I’m sure most of you have heard or read about a recent study linking red meat consumption to heart disease. Entitled, Intestinal Microbiota Metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis (1), it purports to show a new mechanism explaining how consuming red meat increases cardiovascular risk.
First, let me thank my readers for bringing this to my attention. I especially want to thank Ted H., in particular, for emailing me a copy.
Let me just say that this gut-flora hypothesis of heart disease from researchers at the Cleveland Clinic has little relation to what I’ve written about over these past six months. Their hypothesis does not directly deal with gut dysbiosis, increased intestinal permeability, small intestinal bacterial overgrowth, translocation of gut pathogens, lipopolysaccharides, zonulin expression, disruption of tight intestinal junctions, inflammatory cytokine responses, activation of the HPA axis, cortisol release, fatty liver, etc.
No, the hypothesis offered by this group centers on how a byproduct of gut flora metabolism of choline or carnitine, known as trimethylamine (TMA), is converted by a liver enzyme (FMO3) to the oxidizing agent trimethylamine N-oxide or TMAO. It singles out TMAO as the cause of atherosclerosis in a rodent model and makes the case that the same holds true in humans.
These scientists claim that eating foods high in both choline and carnitine, which are found in highest concentrations in animal food, are metabolized by gut flora into TMAO precursors and that this is the reason for high heart disease rates in industrialized countries. Therefore, dear reader, you would do well to shun or drastically cut these foods from your diet, or so the hypothesis goes.
Nevertheless, there are quite a few problems with this theory. First, it assumes that there is a proven link between eating red meat, or animal products in general and heart disease.
And why, pray tell, does this assumption exist among these researchers? Because apparently they don’t understand that association does not equal causation. You see, they’ve fallen in absolute puppy love with confounder-prone nutritional epidemiology, the reigning king of quack research “science.”
It isn’t the purpose of today’s post to recount the many erroneous dietary conclusions derived from these types of studies. Instead, I’ll point you to others who have already done a lot of the leg work.
I recommend Kris Kresser’s recent post on this trial which you can find here. However, for a far more exhaustive review of the limitations of epidemiological studies when it comes to nutritional recommendations, no one has done a better job dissecting these types of studies than Anthony Colpo.
Some classics of his include: Red meat Will Kill You, and other Assorted Fairy Tales, The Full Story: Why Eggs Do Not Cause Cardiovascular Disease, and finally Vegetarian Diets Reduce Heart Disease? Nonsense!
Trust me, by the time you’ve finished reading these posts, not only will you have had a good belly laugh or two, you’ll be far better at evaluating these types of studies than the researchers at the Cleveland clinic.
It’s clear that the authors of this paper have bought into the “red meat kills” meme. That’s apparent from the discussion section of this paper where they write:
“Our results also suggest a previously unknown mechanism for the observed relationship between dietary red meat ingestion and accelerated atherosclerosis. Consuming foods rich in l-carnitine (predominantly red meat) can increase fasting human l-carnitine concentrations in the plasma. Meats and full-fat dairy products are abundant components of the Western diet and are commonly implicated in CVD. Together, l-carnitine and choline-containing lipids can constitute up to 2% of a Western diet. Numerous studies have suggested a decrease in atherosclerotic disease risk in vegan and vegetarian individuals compared to omnivores; reduced levels of dietary cholesterol and saturated fat have been suggested as the mechanism explaining this decreased risk.”
There’s an agenda here just so you know, although it’s not based entirely on warning the public about the supposed hazards of consuming a food that has been part of the human diet for millions of years. No, I believe their motivations are far more base than that, but I’ll get to that near the end of this post.
As an aside, I just had to mention that in the introduction of this paper, the authors state:
“The high level of meat consumption in the developed world is linked to CVD [cardiovascular disease] risk, presumably owing to the large content of saturated fats and cholesterol in meat. However, a recent meta-analysis of prospective cohort studies showed no association between dietary saturated fat intake and CVD, prompting the suggestion that other environmental exposures linked to increased meat consumption are responsible.”
