A meta-analysis including 530,525 people, partly funded by the British Heart Foundation, and published in the Annals of Internal Medicine has just come to this conclusion:
Conclusion: Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats1.
Or to put it another way, there is no evidence that saturated fat consumption has anything, whatsoever, to do with causing heart disease, or strokes. Once again I get to say ‘I told you so.’ Ah, the four most satisfying words in the English language. That is, when arranged in that particular order.
So, eat butter, drink milk, and throw away the horrible sugar-loaded low fat yoghurt. Go to France and enjoy the highest saturated fat diet in Europe and you, too, can enjoy the French rate of heart disease. Yes, of course, the lowest in Europe.
But now what happens? You see, the entire edifice of the cholesterol hypothesis is held together by two links in a chain. Link one is that saturated fat consumption raises cholesterol levels. Link two is that raised cholesterol levels then cause heart disease.
Various ‘experts’ have simplified this to the very simple equation:
A (saturated fat in the diet) > B (high cholesterol levels) > C (heart disease)
This is the cholesterol hypothesis, or the lipid hypothesis, and it has driven medical thinking for the last sixty years.
I have had it painstakingly explained to me, by very clever people, exactly how saturated fat raises cholesterol levels. Indeed, you will find ‘evidence’ for this almost universally accepted fact in literally thousands of clinical studies. Here is what Wikipedia has to say on the matter
‘There are strong, consistent, and graded relationships between saturated fat intake, blood cholesterol levels, and the mass occurrence of cardiovascular disease. The relationships are accepted as causal2.’
Okay, let us accept that eating saturated fat does raise cholesterol levels. However, if consumption of saturated fat does not increase the rate of heart disease then….. Then raised cholesterol levels can have nothing whatsoever to do with causing heart disease. Just keep chasing the implications of that statement around in your head for a while.
So what happens now? We now have a cholesterol/lipid hypothesis that just had its head blown off. Yet, it still continues to wander about, unaware that it is actually dead.
As everyone knows you can chop the head off a chicken and it can wander about for years. I was also informed, when I was an open-mouthed child, that you could shoot a dinosaur through the head and it would continue to blunder about for some time, the rest of its body blissfully unaware that it was actually dead.
Well, the cholesterol hypothesis has just been shot dead, but I suspect it will continue to rampage about, stomping on puny humans for many years, before it finally keels over and admits that it is dead.
But I say, farewell Cholsterolosaurus. You are now a deceased hypothesis. Gone to meet your maker. You just don’t know it yet. Because the people that believe in you do not understand logic.
1: http://annals.org/article.aspx?articleid=1846638
2: http://en.wikipedia.org/wiki/Saturated_fat
Dr. Malcolm Kendrick 
It has been a long time coming but the truth is finally being recognised. Now all that needs to be done is to re-educate the public so that food manufacturers change and medical practice reflects new findings. How long will all that take? Keep up the pressure, Malcolm.
But is high cholesterol bad for you?
Carol Ann Baxter
Document Specialist Supervisor
DAC Beachcroft LLP
T: +44 (0) 113 251 4728
No
Cholesterol is vital for every single organ, for every hormone secretion, and for every cell in your body. It is vital, so, no, it can not be bad. It is life essential.
But the statin makers need not worry that their toxic drug is being dismissed re: cardiac health benefits….’cos the BBC are doing a great job this morning advancing yet another use for statins. Rest assured, once that case is ultimately discredited, there will be another following closely behind. How long before they are used to cure in-growing toe nails? The factories are there making statins, so there must be something they can be used for, for goodness sake. Our precious NHS is the innocent pusher in this sorry, sad fiasco.
Yes I noticed that on one hand they were telling us the ‘sat fat v unsat fat’ story and then I read their story about another use for statins. It is as if they just have to find a way to keep statins top of the drugs table whether or not they are any good.
But is high cholesterol bad for you. And is high blood pressure bad. My cholestorol is 8. I take high blood pressure medication. Doc wants me to take statins.
women with higher cholesterol levels live longer than those with lower cholesterol levels
So 8 isnt so bad. Trying to lower it by diet and losing weight. I have been reading your book so not sure diet is going to lower it. So confusing.
go out in the sun, check your thyroid hormone levels.
Thanks. Cheking thyroid hormone levels doesnt sound good. That will also put me on meds for live if there is something wrong there. Do I just ask the doc for this test.
I think it is worth doing
Thanks I see this can also cause high blood pressure. Been reading about the test and GPs reluctant to test for it. How much does your clinic charge for the test. I live in Leeds.
Carol. Give the clinica a call. The contact details are on my home page. Cheers
Carol,
It was in 1976 researchers identified oxidation of cholesterol as the cause of heart (really ‘arterial’) disease.
It has taken a while but homocysteine (a regular amino acid the body must live with and manage) is now reckoned to be the candidate that can commute oxidative stress to cholesterol and thus ‘damage’ it – much like rust degrades your car. Those cholesterol numbers cannot matter much
You may do well to have an extended consultation with a qualified medical practitioner who understands cholestane triol is atherogenic, while cholesterol is not atherogenic , and that elevated homocysteine is a risk factor in several chronically degenerative conditions due (in all likelihood) to its capacity to oxidise cholesterol. A practice that tests for homocysteine and can interpret results is an essential prerequisite.
In addition the practitioner/practice should have some knowledge of methylation cycles and how they process some of the natural by-products of metabolism that can be toxic if they are not properly processed. knowledge of the bioelectric aspects of physiology would be good, and concern for ‘free-electron deficiency’ would be excellent.
Anything that is a drain on the methylation cycle is a risk factor for several chronic diseases, and risks factors can be physiological, lifestyle, diet, or environmental. Cortisol is a big connection as is the HPA-axis. The stress hormone cortisol, which should follow circadian rhythms that are seasonal and diurnal commands helpful endocrinological cascades that are helpful when in rightful balance, but unhelpful if knocked out of balance.
The practice of ‘Earthing’ helps normalise balance and rhythms of cortisol, so does ample sleep (9-10 hours) and limiting exposure to artificial light is a must, because light received by the retina sends signals that bear upon cortisol levels and rhythms.
Follow the links, have a bash at making sense of what they say, print them off, and take them with you when you go for your consultation.
I cannot recommend a practice that meet all these criteria, but several private practices may test for homocysteine. ‘Clinical Edge’ offer homocysteine testing.
More than anything these steps should put your mind at ease, but suitably informed practitioners may pick up on issues that may warrant attention and may be fixed with naturally oriented fixes, as opposed to pills.
Other than offering direction I cannot dispense medical advice, my qualifications make me a knight of the road and no more.
