Here We Go Again: Another Meat Kills! Study

You’ve got to give the anti-meat hysterics credit for their creativity. Since they can’t prove directly that eating meat will kill you, they’ve become quite adept at stringing unrelated results together into what (almost) looks like a chain of causality.

As I explained in my Big Fat Fiasco speech, this technique is referred to as teleoanalysis. In a nutshell, it works like this: we can’t prove that A causes C, but if we can find evidence that A is linked to B and B is linked to C, we’ll go ahead and declare that A causes C.

Teleoanalysis is partly what has kept the Lipid Hypothesis alive. Studies have failed over and over to prove that a high-fat diet causes heart disease – and in fact, low-fat diets have failed to reduce heart disease in clinical trials over and over. So the anti-fat hysterics trotted out a version of teleoanalysis that looks like this:

  • High-fat diets (A) raise cholesterol (B)
  • Raised cholesterol (B) is associated with heart disease (C)
  • Therefore, a high-fat diet must cause heart disease

If this sounds logical to you, consider my own favorite version of teleoanalysis:

  • Drinking lots of water (A) causes frequent urination (B)
  • Frequent urination (B) is associated with diabetes (C)
  • Therefore, drinking lots of water causes diabetes

With that in mind, let’s take a look at yet another Meat Kills! study that’s making a splash in the media. Here are some quotes from a BBC article online:

A chemical found in red meat helps explain why eating too much steak, mince and bacon is bad for the heart, say US scientists.

A study in the journal Nature Medicine showed that carnitine in red meat was broken down by bacteria in the gut.

This kicked off a chain of events that resulted in higher levels of cholesterol and an increased risk of heart disease.

Can you spot the teleoanalysis? Here it is:

  • Red meat (A) contains carnitine, which when digested kicks off a chain of events leading to higher cholesterol (B)
  • Higher cholesterol (B) is associated with heart disease (C)
  • Therefore, red meat causes heart disease

Here’s the abstract for the study referenced in the BBC article:

Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO). We demonstrate here that metabolism by intestinal microbiota of dietary l-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice. Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of l-carnitine through a microbiota-dependent mechanism. The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status. Plasma l-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels. Chronic dietary l-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed. In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport. Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk.

Allow me to interpret that gobbledygook:

Humans who eat meat have more carnitine-eating bacteria in their guts and therefore produce more TMAO than vegetarians.  TMAO is associated with heart disease.  If we pump mice full of carnitine, they also produce lots of TMAO and get heart disease. So humans should cut back on meat.

More teleoanalysis. It’s just another version of this argument, which helped to establish the Lipid Hypothesis:  lard raises cholesterol, and rabbits get both high cholesterol and heart disease if they’re force-fed lard, so humans shouldn’t eat lard.

The only problem is that lard consumption was plummeting while heart-disease rates were skyrocketing.

The abstract also mentions the “well-established link” between meat consumption and heart disease. Since vegetarians are often more health-conscious in general and therefore less likely to consume sodas, donuts, candy and other junk, I’d expect them to have lower rates of heart disease than meat-eaters who consume the standard western (crap-filled) diet. But is that association consistent?

As I mentioned out in another post about yet another Meat Kills! study, here’s quote from a study titled Mortality In British Vegetarians:

The mortality of both the vegetarians and the nonvegetarians in this study is low compared with national rates. Within the study, mortality from circulatory diseases and all causes is not significantly different between vegetarians and meat eaters.

And here’s the conclusion from a study titled Dietary protein and risk of ischemic heart disease in women:

Our data do not support the hypothesis that a high protein intake increases the risk of ischemic heart disease. In contrast, our findings suggest that replacing carbohydrates with protein may be associated with a lower risk of ischemic heart disease.

In that study, the women who consumed the most protein ate 16.1% more red meat than women who consumed the least protein, but had lower rates of heart disease.

No consistency, no validity.

Enjoy your steak.


56 thoughts on “Here We Go Again: Another Meat Kills! Study

  1. Goose Gander

    Can you spot the teleanalysis

    (a) sugar can elevate levels of glucose in the bloodstream
    (b) elevated levels of glucose in the bloodstream are associated with diabetes
    (c) therefore, sugar causes diabetes

    If you’re gonna (rightly) rip into this sort of crap science when it pertains to red meat, you need to apply the same thinking to the unjustified attacks on sugar by quacks like Lustig.