The meta-analysis they’re referring to contains this quote:
“This study sought to evaluate the effects of dietary saturated fat on CVD risk by summarizing the data available from informative epidemiologic studies and including, where possible and relevant, supplementary information that had been provided on request from investigators of the component studies. The conglomeration of data from 16 studies with CHD as an endpoint and 8 studies with stroke as the endpoint showed no association of dietary saturated fat on disease prevalence after adjustment for other nutrients wherever possible. Evaluation of the subset of studies (n = 15) that adjusted for total energy, which has been shown to be relevant in evaluating nutrient-disease relations, yielded similar findings.” (2)
That’s a pretty damning admission that the last 50 years of sowing fear in the public’s mind about saturated fat and cholesterol was totally unwarranted, unnecessary and very likely sent millions off to an early death. As Kris Kresser puts it:
“If you read the media reports and full-text of this study, you might have noticed something interesting. The study itself, and even most of the media article [sic] about it, quite simply and without much fanfare stated that saturated fat and cholesterol have little to do with the supposed increase in heart disease observed with red meat consumption. Hold the press! Shouldn’t THAT be front-page news?!? Apparently not. Of course, they’re only willing to admit this publicly in the context of an article where they’re proposing yet another mechanism for how red meat will kill you.”
How will they sell statins now I wonder? Like they always do, by ignoring the awkward.
What’s also very bizarre is that one of the papers they cite in support of their crusade against red meat states:
“Consumption of processed meats was associated with significantly higher incidence of both CHD [coronary heart disease] and diabetes mellitus, with 42% and 19% higher risk, respectively, per 50-g serving per day. In contrast, consumption of unprocessed red meats was not associated with CHD and was associated with a nonsigificant trend toward higher risk of diabetes mellitus.” [Emphasis mine] (3)
So consumption of processed meats is associated with higher incidence of heart disease and diabetes, but not fresh meat. And how do these scientists reconcile this with what they report in their study?
The answer is they don’t. They ignore this contradictory evidence and just carry on as if it doesn’t exist, rightly assuming that the idiots in the media who reported these results and many members of the public won’t bother to check the articles they cite in support of their case.
This study builds, as it were, on a previous study released by this group with the catchy title of Gut Flora Metabolism of Phosphatidylcholine Promotes Cardiovascular Disease.
In that paper, these researchers were able to show that raised TMAO levels in mice genetically bred to easily develop atherosclerosis led to a buildup of plaque in their arteries.
When these mice were given antibiotics that completely wiped out their gut flora, feeding them choline resulted in no production of TMA and no conversion of TMA into oxidizing TMAO. Chris Masterjohn recently published a piece on this current study that you can reach here.
As Chris pointed out in that post, there are a number of variables that can account for plasma TMAO levels that were not explored by these researchers. Not least of them being the rate of excretion in urine and feces. I would also add antioxidant status to the mix. This reminds me of those researchers who sound the alarm on plasma lipopolysaccharide levels from fat consumption yet fail to mention that the chylomicrons they’re attached to neutralize their toxic effects.
It’s also an inconvenient fact that seafood, not red meat, contains the highest concentrations of TMAO of any food consumed by humans:
Notice how beef compares to skate, squid, prawns and octopus? Don’t they eat these foods in heart-healthy Mediterranean countries?
And what are we to make of TMAO concentrations in halibut and cod? Are we now to believe that eating fish causes heart disease? Hurry, someone needs to tell this to the Kitavans and Japanese!
Bang. Head. On. Desk.
You see, what gives seafood that fishy smell is, you guessed it, TMA degraded from TMAO. This rapidly happens if fish is not kept fresh.
In people lacking the gene encoding for the FMO3 enzyme that converts TMA to TMAO, TMA creates quite a “fishy” odor in these folks. An odor that closely resembles the stench emanating from both of these studies.