Click to access methylmagic.pdf
Click to access Ghaly__Teplitz_cortisol_study_2004.pdf
(Ghaly, the lead author of this paper was a sceptic when presented with Ober’s ‘earthing’ idea and set out with intent to prove Ober wrong!) His results are another piece of a puzzle of several pieces.
In addition to those links Dr Kendrick may appreciate these slides. Interesting to imagine how Jerry Brunettis narrative might run with them, but note reference to Advanced Glycation End-Products (AGEs) and a term that is new to me if familiar in concept — ALEs (Advanced Lipoxidation End-Products) which meshes with the findings of the late Barry Groves.
Click to access Deep%20Healing%20Doctoring%20the%20Mighty%20Mitochondria.pdf
Cut back on carbs and do not over-consume omega-6 PUFAs, methinks.[I guess that’s in accord with conditions in the stone age when additionally free electron deficiency would be rare, sleep was plentiful, and artificial light was not an issue.]
Oh Christopher!!
What a great answer, and what I would give to have a GP who had an inkling about plain old food let alone the intricacies regarding physiology as mentioned.
And as to taking a Google print-out to a consultation, God forbid! We hear on the news that GPs are working under great strain and are underpaid…..now come on….there is no tickey box payment for reading patients’ Googlies….so that is out of the question.
On the other hand, they are of a mind to suggest to us to look stuff up on NHS Choices, there being not enough time to explain anything to us, (honestly, it happened to my relative, who was given a rarish diagnosis).
And anyone reading Dr Briffa’s blog today, re NHS Choices re Salt, can only be painfully dismayed at what has become of the system which we were brought up to cherish.
So, Christopher, I am pleased to be educated by such info gleaned on the internet, but I wouldn’t raise folks’s expectations that they will be able to educate their hum drum medics, let alone get the type of tests done that you, quite rightly, suggest we ought to have done.
High cholesterol is not bad for you. It is beneficial. I will not get mine checked nor do I worry about any arbitrary numbers.
High blood pressure is something to be concerned about though. When I started eating mostly saturated fat from meat, fish, butter, lard, eggs, eggs, eggs, etc. and cut out most carbs, my blood pressure went down to normal within two weeks.
Well said. Do the cholesterol, fat hypothesis believers also think that the earth is flat and that the only way to save humanity is to take Statins ?
Or maybe the statement could be misconstrued to mean “So no matter what you eat you’re gonna get heart disease, so if you just keep taking these statins I’m sure you’ll be better off….in the long run….possibly.”
When I show this to my doc I’m almost sure that is what he will say!
I read about this yeasterday and had to raise a small smile at the public response by the British Heart Foundation. Did they enthusiastically endorse their findings? No, no, no…
The appropriate quote is given below:
“Professor Jeremy Pearson, associate medical director at the British Heart Foundation which co-funded the study, said: ‘This analysis of existing data suggests there isn’t enough evidence to say that a diet rich in polyunsaturated fats but low in saturated fats reduces the risk of cardiovascular disease.
‘But large-scale clinical studies are needed, as these researchers recommend, before making a conclusive judgment.’”
http://www.dailymail.co.uk/health/article-2582867/Saturated-fat-DOESNT-cause-heart-disease-all.html#ixzz2wOmOMijG
A real grant request operation – more study required plus an element of putting off the evil day of truth.
The recent sudden finding that sucrose is bad for health is another example of ignorance of past research. IT IS NOT NEW! Yudkin back in the 1960s-70s showed that sucrose was “Pure, White and Deadly” (his book title) but was ignored in favour of Ancel Keys “Emperor’s New Clothes” promotion of hicarb/lofat/low cholesterol (aka commercial benefits to pharmaceutical and food companies)
All well and good and a huge relief that we’re not all eating badly, but what about every person who has been put on cholesterol tablets? Do we just come off them? Do we go to our doctors to be told that nothing’s been proved yet, even if it has and then the confusion? Greater to be told that high cholesterol doesn’t lead to heart disease but now what?
Stay on them if you think the probability of benefit to you as a person at p = 0.003 (3/1000) is worth it. Personally I do not the odds are worth it but then having suffered adverse reactions………….
If I were in that situation, where I had started to take statins, I would stop immediately and start eating lots of eggs and other healthy saturated fats. I’ve read up on stopping statins since I know so many people who take them and the article said statins can be stopped immediately. You do not have to be weaned off.
Blood pressure medication takes weaning off.
I would get off, wait several weeks on a new diet approach and then go to the doctor to have blood work done. I would however not tell him what I am doing. But then that’s what I would do! Let they food be they medicine and they medicine be they food ~ Hippocrates
Rosie, My husband took himself off statins because he was having bad pains in his legs. When he went to the GP he was asked to sign a disclaimer to the effect that he had been advised he should continue on statins. How scary is that? His side effects weren’t reported to the relevant body either. I wonder how many others aren’t?
Unfortunately it is likely the current drive to ensure more people are exposed to statin therapy is likely to continue in spite of the lack of independently produced evidence.
I find it particularly distressing the elderly vulnerable people are the most likely to be the victims of statinization. This new paper confirms earlier findings.
Low Levels of Low-Density Lipoprotein Cholesterol: A Negative Predictor of Survival in Elderly Patients with Advanced Heart Failure
C o n c l u s i o n
Low LDL-c levels are associated with a reduced survival in elderly patients with clinically controlled moderate and severe HF.
Statins were independently and significantly associated with a higher risk of mortality
You can’t save everyone Edward. Just make sure your friends and family are on the lifeboat
Yes, and I always wear MY life-jacket… – The big fat, bright yellow one…with “Cholesterol” written all over it ! ;))
I think the return to business as usual is already apparent! Thus in Fergus Walsh’s piece on the BBC, we read:
“It should be pointed out that the authors freely admit their research is inconclusive – the BHF wants to see more studies before anyone considers changing dietary advice.”
http://www.bbc.co.uk/news/health-26622399
Nowhere in his article does he even mention Ancel Keys famous cherry picked graph!
A little later Fergus Walsh tells us:
“The key to a healthy heart remains a balanced and varied diet – with a strong emphasis on vegetables and fruit. Add to that exercise and not smoking.”
To me, that smoothly conceals the central issue – that we were all advised to greatly reduce our intake of saturated fat for decades, and now they can’t find any evidence to back that up! Journalism is supposed to be about pulling out the unpleasant conclusions that others would like to hide – not giving them a helping hand!
It is interesting to imagine how someone might take the raw data and fix it to say the correct thing. Perhaps those in the studies who adopted healthier diets, worried so much about their health that the extra stress predisposed them to heart disease – thus cancelling out the benefit that was conferred by cutting down on saturated fats!