    There’s a difference: chronically elevated glucose IS diabetes, and attempts to reduce diabetic levels of glucose back to normal by restricting refined carbohydrates have (unlike low-fat diets) succeeded.

    1. Goose gander

      And increasing sugar intake has also worked. As far back as the 1800s. The original (and successful) cure for
      Diabetes was to consume more sugar!

      Say what? Are you seriously suggesting diabetics should eat more sugar?

      1. Jason

        Bloodletting and thunder clappers were “cures” in the 1800’s as well. Just because an old wives tale from the 1800’s says its so doesn’t make it correct.

      2. Lori

        It may have been a cure (rather, a treatment) for hypoglycemia, which can accompany diabetes. People get foggy with very low blood glucose, but not everybody goes into “carb comas when their BG is high.

        It’s important to remember that in those days, there was no controlled testing, a low-starch diet was considered odd and expensive, and sugar was seen as “profoundly health-giving substance: Eighteenth century doctors prescribed sugar pills for nearly everything: heart problems, headache, consumption, labor pains, insanity, old age, and blindness.” (from The Black Count–see Dr. Frederick Slare’s 1715 “A Vindication of Sugars Against the Charge of Dr. Willis, Other Physicians, and Common Prejudices: Dedicated to the Ladies”)

        No, sorry, sugar doesn’t really cure diabetes.

      3. Bob Geary

        @GooseGander – could you provide a reference for increased sugar as a treatment for diabetes? I have above-average Google-fu, but I couldn’t find anything of the sort.

  2. charles grashow

    The study shows that bacteria living in the human digestive tract metabolize the compound carnitine, turning it into trimethylamine-N-oxide (TMAO), a metabolite the researchers previously linked in a 2011 study to the promotion of atherosclerosis in humans. Further, the research finds that a diet high in carnitine promotes the growth of the bacteria that metabolize carnitine, compounding the problem by producing even more of the artery-clogging TMAO.

    The research team was led by Stanley Hazen, M.D., Ph.D., Vice Chair of Translational Research for the Lerner Research Institute and section head of Preventive Cardiology & Rehabilitation in the Miller Family Heart and Vascular Institute at Cleveland Clinic, and Robert Koeth, a medical student at the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University.

    The study tested the carnitine and TMAO levels of omnivores, vegans and vegetarians, and examined the clinical data of 2,595 patients undergoing elective cardiac evaluations. They also examined the cardiac effects of a carnitine-enhanced diet in normal mice compared to mice with suppressed levels of gut microbes, and discovered that TMAO alters cholesterol metabolism at multiple levels, explaining how it enhances atherosclerosis.

    Dr. Hazen began his research five years ago with a scientific fishing expedition. He directs a study of patients who come to the Cleveland Clinic for evaluations. Over the years, there have been 10,000. All were at risk for heart disease and agreed to provide blood samples and to be followed so the researchers would know if any patient had a heart attack or died of heart disease in the three years after the first visit. Those samples enabled him to look for small molecules in the blood to see whether any were associated with heart attacks or deaths.

    That study and a series of additional experiments led to the discovery that a red meat substance no one had suspected — carnitine — seemed to be a culprit. Carnitine is found in red meat and gets its name from the Latin word carnis, the root of carnivore, Dr. Hazen said. It is also found in other foods, he noted, including fish and chicken and even dairy products, but in smaller amounts. Red meat, he said, is the major source, and for many people who eat a lot of red meat, it may be a concern.

    The researchers found that carnitine was not dangerous by itself. Instead, the problem arose when it was metabolized by bacteria in the intestines and ended up as TMAO in the blood.

    That led to the steak-eating study. It turned out that within a couple of hours of a regular meat-eater having a steak, TMAO levels in the blood soared.

    But the outcome was quite different when a vegan ate a steak. Researchers had hypothesized that vegans would not have as many of the gut bacteria needed to make TMAO, and indeed virtually no TMAO appeared in the vegan’s blood after he consumed a steak.

    “We did not expect to see such a dramatic difference,” Dr. Hazen said.

