Here is Wikipedia on the wisdom of Karl Popper:
“The classical view of the philosophy of science is that it is the goal of science to prove hypotheses like “All swans are white” or to induce them from observational data. Popper argued that this would require the inference of a general rule from a number of individual cases, which is inadmissible in deductive logic. However, if one finds one single black swan, deductive logic admits the conclusion that the statement that all swans are white is false. Falsificationism thus strives for questioning, for falsification, of hypotheses instead of proving them.”
Sorry, although I am a great fan of Popper, his language is a bit, well, pedantic. What he is saying here is that science starts with a hypothesis e.g. ‘all swans are white.’ If you find white swan after white swan, then you will mildly strengthen the hypothesis. However, once you find one black swan, the hypothesis is dead. (Unless you decree that, as all swans are white, a black swan cannot – by definition – be a swan).
One of the great white swans of cardiology is that Familial Hypercholesterolaemia (FH) causes heart disease. When I give talks to other doctors informing them that the cholesterol hypothesis is bunk, one of the ‘facts’ that is triumphantly used to knock me down is that ‘People with Familial Hypercholesterolaemia die very young from heart disease.’ Case proven, raised cholesterol causes heart disease, now move on.
A little bit of context is needed here. Familial Hypercholesterolaemia (FH) affects about one in five hundred people. It is a genetic condition where those who have it (I refuse to use the words suffer from it) have very high Low Density Lipoprotein (LDL) levels. As everyone knows LDL is known as ‘bad’ cholesterol, which is considered to be the number one risk factor for heart disease. (Of course LDL is not cholesterol at all but, hey, why let scientific accuracy get in the way of…. Well, science).
Goldstein and Brown established that the cause of FH is a lack of LDL receptors on cells. LDL receptors are the things that bind on to LDL molecules and then remove them from the bloodstream. Cells manufacture LDL receptors when they are low on cholesterol and need more.
Once the receptor is made it is pushed out through the cell membrane to attract an LDL molecule. When an LDL molecule has been caught, by binding on to the receptor, the LDL and the attached receptor are pulled back into the cell and broken down. Because they function this way, LDL receptors only work once. If a cell wants more cholesterol, then it needs to manufacture more LDL receptors.
Clearly, if there are not enough LDL receptors being manufactured, the entry of LDL into cells is restricted. This means that blood levels of LDL rise, and you will be diagnosed with Familial Hypercholesterolemia. If, that is, you have a blood test.
Moving sideways for a moment I need to mention that most people with FH are heterozygotic, by which I mean they carry one gene for FH. Their LDL levels are therefore about double that of the surrounding population. However, those with homozygotic FH (carrying both genes) have LDL levels that can be twenty times ‘normal’. More on this group in a later blog.
Back to FH. If you have a heart attack when young, by which I mean under about 55, and you have FH, doctors will nod sagely and that that ‘it was the FH that did it.’ (If you don’t have FH, they will say it was something else that did it).
Sometimes the relatives of those dying young of CHD with FH, are contacted. It is often found that there is a higher rate of FH and premature CHD in relatives. This type of evidence has been used as proof that FH causes CHD. Maybe. Maybe not. If someone dies young from CHD, and has FH, and other relatives have a higher rate of both FH and CHD, what have we actually proved? We have proved nothing – for certain.
All we have done is to establish that relatives of people with FH and premature CHD also have FH (as they must, as it is a dominant gene) and also have a higher rate of CHD. Now, it could be that the FH is the reason for their CHD. Or it might not. It could be that something else, genetic of behavioural, is causing their high rate of CHD.
Given this problem of inherent bias, how could you tell if the FH is causing the CHD or not? Or, better, how could you falsify the hypothesis that FH causes CHD? Can you find a black swan?
Well the best way to find a black swan in this ara is to turn your study inside out. Instead of looking at people with FH and premature CHD, then looking at their relatives to find FH and CHD, you need look for premature CHD first (knowing nothing of FH status), then see if FH is more prevalent in first degree relatives.
