Reversal of CAD: What diet is best? A response to Noakes and Teicholz
A recent interaction on Twitter with Low-Carbohydrate diet advocates Nina Teicholz and Tim Noakes on coronary artery disease gave me some insight into their nutrition world that I feel warrants a more thorough rebuttal than what I could have included in 140 characters. I wanted to learn more and I did not have an immediate answer to their criticisms. I will start with screenshots and an overview of the interaction and then offer the research I was quoting, responses to their criticisms of the research and finally a summary and interpretation of this interaction.
Please follow Screenshots in order of 1-4 for the conversation.
The research I was quoting was written by lead authors Dr. Caldwell Esselstyn, MD(1,2), Dr. Dean Ornish, MD(6) and Dr. Satish Gupta(3). Disclosure; I did not include the Gupta paper in my original twitter thread. Dr. Dean Ornish, MD, has published several papers on the benefits of a plant-based diet, notably regression of Heart Disease(6) and Prostate Cancer(7). This paper(6) was published in 1998, and looked at regression of vessel disease in those with diagnosed heart disease. It was a randomized-controlled diet and lifestyle trial. The experimental group (n=20) received diet modification consisting of a 10% fat vegetarian diet, as well as lifestyle modifications such as aerobic exercise, stress management, smoking cessation and group support. After 1 year, 91% of the experimental group experienced a reduction in frequency of angina, where as control group had a 186% increase (p=.08). There was also a statistically significant improvement of angiographic changes in arterial stenosis in the experimental group after 5 years, but worsening of stenosis in the control group.
The next paper I was referring to was written by Dr. Esselstyn in 2014(2). He built on the experience of Ornish and went a step further with his dietary restriction, withholding all animal products as well as refined sugars, flours, and oils. He encouraged the consumption of whole grains, legumes, lentils, vegetables and fruit. After an average follow-up of 3.7 years adhering to the dietary protocol, Esselstyn reported 99.4% of patients avoided major cardiac events. The adherent experimental group (n=177) reported 1 cardiac event. A small cohort of experimental group participants who admitted non-adherence to the diet protocol (n=16) reported 11 cardiac events in the same time period. “Adherent patients experienced worse outcomes significantly less frequently than non adherent patients (p<.001).
The third paper that is being included in this article is the Mount Abu Open Heart Trial, written by Dr. Satish Gupta, MD(3). In 121 patients with angiographically diagnosed coronary artery disease, 49% had triple vessel disease, 36 had double vessel disease and 17 had single vessel disease. Average percent diameter stenosis at baseline was 65%. After a 2 year follow-up with diet and lifestyle interventions including a low-fat, high fiber diet, sleep education, stress management and aerobic exercise, repeat angiography was performed by 2 independent angiographers. Average percent diameter stenosis decreased by 6.10 absolute percentage points. Adherence was strongly related to changes in percentage stenosis. 31 participants in the most adherent group saw a regression of 18 absolute percentage points. Overall, 37% of diagnosed lesions showed regression of 10% or more, and in those most adherent, 51% of lesions showed regression of 10% or more. After a mean follow-up period of 8 years, cardiac event data was collected. Out of 54 patient in the least adherent group, there were 38 cardiac events, compared to patients who were most adherent (n=31) suffering 11 cardiac events (p<.002).Now, to address Noakes' and Teicholz's critiques of the works of Ornish and Esselstyn.
Teicholz's Criticism’s: (See screenshot 4)
Esselstyn Not controlled with Food Diary:
Esselstyn taught all study participants how to eat, what to eat and what to avoid in a 5-hour seminar. He also confirmed that the participants had a grasp on these dietary principles with the use and review of a 3-week diet diary following the seminar. At follow-up, the study also eliminated 21 participants that, admittedly, were not compliant with the dietary protocol.
Teicholz could be right. The results could be skewed, some of the participants could have been lying because of a lack of a food diary for the trial period. But I contend:
A) they could have lied on a food diary, too.
B) As I outlined above, a reasonable effort was made to ensure participants were compliant.
C) The odds of a significant number of the 177 compliant patients lying is low.
D) The findings supported Esselstyn's hypothesis, they didn't fly in the face of the review of literature and previous findings.
E) Keeping a food diary for the mean length of 3.7 years is not reasonable or realistic.
Ornish control Group not parallel
It is unclear what is being referenced, but am open to further clarification from Teicholz.
Ornish had 2 deaths in intervention group vs. 1 in control group
This is true. Out of an experimental group of 28, there were 2 deaths reported after an average follow-up of 5 years. There was only 1 death in the control group of 20 participants. Was this because of diet? Unlikely, as the p-value of this finding was .81. These deaths were most likely due to chance. However, In Table 6 in this study, the number of cardiac hospitalizations in the experimental group was 23, and in the control group it was 44, with a p-value of .001, which is highly statistically significant. This is just one of many significant findings from this study.