    Then researchers gave meat eaters doses of antibiotics to wipe out almost all of their gut bacteria. After that, they no longer had TMAO in their blood either after consuming red meat or carnitine pills. That meant, he said, that the effect really was because of gut bacteria.

    Researchers then tried to determine whether people with high blood carnitine or TMAO levels were at higher heart disease risk. They analyzed blood from more than 2,500 people, asking if carnitine or TMAO levels predicted heart attacks independently of traditional risk factors like smoking, high cholesterol and blood pressure. Both carnitine and TMAO did. But upon further analysis, they discovered that the effect was solely because of TMAO.

    The researchers’ theory, based on their laboratory studies, is that TMAO enables cholesterol to get into artery walls and also prevents the body from excreting excess cholesterol.

    But what is it about carnitine that bacteria like? The answer, Dr. Hazen said, is that bacteria use it as a fuel.

    Dr. Hazen, though, has taken his findings to heart. He used to eat red meat several times a week, about 12 ounces at a time. Now, he said, he eats it once every two weeks and has no more than 4 to 6 ounces at a time.

    “I am not a vegan,” Dr. Hazen said. “I like a good steak.”

    Mice who were given broad-spectrum antibiotics to wipe out their gut bacteria did not produce TMAO even on a high-carnitine diet, confirming the microbes’ role in linking the two. The group previously found the same result in their lecithin study.

    That doesn’t mean anybody should be taking antibiotics to help prevent heart disease, though, Hazen said. It does mean that a heart-healthy probiotic or yogurt might be a way of modifying the carnitine-TMAO pathway and reducing heart disease risk.

    The group also continues to work on a diagnostic test for TMAO, which should be available late this year.

  3. emi11n

    Thanks again for another great analysis. NBC news just ran a story on this tonight, but of course gave no details or context, just obediently repeated the red meat=death propaganda. Of course they always like to use a human example in their crappy medical stories, so they featured a guy who had a family history of heart disease and had high cholesterol. He was concerned about the hazards of red meat. So at the end of the segment, they show him loading up at the salad bar and state that he went vegan. So now he’s thinner, healthier, and happier. Cue the sound of angelic choruses…(ok, that part was sarcasm). Gee, wonder if they’ll feature him again in a few years when he starts having health issues on his heart healthy vegan diet?
    Head. bang. on. desk.

    Nope, when the guy’s vegan diet doesn’t work out, we’ll never hear about him.

  4. LC

    Nice analysis. The bit on NBC news featured Dr. Hazen, the author, who, with all due respect, reminded me of Nathan Lane when he puts *that* face on. Anyway, and ps, how can something (carnitine) that we use to shuttle free fatty acids into the beta oxidation cycle – the carnitine shuttle – be so bad that it causes heart disease? Doesn’t seem to be evolutionarily smart. Dr. Hazen said (paraphrase) “We make it, so we don’t need to eat it” (yuh, but if we make it how would it make sense that a) it’s bad, or b) when we eat it it’s bad?)

  5. Pierson

    I don’t get it; Do heavy carnivores (Lions, dogs, bears, etc.) have high rates of heart disease? Is this present in other carnivorous Primates, like Chimps? Do low-carb, high-red meat cultures have higher rates of heart disease than those who eat less red meat? How the hell did our ancestors survive during times of famine, when red meat was all that was available to eat at times? Can TMAO production be influenced by exposure to a high-sugar diet?

  6. Stefan

    The German press has picked up this one as well. Same main message. However this article ( however has an interesting last sentence which I didn’t see elsewhere:

    Völlig gelöst ist das Rätsel damit aber noch nicht. So enthält etwa Seefisch relativ viel TMAO. Aber regelmäßig Fisch essen – das gilt eher als gut für die Gefäße denn als schädlich

    Translation: With this the riddle isn’t totally solved yet. Sea fish contains relatively a lot of TMAO. But eating fish regularly – that is considered rather good for blood vessels than damaging.

    Hmm, so now what? Would be also nice to know what kind of beef they looked at (grass fed?)

  7. Nowhereman

    Heads up! There’s another Yahoo bunch of nonsense. This time they’re targeting the Paleo diet:–debunked%E2%80%94what-took-so-long–202100492.html

    This means we must be winning more than I thought since they are actually putting out a major attempt at “debunking” Paleo. Before, “they” had merely treated it as a silly little curiosity, now they’re getting really serious and seeing it for the threat to their status quo that it is.

