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Carnitine, Red Meat and Heart Disease

April 13, 2013 Written by JP    [Font too small?]

It seems red meat is always getting a bad rap – everyone from the American Heart Association to environmentalists to PETA (People for the Ethical Treatment of Animals) has something negative to say about eating beef. From a health standpoint, the cholesterol and saturated fat content of meat is still noted as grounds to avoid it. However, studies examining the link between red meat intake and cancer, cardiovascular disease and overall mortality have consistently yielded mixed results. What’s more, grass fed meat, which contains a significant amount of healthful omega-3 fats, is now quite common in the food supply. This adds yet another wrinkle to the current beef battle.

The latest edition of the journal Nature Medicine offers up a new reason to avoid red meat – the abundance of carnitine (an amino acid derivative) in red meat. This may seem like a bit of head scratcher for those who are familiar with the integrative management of cardiovascular disease. After all, holistically inclined cardiologists such as Dr. Stephen Sinatra have been recommending supplemental carnitine to heart patients for many years. The basis for this recommendation is described in a recently updated review from Oregon State University’s Linus Pauling Institute (LPI). In it, LPI researchers point to scientific studies showing that carnitine benefits patients with various cardiovascular-related ills such as angina pectoris, heart failure and peripheral arterial disease. Nevertheless, the authors of this new study claim that carnitine appears to interact with select intestinal bacteria in such a manner as to cause an increase in, TMAO (trimethylamine-N-oxide), a proatherogenic product.

To a lesser extent, the current study also implicates choline, an essential nutrient mostly found in eggs, fish and meat, as another potentially dangerous component of red meat. This too is quite perplexing. In recent years, there’s been a push within the nutritional community to emphasize the importance of choline during pregnancy to support infant brain development. Additionally, a choline deficiency, which is commonly found in strict vegetarian diets, has been implicated in “liver and muscle dysfunction” and “increased DNA strand breaks” – a cause of carcinogenesis and cell death. Other research indicates that choline, a B-vitamin, helps protect against suspected cardiovascular risk factors, including excess homocysteine and systemic inflammation.

Ultimately, it doesn’t much matter why I think this provocative new finding isn’t the elusive “smoking gun” implicating red meat as a cause of heart disease mortality. If this new theory is indeed accurate, you’d expect to see a pattern of proof in population studies that examine the link between red meat consumption and heart attacks and strokes. In 2013, there have been at least three such studies. They’ve involved a total of approximately 600,000 adult men and women. Two of the investigations found no association between (non-processed) meat intake and cardiovascular mortality. One study demonstrated an increased risk of heart disease deaths in men who ate the most meat, but a lower risk of stroke in the same group. This is far from definitive evidence. In fact, if anything, the weight of the data tips in favor of red meat being an insignificant factor in these findings.

If it seems as if I’m suggesting that everyone eat copious amounts of beef, that is not the case. There’s really little reason to go out of your way to eat large amounts of conventionally raised beef. In my opinion, red meat is best eaten in moderation alongside non-starchy fruits and vegetables, including avocados, broccoli, spinach and tomatoes. I also recommend opting for grass fed beef whenever possible because it has a favorable omega-6/omega-3 fatty acid ratio and lower levels of added hormones and antibiotic residues. Marinating meat in herbs, red wine and spices is another way of improving the health promoting properties of beef by decreasing the amount of toxic chemicals (heterocyclic aromatic amines) which form during the cooking process. Personally, one of my favorite ways to enjoy red meat is at a local chain of restaurants called The Counter. There, I order an organic bison burger in an organic salad bowl with black olives, roasted red peppers, sauteed onions and sliced tomatoes. No bun, no fried potatoes and no soda. Just my burger-in-a-bowl and a glass of red wine. That’s my idea of a healthy meal. And, this latest scare story making headlines in the news hasn’t changed my mind about it.

Note: Please check out the “Comments & Updates” section of this blog – at the bottom of the page. You can find the latest research about this topic there!