How do you do this? Well, firstly you ask hundreds thousands of students if their father had a heart attack, or died of heart attack before the age of 55. Then you measure the LDL level of those students to see if they have FH. At the same time you find age and sex matched control students to see if they have FH.
Now, if FH really were a major cause of premature CHD you would expect to find that FH was far, far, more prevalent amongst those students whose fathers suffered CHD before the age of 55.
Such a study was done once, in the Netherlands. The results were as follows:
In the EARS (European Atherosclerosis Research Society) studies, University students whose fathers had proven CHD before the age of 55 years, were recruited …Age and sex-matched controls were recruited from the same populations for each case.
- 2 of 1089 students with family history of CHD had FH
- 4 of 1727 controls had FH
Thus, the prevalence of FH in both groups was not significantly different at approximately 1 in 500, which is the estimated prevalence of the condition in the general population. The evidence that heterozygote FH is, of itself, a cause of atherosclerosis is unsatisfactory.
In short, when someone finally did a study on the association between premature CHD and FH, where selection bias was removed, they found that FH was no more common in those with, and without, a strong family history of CHD. This was the blackest of black swans.
However, there is a twist to this tale. Which is that this study was never published anywhere. The only reason that I know about it, is that I was reading the responses section in the British Medical Journal, and the lead investigator of the study wrote the above letter in reply to a discussion on FH. (Something more than easily missed).
I contacted him, and asked why the study had not been published. He did not provide any answer that made any sense to me. The end result of the lack of publication is that the blackest of black swans is not actually black. It is invisible. Until now, of course.
P.S. As for homozygotic FH, I shall deal with this later.
Gloomy news for science. Who can you trust I wonder?
Who can you trust? Don’t know the answer to that one.
I’ve just read (devoured, even) your book and am now thoroughly enjoying your debunking of ‘science’ on here. Being from the UK myself it’s refreshing to find an author discussing the state of things over here rather than the US.
If I could get your thoughts on one thing. You’ve proven beyond doubt that traditional cholesterol-based ‘risk factors’ for CHD are useless (at least for anything other than measuring the likelihood your doctor will ever learn to think for himself), but are there any actually meaningful risk factors that can be determined from cholesterol/lipoprotein levels? E.g. we hear about such ratios as (total chol/HDL) or (trigs/HDL) etc, are these overhyped or is there actually a decent measure in there somewhere?
Love the blog, please keep it up!
If you have high trigs/VLDL and low HDL you are almost certainly insulin resistant, may have the metabolic syndrome, and are at increased risk of CVD.
I read the responses at the BMJ link. The first also intrigued me because of the link between statins and neuropathy. I continue to resist the pressure to take statins mainly thanks to the efforts of you and Dr. Ravnskov. Please keep up the good work.
This rings very true to me: few years ago, blood test showed ‘high’ total cholesterol of 9.0 (actually althought LDL was fairly high, HDL was high and triglycerides low – the significance of which I found out myself through research). Immediate response from GP was to suggest referral to lipid specialist, whole family testing and statins for me – this despite no CHD on one side of family (the other side being unknown). The stress this caused at the time was large: imagine feeling you were ‘responsible’ for passing on such a ‘bad’ gene that your children were at risk. Blogs such as this and the books by doctors such as yourself, Dr Kendrick, and Uve Ravnskov, helped me gain a persepctive I would not have had otherwise and helped restore some balance to the ‘diagnosis’. Please don’t stop alerting us to the incompleteness of medical research – we need to know the whole picture and we so very seldom get acccess!
I try my best to dig out the truth. Uffe Ravnskov is my leader and hero.
I hope this isn’t too inane, but I have a reservation about studies where you ask people about family medical history: I know little about my own. My parents just didn’t talk about such things – heavens, my father died before I’d even heard he was unwell. I have no idea of the causes of death of my grandparents. I don’t even know much about my siblings’ health records. Is this unusual? If it is common but not random, could that upset studies such as you describe?