In the earlier rodent study on choline metabolism, there was one curious observation. Female mice expressed far higher levels of FMO3. They had a 1,000 fold higher expression of this liver enzyme. That would suggest that were the observations seen in these rodents also true for humans, women would be far more prone to heart disease than men. That’s contrary to what we know about female susceptibility to heart disease, especially before the onset of menopause.
Returning to the present study, these researchers found that feeding these artherioslerotic-prone mice carnitine also raised their levels of TMAO, but again, only when gut flora was present. Challenging these mice with carnitine after antibiotic administration did not result in TMA or TMAO production.
However, as Chris pointed out in his latest post, the daily amount of carnitine fed these mice would equal the human equivalent of eating 1,000 steaks per day. Daddy does love his steak, really I do, however even I have my limits.
Now I’m sure all of you are wondering what gut flora was specifically causing the production of the TMAO precursor in these choline-fed mice? Well, believe it or not, that was never determined. Shocking, I know.
You would think that in a study showing how gut flora is essential in the production of TMA, and ultimately TMAO from dietary choline, that some time and effort would have been expended to determine that wouldn’t you?
However, even if they did, would it have had any relevance to humans? In this latest carnitine study, the researchers did indeed correct for this earlier oversight and identified a number of mouse-specific gut bacteria that highly correlated with levels of TMAO. Problem is, these gut bacteria are not found in humans, and the researchers admit as much:
“Further analyses revealed several bacterial taxa whose proportion was significantly associated (some positively, others inversely) with dietary l-carnitine and with plasma TMA or TMAO concentrations (P < 0.05) Notably, a direct comparison of taxa associated with plasma TMAO concentrations in humans versus in mice failed to identify common taxa. These results are consistent with prior reports that microbes identified from the distal gut of the mouse represent genera that are typically not detected in humans.” [Emphasis mine]
Hmmm. Now daddy’s really confused.
What, dear reader, does this mean? It means that the results derived from studying rodents in the choline and carnitine study are pretty much useless for identifying which bacteria does the same in humans.
So let us safely squirrel the mice away in their cozy little temperature-controlled cages and focus our attention on the humans.
So, does human gut flora have the ability to increase this oxidizing and potentially arthereogenic agent in the body?
Yes, it does. They were able to induce increased TMAO production from carnitine consumption in humans. Does this have any relevance to heart-disease risk? Well, these researchers are convinced it does, fish consumption and lack of placebo-controlled, randomized clinical trials notwithstanding.
Five omnivores agreed to be tested to determine whether gut flora is necessary for TMA/TMAO production in humans. These participants were fed a large amount of carnitine in the form of an 8-ounce sirloin steak estimated to contain 180 mg of this substance. Along with the steak, there were given an isotope-labeled supplement containing 250 mg of carnitine.
Figuring 22.5 mg of carnitine in each ounce of steak, this is equivalent to the amount of carnitine found in a 19-ounce slab of beef, a favorite meal of petite, omnivorous ladies everywhere I’m sure.
Urinary levels of TMAO were then collected over a 24-hour period. I’ll show you those results in a minute.
These subjects were then asked to return for a second visit after undergoing a week of broad-spectrum antibiotic use to wipe out their gut flora and test what would happen to TMAO production after undergoing the same challenge.
Let me just say here that the use of broad-spectrum antibiotics for non-medical reasons, is, in my opinion, highly unethical. As I’ve tirelessly explained in numerous posts, beneficial gut flora is not some throw away plaything that we can abuse with no health consequences. Far from it.
After the mass slaughter of gut flora, these participants were again challenged with carnitine as in the previous visit. This time, however, no TMAO was produced. This was confirmation that gut flora is necessary for TMAO production from external sources of carnitine.
On the third visit, our hapless volunteers, with guts ever so primed for gut dysbiosis, were once again given their carnitine challenge and lo and behold, TMAO was detected. Hazzah!
