigarette smoking rests purely on epidemiologic, metabolic, and laboratory studies, whereas evidence from clinical trials is largely lacking. The same holds true for the ill effects of physical inactivity, the failure to use seat belts, the consumption of toxic chemicals in foods, and asbestos exposure. None of these conditions has been proven to be unhealthy in clinical trials performed according to the standards for pharmaceutical drugs. I believe that, in all of these cases, we should consider the totality of the evidence, and the totality of the evidence overwhelmingly indicts saturated fat as a cause of heart disease, just as it indicts cigarettes”.
Brown & Goldstein used cell cultures and demonstrated that we are no different from other mammalians when it comes LDL receptor activity. Biologically natural levels of LDL cholesterol for humans ranges from 40 to 70. Lower is better. The LDL receptors get saturized on levels that exceeds 60mg/dl (1,5mmol/l) and start to function less optimally. Good luck getting your LDL down to these digits with use of SFA.
Diethelm et al wrote an excellent piece about scientific denialism.
"The normal academic response to an opposing argument is to engage with it, testing the strengths and weaknesses of the differing views, in the expectations that the truth will emerge through a process of debate. However, this requires that both parties obey certain ground rules, such as a willingness to look at the evidence as a whole, to reject deliberate distortions and to accept principles of logic. A meaningful discourse is impossible when one party rejects these rules.
–Heart Disease, Environment, Stress and Gender [proceedings of the NATO Advanced Research Workshop on Increase in Coronary Heart Disease in Central and Western Europe: Stress and Gender Related Factors, 20-24 May, 2000, Budapest, Hungary]
EXACTLY Pee Pee! I am so gratified to see that you are finally coming around to the realisation as to why you keep getting it so very, very wrong. :-P
Their preamble...
"The metabolic syndrome is a cluster of the most dangerous heart attack risk factors: diabetes and prediabetes, abdominal obesity, high cholesterol and high blood pressure.
* A quarter of the world’s adults have metabolic syndrome
* People with metabolic syndrome are twice as likely to die from, and three times as likely to have a heart attack or stroke compared with people without the syndrome
* People with metabolic syndrome have a five-fold greater risk of developing type 2 diabetes
* Up to 80% of the 200 million people with diabetes globally will die of cardiovascular disease
* This puts metabolic syndrome and diabetes way ahead of HIV/AIDS in morbidity and mortality terms yet the problem is not as well recognised"
Their definition...
"According to the new IDF definition, for a person to be defined as having the metabolic syndrome they must have:
Central obesity (defined as waist circumference ≥ 94cm for Europid men and ≥ 80cm for Europid women, with ethnicity specific values for other groups)
plus any two of the following four factors:
• raised TG level: ≥ 150 mg/dL (1.7 mmol/L), or specific treatment for this lipid abnormality
• reduced HDL cholesterol: < 40 mg/dL (1.03 mmol/L*) in males and < 50 mg/dL (1.29 mmol/L*) in females, or specific treatment for this lipid abnormality
• raised blood pressure: systolic BP ≥ 130 or diastolic BP ≥ 85 mm Hg, or treatment of previously diagnosed hypertension
• raised fasting plasma glucose (FPG) ≥ 100 mg/dL (5.6 mmol/L), or previously diagnosed type 2 diabetes. If above 5.6 mmol/L or 100 mg/dL, OGTT is strongly recommended but is not necessary to define presence of the syndrome."
And since you continually try to refocus back to the "dangers" of LDL-C they give even more detail on cholesterol...
"Atherogenic dyslipidaemia describes the combination of raised triglycerides (TG) and low concentrations of HDL-c together with elevated apolipoprotein B (ApoB), small dense LDL and small HDL particles, all of which are independently atherogenic, and which is commonly observed in patients with both type 2 diabetes and the metabolic syndrome. Low HDL-c and high TG levels are frequently found with insulin resistance, with or without type 2 diabetes, and both are risk factors for coronary heart disease (CHD)."