Yup. Except in this case, I believe, CHD had to be confirmed according to quite strict criteria
On Tue, 16 Jul 2013 20:51:17 +0000
This is a bit off topic but I have a question for you, Dr. Kendrick:
I was reading this paper about omega-3 and heart disease: http://goo.gl/h3gvb
The Data Synthesis section says: “No statistically significant association was observed with all-cause mortality … cardiac death … sudden death … myocardial infarction … and stroke”
and the Conclusion section says: “omega-3 PUFA supplementation was not associated with a lower risk of all-cause mortality, cardiac death, sudden death, myocardial infarction, or stroke”
Maybe I have it wrong, but I think the paper cannot conclude there is no association because the results were not statistically significant. If is not significant it cannot conclude anything at all either pro or against. In other words the paper found nothing. The samples were just not big enough. (although the numbers suggest a positive association in most cases, just not at 95% significance)
But if we look closer at the numbers for Cardiac Death: “RR, 0.91; 95% CI, 0.85 to 0.98” that actually seems to me it says that it is statistically significant at the 95% level, so at least for cardiac death the study seems to have a found a statistically significant association.
Am I confused? I mean this a peer-reviewed, published paper, already referenced in other papers. How many expert eyes have seen this? Yet the abstract seems to show some basic errors in statistical interpretation. Am I wrong?
This is slightly off at a tangent, from the current article Dr K, but as you mentioned Uffe Ravnskov I looked him up as I hadn’t heard of him, and one of his articles made me wonder. He seems to suggest that there are those who are now beginning to suspect that high cholesterol may not be the cause of CHD after all, but that they (scientists etc) “would rather walk down 5th Avenue naked than admit they may have been wrong”. Without condoning that, because people’s health is at stake, I can just about understand their pride, but why do you think they don’t just quietly drop plugging the fat/cholesterol/CHD issue until the public forgets about it (we are very fickle), and then slowly begin to produce articles suggesting new evidence has been found suggesting otherwise. They could probably get away with it and public would naively accept it. But they keep on and on warning us about high fat, and there always seem to be headlines telling us that statins can virtually save your life by just looking at them. Why don’t the higher powers keep quiet until the fuss dies down, do you think?
Not to forget, the USA has lots of grain to sell… cheap carbs & veg oils which go into the “healthy” low saturated fat crap that we’re meant to eat these days.
There’s lots of vested interests making lots and lots of money out of the lipid hypothesis, and let’s not forget, turkeys don’t vote for christmas.
It is now about money. Also, new cholesterol lowering agents are on the horizon, so that cholesterol lowering nonsense needs to be kept alive.
As for fat, just think Flora
On Wed, 17 Jul 2013 13:33:40 +0000
Am I the only one to suspect there is, at least a million slavering ambulance chasers (Sorry! Slip of the keyboard – I meant concerned legal professionals, of course) who are just waiting to cash in with huge class actions as soon as someone admits they have given wrong (possibly harmful?) advice. The myth must be supported because the financial consequences could outstrip tobacco.
Ah yes, I was forgetting about the dollars. Made the mistake of thinking they were concerned about people’s health!
If you were a pessimist you could be forgiven for thinking there was no hope for the future, with all the money involved. If the pharmo companies etc are going to go on and on about high and low cholesterol, thank goodness there are people like you and others who will keep on and on too. Please, all of you who have influence in the medical, keep on with the attitude of ‘Here I stand, I can do no other!’ (Martin Luther), and they may yet be shamed down through sheer persistence! We who have no real influence can at least carry on refusing statins and talking to friends. It works, I know!
#Sue, on the subject of ‘fighting’ back, have you seen the film ‘Statinnation’ on Youtube – this is compelling and very easy to absorb info on the statin/cholesterol debate.
Yes I have, it was so very clear, it would seem impossible to argue against. I really cannot understand anyone who continues to support the statin/cholesterol issue. They must either be deliberately blind or too downright lazy to think things through.