This chart details what happened to one of the five subjects during their three carnitine challenges. During the first visit (far left charts) carnitine challenge resulted in spikes in both TMAO from meat and the carnitine supplement. After wiping out gut flora, the same challenge resulted in no increase in TMAO plasma levels during the second visit. Notice that after antibiotic treatment, the same challenge resulted in TMAO spiking higher than before. Whether or not this is something to concern ourselves with remains an open question.
This graphs TMAO levels in the same subject over twenty-four hours. Again, after wiping out this person’s gut flora, the spike in plasma carnitine was not followed by any increase in TMAO as shown by the flat line in the second chart. The third chart shows what happens after antibiotic treatment. The same carnitine challenge now results in higher TMAO levels.
Here’s what happened to another omnivore who was part of this group:
Unlike the person above, they show no spike in TMAO levels after the carnitine challenge during the first visit. Their levels are pretty much flat. However, note what happens after antibiotic use in the third visit. Twenty-four hour TMAO concentrations are higher than before.
Now, let’s see what happened when one vegan agreed to undergo the same challenge of eating a steak and swallowing a carnitine capsule in comparison to one omnivore:
Here’s another graph showing the difference between five vegan/vegetarians and five omnivores charting TMAO levels when 250 mg of carnitine (but no steak) were ingested. If we assume TMAO is truly harmful, this may be significant.
The researchers note:
“The capacity to produce TMAO (native and d3-labeled) after l-carnitine ingestion was variable among individuals. A post hoc nutritional survey that the volunteers completed suggested that antecedent dietary habits (red meat consumption) may influence the capacity to generate TMAO from l-carnitine (data not shown).”
Data not shown? So we have no idea what different foods either group was eating other than the fact that one group ate red meat and the other didn’t?
No information, say, on whether the red meat typically eaten was fresh or processed? No indication of fiber intake that can dramatically alter bifidobacteria levels in the colon? No information on antioxidant intake from fruits and vegetables? No information on fermented foods other than yogurt that can also shift gut flora populations? No information on levels of processed sugar consumption? Processed food consumption? Alcohol consumption?
Why didn’t they bother sharing this info? Were they afraid to add another page to the forty-page supplement? Were they in fear of my increasing annoyance at having wasted valuable laser toner on printing up this study?
Well, at least they provided us with some other information concerning these participants:
“Male and female volunteers were at least 18 years of age. Volunteers participating in the l-carnitine challenge tests were excluded if they were pregnant, had chronic illness (including a known history of heart failure, renal failure, pulmonary disease, gastrointestinal disorders or hematologic diseases), had an active infection, had received antibiotics within 2 months of study enrollment, had used any over-the-counter or prescriptive probiotic or bowel cleansing preparation within the past 2 months, had ingested yogurt within the past 7 d, or had undergone bariatric or other intestinal (for example, gallbladder removal, bowel resection) surgery.”
But I have more questions I’d like to know the answer to:
- Did the omnivore group include the five members who had their gut flora wiped out earlier?
- Was there a vitamin B2 deficiency in the vegan/vegetarian group (henceforth known as the V/V group) that would impair their conversion of TMA to TMAO?
- Did the V/V group take in more prebiotics from food?
- Did the V/V group consume other fermented foods that were not yogurt?
- Did the V/V group drink less, the same, or more alcohol than the omnivore group?
- Were the number of smokers the same between groups?
- Did the omnivore group contain more current patients of the Cleveland Clinic in contrast to the V/V group?
- Did the omnivore group experience more past hospital stays than the V/V group?
- Did the omnivore group contain older members than the V/V group?
- Were the genders matched between groups?
- Were levels of stress similar?
- Were markers for depression or insomnia similar?
All of these factors, and many more I haven’t mentioned, can affect gut flora composition. All of this assumes, of course, that TMAO levels are relevant to heart disease risk. That would only be true after this hypothesis has been subjected to a randomized, double-blind, placebo-controlled clinical trial.