What has me puzzled in all your talk of logic and being open-minded to the evidence is that neither the IDF nor the WHO definitions of Metabolic Syndrome specifically list an high LDL-C as a factor, instead (evidently) focusing in on Triglycerides and HDL-C. Why is that I wonder? Do YOU really expect us to believe that you (an anonymous, agenda-driven, vegan ideologue) know better that these combined minds? Surely they have access to all the same trials and studies as you do, possibly even more?
interesting association. All free-ranging mammalians have very low blood cholesterol, are they at an increased risk of hemorrhagic stroke or is there something else going on?
Alcohol induces disturbances of the liver resulting on low LDL cholesterol. The combination of low cholesterol and high blood pressure is marker of binge drinking and indeed associated with increased risk of bleeding. People with low cholesterol and low blood pressure are not at increased risk of hemorrhagic stroke. Authors of a huge Korean cohort study with ~800 000 participants concluded:
"In our study, increased risk of hemorrhagic stroke in people with low concentrations of blood cholesterol (less than 4.14 mmol/l) was restricted to those with high GGT values [a measure of alcohol intake]; this relation was less evident when alcohol consumption was measured by self report. The measures of blood pressure might not have been a true reflection of risk, as transient high blood pressure associated with binge drinking may have an important role in hemorrhagic stroke. At low concentrations of GGT, low serum cholesterol was not associated with a higher risk of hemorrhagic stroke.In effect, low blood cholesterol may act as a marker of the health damaging effects of alcohol, rather than be a cause of hemorrhagic stroke".
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1488755/
@FrankG
Diagnostic Criteria for Dyslipidemia
"Low-density lipoprotein cholesterol (LDL-C) is identified in the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) report as the most abundant and clearly causal atherogenic lipoprotein on the basis of many observational and experimental studies over several decades.1 Guidelines from the American Association of Clinical Endocrinologists (AACE) are in agreement with NCEP ATP III that LDL-C is central in the diagnosis of dyslipidemia. Any LDL-C level above 100 mg/dL appears to promote atherogenesis".
http://www.lipidu.com/Pillars.aspx?PillarID=2&ChildID=2
Saturated fat intake is a driver of metabolic syndrome
Saturated Fatty Acid-Mediated Inflammation and Insulin Resistance in Adipose Tissue: Mechanisms of Action and Implications
http://jn.nutrition.org/content/139/1/1.full
I was diagnosed with Metabolic Syndrome in 2003 and was rapidly going downhill health-wise, while strictly following the established advice; including avoiding saturated fat. Since I read GCBC, started questioning the "conventional wisdom" and have significantly increased my intake of Saturated Animal Fat, ALL my health markers have improved, also significantly. How can that be..? Am I yet another oddity, an outlier.. amongst so many other examples that we see here and on other LCHF sites?
What will it take for you to realise that you are wasting your time here? Unless of course you are getting well paid for your efforts :-P
amphetamines were used as weight-loss medication. People taking amphetamines loose weight and see all their biomarkers improving. The same goes with chemotherapy. The difference with amphetamines and low-carb is that amphetamines do not cause adverse effect to number one causal agent influencing CHD, LDL cholesterol. Elevation of LDL cholesterol is often seen on low-carb studies even in the presence of weight-loss (Hernandez et al).
Diet Heart - Problematic Revisit (Jeremiah Stamler)
"As to item 10, the concern (1) about influences of dietary composition on triglycerides, HDL cholesterol, glycemia/diabetes, and “metabolic dyslipidemia” is also one-sided. The evidence is overwhelming that the main “driver” of these traits is caloric imbalance producing overweight/obesity (10). These metabolic traits all respond favorably to even modest weight reduction with diets of varied nutrient composition, including heart-healthy fare (see below) (11, 12)".
You have NO answer to that and you have NO answer to the 137,000 patients hospitalised with CAD where around 50% had low-normal LDL-C.
You just keep hammering away at LDL-C as if that is the answer to everything. BORING!