To learn more about the studies referenced in today’s column, please click on the following links:

Study 1 – Intestinal Microbiota Metabolism of L-Carnitine, A Nutrient in Red … (link)

Study 2 – Linus Pauling Institute Micronutrient Information Center: Carnitine (link)

Study 3 – Dietary Choline Deficiency Causes DNA Strand Brreaks and Alters (link)

Study 4 – The World’s Healthiest Foods: Foods Rich in Choline (link)

Study 5 – Meat Consumption and Mortality – Results from the European … (link)

Study 6 – Meat Consumption and Diet Quality and Mortality in NHANES III (link)

Study 7 – Red Meat and Poultry Intakes and Risk of Total and Cause-Specific (link)

Study 8 – Hass Avocado Modulates Postprandial Vascular Reactivity and … (link)

Study 9 – Red Meat from Animals Offered a Grass Diet Increases Plasma and (link)

Study 10 – Inhibitory Effect of Antioxidant-Rich Marinades on the Formation of (link)

Carnitine and Choline Reduce Lipid Peroxidation, Oxidative Stress

Source: J Am Coll Nutr – June 2005 Vol. 24 No. 3 (link)

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Posted in Food and Drink, Heart Health, Nutrition

9 Comments & Updates to “Carnitine, Red Meat and Heart Disease”

  1. Orna Izakson Says:

    Another great one, JP!

  2. JP Says:

    Thank you, Orna!

    Be well!


  3. liverock Says:

    Chris Masterjohn has done a major debunking of this study.

    According to his research not only does fish have more TMAO than meat, but vegetables such as peas and carrots have more than double the amount of TMAO!

    The trouble with these sort of studies is by the time the media have proclaimed that carnitine will kill you, they never have the space or will to publicise any counter research.


  4. JP Says:


    I think Chris wrote an excellent piece. He’s a wonderful ally for all sensible low carb enthusiasts. I recommend his article to anyone interested in this controversy.

    Be well!


  5. JP Says:

    Update: Carnitine supplementation reduces CAD-related inflammation …


    Nutrition. 2015 Mar;31(3):475-9.

    Antiinflammatory effects of l-carnitine supplementation (1000 mg/d) in coronary artery disease patients.

    OBJECTIVE: Inflammation mediators have been recognized as risk factors for the pathogenesis of coronary artery disease (CAD). The purpose of this study was to investigate the effect of l-carnitine supplementation (LC, 1000 mg/d) on inflammation markers in patients with CAD.

    METHODS: We enrolled 47 patients with CAD in the study. The patients with CAD were identified by cardiac catheterization as having <50% stenosis of one major coronary artery. The patients were randomly assigned to the placebo (n = 24) and LC (n = 23) groups and the intervention was administered for 12 wk. The levels of LC, antioxidant status (malondialdehyde and antioxidant enzymes activities), and inflammation markers (C-reactive protein [CRP], interleukin [IL]-6, and tumor necrosis factor [TNF]-α) were measured.

    RESULTS: Thirty-nine participants completed the study (19 placebo; 20 LC). After LC supplementation, the levels of inflammation markers were significantly reduced compared with the baseline (CRP, P < 0.01; IL-6, P = 0.03; TNF-α, P = 0.07) and those in the placebo group (CRP, P < 0.05; IL-6, P = 0.04; TNF-α, P = 0.03). The levels of inflammation markers were significantly negatively correlated with the levels of LC and antioxidant enzymes activities (P < 0.05). CONCLUSIONS: We suggest that LC supplementation, due to its antioxidant effects, may have potential utility to reduce inflammation in CAD. Be well! JP

  6. JP Says:

    Updated 12/17/15:


    Clin Endocrinol (Oxf). 2015 Dec 15.

    Oral carnitine supplementation reduces body weight and insulin resistance in women with polycystic ovary syndrome: a randomized, double-blind, placebo-controlled trial.

    OBJECTIVE: Limited data are available evaluating the effects of oral carnitine supplementation on weight loss and metabolic profiles of women with polycystic ovary syndrome (PCOS). This study was designed to determine the effects of oral carnitine supplementation on weight loss, and glycaemic and lipid profiles in women with PCOS.