A thought occurred to me today about the Framingham Study. In Ravnskov’s “The Cholesterol Myths”, Figure 2A on page 54 has two curves showing the distribution of cholesterol levels in those with or without CHD. The “with CHD” curve has a bump on the right attributed to FH. So I’m wondering why there isn’t a corresponding bump on the “without CHD” curve, which stops below 400 mg/dl. The bump looks like it represents about 3 or 4 people out of 193, which is not consistent with 1 in 500 having FH.
Also, Ravnskov’s statement about MRFIT on page 53 that the higher mortality in the 10th decile could be attributed to CHD caused by FH cannot be valid.
Does this mean that there is some other cause of very high LDL, other than FH, that does cause CHD?
The lipid hypothesis is a dead duck, it was never accepted by many when proposed, but was driven by vested interests who lobbied the politicians who made it public policy.
Have a read of Malcolm’s idea that CHD is driven by stress. I was a bit sceptical but the more I read around the subject the more convincing his argument becomes.
I’m also a big fan of supplementation, my ethos now is “chill out and take some vitamins”.
As the man said, “don’t worry, be happy…”
P.S. Equally compelling is Barry Groves idea that it’s exposure to sunlight that accounts for CHD – re: high levels of CHD in the North West of the UK compared to elsewhere.
So my ethos is “chill out in the sun and take some vitamins”…. or under a sunlamp (make sure it’s UVB – this is what converts chelesterol into vitamin d). 15mins every other day will do it.
P.P.S. Correction : David Grimes (Barry Groves was cool though – low carb, high fat.)
David Grimes presenting his ideas and some of his clinical experiences:
I have read “The Great Cholesterol Con” and I agree with the stress hypothesis, and I’m a sample of 1 to support stress = CHD. But easier said than solved; I still have living at home three children in their twenties, college graduates, and unable to find employment of any sort!
I’m not convinced about the sun connection; it’s a good idea to get 10-15 minutes of exposure to the midday sun, and there’s plenty where I live, near Baltimore, Maryland.
Alan, Sunlight in the north west of England? You’ve not lived there have you? Manchester and surrounding areas? – not known greatly for the sun! I was brought up there. Doesn’t mean the suggestion is wrong, just possibly move down south instead. I wonder if the folk down there suffer less from CHD? Be interesting to find out
The reason why low vitamin D is correlated with chronic fatigue and other “diseases of civilisation”, cancer and heart disease as main examples – is not because of the mechanism of vitamin D *necessarily* but because the light level is low that is therefore not making vitamin D.
Gilbert Ling proved in the 50s that ATP alone can not possibly the sole “currency of energy” in cells, pumping all ions against concentration gradients.
Structured water and light however do provide for these holes in energy.
Amongst other researchers, Jerry Pollack has proven that the water in cells is structured, but as with the cholesterol hypothesis, ideas about structured water become controversial because it proves the basis of pharma medicine is fundamentally wrong. Pharma based medicine is “riding on the back of a tiger” as the long awaited documentary film title says.
Also explains why certain diseases arent occurring at the equator. But do occur in Finland, Russia etc.
People there are purely dependent on clean fat burning in winter. If something poisons the mitochondria – then disease must happen – if you want to think slightly conspiratorially – population reduction for example – or creating disease to sell drugs to manage symptoms – then attacking the mitochondria would be a “good”=evil thing to do – it just happens that almost all trends in lifestyle, diet, technology and chemical use – do poison and destroy mitochondria with radical chain reactions.
Traditions that have been implementing very long – over one week – fasting or inedia, such as Hindu gurus and sects in India are of course near the equator.