    Yes, it’s a positive sign when people feel threatened by the paleo “fad.”

    1. Nowhereman

      Indeed, Tom. What also heartens me is to see the numbers of comments from people calling out the BS for what it is, and not just blindly accepting the ‘expert’s’ word on it (who also appears to be selling a book from the look of it). Oh and this week there have been several anti-gluten free diet articles as well. Here’s an example to make you want to bang your head on your desk:

      I mean, really? But at least people are tearing this one apart as well.

      That’s what I love about the wisdom of crowds. They can keep printing this nonsense, but people aren’t buying it anymore.

    2. Austin

      “Carbohydrates are necessary for energy and brain function.” *forehead slap*

      I had to comment there to remind readers of a little thing called gluconeogenesis and another little thing called “ample veggies”.

  8. Stan

    It’s funny how their very first sentence is contradicted by their second reference “The high level of meat consumption in the developed world is linked to CVD risk, presumably owing to the large content of saturated fats and cholesterol in meat1,2” and reference 1 is a single epidemiologial study and 2 is a meta-analysis where only processed red meat and not fresh red meat was associated with coronary heart disease risk. So their entire premise is faulty according to the evidence that is supposed to justify it.

  9. Martin Levac

    Tom, if that’s not enough, here’s more:

    Basically, we have a case of a zealous researcher who really really really wants to shine right now because it’s very very very urgent. So, in spite of including a reference (PMID: 20479151 for those interested) in his study that directly refutes the “well-established link between high levels of consumption of red meat and CVD risk” cited in the abstract, he furiously reloads the NYTimes front page to see if the article is posted, and when it does, frantically logs in to Wikipedia, and hurriedly modifies the relevant entries for carnitine and TMAO to include both a direct link to the study and to the NYTimes article, all within hours of first publication. All my other hypotheses incriminate too many innocents.

    Apparently, people always do it like that. As I was told, “somebody reads something online, then modifies the relevant Wikipedia entries accordingly”. Funny, I found out about this “standard practice” while doing my usual routine of checking the sources. I wonder why we think it’s normal.

    Anyway, this researcher got paid a ton of money (several millions of dollars) to research a mechanism (it started with choline, now it’s carnitine, but it was always TMAO) for a non-existing link between red meat consumption and CVD risk. Also apparently, fish contains tons more TMAO right off the bat than any other meat, yet fish intake is inversely correlated with CVD risk. Pfft. Yay for science.

    Ahh, the plot thickens. Thanks.

    1. Walter Bushell

      I should have thought about fish, after all the usual recommendation about choline is to limit consumption so that you don’t smell fishy.

  10. George Wilson

    Goose, goose, goose… You miss the point…

    Teleoanalysis is subject to the classic logic trap…

    A table has four legs
    A cow has four legs
    Therefore a cow is a table

    The difference in the analysis you cite is the experimental data seems to confirm it. It was not the analysis of Keys that was at fault as such posits are a typical way of setting experimental design. The fault was his steadfast insistence that it was true despite the mountain of evidence that it was not true. Wishful thinking is not a substitute for data.

    It was a reasonable posit but, from the evidence, it appears the relation was opposite, Heart disease drives elevated cholesterol.

    On this research there is some potential amplification to be gained. I, for one, would like to see if there is a difference in result between pastured (grass fed) and feed lot (corn/soy fattened) cattle.

    Yup, the experimental data on sugar and diabetes is holding up — data gathered from clinical studies on humans.

    In this case, they’ve pointed out an association between TMAO levels and heart disease in humans and combined that with a mouse experiment. It’s cholesterol/rabbits/lard all over again. The association between TMAO and heart disease could be due to a number of factors. Another reader pointed to this article by Chris Masterjohn:

    “Elevated TMAO could reflect dietary trimethylamine or TMAO from seafood, but it could also reflect impaired excretion into the urine, or enhanced conversion of trimethylamine to TMAO in the liver.

