New paper from Dr. Gundry on stopping progression of CAD

[Verax]

Dr Gundry apparently again misunderstands the PREDIMED study and promotes an unsubtantiated dosage of extra-virgin olive oil. In this report he prescribed 1 liter of EVOO per week per PARTICIPANT. But PREDIMED used 1 liter EVOO per FAMILY per week.
It is possible the extra dosage of EVOO is beneficial, but it changes the macronutrient balance toward more fat; the abstract and poster don't give the balance figures. More likely is that PREDIMED prescribed replacing saturated fat and PUFA with MUFA EVOO (free bottle replacing cooking oil used by family) instead of adding on top of regular Western diet. Weight loss and removal of visceral fat (which PREDIMED did not see) can reduce inflammation markers. even without the fatty acid exchange. The polyphenols in EVOO might not amount to a significant anti-inflammatory effect with any reasonable dosage, as I mentioned earlier elsewhere here. I do feel it is prudent to consume EVOO at 3-4 tbsp/d/person but I would like more evidence before concluding causality.

Meanwhile, I would find it hard to stick to a lectin-free diet. Dr Gundry doesn't seem to include autoimmune thyroiditis and autobody-confirmed celiac disease in his list of diseases, just gluten sensitivity. Autoimmune diseases vary so much by age of onset, gender and geolocation and genomes that they can't all be caused by lectin consumption. His approach might help in preventing Alzheimer's for us ApoE4 carriers, but this study needs more evidence.

https://www.nejm.org/doi/full/10.1056/Nejmoa1200303
https://www.nejm.org/doi/full/10.1056/NEJMoa1800389

[Brian4]

HI Brian, I appreciate your point and especially the humorous delivery. I think your book will be a big hit! Once I finish my experiment with the Gundry diet, I may just try the “Taxonomic Ex-Lover Diet”.

Who knows, the TEL Diet might in fact work in ways independent of the CR effect! But we have to run a prospective trial, if only to set an example for Gundry and Aunt Jemima.

By the way, thanks in advance for sharing the thyroid results when they come in.

Brian

[Julie G]

Brian4, thank you for the clarification! Somehow that was understood to me, but I didn't express it. FWIW, Gundry first drew my attention simply because of the extraordinarily large set of E4 carriers he's working with. That said, I think we all wish he'd subject himself to peer review. Given that we're the largest group of E4 carriers assembled anywhere, we could run our own self-organized collective N=1, using his protocol, and collect the data ourselves. Anybody up for the challenge?

Verax, agree. I'm frustrated that Gundry misuses (the flawed) Predimed trial to justify his extraordinarily high EVOO recommendations. There are so many other studies/mechansims that he could use as a basis for that recommendation. Also, I could be wrong, but I think Gundry's program is designed for all forms of autoimmunity...

Theresa, yes! Glysophate is one of many problems. Modern grains have been successfully engineered to be profitable, but not necessarily good for health. US wheat, as one example, is now bred to be higher in gluten, higher on the glycemic index, to contain more damaging gliadin proteins and wheat germ agglutinin all leading to MORE inflammation. There are many factors -other than just gluten sensitivity- that can impact our health. It's also worth remembering that our genotype preceded grains (only 10,000 years old) by millions of years. Is it a stretch to suggest that non-grain plants may be more evolutionarily in sync with our genotype?

[ApropoE4]

Dr Gundry apparently again misunderstands the PREDIMED study and promotes an unsubtantiated dosage of extra-virgin olive oil. In this report he prescribed 1 liter of EVOO per week per PARTICIPANT. But PREDIMED used 1 liter EVOO per FAMILY per week.

It is a very generous reading to say he "misunderstands" it, because by ignoring the nut consuming arm of the study, he bases his anti-lectinism on a study that shows exactly that lectins make no difference.

[ApropoE4]

Glysophate is one of many problems.

You say that, but it is in fact the opposite of the truth. Glyphosate saves tens of thousands of lives directly by replacing highly toxic and certainly carcinogenic herbicides.

There is a lot of detail on that here, for example:

http://www.crediblehulk.org/index.php/2 ... ible-hulk/

Glyphosate does not cause any disease or condition in humans in doses any of us are likely to encounter and the abuse of the trial results (which will be reversed on appeal), which circled around exposure to extremely high dosages, is the same old tactic used by commercial enterprises like the one with the Gundry figurehead.

As a side note, after looking at the Gundry website to research why he's suddenly such an olive oil fan, I got an ad today saying "Cardiologist tells you what happens when you eat steak" with Gundry's image and a steak. I clicked the ad and it directed me to the mercola site (I'm not sure what that is, seems like a clearinghouse for non-fact based medicine) and from there to a generic blurb about "this one thing you should avoid to make your diet work" and from there to a video by gundry badmouthing lectin.

I'm going to guess this means there was previously something about the horrors of acrylamide and that they forgot to change the ads to show beans instead of steak.

About non-celiac gluten sensitivity - unfortunately for those who believe they have it based on not generally accepted lab tests, there remains no evidence for it.

Stefano Guandalini: Not necessarily. It does mean, however, that what we now call non-celiac gluten sensitivity is likely to be a mixed bag of issues. Interestingly (and I was able to convince a panel of experts in Italy of this during a round table last week) there is to date not one scientific proof that gluten as such is involved in any of the patients reporting gluten sensitivity.

[floramaria]

Meanwhile, I would find it hard to stick to a lectin-free diet. Dr Gundry doesn't seem to include autoimmune thyroiditis and autobody-confirmed celiac disease in his list of diseases, just gluten sensitivity. Autoimmune diseases vary so much by age of onset, gender and geolocation and genomes that they can't all be caused by lectin consumption. His approach might help in preventing Alzheimer's for us ApoE4 carriers, but this study needs more evidence.