EMF, high carb diet, circadian mismatch, sitting, too much “comfort” low activity / warmth – i.e. no cold tolerance, lack of good fats, DHA, trace metals – toxic metals filling the gaps – Al, Hg, Cd, Pb, As, too much Fe, Ni, Cu, glyphostate, DDT, atrazine, statins, low cholestrol, lack of natural B vitamins, lack of PQQ, vitamin K, vitamin A and E from organ meat, too much blue light, toxins from unacknowledged and undiagnosed infections – Lyme and similar Bartonella, mycoplasma/GWS, Candida, chronic EB and other herpes infections, mold toxins, list goes on.
Also > Amy Proal and Trevor Marshall for the interaction between Lyme and L form bacteria and vitamin D.
Dr Richi – what would ‘Weakly sensitive for mitochrondria’ mean ? Curious.
I must confess, I was just writing something (yet basically an honest contribution) to test if it is possible to comment on old posts – I was surprised.
I did a page search for the term “Weakly sensitive” and only got one match. It was your comment.
I was first to suspect that I must have wrote something retarded late last night – but I cant honestly find what you are referring to.
Problem with the format of “blog + comments” as opposed to the “DrMalcolmKendrick.com/membersforum” or Malcolm Kendrick plus guest contributions…
is 1. is the discussion closed?, 2. are people interested? 3 Is there a new point to make – that hasnt been made on an other page? – would take long to search for.
Am just catching up on some old posts in case people have discussed certain areas before or the opposite, if I could humbly contribute to an old thread.
It was a little test because if no one can comment, then no point and if no one gets alerts or cares about a comment, then no point.
Hence to explain this area would require a “comment” i.e. essay, much longer than the original post – which to presume to write impromptu to no one or people who prefer to discuss tabloid fearmongering about relative risk – well I would be the mental one, almost.
I believe my points are valid – if you want a mechanism – and proof, am not sure it exists outside of PhD theses or classified documents – not on a basic websearch.
If you search for “ubiquitination-8-the-mammalian-battery” you’ll find that egoist gas bag Jack Kruse spouting his theories. Without references, but charging a membership fee. Indeed he is the only reference to the same idea here:
“This is why health metrics in humans are always tied to high tissue DHA status. The more DHA you have in your tissues the more back up power source you have to generate a larger electromotive force in your mitochondria to generate the DC electric current. If your battery cannot hold the charge from the Earth of sun, for any reason, you get ill.”
Despite that, am sure there is truth here, meaning mammals get energy from light but in ways not accepted or comprehended by the mainstream – this would necessarily cross the woo-line, since rather than there not being references or science, I just think the evidence is well buried, classified or in Russian https://www.ncbi.nlm.nih.gov/pubmed/1667719.
Mammals can too get energy from light in ways known to science http://jcs.biologists.org/content/joces/127/2/388.full.pdf but this is unnecessary when you understand going around the Grand Tour of the Krebs cycle, and electron transfer chains and ATP recycling is NOT necessary – ATP can be also regenerated by light – see Russian reference
On the case of Prahlad Jani
Dr. Sudhir Shah, the initiator of the study and Neurologist at the Sterling Hospital said :
“Mr. Prahlad Jani did not take anything orally, neither fluid, nor water, nor food – during these 10 days of our project – and Mr. Jani did not pass urine or stool during these 10 days”.
“We are all scientifically educated and research orientated doctors. We racked our brains and it was the greatest surprise of our hitherto existing life… As if a bomb had hit us! The complete history of science has to be written anew. And our entire knowledge has been shaken to the core”
There are multiple theories about energy from light or the “quantum background/field” –
if there is a mechanism within current materialist thinking, it almost assuredly includes the mitochondria and structured water. If you think why food is meant to be needed – at the atomic level and below – then you can imagine how all of this is likely to be unnecessary given certain assumptions about life – i.e. evolving under the sun. Any mechanism to use energy from light would be more ancient than the first plant cell – and of course be conserved indefinitely.
The buzz word that Kruse and his cult followers use is whether one is “uncoupled” or not. I tend to agree without using these cool buzzwords.
