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Food & Drink

Eating Cloned Beef

Every neurotic nutcase in Britain is quivering in fear because they might have eaten a cloned hamburger.  They’re terrified. You’d imagine they were just injected with concentrated bubonic cancerous AIDS-leprosy.

What the fuck do they think is going to happen?  Do they think they’re going to grow another shoulder?  An extra knee?  A chin at the back of their head?

It’s just beef.  Delicious, juicy, burger beef.  It’s bad for you, but not in a Doctor Evil Mwooohahahaha kind of way.  It’ll up your cholesterol and zap you in the end, but at least you had a couple of beers at the barbecue, sang a few songs and chilled.

Oops.  Did I say chilled?

These eejits wouldn’t know the meaning of chilled.

They think they’ve just eaten a bit of Jeff Goldblum.  When the waiter brought their steak, he leaned close and whispered Be afraid.  Be very afraid. Next thing you know, they’ll be clinging to the ceiling, vomiting acid on their food to digest it, but considering the stupidity of these people, maybe that’s how they’ve always eaten.

Now I see the British government is issuing statements to calm them down : No danger from eating cloned meat, says food-safety Czar.  It’s always a Chief or a Czar or a Baron.  Never a Sheikh, or a Sultan or a Nabob, for some reason, but I digress.

There’s no danger from eating cloned meat because it’s just fucking meat, meatheads!

This is what happens when people get their education from Hollywood. They think the cow walked out of a spaceship and said Klaatu Barada Nikmoo.

Jesus Christ, it’s just a cow.  A cow.  A fucking unlucky cow who got whacked to put burgers on our tables, but a cow nonetheless.

Imagine if you told these people they were surrounded by clones? There wouldn’t be an identical twin safe in the whole of Britain.  They’d be out with burning pitchforks marching on the homes of known multiple pregnancies.

Give out your radioactive Satan-children!  They must die!

Morons.

42 replies on “Eating Cloned Beef”

So people put up with all the steroids pumped into animals to make them plumper and give them a shortened crappy lifespan so they can make triple the output but a clone burger is wrong? The food chain is already well poisoned so caring at this stage is well pointless.

This is the same Brit government what spent millions on the Swine Flu pandemic.Remember that. Thousands. Millins even, were doomed. Oink oink

The food safety crowd, as suuposed scientists, should be taking a lead here and explaining to people that there is no harm in this, but they seem to be taking the “don’t spook the horses route” instead, and issuing “this will never happen again” type statements, in order to protect consumer confidence. Like the way they banned T-bone steaks even though the chances of getting BSE from eating one was about a billion to 1.
You can see why it would be easy to be confused if you had no understanding of genetics

It’s just beef. Delicious, juicy, burger beef. It’s bad for you, but not in a Doctor Evil Mwooohahahaha kind of way. It’ll up your cholesterol and zap you in the end…

Actually, Bock, this is wrong. Beef, especially fatty beef, is very healthful food. It doesn’t do anything bad to your “cholesterol”*, and is chock full of vitamins, especially fat-soluble vitamins, and minerals, and both protein-y and fatty building materials for your muscles, bones and organs. Humans (and their direct ancestors) have probably been eating meats quite similar in composition to beef for around 2 million years or more, and the idea that there is any threat to our health from eating either the meat and/or the meaty saturated fat to which we are so well adapted is a huge claim, for which next-to-no evidence has actually ever been advanced.

*cholesterol – has two modern meanings.
a) an essential molecule for building cell walls, an essential precursor for several steroid hormones, including human sex hormones, and the essential substrate your body needs in order to make Vitamin D in your skin under the influence of sunlight, among other things. (Also appears to be used by the body as “patch” material in repairing damaged arterial walls). So essential is it that your liver makes it continually to ensure you have enough for all necessary purposes – there isn’t nearly enough of it in your diet.
b) a magical number that doctors persist in measuring and frightening their patients with, even though its ability to predict anything useful or treatable about anyone’s health has been thoroughly debunked, possibly because certain drug companies have discovered that they can reduce it in a hugely profitable way, even though they have also not yet been able to provide any evidence to show that reducing it is in any way beneficial or likely to prevent disease or death.

a magical number that doctors persist in measuring and frightening their patients with, even though its ability to predict anything useful or treatable about anyone’s health has been thoroughly debunked, possibly because certain drug companies have discovered that they can reduce it in a hugely profitable way, even though they have also not yet been able to provide any evidence to show that reducing it is in any way beneficial or likely to prevent disease or death.

Really?
Elevated levels of LDL cholesterol (low-density lipoprotein) in the blood, has been strongly, directly linked to cardiovascular diseases, through reviews and meta analysis, for some time.

[Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III)?Final Report. Bethesda, MD: National Heart, Lung, and Blood Institute; 2002. NIH Publication No 02-5215.
Cui Y, Blumenthal RS, Flaws JA, et al. Non-high-density lipoprotein cholesterol level as a predictor of cardiovascular disease mortality. Arch Intern Med. 2001;161:1413-1419.
Frost PH, Davis BR, Burlando AJ, et al. Serum lipids and incidence of coronary heart disease. Circulation. 1996;94:2381-2388., Von Muehlen D, Langer RD, Barrett-Connor E. Sex and time differences in the associations of non-high-density lipoprotein cholesterol versus other lipid and lipoprotein factors in the prediction of cardiovascular death. The Rancho Bernardo Study. Am J Cardiol. 2003;91:1311-1315.
Pedersen TR, Olsson AG, Faergeman O, et al. Lipoprotein changes and reduction in the incidence of major coronary heart disase events in the Scandinavian Simvastatin Survival Study (4S). Circulation. 1998;97:1453-1460.
Manninen V, Elo MO, Frick H, et al. Lipid alterations and decline in the incidence of coronary heart disease in the Helsinki Heart Study. JAMA. 1988;260:641-651.]

Irate Chemist – hello!

“Linking” – another term for “correlation.” Repeat after me, class: “correlation is not the same as causation.”

Firstly the evidence base for the links between dietary fats and serum cholesterol are all over the place. You can cherry pick the epidemiological evidence one way or the other way (which Ancel Keys demonstrably did in his Seven Countries study). The fact is that when all evidence is taken together, there is no clear link between any particular dietary pattern and serum cholesterol and/or blood lipid concentrations. There are extremely high saturated fat human diets (notably the Masai and the Inuit) which do not lead to noticeably elevated cholesterol levels, and vice versa, as well as every variation in between. In other words, no correlation at all.

Also, “cholesterol” and LDL are not the same thing. LDL = low density lipoprotein, one of a suite of fatty-protein complexes in which cholesterol may travel in the blood (cholesterol is only slightly soluble in the blood serum, which is one reason it is useful as a cell membrane component). When cholesterol travels in a different complex, known as HDL, high density lipoprotein, it is reputedly “linked” with a LOWER incidence of cardiovascular disease (although some argue that this conclusion is simply an attempt to “save” the cholesterol/heart association in the face of contradictory evidence). Clearly when speaking about cholesterol it is important to be precise about what we are actually talking about, since not all cholesterol is equal, and not all is “linked” to cardiovascular disease.

But to go back to the LDL/cardiovascular disease link which you highlight above. IF a high concentration of LDL WERE a causative risk factor for cardiovascular disease, THEN lowering it would have a beneficial effect on the hard clinical endpoints of cardiovascular disease. This paper documents how that assumption began to come unstitched in drug trial after drug trial, within the last few years.

As it points out:

“As a matter of fact, ezetimibe was approved and marketed in 2002 based solely upon a 20% reduction of cholesterol, but not on data related to its effectiveness on any clinical endpoint, as if cholesterol levels by themselves could be a surrogate of CHD. In addition, the effectiveness of the ezetimibe+simvastatin combination against hard clinical endpoints has never been demonstrated, as discussed below about the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) trial. As a consequence, many physicians and scientists rightly questioned why the combination tablet already was
on the market if there was no proven effect on clinical CHD complications”

Hello Scotlyn!

High blood cholesterol is a major risk factor that has been shown to significantly increase the risk of heart disease, by extensive clinical and statistical studies. As for cherry-picking, I picked the papers above at random–i’ll leave you to balance the discussion.

The fact is that when all evidence is taken together, there is no clear link between any particular dietary pattern and serum cholesterol and/or blood lipid concentrations.

You obviously read a meta-analysis of the data–could you provide a link to the peer reviewed paper?

I read a book a year ago that gave a very plausible theory to why Inuit’s can deal with high levels of fat and african americans cannot, it was based on their respective climates and cellular metabolism–the author also made some predictions based on his theory. One point; I don’t know if Inuits eat alot of animal “fat” –it was noticed many decades ago that visiting explorers were dropping like flies and it was discovered that they were eating alot of animal blubber. They died of a condition known as hypervitaminosis. It’s basically too much fat soluble vitamins, unlike water soluble vitamins which are excreted in urine they can build up in the body if taken in large quantities.

Scotlyn, I specifically addressed LDL cholesterol. Where did I say LDL and cholesterol were the same thing? The more cholesterol a lipoprotein complex has the less dense, hence LDL has more cholesterol molecules present in the complex than HDL cholesterol complex. More research is pointing toward all non-HDL cholesterol as being a major risk factor.

Just read the paper that you linked to above–was an interesting read, i’m not surprised that certain pharmaceutical companies, or their representatives, are up to their old tricks. It’s a huge problem; thorough well conducted studies are very expensive and are hence funded almost exclusively by pharmaceutical companies. This is not good.

Irate Chemist

The polar explorers died because they ate things like polar bear liver and died of massive vitamin A overdoses—the natives never eat the liver they do eat blubber and use it for fuel.