    The enzyme Fmo3 carries out this conversion, mainly in the liver, as reviewed here. There are a number of genetic variants affecting the activity of this enzyme, some of which appear only in certain ethnicities, and the enzyme also processes a number of drugs used to treat psychoses, infections, arthritis, gastro-esophageal reflux disease (GERD), ulcers, and breast cancer. Iron or salt overload may also increase the activity of the enzyme. TMAO could, then, be a marker for ethnicity, drug exposure, genetically determined drug efficacy, or other conditions.”

  11. Charlie

    The authors did something similar with choline to what they are doing now with carnitine. Chris Masterjohn did a block on it.

    In fact, these authors even fed 46 different foods to humans and looked at the subsequent excretion of trimethylamine and TMAO. Choline-rich foods like liver and eggs did not produce any increase in urinary trimethylamine or TMAO over control levels. In fact, even carnitine-rich meats failed to increase excretion of these compounds. The only foods that increased excretion of TMAO were seafoods, which naturally contain some trimethylamine, giving them their “fishy” smell.


    Perhaps future work will in fact elucidate a role for harmful gut bacteria in increasing TMAO levels and subsequent development of heart disease, in which case the clear implication would be that we should figure out how to normalize the gut bacteria. Right now, we have no evidence that eating choline-rich animal foods increases TMAO at all, so a hypothesis dependent on this apparently fictitious process is as yet an impotent one.

  12. Jess

    I actually looked up the study yesterday at work when I saw an article on it ont he Time website. This was my favorite part:

    “An analyte with identical molecular weight and retention time to
    l-carnitine was not in the top tier of analytes that met the stringent
    P value cutoff for association with CVD. However, a hypothesis-driven
    examination of the data using less stringent criteria (no adjustment for
    multiple testing) revealed an analyte with the appropriate molecular
    weight and retention time for l-carnitine that was associated with cardiovascular event risk (P = 0.04).”

    So… we didn’t see what we wanted with the really stringent tests, so we loosened up our standards and found what we wanted to find?

    I couldn’t get away with that sort of response in research in the lab I work in. Some scientists are quite sloppy and don’t really follow the scientific method very well at all.

    One of my favorite lines from Dr. Mike Eades: If you torture the data long enough, it’ll tell you what you want to hear.

  13. Jim

    I heard the same NBC story last night. I actually overheard it as I never watch that news. It was literally maddening to hear how they reported it. So irresponsible. Many people will make diet choices based on that lousy report. It was a very slick presentation. A co-worker of mine is a vegetarian and he is often asking me (respectfully so far) if I am concerned with all the problems with meat. I usually just dispense with his question in a sentence or two. I honestly don’t want to debate with him. He isn’t going to change my mind and I won’t change his so why bother.

    The most interesting aspect of this person is that as a vegetarian he never eats vegetables. Lots of pasta, processed foods and mountains of candy. He recently ended up in the ER with severely high blood pressure. So now he is on BP meds and cutting back his sodium intake. Even so his BP still soars from time to time. The candy eating hasn’t stopped. The other critic of my diet in the office is on statins and bp meds too. I take none and I eat a high fat diet with lots of red meat. I feel great and my health markers are normal or great. Doesn’t convince these guys though. This is the kind of thing we are dealing with. I just say let the results speak for themselves. A few months ago when they were both trying to talk to me about diet I pointed out that I was the only one not on prescription meds. My comment brought immediate silence. They have not said too much since then. Yeah that was fun.

    I get that one too. People who are popping statins, painkillers and other prescription drugs still believe my fatty diet will kill me.

    1. Catherine

      A vegetarian who doesn’t eat vegetables – I love that! Jim – my darling hubby is on BP tablets (two different ones), and has just been prescribed Atorvastatin. He suffered a minor heart attack on New Year’s Eve 2011, and really, apart from quitting smoking, the best thing he could do is lose his excess weight. He flatly refuses to believe that my eating plenty of fresh meat, eggs, butter, cream, fish and vegetables is a good diet. He is addicted to sugary foods – cake, biscuits, sweets – you name it! Yet I am not the one who has high blood pressure (I don’t believe that very many people actually need to take statins, him included, so I don’t count those as “needing” to be taken). Our GP (new to us) has, of course, told him to cut down on the fat, and eat wholemeal bread rather than white, etc etc. I have to say it really does worry me.

  14. Brandon

    I did some research on this, apparently TMAO reduces ER (endoplasmic reticulum if I remember correctly) and oxidative stress in certain cell types. Maybe this makes sense with all the inflammation going on in the blood vessels.