Anyway a real discussion of this para-biology is “beyond the scope of this comment section, and probably this page”
Anyway, within this “pseudoscience” and “woo” is going to be a revolution in biology sooner or later. But for now it suggests some simple directions for research into CHD and mitochondrial disease – sunbathing, fish oil, iodine etc
PS just occurred to me that perhaps just living in the north west of England could be stressful? Joking of course – or am I?
Hi, I do in fact live in the northwest – Stockport. We suffer from a lack of sun generally – the last week or so has been a welcome exception! Grimes has made the link between lack of sun and consequent vitamin d deficiency and heart disease. It seems to me to be a good bit of reasoning, maybe Malcolm would like to comment on it?
By the way, whereabouts did you live in the northwest?
Hi again Sue,
Just re-read my comment regarding CHD & sun.
Your reply makes more sense to me now lol. I should have said that according to David Grimes LACK of sunlight causes CHD. What did you think of his video?
No I hadn’t seen David Grimes’ video re lack of sunlight, but having read your post, I have now. VERY interesting and it does make sense. It made me appreciate the fact that I now live in by the seaside, and can nip down to the prom and get a kipper bap whenever I want. Re where I lived in the north west, this is spooky – until I was married I lived about half a mile away from Manchester Airport, and then lived in Edgeley. You will know where that is if you live in Stockport!
Absolutely, used to live nearby in Davenport… before that sunny Brighton. How weird we’ve moved in opposite directions lol. I do miss the sun!
Hi Malcom. I have just been diagnosed with Kidney Disease and there seems to be some thought around that people with this need to keep their Cholesterol down. I have FH. Have read your books, been in trouble with the lipid specialist because I refuse to take anything. Would value your opinion. I am also a great fan of Zoe Harcombe. Will be listening to you in September at the Harcombe Conference! Meanwhile what do you think?
There is a thought, among all doctors, that cholesterol should always be kept down – in all conditions. It isn’t a thought, it is a pavlovian response. In certain types of kidney disease the cholesterol level becomes very high….it is a repair system.
Apparently I have had kidney problems all my life according to the Consultant that operated on me. But only had kidney infections in the last few years. So perhaps I don’t have FH but my Cholesterol is high because of the kidney complaint. Thanks Malcom. Quite an eye opener.
New to this blog, but familiar with the GOod Doc Kendrick and enjoyed “The Great Cholesterol Con”. Cholesterol is the most common organic molecule in our brain. Water is the most common overall. Cholesterol is never fuel, only raw material. The velvety , cholesterolly axonal membranes in the average human, if laid out, would wrap around the earth 4 times. Cholesterol was ‘discovered’ by proto-animals 3/4 of a billion years ago when animals were beginning and diverging from plants- plants have very little, just some for waterproofing. The human brain is so powerful because it is and exploits cholesterol, and the water it structures (see Gerald Pollack PhD.). Just an anecdote (but a mass of anecdotes is ‘data’)- the one person I know who has FH and ‘high cholesterol’ (no idea if hetero or homozygous for it), is the smartest most entrepreneurial, success I’ve ever personally met.
What you say is true. I am a bit worried my cholesterol level might be low (never had it measured of course), as a high cholesterol protects against Parkinson’s, MS, Huntington’s Chorea and – of course – dementia. (To name but four neurological conditions). You forgot to add that serotonin is made from cholesterol, as are synapses.
I thought serotonin is made of the tryptophan amino acid.
Dear Dr. Kendrick, I found out last week that I have heterozygous FH (ApoB mutation) by genetic screening. Since there was a suspicion for this I started reading books (Hartenbach, Ravnskov) and articles which of course make me feel a bit better (also this page, thanks for that!). I really worry about the damage in my body due to this mutation. I am apparantly an healthy man, age 40, normal BMI. I have no symptoms of any disease. My cholesterol is measured twice. First time TC=6.2, LDL=4.4, HDL=1.3. Two months later after dieting TC=5.2, LDL=3.9, HDL=1.09. Triglycerides were both very low.