Native Americans and Pacific Islanders have a massive problem with obesity because they adapted genetically to survive famines by bulking up fast to deal with the lean times–there are no more lean times so they keep on bulking up

The main problem with modern beef is that it is corn and soy fed in lots rather than grass and pasture fed.
Genetically the Irish adapted to thriving on beef and milk–they have been breeding and herding cattle for many thousands of years–part of this genetic mutation also leaves them vulnerable to alcoholism, you see the same phenomena in Scandinavia and Scotland—the average life expectancy for male Scots in now down to the mid to late 50s

How is being adapted to thriving on beef and milk related to being vulnerable to alcoholism?
The average life expectancy for a Scotish man is mid to late 50s.. I don’t think so.

It’s kind of annoying Bock, because you have such an informed and knowledgeable readership, that I trust a lot of what is written in comments. Valiant, however – you can’t trust a word.

So in terms of her saying the life expectancy for a Scottish man being mid to late 50s. Jesus, you’d have to go back a century or two for that figure to be accurate.

http://www.dailyrecord.co.uk/news/scottish-news/2010/08/06/scottish-life-expectancy-rates-still-lower-than-most-of-europe-survey-finds-86908-22469260/

“It shows life expectancy rates are creeping upwards. A man born in 1981 could expect to live until 69 and a woman to 75, but for those born in 2008 it rose to 75 and 80 respectively.”

Also it would appear any lower comparable life expectancy average is related to poverty.

Actually I confused the statistics from Russia with Scotland–Scotland does in fact have one of the lowest life expectancies for males in Europe but is not as bad as Russia and hopefully will never get that low.
A big issues in Russia is the heroin that comes from Afghanistan and the sharing of needles that is spreading HIV, truly a tragic situation with so many young men dying in Russia from heroin.
I do not know why Scotland has such a high male mortality rate, smoking, binge drinking and deep fried Mars Bars must contribute. Glasgow has the worst statistics so it is poverty is also a factor.
Re Milk and alcoholism—nobody knows for sure what the connection is –at this point it is a correlation, studies in Iceland are looking into it and will have the answers soon.
The vast majority of the worlds population cannot tolerate fresh cows milk, but those that can–Irish, Scandinavians etc have much higher rates of alcoholism.
The best genetic studies are done in Iceland—they have a homogeneous population and have been collecting good health statistics for a long time and it has been genetically isolated for a long time.

The Genetic heritage of Iceland is Scandinavian and Irish, the raiding Vikings took Irish women to Iceland.

Irate Chemist –

The main problem with modern beef is that it is corn and soy fed in lots rather than grass and pasture fed.

Hey, I absolutely agree with this! – corn and soy are not good foods for cattle, (or people except for an occasional side dish), and soy particularly should be kept for industrial uses. (Israel issued a health warning against the frequent use of soya based foods, particularly for children and babies, in or about 2005).

HOWEVER, we are still fortunate in Ireland in that our cattle and sheep are still reared on grass and not on feedlots. This makes their meat, butter and cream much more healthful – and their fatty makeup includes a very good ratio of omega-6 to omega-3 fats.

Writing this at work, so gotta run without posting any links, but I’ll be back.

“and soy particularly should be kept for industrial uses”. That rules Tofu out then huh. I had heard too much of it is not good all right. Too much estrogen in it. Which is linked to cancer.

RE: cholesterol
I was at the doctor a while back and thought I’d get my money’s worth. So said to her to do a full check up. Blood pressure, bloods for cholesterol, iron/hemoglobin level.. (1 in 5 women have low iron levels)
So anyways she leaves a voicemail for me when the results come back saying everything’s fine. Call her back and get this dumbed down explanation – a figure that means nothing to me.. “5 or under is good, you’re fine” That annoys me. I want to know the exact calculation of the levels for cholesterol testing. Have to rely on the internet again. Jesus if only we made them work for their €50/€60 – we should be at least getting a half hour to an hour for that. Not 5/10 minutes.

I think that Valiant posted that comment, Scotlyn. But yeah, grass reared cattle does sound much better.

I agree with you that soft surrogate endpoints tell us very little about the effectiveness of a particular intervention–it’s one of a bag of tricks that some researchers use to arrive at more positive result.
However,

..its ability to predict anything useful or treatable about anyone’s health has been thoroughly debunked..

I don’t agree with you unless you can provide more literature. The above paper looks to be sound but there needs to be more research. Lets see the data pre-Vioxx, there needs to be more trials with better methodology and transparency. The authors were very tentative in their conclusions, unlike your statement of “thoroughly debunked”.
As the Authors said in the closing sentence

The next question would then be: is it not time for a full reappraisal of the choles-terol theory?

Why not?

I’m sure they wouldn’t mind giving you a copy of the lab results, FME. Squeeze your GP like a sponge, ask as many questions as you like–you’re paying for it after all.