The researchers then proceed to tell us how elevated plasma concentrations of carnitine are significantly associated in a dose-dependent manner with heart disease in an independent cohort of patients:
The first column is an aggregate of the entire study cohort of 2,595 people. These people were then divided into four quartiles based on fasting carnitine plasma levels. And indeed, those in the highest quartile had the most cardiovascular disease. Moreover, note that carnitine seems to cause people in this group to smoke more as 77% were classified as smokers in contrast to 69% in the lowest group.
Perhaps Phillip Morris needs to add some carnitine to their cigarettes to increase sales.
So what else do we notice in this group? Well, they had the highest levels of type 2 diabetes, hypertension, hyperlipidemia, prior cardiovascular disease, coronary artery disease and peripheral artery disease.
I do find the total cholesterol numbers amusing, however. Shouldn’t their below 200 numbers keep them free from heart disease? Aren’t those statins working? Apparently not. Must be the red meat.
Now the authors assure us that after adjusting for traditional risk factors, the association of plasma carnitine and heart disease was still significant. The risk factors adjusted for were: age, sex, history of diabetes, smoking, blood pressure, LDL and HDL cholesterol.
However, these are far from the only risk factors for coronary heart disease. Tooth and gum disease, pattern and amount of alcohol intake, sugar intake, plasma cytokine levels, fatty liver disease, use of polyunsaturated omega-6 fats, omega-3 status, stress, antioxidant intake, anxiety, depression, insomnia, thyroid function—all of these are verified risk factors for cardiovascular disease.
And of course, I would add in the most important risk factor of all, gut dysbiosis. Most of these risk factors can be explained by the theory of metabolic endotoxemia. The only thing their theory can account for is increased levels of oxidation, and that still needs to be proven in humans eating real food.
Increased TMAO levels may be a sign of gut dysbiosis or nothing at all. The fact that fish contains the highest concentration of TMAO of any food omnivores eat and that seafood consumption is inversely correlated to heart-disease risk leaves me a tad bit skeptical. But hey, I could be wrong.
OK, I want to focus in on the issue of gut flora. Did these researchers study what gut flora was associated with TMAO production?
Why yes they did. However, they didn’t put that chart in the published paper. The chart in the published paper is for the mice. You know, the mice that the researchers said had gut flora not found in humans. Instead, they relegated the human gut flora findings to the supplementary material:
This may be a bit difficult to make out, but I just want to point out that those bacterial strains with red bars next to them containing asterisks had the greatest statistical association with TMAO production. These were all classes of Clostridia. However, note that other strains of Clostridia showed no correlation whatsoever. So assuming TMAO is a relevant marker, it might be helpful identifying the strains of Clostridia that elevate risk for heart disease. However, we already know one well-known cause of Clostridia-specific dysbiosis and it doesn’t have anything to do with red meat consumption:
“This study investigated the relationship between hospital exposures, intestinal microbiota, and subsequent risk of Clostridium difficile–associated disease (CDAD), with use of a nested case-control design. The study included 599 patients, hospitalized from September 2006 through May 2007 in Montreal, Quebec, from whom fecal samples were obtained within 72 h after admission; 25 developed CDAD, and 50 matched controls were selected for analysis. Nonsteroidal anti-inflammatory drugs and antibiotic use were associated with CDAD. Fecal specimens were evaluated by 16S ribosomal RNA microarray to characterize bacteria in the intestinal microbiota during the at-risk period. Probe intensities were higher for Firmicutes, Proteobacteria, and Actinobacteria in the patients with CDAD, compared with controls, whereas probe intensities for Bacteroidetes were lower. After epidemiologic factors were controlled for, only Bacteroidetes and Firmicutes remained significantly and independently associated with development of CDAD. Hospital exposures were associated with changes in the intestinal microbiota and risk of CDAD, and these changes were not driven exclusively by antimicrobial use.”