My father also has this mutation, he is now 67, taking statins for I believe over 20 years. He never had heart problems. But my grandfather had multiple heart attacks, operations and a stroke, died 20 years ago in his 60s (FH-mutation was not tested).
I feel very bad with the knowledge I have FH. I am very scared and don’t want to take statins, but also think it is unwise not to do it in my situation. So basically whatever I do, I feel bad about it. What suports me is sites like this, the thought my father has no problems yet, and the fact that my cholesterol is not that high (I read that 10-20% of FH patients have not very high cholesterol levels and treatment with statins is not necessary).
I only don’t understand a few things, which I hope u can clear up for me.
-1- If the cells have not enough cholesterol, they increase synthesis of LDL-receptor. Why don’t they increase synthesis in case of FH? They can not have enough cholesterol, so if they increase transcription of the good and the bad allel equally, they nett increase the amount of good LDL-receptors.
-2- I certainly believe that higher cholesterol has a function and that lowering it in non-FH, healthy lifestile practicing individuals is mostly working against nature. But in the case of FH, the LDL-C levels are higher then they should be! So the higher LDL-C in FH-patiënts is always pathological, especially because it is elevated from birth!
-3- I have the idea there is something wrong with the logics behind the claim that if we screen a group of persons with CHD, and find that most individuals have FH, that it is the selection of CHD-patients. Why does the selection of CHD-suffering people has a bias on FH? Is it not strange that the occurence of FH in this group is so high?
Pingback: Cholesterol Primer - Page 10
Hi Dr. Kendrick. Please please please can we have some (a lot of) science for uswise. I am so thoroughly heartsore. My family carries Heterozygous FH and thing is my mom (with the disease) is turning 83 this year and she doesn’t have heart problems. BUT BUT … my son, my beautiful, clever son (he belongs to mensa – sorry I need lots of adjectives for this gentle, fantastic kid) is 34 and just this past Christmas had QUINTUPLE bypass surgery (without suffering a heart attack first – only fatigue and numbing fingers brought him to the doc). I went on LCHF diet on 1 February 2012 (only I did) and for the first time ever (even on every pill in high dosages) very quickly my numbers plunged to (metric) 6.1 (without meds it is 13 and never went lower than 8.8 on the worst of the worst stuff). Can’t find any other person of my ilk in cyberspace who had gone onto this diet – they are terrified. But my son! and no-one talks about the elephant in the room, my youngest also has it and no-one says anything because SURELY nothing will happen to our Jake, who is now 28. I feel so floored and really -QUINTUPLE bypass? never heard of it, but now I know that means almost every artery beyond the chest wall has been grafted into the aorta, or some such. Help us please. Tell me that I’m right about my diet – MY doctor was astounded with my numbers and said the blood cannot lie – so do we or don’t we. Michael’s surgeon and cardiologist are morosely against any fat for him. It’s a case of off to the low fat nutritionists and don’t forget your statins (which he didn’t even bother to tell them, gives him rhabdomyolises within a week – he will much sooner die of kidney failure on those – so he kept quiet and left) and never returned, not even for his follow-up. My happy boy is crest-fallen and I can’t find anything. Thank you for your goodly writ.
Can’t help wondering. Is FH really ‘genetic’ or is it nutritional? After all, families often eat a similar diet – and have dietary ways handed down through maybe two or three generations.
We now know how problematic modern grains, especially wheat is for many. And in its modern form it has been eaten for several generations, as too have processed seed oils and margarines.
It is easy to put a ‘genetic’ label onto these seemingly ‘familial’ diseases, but we are the product of not only two World Wars with all their rationing and nutritional restrictions but also high degrees of food-meddling and factory-based ‘food industry’ processing and procedures.
As Ocean Robbins said recently on a broadcast, the ‘Health Industry’ is not interested in food, and the ‘Food Industry’ is not interested in health. And we are all piggies-in-the-middle of it all…..
All topics covered in the latest book of french veteran cardio researcher M de Lorgeril: The new mediterranean diet