The BBC used to be lauded the world over for being neutral and putting both sides (or all sides) of an argument. But it has been a long time since that was true (if it ever really was). Now they post articles on their website and make programmes for TV that are bland, avoid controversy, don’t rock the boat, don’t upset the government of the day (most particularly if the government is Conservative), and generally have as much substance as candy floss and clouds.
I got this PLOS study yesterday. Of those that took statins one in four had adverse reactions. Palamaner Subash Shantha G, Ramos J, Thomas-Hemak L, Pancholy SB (2014) Association of Vitamin D and Incident Statin Induced Myalgia—A Retrospective Cohort Study. PLoS ONE 9(2): e88877. doi:10.1371/journal.pone.0088877
On the Wright Stuff (channel 5) today Dr Rosemary Leonard (express correspondent) was claiming that adverse reactions to statins was rare! Clearly a Big Pharma KOL.
Best wishes
Mike CAWDERY
________________________________
I thought a while ago that it wouldn’t be too long before some ‘backtracking’ would begin, but it came sooner than expected! First the “hey,you know what, we think it might be sugar that’s the problem” not much said about the fat at this point. Now it’s “oh look, we’ve discovered it isn’t the fat after all”. The low fat diet related food industry must be quaking at the knees at what’s coming next. I suspect we’ll see a flurry of articles in the news from the cholesterolasaurus lovers desperate to save it’s sorry little life.
dam it….shouldn’t have read this before going to bed as i can’t stop laughing
PS. Oh sorry, I worded the last post incorrectly. I should have said that they would be desparate to revive the cholesterolasaurus, because of course it’s DEAD!
Except… sugar in and of itself isn’t the problem. It’s highly processed fat and highly processed sugars.
See that Sue ? – Even you didn’t realize it was extinct! What chance the True Believers ???
Goodbye-ee!
Cholesterolosaurus – I’d love to see that word enter the Oxford English dictionary.
It should be put in a cabinet of curiously untenably beliefs, next to phlogiston and luminiferous aether.
Dr Kendrick, when you say that you accept that dietary saturated fat may raise blood cholesterol levels, aren’t you implicitly accepting the idea that there is a single thing called “cholesterol” that is medically significant? Surely some lipoproteins may rise, while others fall? As long as the medical establishment continues to believe that it can meaningfully measure “total cholesterol”, won’t it go on blundering up the blind alley of the lipid hypothesis?
Tom. You are right, of course. There is no such thing as a cholesterol level, really. But explaining lipid metabolism is a bit complex, and most people just fall asleep when such things are described. My blog is, by its nature, a bit broad brush.
Let it not be forgotten that when transplant surgeons where in search of an immune suppressor that the most potent discovered was PUFAs! When plague was analysed it was discovered that a massive 70% arose from PUFAs. It is also stated that MUFAs, olive oil in particular, causes masses of those nasty wee free radicals that are bodily harmful. We are also informed that cholesterol provides the body with its essential hormones which produces us with that feel-good factor; need more be said? I will stick to my steaks with lashing of saturated fats thank you!
Apologies for the obvious spelling error folk (stupid spell checker)!
Dear Dr Kendrick,
The Fanatic Cook suggests that “A Meal High In Saturated Fat Increases Inflammation”:
“This post describes a study that found eating a meal high in saturated fat increased systemic (whole body) inflammation. Consistent, low-grade inflammation is thought to contribute to atherosclerosis, and so, to heart disease”:
http://fanaticcook.com/2014/03/17/a-meal-high-in-saturated-fat-increases-inflammation/
If this is true, might those of us who haven’t bought into the high cholesterol theory of heart disease and eat high fat diets want to keep an eye on our CRP. My experience is that in my ten or so years on a high fat diet, the annual measure of my CRP has been below 1 (.3 in my last several physicals). But if true about the CRP’s spiking after a high fat meal, might that be of some concern, even with the CRP measure’s being very low otherwise?
Regards,
Dave
Inflammation might be good, it might be bad. The most potent anti-iflammatory agent known to man is cortisol (made into corticosteroids a.k.a. steroids). Steroids vastly increase the risk of heart disease, as do many other anti-inflammatory agents
Not all inflammation is bad, as it is created by the body when the body needs to heal itself. Too much of any substance that stops this process can be a problem. Plants and sugar can make us feel better, reduce our pain, but that feeling too good or too high, much less pain, comes at a price. Aspirin can reduce fever and pain, but too much and you can bleed to death.
Protein is especially needed for the body healing itself. The body can get stuck-into just more and more inflammation if the healing is too much interfered with, or too much sugar and toxins keep the body in perpetually trying to heal itself, when no nutrients are present. Meat and fat are said to be inflammatory, but the article explains that they start the inflammatory response (which is needed), but also determine the switch to the next phase, the resolution of the inflammation.
http://www.nutritionandmetabolism.com/content/9/1/32
http://woundcareadvisor.com/how-dietary-protein-intake-promotes-wound-healing-vol2-no6/
http://www.nursingtimes.net/home/clinical-zones/wound-care/understanding-wound-inflammation/205361.article
http://en.wikipedia.org/wiki/Inflammation
Malcolm,
I love the way you are undressing the emperor.
Thanks. But he seems to have a lot of invisible cloaks up his sleeve.
…. must have access to the global warming wardrobe.
The American Heart Association responded by stating that they will not change their guidance. Their cognitive dissonance is showing. They state that this meta-study only highlights that we don’t have enough evidence, then they state that “we must rely on existing science that suggests that saturated fat is atherogenic.” Even though the “existing science” they reference is the same science the meta-study just took to task. http://blog.heart.org/study-raises-questions-about-good-and-bad-fats/
It woudl be funny, if it were not so serious. It just shows that effective brain programming is irreversible.
I think it’s more vested interest than cognitive dissonance that drives the debate.
Big pharma don’t pick the footsoldiers they pick the opinion formers and woe betide anyone who disagrees with them, careers can be ruined. All the sciences are the same, higherarchial, sadly most scientific opinion is formed by paying scientists to promote the required. Many empires have been built and most of them have become so large as to be virtually unassailable.
Afterthought, as Malcolm asserts it’s dead but rest assured it not going to lie down any time soon.
I used to have a colleague who talked darkly of anyone whose work wasn’t “mainstream”. Fortunately he was rather stupid and nobody respected him. But what if someone clever, in a position of power, had had that dim belief? Trouble.
They are already questioning this study, because it is a study of studies. In some of the studies the participants self reported what kind of fat the consumed. They are saying that the participants were too stupid to correctly report the kind of fat they consumed.
This is just like the UCLA study that showed 75 percent of those hospitalized for heart attacks had low to normal cholesterol. Their conclusion, reduce cholesterol even more.
http://www.fathead-movie.com/index.php/2010/03/02/ldl-nonsense-is-taxing-my-sanity/
Ignore the facts, nothing to see here, move along.