Will do Irate. Thanks. Maybe I’ll post the results here and you can decipher them for me.. ha.
RE: “The fact is that when all evidence is taken together, there is no clear link between any particular dietary pattern and serum cholesterol and/or blood lipid concentrations” I don’t have the inclination right now to check out the links.. too busy.
But I’m not convinced a diet high in dairy/animal fat is not a cause of high cholesterol.
The Irish diet compared to that of the mediterranean diet for instance and the comparible rates of heart disease for each, would indicate their diet is much healthier/doesn’t result in high cholesterol/heart disease.

I’d bet that there is, somewhere on the inter-highway, a calculator that can do that for you. If there isn’t then there should be!

I agree, we spread butter on our toast, they use olive oil. I think their climate has a lot to do with the whole business too. Having sunshine for days on end makes me want to get out of the house and do something–I feel like hibernating here.

I’ll have a search for it IC. It really is great to get such easy access to information from the web. I think if we were to depend solely on doctors we’d be none the wiser.

Yeah, their diet has been shown to be one of the healthiest. With low rates of heart disease and certain cancers. They’re definitely doing something right. The monounsaturates as far as I know in olive oil help reduce LDL cholesterol and contain a lot of antioxidants.

Would be an interesting discussion on the molecular bonding of monounsaturates with LDL to explain why it’s so beneficial. Or maybe not. :)

The web is a huge asset to anyone who wants to know more about everything, I don’t know what I would do without it.
I remember reading somewhere that it’s the double bond between two carbon atoms in the fatty acid chain of monounsaturated fats (1 double bond) and polyunsaturated fats (many double bonds) that the body finds easy to target and to breakdown, I might be wrong but that’s what I first thought of.

I’d forget about the antioxidants though, FME–it’s a load of codology.

Yeah. The antioxidant thing really annoys me. Fake science to sell products, dressed up in important-sounding, but spurious, language.

A bit like L Casei Immmunitass and all that bollocks.

Exactly, Bock. The fundamental science behind the mechanism of antioxidant action is so deeply flawed it’s comical. All the while these companies enjoy huge profits for selling snake oil, essentially. It was disproved years ago yet people are cramming them into as many different foods as they can. I wouldn’t be surprised if you can get an antioxidant injection or IV.

You hit the nail on the head with L. casei–I don’t think i’ve ever seen compelling evidence to substantiate the claims made on the TV ads. It’s only a matter of time before the wheels come off that charade.

Irate Chemist

Exactly, Bock. The fundamental science behind the mechanism of antioxidant action is so deeply flawed it’s comical. All the while these companies enjoy huge profits for selling snake oil, essentially. It was disproved years ago yet people are cramming them into as many different foods as they can. I wouldn’t be surprised if you can get an antioxidant injection or IV.

Irate Chemist, you’re quite happy to make a sweeping statement and you’re not at all bothered about all of the epidemiological studies these folks have done to “prove their case,” since you realise that when tested in intervention studies there is no case to prove. Now substitute the word “statin” for “antioxidant” – the same argument applies.

Heart disease is not caused by statin deficiency.

Re the data in the paper I attached above, what has clearly been shown in all cholesterol/statin studies completed and published since the rules made it harder to “hide” or “lose” negative results, is that lowering cholesterol levels by as much as 50% does not improve intima media measurements, nor does lowering cholesterol levels by as much as 35% improve the mortality rate. (And there is no harder clinical end point than mortality). For an even better rebuttal of the idea that lowering cholesterol must be “a good thing” – see the J-LITT study. Japanese researchers controlled for the dosage of simvastatin (either 5 or 10 mg) and compared outcomes for sub-groups within the treatment population of 47,000+ Japanese males on the basis of how successfully their medications lowered their cholesterol – as with other medications, people will have a “bell curve” type range of responses. In this case the population was sub-divided by TC (total cholesterol) levels as follows:
280mg/dl – keeping in mind that most doctors would like to see their patients achieving the lower values in that scale. In this study, the risk of all-cause death in the <160mg/dl group was 2.76 compared to the mean rate of death of 1.00 in the 200-219/mg/dl group. But the rate of cardiac deaths in the <160mg/dl group was 6.23 compared to the mean rate of cardiac deaths of 1.00 in the 200-219 group! In other words, the people for whom the statin was most successful in lowering cholesterol, were those who died in much greater numbers!

Cholesterol is a molecule we require to build cell walls, protect nerve cells, make steroid and sex hormones, make Vitamin D and countless other necessary functions. 97% of it is not in our bloodstream, but currently being put to use within our cells throughout our bodies. The levels in the blood are determined by very complex interactions within and between cells. It would be useful to try to understand these interactions in much more detail, before recommending the use of a medication which can indiscriminately blast down our cholesterol levels, interfering with all these metabolic processes. With this basic biochemistry info to hand, the results of J-Lit are not in the least surprising.