Comparative Metagenomic Study of Alterations to the Intestinal Microbiota and Risk of Nosocomial Clostridum difficile–Associated Disease (5)
So wouldn’t that mean that the 2,595 cardiovascular patients who had raised carnitine levels were more likely to have been under the care of a doctor and spent more time in the hospital? Could the elevated carnitine levels be nothing more than a marker of gut dysbiosis caused by medical treatment, i.e. iatrogenic disease? Last time I checked Wikipedia, iatrogenic diseases cause 225,000 deaths a year in the United States alone.
Gee, I guess we wouldn’t want to highlight that. Better to blame the meat.
And what of kidney function in these patients. As Chris Masterjohn pointed out, plasma levels of carnitine, or uric acid or many other plasma makers, depends not only on rate of production, but also on rate of excretion either in urine or bile or both. Could the higher carnitine levels be nothing more than an indicator of compromised renal function?
Further issues making me question this particular heart-disease hypothesis comes from placebo-controlled trials that show real benefit when supplementing with carnitine. Unlike a confounder-prone epidemiological study, or a totally uncontrolled, non-randomized study like this one, a double-blind, placebo-controlled trial controls for a great many confounding variables, including the confirmation bias that seems to be at the very heart of this carnitine study.
In one Italian trial that lasted six months, recently diagnosed type 2 diabetics were randomized into either a group receiving a placebo or a group receiving 1 gram of carnitine twice a day. I think we can all safely agree that type 2 diabetics probably have some serious endotoxemia issues going on, not to mention a significantly higher risk for developing heart disease.
So what were the results? Did the carnitine they took in this supplement and ingested in food worsen their markers for heart disease?
“In this preliminary study, after 3 and 6 months, L-carnitine significantly lowered the plasma Lp(a) level compared with placebo in selected hypercholesterolemic patients with newly diagnosed type 2 DM.” (6)
Elevated LP(a) has been identified as a risk factor for coronary heart disease and stroke for quite a long while now. So let me get this straight. Supplementing with carnitine in a double-blind, placebo-controlled trial improved a marker for heart disease. However, it was shown to be associated with increased risk for heart disease in this non-placebo, non-randomized carnitine study. And you want me to believe which study now?
Well, maybe six months wasn’t enough time to induce heart attacks in people with improving heart-disease markers. I know, what about we study a group that already has weakened hearts and is at very high risk for heart attacks? I betcha supplementing these folks with carnitine in another placebo-controlled, randomized trial would cause them to buy that farm in the sky faster than you can yell soo-ee!
“We examined the efficacy of long-term L-carnitine administration for the treatment of heart failure caused by dilated cardiomyopathy in adult patients. To accomplish this, we studied 80 patients with moderate to severe heart failure (New York Heart Association classification III to IV) caused by dilated cardiomyopathy. This article reports on the nearly 3 years of follow-up data on patient mortality. Primary results will be published in the future. After a period of stable cardiac function up to 3 months, patients were randomly assigned to receive either L-carnitine (2 g/d orally) or placebo. There were no statistical differences between the 2 groups at baseline examination in clinical and hemodynamic parameters, such as ejection fraction, Weber classification, maximal time of cardiopulmonary exercise test, peak VO(2) consumption, arterial and pulmonary blood pressure, and cardiac output. [You see in real science, making sure that the two groups of people you are studying are similar in as many ways as possible before the trial begins is very, very important so as not to be perceived as a complete and utter moron by your peers, RM]
After a mean of 33.7 +/- 11.8 months of follow-up (range 10 to 54 months), 70 patients were in the study: 33 in the placebo group and 37 in the L-carnitine group. At the time of analysis, 63 patients were alive. There were 6 deaths in the placebo group and 1 death in the L-carnitine group. Survival analysis with the Kaplan-Meier method showed that patients’ survival was statistically significant (P <.04) in favor of the L-carnitine group. L-carnitine appears to possess considerable potential for the long-term treatment of patients with heart failure attributable to dilated cardiomyopathy.” (7)
What, what, WHAT? You mean more people died in the placebo group than in the dreaded carnitine group? Oh, oh. I can hear our Cleveland Clinic scientists yelling for another epidemiological study to drown out these placebo-controlled results. We can’t have this widely known otherwise what will become of our patents.