Well stated Dr. Kendrick.
Here are some questions that I have never found an answer to with regard to so-called “familial hypercholestrolemia” where it has been thought, or said, that the person’s overall serum “cholesterol” level is grossly abnormally “high” and can thus lead shortly to death in those unfortunate souls who are said to “have” it.
In light of what is becoming known about the now-discredited lipid hypothosis, do you think “familial hypercholesterolemia” is (or was ever) a legitimate disease state (i.e., based purely on some supposed cholesterol numbers)? In the course of diagnosing such an (alleged) malady, is it known whether an effort has ever been made to distinguish between the types of LDL particles – e.g. large particle vs. small particle? Or between HDL and LDL? If HDL is considered by mainstream medicine to be “good” cholesterol (vs. the supposedly “bad” LDL), was the HDL number at least subtracted from the LDL number in order to determine whether there really was a problem?
I guess what I’m thinking at this point is that “familial hypercholestrolemia” might in some cases (all cases?) be something much less (or at least much different) than what meets the eye of a lipophobe? Along the same line, I’m also reminded of the adage to the effect that when the only tool a man has at hand is a hammer, every problem starts looking like a nail.
Warm Regards,
Wil from USA
The closer I get to the end of school the more worried I become about adhering to guidelines and what might happen if I don’t. This is one of the biggies for me.
I know you in the UK have much higher standards regarding the processing of meat and the hormones/feed used to feed the animals before slaughter but here in America I really think there’s a huge correlation between factory farmed meats, simple carbohydrates and sugars, and heart disease. I don’t think it’s the meat as much as how it’s made ready for the table. I think the sheer numbers of simple carbs people eat (and we know they raise triglycerides mightily – and high triglycerides are somehow connected with higher levels of heart disease) along with meat from animals raised in factory farmed conditions, as well as general levels of NON activity contribute far more than realized.
It’s too bad there couldn’t be a large study comparing people who eat grass fed meat and high natural fats like butter and cheese against those who eat factory farmed stuff. I suspect there would be a difference even after allowing that someone who chooses higher quality foods probably also exercises more.
Um, and we get a wee bit of horse in our meat too. Delicious. But joking aside: a young friend was recently on his first business trip to the US and had to reject several main course as being unpalatably sweet. Mains!
As for factory farming, my wife won’t buy factory-farmed chicken, principally on grounds of cruelty. If we get a health benefit in addition to better flavour, yippee!
So if half a million people isn’t a big enough study, what would be?
On a different point, I wonder if perhaps there is a big silent medical majority out there… I told my GP today that I’d stopped taking statins, expecting him to argue with me – he just said, “Fine, there’s no easy answer..” (i.e. to controlling CVD), which left me wondering why he and his colleagues had been so keen for me to take them in the first place!
You lay contradictory studies on the Procrustean bed. If to small they must be stretched, if too long, bits must be chopped off. No study can be the correct size to fit.
On a financial note. I suspect that the potential change in health advice, could blow the food manufacturers into total turmoil. How much have they invested in “low fat” junk over the last 40 years??? How can they “unpick” this?? Poor old Flora and Benecol – what will their angle and sustainability be without a place in the so called “heart healthy diet”
OOOh, I hope so. I want my food to be about delicious and natural, not about some sort of cardboard/benzine substitute that lowers a biomarker I could care less about and tastes like vom.
Get TWo teaspoons from the drawer fill one with BUTTER and one with MARGE place them in the shed ,or outside for three days , then tell me which one is left when the BEE’s have finished having a go at them. That will answer your question.
This hypothesis works quite well under one, quite broad assumption: that people eat modern, agricultural diet. Your question actually dives way deeper than cholesterol. It goes to the heart of the question: What is the natural, evolutionary determined human diet?
I, personally for the last 12 yrs am on a diet that challenges both and my (anecdotal but science supported) results speak to both issues. I predominantly eat animal fats, fats and proteins. You could call it Atkins, low-carb, paleo,… but essence of it is not eating carbohydrates unavailable to us without invention of farming (which is evolutionary recent). Metabolically speaking, my metabolism is keton(ic). In modern science, assuming that agricultural diet is normal experts call it “starvation diet”/”starvation metabolism”. I would claim it to be a natural, evolutionary developed normal human metabolism.
My personal results over 12 yrs match with scientific expectations: despite eating all kind of fats in great quantities, my total cholesterol was falling for about 1 yr and than stabilized at very healthy levels (both as total and good/bad/…).
One must underline that scientifically one must expect exact opposite result if significant amounts of carbs/sugars/grains/… were eaten along. That is the difference. Yet, modern medicine is reluctant to spell it out.
So, fats and sugars together is the key. Eat that and you’ll eat diet human species is NOT accustomed to, yet. Eat that and you’ll cause cravings for carbs (as it should mimicking Fall diet of plenty resources in preparation for lean Winter) and related weight gain and likely diabetes. Eat that and your cholesterol will indeed raise with all consequences.
You nailed it. The carb craving is so universal it may have been an evolutionary necessity to get us through the lean times (winter). So the insulin respone to a carb load would be vital. Rapid ingess of glucose into the blood stream is toxic: a swift release of insulin to rid the blood stream of glucose would be a good thing! The liver and muscles become full od glycogen, the rest goes off to the adipocytes- they are NEVER full. Carbs result in a response that is meant to be short lived and our bodies do not expect to see this response repeated 3 to 4 times a day ALL YEAR LONG!!! When our physiology has to cope with a constant insult like this, trouble occurs. Homeostasis is disrupted: Nature hates that.
Modern medicine is reactionary, not visionary: i.e., DO NOT disrupt the staus quo. After all, we must show that endless studies repeated over and over again until they meet the satisfaction of the Professorial Gods, finally PROVE that A is better than B. This cannot be achieved with any degree of scientific integrity in the usual epidemiological studies that are used to prove what foodstuffs cause heart disease. Or that statins don’t work; or are dangerous. Not enough studies; not enough studies. How many times have I heard that one?
Vested interests need to be exposed. Rip off their flimsy garments and expose their “short comings.” We are on the verge of getting the truth out. This is an exciting time to be involved in this part of medicine.
Malcolm, I like to get big with my arguments nowadays. I just say, “you know,, someone should tell the French and the Swiss that they should all be keeling over, because they don’t appear to have got the message.”
I like it. Those damned foreigners just don’t know what’s bad for them.