    DESIGN, PATIENTS AND MEASUREMENTS: In a prospective, randomized, double-blind, placebo-controlled trial, 60 overweight patients diagnosed with PCOS were randomized to receive either 250 mg carnitine supplements (n=30) or placebo (n=30) for 12 weeks. Fasting blood samples were obtained at the beginning and end of the study to quantify parameters of glucose homeostasis and lipid concentrations.

    RESULTS: At the end of the 12 weeks, taking carnitine supplements resulted in a significant reduction in weight (-2.7±1.5 vs. +0.1±1.8 kg, P<0.001), BMI (-1.1±0.6 vs. +0.1±0.7 kg/m2 , P<0.001), waist circumference (WC) (-2.0±1.3 vs. -0.3±2.0 cm, P<0.001) and hip circumference (HC) (-2.5±1.5 vs. -0.3±1.8 cm, P<0.001) compared with placebo. In addition, compared with placebo, carnitine administration in women with PCOS led to a significant reduction in fasting plasma glucose (-0.38±0.36 vs. +0.11±0.97 mmol/L, P=0.01), serum insulin levels (-14.39±25.80 vs. +3.01±37.25 pmol/L, P=0.04), homeostasis model of assessment-insulin resistance (-0.61±1.03 vs. +0.11±1.43, P=0.04) and dehydroepiandrosterone sulfate (-3.64±7.00 vs. -0.59±3.20 μmol/L, P=0.03).

    CONCLUSIONS: Overall, 12 weeks of carnitine administration in PCOS women resulted in reductions in weight, BMI, WC and HC, and beneficial effects on glycaemic control; however, it did not affect lipid profiles or free testosterone.

    Be well!


  7. JP Says:

    Updated 03/07/16:


    J Am Coll Nutr. 2016 Mar 2:1-7.

    Effects of l-Carnitine Supplementation on Serum Inflammatory Factors and Matrix Metalloproteinase Enzymes in Females with Knee Osteoarthritis: A Randomized, Double-Blind, Placebo-Controlled Pilot Study.

    OBJECTIVE: Considering the importance of inflammation in the pathogenesis of osteoarthritis (OA) and induction of pain, this study was aimed to investigate the effect of L-carnitine supplementation on serum inflammatory mediators and OA-associated pain in females with knee OA.

    METHODS: In this clinical trial, 72 females with mild to moderate knee osteoarthritis started the study, divided into 2 groups to receive 750 mg/day L-carnitine (n = 36) or placebo (n = 36) for 8 weeks. Serum levels of Interleukine-1β (IL-1β), high-sensitivity C-reactive protein (hs-CRP), matrix metalloproteinases (MMPs)-1 and -13, and visual analog scale (VAS) for pain were assessed before and after supplementation. Data were analyzed by t test, Wilcoxon signed rank test, Mann-Whitney U test, and analysis of covariance.

    RESULTS: Only 69 patients (33 in the L-carnitine group and 36 in the placebo group) completed the study. L-Carnitine supplementation decreased serum IL-1β and MMP-1 levels significantly (p = 0.001 and p = 0.021, respectively); however, serum hs-CRP and MMP-13 levels did not change significantly (p > 0.05). In the placebo group, serum IL-1β levels increased significantly (p = 0.011), whereas other studied biomarkers did not change significantly. The mean VAS score decreased significantly in the L-carnitine and placebo groups by 52.67% and 21.82%, respectively (p < 0.001). Significant differences were only observed between the 2 groups in serum IL-1β (p < 0.001) and MMP-1 (p = 0.006) levels and mean VAS score (p = 0.002) after adjusting for baseline values and covariates. CONCLUSION: Despite observed beneficial effects of short-term supplementation of L-carnitine in decreasing serum inflammatory mediators and improving pain in knee OA patients, further studies are needed to achieve concise conclusions. Be well! JP

  8. JP Says:

    Updated 05/30/16:


    J Int Soc Sports Nutr. 2015; 12(Suppl 1): P11.