In relation to diet, with so many modern foods, never before encountered by gut of man, from which to choose in deciding what dietary elements may contribute towards the aetiology of modern disease – eg. sugar, high fructose corn syrup, highly processed vegetable oils, extruded soya proteins, white wheat flour, etc, etc, – it beggars belief that we have chosen to blame all our ills on a type of food that our ancestors have consumed in large quantities for a length of time that may be as long as four million years ago, but certainly no less than two – plain, simple fatty meat.

Meat does a body good.

What sweeping statement did I make, Scotlyn? I made a very specific statement about antioxidants, do you disagree with what I have said? Why do you consider it to be a sweeping statement?

Again, you said that the cholesterol theory was thoroughly debunked–where is the proof?

I don’t think that you have read what I have said previously, Scotlyn. I don’t understand why you say that i’m not bothered about the paper that you posted–it’s a start, but there needs to be more data collected and previous trials have to be re-assessed. I personally would not stop taking a statin after reading the paper above.

Heart disease is not caused by statin deficiency

Headaches are not caused by aspirin deficiency. Pain is not caused by morphine deficiency, nor is it caused by lack of acupuncture treatment. Asthma is not caused steroid deficiency. What is your point?

Cholesterol is a molecule we require to build cell walls, protect nerve cells, make steroid and sex hormones, make Vitamin D and countless other necessary functions. 97% of it is not in our bloodstream, but currently being put to use within our cells throughout our bodies. The levels in the blood are determined by very complex interactions within and between cells. It would be useful to try to understand these interactions in much more detail, before recommending the use of a medication which can indiscriminately blast down our cholesterol levels, interfering with all these metabolic processes. With this basic biochemistry info to hand, the results of J-Lit are not in the least surprising.

Where is the basic biochemistry?

Whoops, just realised another bit of a phrase got left out – the study group was divided into sub-groups starting at total cholesterol (TC) values under-160mg/dl and going up in 20 mg increments to over-280mg/dl.

This will teach me to post and run away to eat dinner without checking and editing!

I’m wondering did I read the same paper.
“For an even better rebuttal of the idea that lowering cholesterol must be “a good thing” – see the J-LITT study.”

From the article: “Hypercholesterolemia is a known and significant risk factor for the development of coronary heart disease (CHD) and death.1 Epidemiologic studies from Western countries, such as the Framingham Study, have established that a high concentration of serum cholesterol confers a high risk of CHD. The incidence of CHD in the Japanese population is relatively lower than that reported in the Western countries.Cholesterol-lowering therapy with resins and fibrates has been shown to reduce the risk of CHD. Recent primary and secondary prevention studies have indicated that **statins** also reduce the incidence of CHD…

“The present study demonstrates a relationship between serum lipid concentrations and the incidence of coronary events in Japanese patients with hypercholesterolemia under low-dose simvastatin treatment. A reasonable strategy to prevent coronary events in Japanese hypercholesterolemic patients without prior CHD under low-dose statin treatment might be to regulate the serum lipid concentrations to at
least <240 mg/dl for TC, <160 mg/dl for LDL-C and 40 mg/dl for HDL-C.”

In other words, lower their serum lipid concentrations further.. Lipids including: TC – LDL-C , TG and HDL-C. So there has been no debunking of the fact that high cholesterol, particularly LDL is linked to heart disease. – It is.
(from Scotlyn above “they have also not yet been able to provide any evidence to show that reducing it is in any way beneficial or likely to prevent disease or death”)

Also in the article:
“Dietary changes and exercise therapy for hyperlipidemia were recommended to the patients by the investigators.” Why would dietary changes be recommended? I would presume those changes would include less saturated fat intake – of which meat has a relative high concentration of. All good things in moderation as they say. Just google red meat consumption linked to cardiovascular disease and you will find a million studies and articles which has proven it is.

Irate Chemist
The point I am making is this.

I do agree with you that the science behind the use of anti-oxidants is fundamentally flawed. And yet, as you say, studies (mainly epidemiological) continue to find benefits for them, doctors continue to recommend them, people continue to pay for them, and billions are made.

It appears to me that you consider my contention that the science behind the diet-lipid-heart hypothesis is equally flawed, is too sweeping, and you ask me to provide links – which I’m happy to do, but it will take a while to get through all the points.

Meanwhile, though, if someone held you to an equal requirement to underpin your dismissive statement re anti-oxidants (which I agree with), with all the relevant studies, this would also take you a while. There is a lot of material out there. And dissenters with your opinion might ask similar questions to the ones you are asking here. So, I’ll work at this a bit, and provide some links as and when I can dig them up, so long as you remain interested.

But consider that for this hypothesis to work, ALL of the following must be true:
1. Saturated fat in the diet must elevate cholesterol levels.
2. High cholesterol levels must CAUSE (note this does not say – be linked to) heart disease.
3. Increases in dietary saturated fat must be independently shown to CAUSE (not be linked to) heart disease
4. Low cholesterol levels must prevent heart disease (it would be useful if low cholesterol levels also improved health generally and did not lead to death by other causes instead instead of death by heart disease).
5. Lowering previously high cholesterol levels through medications must also help to prevent heart disease and death.
6. (And for statins to be acceptable as “preventive” medicine, they must be further shown not only to work to prevent what they are supposed to, but also to cause no alternative harm – the risk profile for a preventive medicine must be much lower than the risk profile of a medicine for treating an actual illness which is already causing harm).