Sadly the statinators are casting around for new markets for their drugs. Advanced MS sufferers are the next target, apparently.
http://www.independent.co.uk/life-style/health-and-families/health-news/surprise-discovery-shows-multiple-sclerosis-sufferers-lives-are-significantly-improved-by-taking-statins-9200117.html
Clever right? Target a group whose symptoms would surely be hard to distinguish from the side effects?
Get the early stage MS sufferers out into plenty of sunshine, give them large daily doses (20-40,000 IU) of vitamin D if that isn’t possible (or even if it is) and they won’t progress to late stage.
But statins are for [i]late stage[/i] MS. Oh, I know, don’t prevent progression.
….and buy Terry Wahls latest book
Pingback: Although now dead, the Cholesterolosaurus will march on | Bydio
We can keep the cholesterolasaurus alive a little longer if sugar raises cholesterol, because now they’re looking at sugar, it’s starting to generate CHD ORs that lipophobes only dreamt of attaching to fat.
So high cholesterol from sugar is a bad thing. Mainly because that much sugar is a bad thing anyway.
Sugar IS the demon. Until sugar began to permeate the human diet in large quantities, coronary thrombosis was almost unknown. There was, apparently, a 20 year lag between an big increase in sugar consumption and the appearance of coronary artery disease (smoking a separate factor). Yudkin went into all of this as did that much maligned man, Atkins. I still have the 1992 book and in it he outlines his theories about coronary artery disease and it’s totally spot on. Every line. Of course, so was Yudkin.
The answer was simple all along.
Insulin is the big key everyone was looking for. Insulin drives hunger, and obesity, and artery damage and coronary artery disease and metabolic syndrome. It, in turn is driven by sugar/carbs.
It’s that simple. How this happens is irrelevant because by dealing with this fact, it’ll all go away.
The Triad is therefore, Hunger, Insulin, Sugar.
I do not think it is that simple
If sugar caused CVD, why did heart attack rates (corrected for age and smoking) collapse from the sixties onward? The notion is clearly wrong.
Yudkin thought that sugar changed blood lipids in a bad way. To be fair he did show that fructose raises cholesterol. But having low cholesterol is pretty bad news, and having a simple mechanism for raising cholesterol seems like really nice thing to know about in that light.
To my mind, really most of the the war on sugar in the extreme camps where a banana is given the same status as a hfcs soft drink, is just another squirming tentacle of the lipid hypothesis.
Dr Lee,
You may find it interesting to read into the methylation cycle.
Several stress provoked biochemical stressors require the donation of a methyl (CH3) group to ‘detoxify’ their radical aspects. B complex vitamins are big donors of of methyl groups (CH3). It is as if oxidative stress may rise up hierarchically, and poor detoxification by compromised ability to ‘detoxify’ through this methyl donation appears to permit oxidative stress to climb the hierarchy steps. In the event if aspects of the HPA axis are communicating stress, and if cortisol may be high, demands on detox by methylation may be high, and the count of antioxidant ‘methyl donors’ may not match demand. It seems in this instance metabolism of homocysteine (by methylation) may be inadequate, permitting homocysteine levels to rise, and homocysteine, it is said, ranks of one of the most powerful oxidants in the body we know of. On contact with cholesterol homocsyteine is said to be capable of converting (oxidising) cholesterol to oxycholesterols including the highly atherogenic cholestane triol.
Pleas, do not take my word, but it’s my belief the contemporary state of the homocysteine theory runs along these lines. Cholesterol is not at all atherogenic (Imai 1976) but cholestane triol is.
The capacity for methylation can be compromised by too few donors (poor supply), or by the proliferation of radicals in need of a donor (high demand).
I’m inclined to agree, high supply of glucose (from excess carbs), scope for lost of AGEs, scope for lots of ALEs, and hyperinsulinemia, likely feeds into the oxidative stress as it closes upon atherogenicity, but I haven’t read into these aspects yet, hence I don’t actually ‘know’.
You’re over-simplifying it. Sugar is NOT the demon. Highly processed fats and sugars are.
How do you know?
I am following the whole cholesterol-diet-heart disease-statin debate with great interest. I’m male, 52, and had a heart attack a year ago, resulting in two stents to fix blockages in the LAD and LCX arteries. At that time I considered myself in pretty decent shape for my age – I exercised regularly, my weight was about right, I had a good diet, used to smoke but stopped 17 years ago, no history of anything bad health-wise in the family history. Of the usual causes for a heart attack, high cholesterol was the only box I could tick. At the time of the attack my LDL was 4.5, HDL 1.8 and tri 0.6. Overall 6.6 – quite high in other words, though not astronomically high. I had also had detailed health check-ups about 1 year before the attack, 3 years before and 7 years before. I was given a clean bill of health each time except for high cholesterol, which was similar to the level at the time of my attack for each check-up. In other words, I’ve had fairly high cholesterol for years, and probably for most of my adult life. Naturally then, when I had the heart attack cholesterol was deemed to be the main culprit. I’m glad to say that today I feel in just as good health as I did prior to the attack, though obviously some damage must have been done and I don’t like the fact that I now have two stents in my heart. Following the attack the doctors here in Hong Kong prescribed a daily course of aspirin, a beta-blocker and of course a statin (also an anti-coagulant but I’m already off that). I don’t like medication generally, and I especially don’t want to be taking statins if they are doing me no good. I’m tempted to stop taking them, because from what I’m reading here and elsewhere there is no point in reducing my cholesterol level – cholesterol was not to blame. But how can I be sure that my high cholesterol level was simply coincidental? And if cholesterol wasn’t to blame for my MI, then what did cause it? And if I forget about trying to control my cholesterol level, what then should my strategy be for avoiding another attack? Apologies for the long post, but this is important stuff – and not just for me.
Your questions are very pertinent to you, and many others. If not cholesterol, what? There are many other competing hypotheses out there. The current favorite culprit it sugar. The ‘sugar hypothesis’ has some merit – no doubt. However, moving back to your situation. If the only risk factor you had was raised LDL/cholesterol, even if the current orthodoxy is correct, you only had a very marginal increased risk. (Average cholesterol in Switzerland is 6.4mmol/l and they have the second lowest rate of CHD in Europe). In fact, if you fed your risk factors into the new US risk calculator you wouldn’t, yet, trigger to go on a statin – had you not already had a heart attack. In short, your heart disease is due to something else. I don’t know what, and I do not do individual ‘consultations’ on-line. However, my own view is that negative ‘stressors’ enough to overwhelm your neurohormonal homeostatis create a series of pathophysiological steps that will lead inevitably to a heart attack/severe narrowing of arteries. To oversimplify horribly – call ii stress.