Noakes' Criticism’s: (See Screenshot 4)
Ornish- Not a diet study & incomplete
It was a diet and lifestyle study. When we're dealing with chronic diseases that take a lifetime to manifest, it's unlikely that a single factor caused that disease. So, when trying to reverse, in this case heart disease, it makes sense to look at all of the factors that have been shown to effect ones health.
Ornish wanted to look at someone's life holistically. What Noakes may be arguing is the diet aspect might not have had anything to do with the significant findings. In other words, the significant finds may have been attributed to the other factors that the experimental group undertook, like aerobic exercise, stress management, smoking cessation and group social support. This assertion, though plausible, is unlikely. I'm sure Ornish and Noakes both agree that diet plays a large role in heart disease progression, so then why would initiation of meditation and aerobic exercise in the experimental group be the sole cause of the statistically significant results?
By comparison, the study by Esselstyn(2) did not have the number of non-dietary interventions and found more significant results.
It's unclear what is being references in Noakes' assertion that the Ornish study was incomplete, but am open to further clarification.
Esselstyn: Published limited angiograms in 4 patients with minor single vessel disease
This1 is the study that I believe Noakes is referring to. This study, by Esselstyn(1), looked at 11 patients with "triple-vessel coronary heart disease documented by angiography", with a mean percent stenosis of 53%. I'm not a cardiologist, but I wouldn't consider this minor single vessel disease. I am open to further clarification.
Results could be spontaneous.
I respectfully and strongly disagree. The studies I have cited have all found statistically significant results within the intervention groups.
Additionally, the link provided by Noakes in Screenshot 3 backing up his assertion that more saturated fat is better at preventing arterial plaques (bit.ly/2rubfEU) is not a particularly strong article. The findings of Mozaffarian(4) suggest that, according to angiography, higher intakes of saturated fats is associated with less progression of coronary artery disease in. And high intake of carbohydrates is associated with more plaque formation. A paradox. There are several things with this article that I call into question:
A) This study was not an interventional trial. It employed a food frequency questionnaire, watched a cohort of post-menopausal women over time, and drew correlations about diet and coronary atherosclerosis. No intervention was provided.
B) This study just looked at postmenopausal women who were on a host of medications and had multiple metabolic disorders.
C) Although fats were delineated into SFA, MUFA and PUFA, there was 1 category for ‘carbohydrates’. As we know, there is a huge difference between carbohydrates coming from refined white bread or whole sweet potatoes. Judging by average fiber intake in all quartiles, whole plants foods were sparse.
D) The classic results of saturated fats increasing the incidence of coronary artery disease were likely blunted in this article. The effects of low fat and high carbohydrate, seen in this study to create additional stenosis, appear exaggerated by female sex hormones, exogenous sex hormones and metabolic syndromes present in these women (diabetes, hypertension, CAD, hyperlipidemia)5.
E) The study could have been better, but we shouldn't throw out the findings. These data may offer insight into different treatment options for various genders and demographics who are affected by CAD and other comorbidities.
In all three interventional trials, a vegetarian (Ornish, Gupta) or vegan diet (Esselstyn) was used. Results were significant and noteworthy. The critiques to offered by Noakes and Teicholz were superficial, insignificant, unrealistic or simply wrong. The studies cited are not perfect by any means, but they're the best interventional trials we have at showing optimal outcomes to the #1 killer of men and women in the western world. Where there’s smoke, there’s probably fire. To my knowledge, there are no interventional studies showing that high fat, low carbohydrate diets lead to the same clinical regressions of atherosclerotic plaques or reduction in cardiac events. The onus is on those denying the current evidence to provide better science that validates their hypothesis. Otherwise, should we not use the best available data to prevent and reverse this nations #1 killer? According to Noakes and Teicholz, these high carbohydrate interventions (coming from whole, unrefined plant foods) should have been killing participants, or at the very least causing progression of symptoms and plaques. These data suggests that a whole-foods plant-based diet that is relatively low in fat (saturated in particular) and high in unprocessed, natural carbohydrates is the best diet at this point in time for reversal, and likely prevention, of heart disease.
Why hold out on prescribing this when there are no side effects? What's the side effect of eating more greens, beans and broccoli? Why deny these lines of evidence?
I think we should be critical of research. I think we should be critical of claims and do what is best for people’s health. I think we should ask more questions to come to a greater understanding of what is helpful or harmful to our health. I think we should listen and learn more from experts with many views on diet and lifestyle (shameless plug-this is the mission of The Ian Cramer Podcast). Could I be wrong with writing this whole article? Yes. Could Ornish, Esselstyn and Gupta be wrong? Yes, but unlikely. Through these papers and the conversations I've had with many cardiologists in direct patient care as part of my podcast (8, 9, 10, 11, 12, 13, 14, 15, 16), I know that these studies are not isolated incidents that have shown these results by chance. Why would a cardiologist or advocates of health actively ignore and discard these results? Professionals dedicated to healing those around them and doing what is best for the patient are obligated to pay attention.