Earlier I wrote that what motivated these researchers was not concern for the hazards of red meat consumption in the general population, but something much closer to their wallets.
When I was emailed this study, I almost decided against driving to my local medical library to retrieve the online edition. I’m glad I didn’t give in to that decision.
In the print version of this study, under the heading of “Competing Financial Interests”, the following statement appears:
“The authors declare competing financial interests: details are available in the online version of the paper.”
However, unless you’re a subscriber to Nature, the online paper is behind a pay wall. So what, dear reader, did I find when I accessed the online edition at my local medical library?
“Z.W. [Zeneng Wang] and B.S.L. [Bruce S. Levison] are named as co-inventors on pending patents held by the Cleveland Clinic relating to cardiovascular diagnostics and have the right to receive royalty payments for inventions or discoveries related to cardiovascular diagnostics from Liposciences. W.H.W.T. [W. H. Wilson Tang] received research grant support from Abbott Laboratories and served as a consultant for Medtronic and St. Jude Medical. S.L.H. [Stanley L Hazan] and J.D.S. [Jonathan D Smith] are named as co-inventors on pending and issued patents held by the Cleveland Clinic relating to cardiovascular diagnostics and therapeutics patents. S.L.H. [Stanley L Hazan] has been paid as a consultant or speaker by the following companies: Cleveland Heart Lab., Esperion, Liposciences, Merck & Co. and Pfizer. He has received research funds from Abbott, Cleveland Heart Lab., Esperion and Liposciences and has the right to receive royalty payments for inventions or discoveries related to cardiovascular diagnostics from Abbott Laboratories, Cleveland Heart Lab., Frantz Biomarkers, Liposciences and Siemens.”
It appears that a number of these researchers are developing a diagnostic tool for LipoScience.
How much do you want to bet that the patents held by the authors of this paper have something to do with measuring plasma levels of carnitine and/or TMAO? And how successful do you think they would be in marketing this diagnostic test if they were unable to convince their fellow health-care providers of its necessity, or scare the public into demanding this test when visiting their doctors?
Look, if, and that’s a big “if”, this turns out to be a valid marker for gut dysbiosis and heart disease, then I say go for it gents. Why not. I sure as hell would.
I can assure you that selling probiotics and prebiotics is not where the money is. If I could develop a valid diagnostic test that determined future risk of heart disease, reap millions and retire, I would jump at the chance in a New York minute.
However, given what I’ve just told you about this study, I’m highly doubtful such a test would have any useful clinical application. You’d be better off visiting a gastroenterologist and undergoing tests for increased intestinal permeability.
One last note. In their choline paper, these authors noted how probiotics are capable of altering intestinal gut flora. In this latest paper, not a word is mentioned about either probiotics or prebiotics.
Don’t you find that odd?
Every, and I mean every, paper I’ve read about how metabolic endotoxemia can account for many chronic medical conditions, including heart disease, always mentions the role of beneficial gut flora. They also typically mention how probiotics and prebiotics may play a therapeutic role in mitigating many of these diseases. So why not this paper?
Perhaps they fear that people might come to some unprofitable conclusions, unprofitable, that is, for the medical industry and LipoScience in particular. Nurturing your gut flora with fermented foods, probiotics, prebiotics and making healthy lifestyle and dietary changes that foster the same eliminates the need for expensive drugs or medical testing.
But what then becomes of the patents held by these scientists?
Yes, what would become of them indeed.