My heart attack, which was entirely unpredicted and unforeseen – average cholesterol levels, active, lots of exercise – followed a period in which I had narrowly escaped being mugged while traveling alone in Italy, had to fly back (I hate flying, and the plane was delayed, diverted and the journey full of complications) at short notice because my partner was in intensive care with kidney failure (now thankfully recovered) and my much younger brother was then admitted to hospital with liver failure and was clearly dying. My stress levels must have been astronomical and there is no doubt in my mind (and my GP’s mind) that they played a hugely contributing factor in the MI. I think we should be looking harder at the role of stress, as you suggest.
But, doc, how would that explain the rise and fall of heart attack rates? Did stress really rise 1920-1960 (roughly) and fall thereafter?
You may have noticed, in the USA at least, mass immigration, the great depression, then the second world war.
Well I did simplify it somewhat. If you want the fuller picture as I believe it to be.
Sugar plus refined carbs cause metabolic syndrome in those who’re genetically insulin resistant. They get higher insulin levels in response to carbs. They trap their lipids in cells thus, stimulating hunger and they get fat. Their higher average and spiking blood sugars cause a low-grade inflammation in the arteries, facilitating a leakage of small particle LDL into the wall of the artery, initiating the plaque. At the same time, the consumption of sugar (as demonstrated by Yudkin) makes the blood more liable to clot, with platelet aggregation etc. Not only that, but it is the ingestion of sugar/carbs which turns the cholesterol bad, i.e. raises the TG, lowers the HDL and promotes the small particle portion of the LDL . So, the attack is from three sides as it were.
Thrombosis, Leak and burrowing cholesterol.
Statins do work but it’s highly probable that their main function is other than the lowering of cholesterol, i.e. anti-inflammatory. This was shown in a paper by Murphy, Vaughan and Buckley (from Cork, I know all three) in the Lancet in 1996. They weren’t sure how they worked but they were full sure it was far too fast for the lipid reduction to have worked.
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Many thanks for your reply Malcolm. Yes, I have been wondering whether stress might be the cause. The things is, I wouldn’t say I fall into the classic notion of someone who is stressed. I don’t have a stressful job and I don’t have a stressful life (no kids!). My wife and I earn good incomes and live in a nice apartment. I walk my dog to the local beach each morning before I go to work – all in all not a bad life. Having said that, perhaps I do suffer from stress in a low key kind of way. I am a self-conscious person and I suppose it’s true to say I have a habit of dwelling on things, which perhaps goes some way to explaining why I’m a bad sleeper. My mother is a somewhat nervous person – some would call her a “worrier” – and it is obviously possible I have inherited some of her characteristics. (Though I’m glad to say she is alive and well at 77 years of age – as is my father. And interestingly – or not – neither of them has high cholesterol.) But coming back to me, if it is true that stress caused my heart attack, I have no idea what I can do – because I cannot see how I can appreciably alter my own character. If stress is the cause, then perhaps it will just be a matter of time until the next attack. What I have done – what I am doing – is more heart and lung exercise than before. I suppose that will help. I also imagine that continuing with a small dose of beta-blocker might be wise – and continue the aspirin. But I think I might ditch the statins. I will of course consult again with a cardiac doctor here before making any major decisions, but I’d be grateful for further input.
The hypothesis that one’s predisposition to cardiac events is in your genes is not a complete picture, never mentioned is the inheritance of personality traits. My son was brought up by his mother, failed teenage marriage, almost without any of my influence for over 20 years, I thought it only fair to leave it to his mother and step father who I hasten to add is nothing like me at all in fact opposites in almost every area. He’s 42 this year and as anyone who knows us will attest in personality we are like clones, poor lad. So if you have a worrywort parent there is every chance that you’ll be one also. This will appear so normal to you, you won’t recognise the trait.
In the nature of things you now seem to be worrying about worrying. My wife worries if she hasn’t got anything to worry about.
Yoga or meditation might be avenues to persue.
Best way to fry the eggs to go with my bacon?
Have just read that Oilve Oil turns into a trans fat when heated!
Confused now
I’ve read that coconut oil is a very stable oil at high temperatures. Olive oil should be kept for salad dressings.
The only problem I have with coconut oil is that it can impart a flavour of its own to the food, and I’m having trouble adapting to it.
Ignore any references to “Extra Virgin” – it is meaningless in the context of coconut oil and is just marketing hype. Organic is good though, and in terms of quality, you get what you pay for.
Apparently, it has to be really hot (smoking) to do this. The Spaniards use it..
Avocado oil is supposed to remain stable at high temperatures; it’s high in mono-unsaturates and doesn’t have a strong flavour.
Good old fashioned lard!
Butter sunshine. 🙂 Actually my favourite is bacon fat, but modern farming practices have meant that now most bacon is high in O6, which many of us get too much of anyway. Butter, ghee, coconut oil (refined has no flavour, so it’s quite neutral) are all good, and apparently handle they heat pretty well without turning into horrible carcinogens.
Ghee (butter with proteins/etc removed) or lard (leftover bacon fat).
Ghee is what I use as coconut oil leaves them tasting odd?
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Smoking was very prevalent in the US and that was behind an awful lot the the increase..
My high horsing detector is being stimulated again, as a lifelong smoker fron the age of 11 ish, I’m now 62, I wish I’d never seen the things, but that aside.
The French, often cited as a reduced CVD occurence are still smokers in very large numbers, I’m not suggesting for a moment that there is not some correlation between tobacco use and CVD, what I’m insisting is all proportionality has been lost to the cause. Notwithstanding that apart from the net contribution to the UK economy, circa 5bilion pounds, probably the entire ENT budget, disregarding the inferred life reduction, read pension liability, of some 10 years the non smoker should be grateful of our efforts.
Malcolm has cited stress as a principal factor, how much greater would that be if we all ceased smoking, unquatifiable I’m sure.
Another factor to bear in mind is smoking has been, quite rightly, as damaging to health probably lobbied for by the manufacurers of zyban et al but on the back of opportunity, vested interest, not in any way the common good. They neither see or want to see the bigger picture they wish to avail themselves to the, government sponsored, opportunity. Hard cash again.
My contention is the more you demonise it, plain packaging et al, the more you promote it, it’s rebelion innit, this ‘ll annoy em.
Sugar, what do you propose, a tobaccoesque tax on it? Leave us alone you are not enhancing our lives you,re ruining them. Life is life, live as you want to live and live as long as you do is a much bettter option and as a bonus it disempowers you.
Best way to fry the eggs to go with my bacon?
Coconut. Failing that, butter, from cows allowed to eat what they were designed to eat – grass!
Throw all your margarines and vegetable oils away and don’t buy them or eat them ever!
http://www.modernhealthcare.com/article/20140319/NEWS/303199957/new-heart-guidelines-would-qualify-12-8m-more-for-statin-therapy?AllowView=VXQ0UnpwZTVDZldYL1IzSkUvSHRlRU9xamtVZEErTmE=&utm_campaign=am
A thought occurred to me: if the evidence in the 1960s / 70s etc was at best circumstantial and ad hoc regarding fat causing heart disease, then why is the burden of proof which is now required to kill the myth so high?