    1. Pierson

      The endoplasmic reticulum is the organelle that makes mitochondria, though, so I hope TMAO doesn’t reduce it…

      1. Martí

        I thought the mitochondria were responsible for reproducing themselves (they have their own distinct DNA), the endoplasmic reticulum either produces proteins and hormones if it is a rough endoplasmic reticulum (has lots of attached ribosomes) or removes toxins if it’s a smooth endoplasmic reticulum (little to no ribosomes attached). Still less than fun side-effects from losing either of those though…….

        1. Brandon

          Ok, since my second post was without context, I’ll say this again:

          TMAO seemed to reduce ER stress and oxidative stress in certain cell types. It has nothing to do with ‘reducing the ER.’

          1. Martí

            Ah, thanks for the context! (sorry, must’ve misread your first comment) 🙂 In that case what I said is reversed, if the stress is reduced for oxidation and ER stress the cells should have better protein synthesis, detoxifying processes, and also be better protected against cancer. Thanks for sharing! 🙂

  15. George @ the High Fat hep C Diet

    Isn’t fish (the richest source of TMAO) supposed to be good for the heart?
    Isn’t there less carnitine in processed meat? (pork and chicken, the main ingredients in processed meat, have about 1/4 the carnitine of red meat)
    Doesn’t ALCAR, acetyl-l-carnitine, extend life in rodents (or at least not kill them)?
    What about homocysteine, trans fats, iron, cholesterol, omega 6, and every other candidate for the cause of heart disease – isn’t TMAO just joining the end of a very long queue?
    What is the chemical reaction by which TMAO produces these effects?

    “Some osmolytes, such as trimethylamine-N-oxide (TMAO), are known to protect proteins against harsh environments (1, 2). In particular, TMAO counteracts the destabilizing effect of urea on protein structure (3–5). Addition of TMAO to a protein solution usually results in increased protein stability against denaturation (6, 7), and higher rigidity of the protein backbone (8, 9). Mechanistically, TMAO compacts a protein globule, while urea does the opposite (8, 10, 11).”

    Sure, and a high-fat diet will lower your triglycerides and raise your HDL, but we all know a high-fat diet will kill you anyway. You can’t expect consistency from these people.

  16. Martí

    Maybe I missed it, but is this the same type of carnitine that clinical studies have shown to improve lipid profiles, decrease the pains of angina, and increase heart recovery during exercise in patients with heart disease?

    “The authors conclude, after having discussed the particular metabolic mechanisms, that L-carnitine undoubtedly represents an interesting therapeutic drug for patients with exercise-induced stable angina.”

    “Thus, LPC [L-propionylcarnitine] prevents ischemia-induced ventricular dysfunction, not by affecting the myocardial oxygen supply-demand ratio but as a result of its intrinsic metabolic actions, increasing pyruvate dehydrogenase activity and flux through the citric acid cycle. Because it is well tolerated, it may be a valuable alternative or addition to available antiischemic therapy.”

    Gotta love the consistency of medical science, its healthy for you if its a drug but if it comes from its natural source in meat, then heaven help you that nutrients a heart attack waiting to happen! Lord knows how we survived before Big Pharma put all our nutrients in pills ^_^

    Does seem a bit inconsistent, doesn’t it?

  17. Pierce

    From a previous comment: “Anyway, this researcher got paid a ton of money (several millions of dollars)”


  18. K2

    Hi Tom,

    This might have no bearing on the study or the outcome, but I couldn’t help but immediately think something was up when I saw the location: Cleveland Clinic. Yep, the home of Dr. Caldwell Esselstyn, the vegan doctor who promotes a zero fat vegan diet to heart patients, even though he is not a cardiologist. He didn’t conduct the study, but I have to wonder if there might be an association with the clinic’s vegan heart patient program. Again, it might be a coincidence, but it threw up a big red flag for me.

    Personally, I don’t eat beef (or much meat period) because it bothers my stomach. Otherwise, I load up on eggs, butter, cream cheese, goat cheese, veggies, yams, some fish, etc. Honestly, I think the bottom line is eat real food that suits your individual life, just enough to meet your daily needs, and get on with life.