As shown in the link I provided above, number 5 has been massively disproved by several of the drug companies’ own studies – it only takes one negation to disprove the point, and we have several. The J-LIT study – also linked above, disproves both number 5 and 6 – the more effectively your medicine lowers your cholesterol (keeping the dosage equal), the more you INCREASE your risk of death, especially cardiac death.

Re the association between cholesterol levels and death, including death from heart disease, see this link. In 1989 a population of 350,000 men were screened for their cholesterol levels and other risk factors. A sub-group of 12,000 or so was selected for an intervention trial known as MRFIT, but all 350,000 were followed up for six years. Interestingly, the all-cause death rates in the low cholesterol cohort were much higher than those in the mid-level cholesterol cohort, and still somewhat higher than in the high-cholesterol cohort, although the heart-related deaths, when viewed on their own, showed a slight trend towards increasing in the higher cholesterol cohorts than in the lower cholesterol cohorts. Again, this study shows that low cholesterol levels are NOT associated with increased longevity. (Note that this study cannot now be replicated, since elevated cholesterol levels are now invariably medicated as part of standard treatment. There are no longer any unmedicated high cholesterol cohorts “in the wild,” as it were, to study).

Irate Chemist, re the references you provided, I will try to track them down, as you provide no links. Will revert to you on these.

Re the complex effects of different types of fatty acid proportions in dietary intervention studies, this meta-analysis, which is unfortunately locked behind a paywall, is discussed here. According to them, to date, no dietary fat intervention study has eliminated or reduced animal fat alone. All have replaced BOTH animal and trans-fats with varying combinations of polyunsaturated fats. It would be useful to have a study which allowed us to draw conclusions about animal fats independently of trans-fats (which is the basis for all this health advice we keep receiving re the “unhealthiness” of animal fats), but we do not. Meanwhile, those studies which have replaced animal and trans-fats with a high ratio of omega-6 to omega-3 polyunsaturated fats showed a slight increase in heart disease, while those which replaced animal and trans-fats with a high ratio of omega-3 to omega-6 polyunsaturated fats showed a decrease in heart disease. Since animal fats (particularly those of grass-fed ruminants) also have a high omega-3 to omega-6 ratio in their polyunsaturated portion, it would be useful for a study to actually address the issue of animal fats separately to trans-fats, in order to discover where the real “fatty” culprits lie.

The references I provided are from the article you gave the link for Scotlyn.

From the article: “Hypercholesterolemia is a known and significant risk factor for the development of coronary heart disease (CHD) and death.1 Epidemiologic studies from Western countries, such as the Framingham Study, have established that a high concentration of serum cholesterol confers a high risk of CHD. The incidence of CHD in the Japanese population is relatively lower than that reported in the Western countries.Cholesterol-lowering therapy with resins and fibrates has been shown to reduce the risk of CHD. Recent primary and secondary prevention studies have indicated that **statins** also reduce the incidence of CHD…

“The present study demonstrates a relationship between serum lipid concentrations and the incidence of coronary events in Japanese patients with hypercholesterolemia under low-dose simvastatin treatment. A reasonable strategy to prevent coronary events in Japanese hypercholesterolemic patients without prior CHD under low-dose statin treatment might be to regulate the serum lipid concentrations to at
least <240 mg/dl for TC, <160 mg/dl for LDL-C and 40 mg/dl for HDL-C.”

In other words, lower their serum lipid concentrations further.. Lipids including: TC – LDL-C , TG and HDL-C. So there has been no debunking of the fact that high cholesterol, particularly LDL is linked to heart disease. – It is.

What sweeping statement did I make, Scotlyn?

And yet, as you say, studies (mainly epidemiological) continue to find benefits for them, doctors continue to recommend them

Where did I say this?

On antioxidants–the science is not just flawed, its incorrect. The theory was disproved, possibly decades ago. It’s mumbo-jumbo.

Irate Chemist, re the references you provided, I will try to track them down, as you provide no links. Will revert to you on these.

Copy and paste to google.

Re the complex effects of different types of fatty acid proportions in dietary intervention studies, this meta-analysis, which is unfortunately locked behind a paywall, is discussed here. According to them, to date, no dietary fat intervention study has eliminated or reduced animal fat alone. All have replaced BOTH animal and trans-fats with varying combinations of polyunsaturated fats. It would be useful to have a study which allowed us to draw conclusions about animal fats independently of trans-fats (which is the basis for all this health advice we keep receiving re the “unhealthiness” of animal fats), but we do not. Meanwhile, those studies which have replaced animal and trans-fats with a high ratio of omega-6 to omega-3 polyunsaturated fats showed a slight increase in heart disease, while those which replaced animal and trans-fats with a high ratio of omega-3 to omega-6 polyunsaturated fats showed a decrease in heart disease. Since animal fats (particularly those of grass-fed ruminants) also have a high omega-3 to omega-6 ratio in their polyunsaturated portion, it would be useful for a study to actually address the issue of animal fats separately to trans-fats, in order to discover where the real “fatty” culprits lie.