Where were the meta studies in the 60s / 70s?
Where were the 500,000 people taking part in those meta studies then?
All we had then was cherry picked data from Seven Countries and even though that was soon shown for what it was, the “advice” didn’t change.
Now we have studies with evidence to refute the previous “advice”, we have the consequences of dietary advice leading to all sorts of metabolic problems and yet, the “official advice” isn’t changing because “we need more studies”. What is going on?!
That is exactly the question that decent science journalists should be asking – if we still had any! There are so many areas of science that are let off the hook by lazy journalists. I’d love to hear the answer to your question, and I’d add some more of my own, such as:
1) If we don’t have proper data on statin side effects, how would we know if they were having horrible consequences? (Heart failure for instance).
2) How do we know if some people with apparent dementia, aren’t actually suffering cognitive statin side effects?
3) How many muscular/ skeletal problems of later life might be wrongly diagnosed when statins were the true cause?
4) How much extra life expectancy would a person gain from taking a statin after 60?
Then we could go onto global warming, the effects of salt, etc. etc.
Part of the scandal is that journalists simply let these ‘scientists’ get away with it!
David – I have asked my doctor these questions and his answer – ‘But the benefits so far outweigh the risks’. I got so tired of hearing those words that I stopped taking statins about 5 months ago. Except for some leftover muscle pain, I feel great! I am now hoping the muscle pain will subside but sort of suspect it might be permanent.
Re 4) How much extra life expectancy would a person gain from taking a statin after 60?
I think you have TOTALLY failed to read or understand the evidence I linked to earlier in these comments.
Please read Low Levels of Low-Density Lipoprotein Cholesterol: A Negative Predictor of Survival in Elderly Patients
with Advanced Heart Failure and explain to me why you think it is the case that lowering cholesterol extends life in the elderly when in practice we know this isn’t the case?
Association between serum cholesterol and noncardiovascular mortality in older age.”
Higher total cholesterol was associated with a lower risk of noncardiovascular mortality in older adults. each 1-mmol/L increase in total cholesterol was associated with an approximately 12% lower risk of noncardiovascular mortality
Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 studY
“Part of the scandal is that BY ASKING THE WRONG QUESTIONS we simply let these ‘scientists’ get away with it!
Increasing cholesterol in the elderly LOWERS all cause mortality.
Lowering cholesterol in the elderly INCREASES MORTALITY.
The question should be
WHY IS ACCEPTABLE TO KNOWINGLY INCREASE RISK OF MORTALITY IN THE ELDERLY?
While there seems to be a consensus in the thread on the statin question people don’t seem to be able to apply it in other areas, global warming, whether it’s true or not but noticably absent for some 17 years, is driven by identical mechanisms, though they have had to change its name to climate change ie: vested interest, by driving the perception that we are about to run out of fossil fuels and kill the planet the energy companies can increase prices whereby they can reduce consumption but maintain profits. Followed by governments who see this a tax revenue opportunity. I’m all for stewardship but not hysteria.
Salt, there has been some research, off message so ignored and reviled, that reducing salt levels excessively can lead to type two diabetes and very quickly. Theres a simple, never mentioned solution for salt intake. If you want more salt drink more water.
“All we had then was cherry picked data from Seven Countries and even though that was soon shown for what it was, the “advice” didn’t change.”
Not quite, see http://group.bmj.com/group/media/latest-news/study-raises-questions-about-dietary-fats-and-heart-disease-guidance
I think the missing data from the Sydney Diet Heart Study turned up a little while ago and was reported on in Feb 2013. But is does make one wonder just why the evidence showing polyunsaturated fat was worse for you than saturated (some particular PUFAs admittedly) went ‘missing’ for so long when it clearly wasn’t lost or destroyed.
It didn’t fit with the fairy story but surely that couldn’t be why it ‘got’ lost for so long… could it?
Mark Jan
You end with the question – “What is going on?”
Simple answer – Money. Billions of the stuff.
The American Heart Association, based on the fact that Cheerios are low in saturated fats, gives General Mills its seal of approval and proclaims Cheerios “Heart Healthy. Will the AHA do an about face. I doubt it because the AHA knows where it’s bread is, “I Can’t Believe It’s Not Buttered.”
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Cholesterosaurus – AKA Zombie Hypothesis – even though it’s dead it’s still going to keep coming back to eat your brains, dumbly slogging along infecting others.
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Thanks again Malcolm. To add to my posts above … My beef (pun intended!) with stress as the main (or a major) cause of MI is that it seems to be unquantifiable. I have read that blood pressure can be an indicator of stress, but again, in my case, my blood pressure was good both before and after my MI a year go – averaging 115/70 then as now. As mentioned above, of the usual suspects only my cholesterol was out of whack (6.6 overall, LDL 4.5). All other indicators where good. I accept that, as you point out, that is actually not a very high level of cholesterol and can perhaps be discounted as a cause of my MI. But if stress is the culprit, how can I identify it and how can I prevent it?
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Just in case it gets missed, I found an article about statins in the Society pages of The Guardian which I thought was an odd choice of section to publish it : http://www.theguardian.com/society/2014/mar/21/-sp-doctors-fears-over-statins-may-cost-lives-says-top-medical-researcher
“Doctors’ fears over statins may cost lives, says top medical researcher”
We’re being made too suspicious, apparently. I wonder if there is a pill for that too?
I knew it was coming, I spent quite a while talking to the health editor. Rory Collins is using tactic number 2: Accusing people who attempt to engage in scientific debate of ‘killing people.’ My, my. Very hackneyed. Though, it seems, works every time.
Yes…just as my GP dismissed my essential debate, by threatening me with self inflicted debilitating illness, ( meaning death), should I dare to deviate from the script.
Why have some docs morphed into scaremongers? Where has care and concern gone? This new form of medical business, based on crystal ball gazing, is encroaching on precious time needed to help the already sick and needy. It just has to be less stressful dishing out scripts to the otherwise well, whose only problem is that their computer printouts slightly deviate from the norm, rather than to actually confront the problems of the very sick. Oh sorry, I forgot….that job has been delegated to the Practice Nurse.
A visit to the GP these days seems to resemble a game of Deal or No Deal scenario.