In the past year I was referred to a Lipidologist -- a clinician specialising in the area under discussion -- as my Endocrinologist was still trying to convince me to go back on statins as a primary prevention precaution, despite the side effects I had experienced. The lipid specialist also was more interested in my high HLD-L and low Triglycerides that he was in my LDL-C. He did NOT prescribe me statins, nor recommend any change to what is clearly already working very well for me -- and evidently is working well for many, many others.
Between a clinical specialist who has met me, knows my case, and an anonymous, vegan ideologue, where do YOU guess I put more trust?
Whatever musings you entertain about smoking is not evidence against saturated fat. You are making a claim about saturated fat, therefore you have to provide positive evidence against saturated fat, not provide some faulty analogy with smoking.
Many people agree that passive smoking is harmful because of the known risk of active smoking (and dose response relationship) in relation to lung cancer where the risks are really large. In this case the analogy is valid. Incidentally, smoking is also associated with increased oxidative stress which supports my case even more.
Richard: "we should consider the totality of the evidence, and the totality of the evidence overwhelmingly indicts saturated fat as a cause of heart disease, just as it indicts cigarettes”.
When the majority of observational studies and clinical trials fail to find any link between saturated fat and heart disease it can only be a sad joke to suggest "the evidence overwhelmingly indicts saturated fat". Katan, Stamler and friends have a lot of talk but very little substance.
Richard: "Diethelm et al wrote an excellent piece about scientific denialism."
Scientific Denialism is not following scientific principles. Hint: it is not me that is gulity of this but you and your "experts".
So far as I am concerned "High Cholesterol" is the biggest insult to anyone's common sense out there... it tries to simultaneously contain the concept that "High is bad" while including HDL-C where "High" is supposed to be "good" ?!? It CAN'T be BOTH! That is utter nonsense.
Then again LDL-C as reported is not even usually directly measured but is rather a calculated VOLUME. Being a VOLUME it ought to take into account the different particle sizes but it DOESN'T.
It is like saying that I have a garbage bag full of sports balls here, who many do you want..? without identifying if they are beach balls or golf balls. The garbage bag may be the same VOLUME but the number of balls (or LDL particles) it contains is vastly different.
By the same token if I had say 1,000 small dense LDL-C particle per litre of blood (not related to actual numbers, just for illustration) and the way I ate (for example) caused them to change from being small dense to large buoyant particles, then any reasonable person ought to see that the VOLUME of LDL would increase. Is this what we see initially with an LCHF diet... I am convinced that indeed it is. Given time in many (most) cases it will normalise.
Some authorities focus on the LDL particle size only, claiming that the small dense are up to 300% more damaging than the large buoyant which are relatively harmless, others (like Peter Attia MD, for example) will focus on LDL particle count.. which is not yet routinely measured -- although I note it WAS mentioned in the IDF definition I cited above. Meantime a low TG and high HDL-C are a fair way to estimate both a low LDL count AND large buoyant particles.
I know you thrive on obfuscation Pee Pee but once again I'd point out that you made a big mistake in thinking folks here as gullible or malnourished as your usual vegan crowd :-P
http://www.centerforpreventivemedicine.com/04114med_messenger.pdf
At a bare minimum there is controversy over the role of LDL-C in CHD/CVD etc... to deny that simple fact is the worst kind of "denialism". It is not a done deal... it is antithetical to the scientific method to even suggest that we have all the answers on any given subject.
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A fascinating story that I think would play well to audiences with someone like Meryl Streep as Dr. Dahlquist!
So how is it that my father 26 years ago ( at the age of 56) leading physically active life and eating healthy low fat foods had a massive heart attack after which, on the advice of his cardiologist, eliminated fats from his diet. Few years on fat free diet he was advice that his heart is in real bad shape and he will need multiple by-pass surgery. By quirk twist of fate (details are not important here) he started extreme LCHF diet. Today at he age of 82 his heart works as that of 20 years old. He never underwent by-pass.
Is my father a freak of nature?, one in a million?
or all that all Richards on this blog are saying is:
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