If its behind a pay wall, how did you get the conclusions? The abstract and conclusions usually offer little–the experimantal section is usually where the meat is.

FME–this isn’t the first time Scotlyn has extrapolated or misinterpreted the conclusions of a paper.

FME – lets turn this around.

Just google red meat consumption linked to cardiovascular disease and you will find a million studies and articles which has proven it is.

Can you please link to an intervention study which shows that a reduction in the consumption of meat has led a reduction in cardiovascular disease? And, if you wish to translate such information into general health advice, then please link to an intervention study which shows that a reduction in the consumption of meat has led to a reduction in any disease and in all-cause mortality. (It is no good telling someone that they should do something to reduce their heart disease risk, if they will be increasing their risk of dying of something else instead).

Re the J-LIT trial – did you read the data tables? (Sometimes what the researchers say in words belies or “spins” what is contained in their data – they are being paid to produce reasons for people to take this drug, after all). What I summarised above was only the TC cholesterol levels. The data clearly show that lowering Total Cholesterol (TC) levels below 240 is beneficial, but lowering it below 200 is increasingly harmful and increasingly likely to cause cardiac (and other) deaths the MORE it is lowered.

And, re the association between elevated levels of cholesterol and heart disease, this is an association only. If there was a causal link, then lowering these levels would reduce heart disease – the J-LIT data clearly shows that lowering cholesterol by too much can increase either heart disease-linked deaths and/or increase deaths by cancer. Other recent trials of statins and/or fibrates have shown no reductions in mortality despite quite large cholesterol-lowering effects, possibly because at the lower levels, cardiac deaths are less likely, but deaths by cancer or other causes are more likely.

Think of it in this way. There is a strong association between firemen and fires. The more fires there are, the higher the rate of the appearance of firemen. If you find that this association is strong, you might think it a logical idea to remove the firemen in order to have fewer fires. In the same way, whatever is the reason there is some association between very high cholesterol levels and heart disease (and this association is strongest in men under 50, and hardly noticeable in women over 70), it may be that some other, as yet undiscovered process is bringing about both the heart disease and the elevations of cholesterol in the blood. J_LIT’s data would seem to suggest, though, that cholesterol is more like the firemen than the arsonists – if you reduce it too much, you get more disease, not less.

Irate Chemist, do you think you and I could start again? I know you and I had at it before on a different subject. In that case, I was admittedly less well-informed than you, and I granted you every correction you made to my errors with, I hope, some grace. I also went away and became better informed in the areas you pointed out to me, and hope to continue to do so if you should give me reason to do so in future.

It seems, however, that there is something in that history that colours your approach to what I am saying. Perhaps if someone else was making this argument you would respond differently? (Just saying.)
(So, how do I put a tongue-in-cheek smiley thingy in here to indicate basic good faith here?)

The paywall article is unfortunate (I hate these paywalls which prevent plebs like me gaining access to research), but the second associated link to a discussion of that article, which I also included, is very well researched and presented, and raises the points I made.

The original point I wish to make is that (contrary to Bock’s throwaway comment that meat is unhealthy as it raises your cholesterol)

1. Meat is a healthy food for humans. (There is abundant archeological, ethnological, nutritional evidence for this).

2. Cholesterol (the molecule), is an essential molecule for healthy cell membranes, for the production of useful hormones, and for the proper maintenance of brain and nerve tissue and other functions (its biochemistry is fairly well understood and very complex, connected in some way to every tissue in the body).

3. Cholesterol (the blood-borne cholesterol-carrying lipoprotein complex, in its various grades, which is actually measured in a doctor’s blood test), has, at best, an uncertain relationship to disease risk, and the idea that lowering it can only be beneficial is highly questionable. No causal link has yet been established, in fact the demonstration in drug trials that lowering cholesterol can have either no beneficial effect, or that it can be harmful, would tend rather to support the idea that the link between cholesterol levels and disease is NOT causal.

Re your first (unlinked) reference above, which I have tracked down, you have cited the National Cholesterol Education Project – a project whose members have strong ties with the pharmaceutical industries who produce the cholesterol-lowering medications which its clinical guidelines propose should be used.

I will get to the others sometime soon, but probably not tonight. Nancy’s, and a hot whiskey beckons, now that the roads may permit.

Good night.

Scotlyn RE:
“Re the J-LIT trial – did you read the data tables? (Sometimes what the researchers say in words belies or “spins” what is contained in their data – they are being paid to produce reasons for people to take this drug, after all). What I summarised above was only the TC cholesterol levels. The data clearly show that lowering Total Cholesterol (TC) levels below 240 is beneficial, but lowering it below 200 is increasingly harmful and increasingly likely to cause cardiac (and other) deaths the MORE it is lowered.”