Dietary fat and heart disease study is seriously misleading | The Nutrition Source | Harvard School of Public Health
https://www.hsph.harvard.edu/nutritionsource/2014/03/19/dietary-fat-and-heart-disease-study-is-seriously-misleading/
Says a man whose entire reputation rests on the hypothesis….ho, hum. Walter Willett is man who has several horses in this race. If the dietary fat and heart disease study is right – he is wrong – and all of his status and dietary advice is wrong. Although he doesn’t know it, his refutation primarily rests on the Mozafarrian meta-analysis. This, in turn rests on the Finnish mental hospital study – just about THE most ridiculous scientific study published in recent memory. Perahps you could write to Walter Willett and ask him why uses the Finnish Mental hospital study, and ignores the Sydney study?
Dietary advice about fats and the risk of heart disease is called into question on bmj.com today as a clinical trial shows that replacing saturated animal fats with omega-6 polyunsaturated vegetable fats is linked to an increased risk of death among patients with heart disease.
The researchers say their findings could have important implications for worldwide dietary recommendations.
Advice to substitute vegetable oils rich in polyunsaturated fatty acids (PUFAs) for animal fats rich in saturated fats to help reduce the risk of heart disease has been a cornerstone of dietary guidelines for the past half century. The most common dietary PUFA in Western diets is omega-6 linoleic acid (n-6 LA for short).
UK dietary recommendations are cautious about high intakes of omega 6 PUFAs, but some other health authorities, including the American Heart Association, have recently repeated advice to maintain, and even to increase, intake of omega 6 PUFAs. This has caused some controversy, because evidence that linoleic acid lowers the risk of cardiovascular disease is limited.
An in-depth analysis of the effects of linoleic acid on deaths from coronary heart disease and cardiovascular disease has not previously been possible because data from the Sydney Diet Heart Study – a randomised controlled trial conducted from 1966 to 1973 – was missing. http://group.bmj.com/group/media/latest-news/study-raises-questions-about-dietary-fats-and-heart-disease-guidance
It is very frustrating when someone like Willett uses selective research that he likes, and ignores stuff he doesn’t to make his points. Most people have no idea if he is talking bollocks or not. BTW, he is.
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Hello Dr. Kendrick
After reading your last two posts, I have to wonder if you are correct in stating that there is no link between high cholesterol levels and heart attacks but incorrect in stating that the use of statins does not help reduce that risk. Perhaps there is something else going on such that the use of statins, especially in persons who have a history of heart disease, is beneficial.
I myself was diagnosed with coronary heart disease via an angiogram 13 years ago. No stent was put in but I started on Lipitor, lost weight, changed my diet and started exercising more. I also stated taking Niacin about 10 years ago and now take 3,000mg daily. An angiogram two years ago showed my blockages had declined from 90% to 70%. Because of all the changes in my lifestyle, it’s had to attribute this improvement to just one thing but my doctors feel the Lipitor has helped.
This is, of course, anecdotal evidence but I am reluctant to change anything, including my 10mg daily dose of Lipitor. I don’t know if you read these replies or not or if you respond but I wanted to contact you with my story as well as to say I enjoy your posts on this subject.
Best regards, Gerry Gabel
__________________________ … sent from our Mac at home … __________________________
Gerry. Firstly, of course I read them. I am the all-powerful moderator. And nothing goes up without me allowing it. I have only blocked adverts (a couple have slipped through), personal insults from anyone, about anyone, and some completely mad ones. Because I get a bit bombarded, there are probably comments that I have just, plain, missed.
Your point that statins may have other effects is completely valid. [I have never said that statins do not reduce the risk of CVD (they do – a little bit).] Statins have many other effects, key among them is probably stimulation of nitric oxide synthesis in the endothelium. Nitric oxide is a potent anti-coagulant, and may well stop thrombi forming inside critical arteries. That is how, I believe, they work. Although I do not think that – for the vast majority – the benefits outweigh the adverse effects.
Hi
I have been following previous posts but I am still sitting with one very big question. I have a family who has FH cholesterol therefore they have all been prescribed statins. my husband has had two stent surgeries so it is crucial to control his levels. I am confused with so much media and information that I worry with the side affects that i don’t want them to be taking statins but what is a health safe alternative that will keep cholesterol levels low and give them safe levels to avoid any artery blockage and the acceleration of CVD?
we are a vegetarian family who don’t smoke or drink or eat fish and eggs. preparing meals is so confusing I don’t know what to cook anymore.
please can you give a more update on a way forward from here as I am struggling here.
Sure hope someone responds to question by sjan. I have the same questions.
Sjan, When it comes to genetics, you husband is not your family, he is a genetic stranger that you me. I am confused. Who has FH? Your husband, you, others?
Hi thank you for answering. My husband has FH with two stent surgeries. His siblings are all on statins. My children age 23 / 25 have both received their blood test results which were at 9.3 and 8.6. I was hoping they would be clear but now I guess I have to assume they have it too. they ( my husband and kids) are being referred to guys for lipid clinic but I am sitting with which way to go. I am not happy any of them taking statins but then whats the alternative?
I have been searching and have come across Serrapeptase and wonder, if there is research, that backs the claim it is the wonder enzyme that dissolves and cleans arteries? I sit with caution because if it is the wonder drug then why is it not prescribed by doctors? Surely then the need to take stains can be stopped .
Hi, I came to see you in March. I told you my cholestrol was 8.4 and you said you were not interested in levels. Advised not to take statins which I really dont want to take. I have just been for an eye test and was told they could see I had high cholestrol from this in my eyes. Should I be worrried about this.
Hi Carol,
How is your vision? Studies show lysine(high in meat) can lower blood sugar, and prevent cataracts. Taurine(from animal foods) is helpful to the eyes and heart.
http://www.ncbi.nlm.nih.gov/pubmed/9878222
http://www.ncbi.nlm.nih.gov/pubmed/3888464
http://www.ncbi.nlm.nih.gov/pubmed/19343117
http://www.ncbi.nlm.nih.gov/pubmed/1760655
In this article, cholesterol in the eye, does not seem to be the problem, The immune system , aging, and perhaps genetic defects affect the eyes. Lack of zinc,and A (from meats) are a known factor for macular degeneration
http://nih.gov/news/health/apr2013/nei-03.htm
https://www.nei.nih.gov/news/pressreleases/101201
http://onlinelibrary.wiley.com/doi/10.1002/mnfr.201100511/abstract;jsessionid=D12689805BAF1C79B61DAF7A9825C199.f01t02
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0003068/
If you want good vision, and in extension, good arteries, just stay away from sugar and high carrbs.
http://www.webmd.com/eye-health/macular-degeneration/news/20070713/high-sugar-foods-may-affect-eyesight
Hi, I came to see you in March with high cholesterol. 8.4 You said not to worry about this. Just been for an eye test and was told they could tell I had high cholesterol because they could see it at the back of my eyes. Should I be worried about this.
Thanks.
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