    The effects of beef protein isolate and whey protein isolate supplementation on lean mass and strength in resistance trained individuals – a double blind, placebo controlled study

    Background: Consumption of moderate amounts of whey and animal derived protein has been demonstrated to enhance short and long-term protein balance over a placebo matched control. However, to date no study has comprehensively compared high quality beef based protein supplementation with whey based protein sources following a resistance training protocol. The purpose of this study was to determine the effects of post-exercise consumption of two servings of beef protein isolate (BeefISO) or whey, compared to a maltodextrin control on lean mass and strength during 8 weeks of resistance training.

    Methods: Thirty college-aged, resistance-trained males and females were randomly assigned to one of three treatment groups. Subjects consumed two servings (46g) of Beef Protein Isolate (BeefISO™), Whey Protein isolate or maltodextrin. Subjects trained 5 days per week (3 resistance training, 2 cardio) for 8 weeks as a part of a daily undulating periodized resistance-training program. Two servings of protein were consumed immediately following exercise or at a similar time of day on off days. Dual emission x-ray absorptiometry (DXA) was used to determine changes in body composition. Maximum strength were assessed by one-rep-max (1RM) for bench press (upper body) and deadlift (lower body). A two-way ANOVA with repeated measures model was used to identify group, time, and group by time interactions. The significance level was set at p < 0.05. Results: Both beef protein isolate (↑5.7%) and whey protein isolate (↑4.7%) each lead to a significant increase in lean body mass compared with baseline (p < 0.0001). Fat loss was also significantly decreased at 8 weeks compared to baseline for beef protein isolate and whey, 10.8% and 8.3% respectively (p < 0.0001). 1RM both deadlift and bench-press were both significantly increased for all treatment groups when compared to baseline. However, no significant differences in increased strength as measured by deadlift (↑11.6%-19.3 %) or bench-press (↑11.4%-17.6%) were observed between beef protein isolate, whey, or maltodextrin groups over the 8 week training regimen (p < 0.0001). Conclusion: The results of this study further support the benefits of protein supplementation following resistance training. Specifically, in this study consumption of two-servings of beef protein isolate or whey resulted in significant gains in lean body mass over time, which outpaced gains resultant from resistance training alone (maltodextrin supplementation). However, all experimental groups increased strength equally. It is plausible that the uniform strength gains were explained by both increases in neural and morphological adaptations negating the effect of protein supplementation. Overall, the results of this study demonstrate that consuming two servings of either beef protein isolate or whey protein isolate following resistance training lead to significant increases in lean body mass and strength. Be well! JP

  9. JP Says:

    Updated 08/30/16:


    Mol Nutr Food Res. 2016 Aug 28.

    Plasma trimethylamine-N-oxide following supplementation with vitamin D or D plus B-vitamins.

    SCOPE: We compared the effect of supplementation with vitamin D+B or vitamin D on plasma trimethylamine N-oxide (TMAO) and choline metabolites.

    METHODS AND RESULTS: This is a randomized single-blinded non-placebo controlled study. 27 participants received 1200 IE vitamin D3 and 800 mg calcium and 25 received additionally 0.5 mg folic acid, 50 mg B6, and 0.5 mg B12 for 1 year. Plasma Hcy, TMAO, and choline metabolites were measured at baseline and 12 months later. TMAO declined in the vitamin D arm by 0.5 vs. 2.8 μmol/L in the D+B arm (P = 0.005). Hcy decreased and betaine increased in the D+B compared with the D arm. Within-subject levels of plasma choline and dimethylglycine and urine betaine increased in both arms and changes did not differ between the arms. TMAO reduction was predicted by higher baseline TMAO and lowering Hcy in stepwise regression analysis. The test-retest variations of TMAO were greater in the D+B arm compared with vitamin D arm.

    CONCLUSION: B-vitamins plus vitamin D lowered plasma fasting TMAO compared with vitamin D. Vitamin D caused alterations in choline metabolism which may reflect the metabolic flexibility of C1-metabolism. The molecular mechanisms and health implications of these changes are currently unknown.

    Be well!


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