That’s not what you said initially. You say above – “For an even better rebuttal of the idea that lowering cholesterol must be “a good thing” see the J-LITT study”. A bit of a general sweeping statement there I would say. So you are now saying it’s beneficial to have TC levels below 240.

Ok, here’s what’s in the article to be exact:
“The aim of the study was to determine the relationship between the occurrence of CHD coronary heart disease and the serum lipid concentrations during low-dose simvastatin treatment. Simvastatin reduced serum concentrations of total cholesterol (TC), low-density lipoprotein- cholesterol (LDL-C) (Bad cholesterol ) and triglyceride (TG), by 18.4%, 26.8% and 16.1% on average, respectively, during the treatment period.

“The risk of coronary events was higher when the average TC concentration was ?240mg/dl and the average LDL-C concentration was ?160mg/dl.” So when the concentration of total cholesterol was greater or equal to 240mg/dl and LDL (bad cholesterol) greater or equal than 160mg/dl there were higher instances of coronary events.

“The incidence of coronary events increased in the patients with TG concentration
?300mg/dl compared with patients with TG (triglyceride) concentration <150 mg/dl." In other words, more coronary events when TG was greater or equal to 300mg/dl compared to when concentration was less than 150mg/dl. High bad, low not so bad.

And:
"The high-density lipoprotein cholesterol (HDL-C) (that'd be the good stuff) inversely correlated with the risk of coronary events." "Inversely correlated" – in other words, coronary events were reduced when HDL was high.

I've looked at the data tables. Is there something in them that contradicts what I've just posted – from your article? Are you saying the article you've posted is now unreliable?
Regarding the firemen analogy. That's a little simplied really.
"cholesterol is more like the firemen than the arsonists". LDL Cholesterol – (the bad stuff along with triglycerides) can slowly build up in the inner walls of the arteries, leading to coronary heart disease.

RE:
"it may be that some other, as yet undiscovered process is bringing about both the heart disease and the elevations of cholesterol in the blood." What do you think it could be Scotlyn? Yeah, let's ignore all the studies out there that show the risk factors for heart disease and keep guessing.

It's very simple.Diet high in saturated fat – bad. Little exercice- bad. Smoking -bad. Too much alcohol – bad.

On meat. Here's something from Harvard. Studies are really all over the internet if you want to google yourself.
http://www.hsph.harvard.edu/news/press-releases/2010-releases/shifting-protein-heart-disease-risk-women.html
"During that time the researchers documented 2,210 non-fatal heart attacks and 952 deaths from CHD. After adjusting for age, smoking and other known cardiovascular disease risk factors, the researchers found that higher intakes of processed (such as bacon and salami) and unprocessed (such as steak and pork) red meat and high-fat dairy were significantly associated with an elevated risk of CHD. Higher consumption of fish, poultry and low-fat dairy was significantly associated with a lower risk of CHD.

A number of factors may account for the link between red meat intake and higher risk of heart disease. For example, many previous studies had found an association between the form of iron in red meat and risk of CHD; saturated fat and cholesterol may also contribute to greater CHD risk. The high sodium content of processed meats may also lead to heart disease."

I’m just responding to the points that you have raised, I don’t have a grudge against you–if that’s what you think, Scotlyn. I don’t even know you–i’m sure that you are a nice lady. But expect to be challenged.

Re your first (unlinked) reference above, which I have tracked down, you have cited the National Cholesterol Education Project – a project whose members have strong ties with the pharmaceutical industries who produce the cholesterol-lowering medications which its clinical guidelines propose should be used.

I don’t know how to link files, or had been told and have forgotten. As I said, copy and paste into a search engine–just as good. Any analysis of the actual content of the paper? Or just that the members have strong ties with the pharmaceutical industry? Not all pharmaceutical companies manufacture statins, by the way. I have to admit that I have worked in R&D on the synthesis of a statin for one of these companies. But I have no bias, i’m just interested in the chemical transformations and methods involved in making these compounds, its all very elegant.

On your points (comment 36): don’t disagree with 1, never did, but in moderation.
3-can you really make that call–based on the one paper that you have linked to, whose authors were very tentative in their conclusions. How are you so convinced?

Enjoy your whisky–I think i’ll have one myself.

FME–looks like a good paper, the full version is free too!

It is? The Harvard one? I can only see the abstract of it. Could you copy/paste the full link here for me please? (blind as a bat)
Enjoy your whiskey. I’m house bound all day due to 12 inches. (of snow) and enjoying a nice glass of merlot after my lovely (yuck, really) spinach lasagne I cooked for a fussy vegetarian.

My apologies FME, its not free. I was clicking on a page number at the bottom of the abstract and it took me to a related full paper that was free. No more snow down here, although we have no water either. Again.

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