Could these results be replicated with other diets? Perhaps. But like many before me, I asked Noakes, Teicholz and those who share similar dietary philosophies ‘Provide the research that shows an intervention resulting in regression of atherosclerotic plaques and/or significant reduction in cardiovascular events in those on a low-carbohydrate, high-fat diet’. Until that time, shouldn't we use these interventional protocols as the 'default' until better research comes along? What I am suggesting isn't dogma, it’s not an agenda and it’s not blind zealotry. This is science and an interpretation shared by many. To my knowledge, it's the best available science that we have and it should at least be part of the conversation, if not standard practice.
-Ian M. Cramer, MS, ATC
Thank you to Nina Teicholz and Tim Noakes for engaging with me in a collegial conversation. Thank you to Dr. Evan Allen, MD for his help.
Esselstyn, Caldwell B, et al. “A Strategy to Arrest and Reverse Coronary Artery Disease: a 5-Year Longitudinal Study of a Single Physician's Practice.” Journal of Family Practice, vol. 41, no. 6, Dec. 1995, pp. 560–568.
Esselstyn, Caldwell B, et al. “A Way to Reverse CAD.” The Journal of Family Practice, vol. 63, no. 7, July 2014, pp. 356–364.
Gupta, Satish K. “Regression of Coronary Atherosclerosis through Healthy Lifestyle in Coronary Artery Disease Patients- Mount Abu Open Heart Trial.” Indian Heart Journal, vol. 63, 2011, pp. 461–469.
Dariush Mozaffarian, Eric B Rimm, David M Herrington; Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women, The American Journal of Clinical Nutrition, Volume 80, Issue 5, 1 November 2004, Pages 1175–1184, https://doi.org/10.1093/ajcn/80.5.1175
Knopp, Robert H, and Barbara M Retzlaff. “Saturated Fat Prevents Coronary Artery Disease? An American Paradox.” The American Journal of Clinical Nutrition, vol. 80, no. 5, 2004, pp. 1102–1103., doi:10.1093/ajcn/80.5.1102.
Ornish, Dean. “Intensive Lifestyle Changes for Reversal of Coronary Heart Disease.” Jama, vol. 280, no. 23, 1998, p. 2001., doi:10.1001/jama.280.23.2001.
Ornish, Dean, et al. “Intensive Lifestyle Changes May Affect The Progression Of Prostate Cancer.” Journal of Urology, vol. 174, no. 3, 2005, pp. 1065–1070., doi:10.1097/01.ju.0000169487.49018.73.
Cramer, Ian. “Dr. Caldwell Esselstyn || Ian Cramer Podcast 26.” Ian M. Cramer || Rochester, NY || Podcaster/Public Speaker, 2017, www.plant-basedcyclist.com/icp26-dr-caldwell-esselstyn.
Cramer, Ian. “Dr. Chad Teeters || Ian Cramer Podcast 5.” Ian M. Cramer || Rochester, NY || Podcaster/Public Speaker, 2017, www.plant-basedcyclist.com/icp5-dr-chad-teeters.
Cramer, Ian. “Dr. Heather Shenkman || Ian Cramer Podcast 17.” Ian M. Cramer || Rochester, NY || Podcaster/Public Speaker, 2017, www.plant-basedcyclist.com/icp17-dr-heather-shenkman.
Cramer, Ian. “Dr. Jami Dulaney || Ian Cramer Podcast 3.” Ian M. Cramer || Rochester, NY || Podcaster/Public Speaker, 2017, www.plant-basedcyclist.com/icp3-dr-jami-dulaney.
Cramer, Ian. “Dr. Joel Kahn || Ian Cramer Podcast 2.” Ian M. Cramer || Rochester, NY || Podcaster/Public Speaker, 2017, www.plant-basedcyclist.com/icp2-drjoel-kahn.
Cramer, Ian. “Dr. Kim Williams || Ian Cramer Podcast 13.” Ian M. Cramer || Rochester, NY || Podcaster/Public Speaker, 2017, www.plant-basedcyclist.com/icp13-dr-kim-williams.
Cramer, Ian. “Dr. Koushik Reddy || Ian Cramer Podcast 51.” Ian M. Cramer || Rochester, NY || Podcaster/Public Speaker, 2018, www.plant-basedcyclist.com/icp-51-dr-koushik-reddy.
Cramer, Ian. “Dr. Robert Ostfeld || Ian Cramer Podcast 44.” Ian M. Cramer || Rochester, NY || Podcaster/Public Speaker, 2018, www.plant-basedcyclist.com/icp-44-dr-robert-ostfeld.
Cramer, Ian. “Dr. Steve Lome || Ian Cramer Podcast 40.” Ian M. Cramer || Rochester, NY || Podcaster/Public Speaker, 2018, www.plant-basedcyclist.com/icp-40-dr-steve-lome.