    I really love your common sense, down-to-earth and humorous responses to the “science” out there. Keep up the good work! 🙂

    There certainly could be a connection, but I don’t know.

  19. Paul B.

    The dramatic increase in sugar consumption over the last few generations is remarkable. And just as remarkable is the decrease in consumption of saturated fat, paralleled by an increase in vegetable oil consumption. It would be interesting to see some charts illustrating this.

    Im 46 years old so I remember the days when fast food restaurants fried stuff in beef tallow, and Mom cooked stuff in butter and lard. Now it seems to be all vegetable oils–corn, soy, canola, safflower, etc. Not only do these foods just not taste as good, we do have a lot more fat people walking around these days. Some researchers think all of the high omega 6 oils may be contributing to obesity as these fats are virtually unknown to the human body until recent times.

    So maybe PUFA’s can give you a FUPA?

    And then you’re FUBAR.

  20. neal matheson

    The health bit on BBC radio 4 featured a section on this study, I only caught the end but the potential “paradox” with fish was mentioned as was another marker of heart health. So expect a new drug soon then.
    I have been suprised at the reaction of many in the Paleo world at this article thanks Tom and Chris for your critical view of it.

    And the paradoxes just keep piling up.

  21. Ted Hutchinson

    Here is another detailed rebuttal of this paper highlighting other aspects of bad science not discussed in other blogs on this paper.
    Are Red Meat And Your Gut Flora Killing You? Or Do I Smell Some Rotten Fish?
    It worth reading to the end of the blog where “Competing Financial Interests” of the researchers are discussed.

    So it’s not just the TMAO-raising fish that smells rotten.

  22. Ted Hutchinson

    Just in case anyone has any lingering doubts that this red meat, carnitine, study has any validity at all you may care to read this study which comes from people totally outside the paleo/low carb community.

    L-Carnitine Significantly Improves Patient Outcomes Following Heart Attack

    This systematic review of the 13 controlled trials in 3,629 patients, involving 250 deaths, 220 cases of new heart failure, and 38 recurrent heart attacks, found that L-carnitine was associated with:

    · Significant 27% reduction in all-cause mortality (number needed to treat 38)

    · Highly significant 65% reduction in ventricular arrhythmias (number needed to treat 4)

    · Significant 40% reduction in the development of angina (number needed to treat 3)

    · Reduction in infarct size

    There were numerically fewer myocardial reinfarctions and heart failure cases associated with L-carnitine,

    L-carnitine is proven to be safe and is readily available over the counter. The investigators agree that the overall results of this meta-analysis support the potential use of L-carnitine in acute myocardial infarction and possibly in secondary coronary prevention and treatment, including angina.
    If it was true that Carnitine, either as a supplement or in red meat was a factor in heart disease then giving carnitine to people who have just had a stroke would make matters (their survival) worse.
    In practice carnitine improves survival.

  23. Fauna V

    Follow the money…

  24. Nowhereman

    This reminds me of Chris Masterjohn’s analysis of T Colin Campbell’s studies of rats being fed casein protein where he pointed out that Campbell came to a false conclusion that the protein casein and therefore all animal-based proteins by extension caused cancer because he fed the rats a purified casein and combined it with aflatoxin to form a complete protein that then induced tumor growth. However, in order to come to this conclusion, he ignored many other factors that came up during this test and subsequent other ones, such as the control rats on minimal protein levels dying of liver failure much sooner than the aflatoxin/casein rats. Campbell also ignored that while wheat protein when combined with aflatoxin did not cause cancer, when combined with lysine it also produced carcinogenic effects very similar to what the casein-aflaxtoxin did.

    It’s really just amazing what hoops a person who’s come to a foregone conclusion will do to force the data to fit their preconceived view, even going to the point of lying about their results.

    Sad but true.

  25. Juia Wilson

    It’s getting to the point where you can’t believe anything. Any study can be skewed to whatever result they want, plus like you have mentioned the analysis is usually being done to benefit one side. Hey, I don’t want to live to be 90 anyway so give me some steak!

  26. WesSeid

    In case anyone missed the most interesting part of this study, here it is:

    The study found that saturated fats and cholesterol aren’t a major cause of heart disease! …Who knew?

    You’d think that little revelation would be the headline of every newspaper.

    I keep waiting for that …


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