The blog

An Open Letter to Bart Kay

by on March 21, 2019

Hey Bart,

I saw your video on me. Gonna assume it was the usual youtube theatrics. You may not know me. My bio is online and all over. I am board certified in both the surgical and the medical management of obesity. My interest really shifted to nutrition in 2007 when I started pursuing more medical/nutritional methods of addressing obesity. At that time I had been involved in some work on evidence based medicine and decided that we were extremely deficient in evidence based medicine in obesity. I therefore when fanatical on studying lifestyle methods for handling western disease.

Wrote a book called Proteinaholic, with extensive references.  Currently, I run a lifestyle medicine clinic as well as do weight loss surgery. I am a key note lecturer to major medical societies on topics of nutrition. Gave keynote at the American College of Lifestyle Medicine. Will be giving the keynote at the American College of Obstetrics and Gynecology, as well as lecturing at medical schools and dietitian schools.  I am personally vegan though I do not teach my patients to be vegan. Not because I believe it is in any way unhealthy, it is just that vegan is about ethics but patient care is about science.

You questioned  where I got the science in my video. I am now going to provide you with a huge list of papers. It may be too much. We can talk broadly tomorrow and then reconvene after reviewing studies.

You state that antioxidants aren’t absorbed. Actually there are MANY MANY studies showing antioxidant absorption and its effects on oxidative stress. These are just a few.

When it comes to microbiome and the effect of low fiber and high fat the research is just so huge. Hard to know where to begin.  This study shows that in one week you can decrease bile acid and bile acid bacteria and thereby dramatically reduce ROS:  This study shows in 2 weeks of plant based diet you completely change your microbiome to a higher butyrate producer. This was published in Nature and includes a cross over which was exceedingly impressive.

Likewise TMAO has a HUGE body of work that shows TMAO effect both in animals and in humans. Interestingly, TMAO was an independent factor in this study even after controlling for confounders INCLUDING LDL. Most of the better studies have come out of The Cleveland Clinic which is our top cardiovascular research institute.

This from NEJM:

I know you have a video on liptoxicity which I did not watch. There is considerable interest in lipotoxicity among many people I work with. This paper has a treasure trove of references:  In your video you questioned the saturated fat causing gap junction separation. This is a little bit more complex than I made it out to be on the video. There is suggestion of translocation due to saturated fat but the evolving thought is that fat induces Bile acids which change microbiome to non butyrate producing microbiome which interfere with gap junction and mucin production as barrier.,, These 2 papers are interesting because they show the increase in inflammation with a fatty meal. Now interestingly, the inflammation is very fast. It was thought that this was because a meal makes the gut permeable due to fat and that allows LPS to translocate but the second study shows it may actually be the LPS in the food itself.

As far as the epidemiology, I am not sure how much you want to see. You make it sound in your video that I am making univariate analysis. Couldn’t be further from the truth. I am only interested in epidemiology that is prospective and subjected to multivariate regressions analysis with as much a control on confounders as possible.  I only use this as a starting point. The epidemiology I use is not a single study but multiple done in multiple settings and consists of large databases. My interests have been in The Nurses Health Study, Harvard Health Professions, EPIC Data study, NIH AARP, and the Adventist Health 1 and 2, and 3 is coming.  I can provide specifics references if you want or simply discuss how I use them as a guide.

Finally, cholesterol.  The study I cited was the Cooper study which looked at healthy people very well controlled for weight, exercise, smoking, etc.  Only variable was LDL and none of the 30,000 had any metabolic diseases. Followed 10 yrs. People with 160 LDL vs 100 LDL had 40% increased risk of CV mortality over 10 years, and if over 160 it jumped to 70%.  I do believe cholesterol plays a part in atherosclerosis and can back that with library of papers BUT it is NOT the inciting event. Rather, the inciting event has to do with endothelial damage from flow and inflammation with the formation of foamy macrophages which then incite an inflammatory lesion. Here is where TMAO may play a role as it does compete with arginine and blocks NO, it prevents extraction of cholesterol from plaque, and promotes inflammation by promoting macrophage scavenging. Heme iron also has large effect as it oxidizes fat,  and can change BH4 to BH2 preventing NO formation and thereby causing vasoconstriction.  This is seen in the fact that high fat eaters have impaired flow mediated dilation.

Looking forward to a good chat. Some of the things you said I have honestly never heard and open to learning.

Garth Davis