Just for clarity: on page 85 of The Plant Paradox Dr Gundry: "If you suffer from..."
and goes on for 5 lines of of AI diseases including autoimmune thyroiditis and continues,
"that's right anyautoimmune disease-the good news is you can eliminate it without using drugs. I see it everyday. The answer lies in healing your leaky gut...."

He doesn't say lectins are the cause of autoimmunity, but rather that lectins can cause leaky gut, and leaky gut is the cause of autoimmunity.
My feeling as I read the arguments on this thread is that to some extent there is the opposite tendency to the old "shoot the messenger" idea, where the carrier of bad news is punished for the content. In this case Gundry's message may be undervalued because of the appearance of his being a compromised messenger due to his marketing. "Shooting down the message" what I have to pvercpome in myself anyway.
I am not a personal fan of Dr Gundry; since I don't like his marketing tactics or his videos, I am somewhat biased against him as a messenger. But I am experimenting , following the Plant Paradox diet, because he has a tremendous amount of clinical experience,
and, in my opinion, makes a impressive case in his book for the improvements in his patients when they remove lectins.
In this thread and elsewhere on the Forums, there are personal testimonies of people in this community who have had health improvements after eliminating lectins. So I am willing to give it a try.
If my autoimmune thyroiditis (Hashimoto's) is cured, it won't prove anything. But I am willing to make the dietary changes Dr Gundry recommends and hope for a good outcome. I don't think it will prove anything if it is not cured either.

FWIW, A messenger I prefer, microbiologist Kiran Krishnan, agrees that leaky gut is a factor in AI disease. Based on notes I took last year during his talk on the microbiome and autoimmune disease, presented by Rebel Health Tribe, he said "If you have autoimmune disease, you have leaky gut."
(He is probably a "compromised messenger" too since he may profit from sales of MegaSpore probiotic )
His interventions do not include avoiding lectins but he was very strong on the need to repair leaky gut to recover from any autoimmune disease.

[Verax]

I hesitate to wade into the debate that has been going on here for some time about leaky gut allegedly caused by lectins or gluten or glyphosate, all leading to toxins crossing the blood-brain barrier and causing neuroinflammation leading to neurodegeneration such as AD. Each of us is entitled to do an n=1 experiment on herself and share the results. Having risk factors for AD such as ApoE4 might stimulate such experiments even if there is little evidence or biomarkers available. JulieG is wise in suggesting that if we don't like Dr Gundry's manner we do the studies ourselves, we are certainly capable.

In that connection, I note with interest Carl Zimmer's recent article in The New York Times, "Marine Mammals Have Lost a Gene That Now They May Desperately Need" at https://www.nytimes.com/2018/08/09/scie ... cides.html (sorry if it is behind a paywall). He reports studies of the PON1 gene (Serum paraoxonase/arylesterase 1 gene). PON1 is responsible for hydrolysing organophosphate pesticides such as glyphosate. Polymorphisms in the PON1 gene significantly affect the catalytic ability of the enzyme as PON protects lipoproteins from toxic oxidative modifications and has an antiatherogenic mechanism; variations affect a major antioxidant function of high density lipoprotein, and so this pathway is particularly important to ApoE4 carriers. PONs also hydrolyze lactones serving as quorum-sensing signals for biofilms, which might be important in the gut (sprue). Zimmer reports that many marine mammals have long ago moved from land to sea and in the process of adapting to oxygen levels and diving lost PON1 function (perhaps replaced by other ROS-defending reactions).

What interested me was that there is such variation in PON expression and whether or not that correlates with disease prevalence such as autoimmunity. Zimmer postulates that manatees lacking PON1 are exposed to more organophosphates in Florida canals, so they should at risk. http://science.sciencemag.org/content/361/6402/591 But, instead, the manatee population has grown, and I know of no studies on marine mammals or humans with PON risk alleles that show effects from glyphosates such as autoimmunity.

It might be worth checking your own PON1 status. I have a couple of risk alleles and Hashimoto's, which runs in my family rather than correlates with chemical exposure.

[floramaria]

It might be worth checking your own PON1 status. I have a couple of risk alleles and Hashimoto's, which runs in my family rather than correlates with chemical exposure.

Very interesting, Verax.
Where did you check your PON1 status?

[Verax]

I checked my PON1 status on selfdecode.com with 23andMe data loaded. rs662, rs854571, rs854555 (risk allele A), rs4242382 (risk allele A), rs2057681 (risk allele G). PON1 is more important than PON2 and PON3, I understand.

Oxidised-lipids are the major cause of inflammation and are responsible for the initiation and/or propagation of several inflammatory diseases including atherosclerosis (heart disease and stroke), diabetes, liver and kidney diseases, rheumatic diseases, eye diseases (macular degeneration), cancer and HIV infection [citation needed]. Because of its ability to destroy oxidised-lipids PON1 appears to play some role in all these diseases.

https://en.wikipedia.org/wiki/PON1

The exact mechanism by which paraoxonase is cardioprotective is not clear, although it is likely to be related to its antioxidant properties especially on LDL. PON1 levels are influenced by a variety of environmental factors, including statins and cytokines. The preferential association of PON1 with HDL is mediated in part by its signal peptide and by desorption from the plasma membrane of expressing cells by HDL or phospholipid. Apolipoprotein A-I is not necessary for PON1 association with HDL, but its activity is stabilized in the presence of the apolipoprotein. Only in the absence of both lecithin cholesterol acyltransferase and apolipoprotein E is paraoxonase associated with non-HDL lipoproteins. The displacement of paraoxonase by serum amyloid A may explain in part the proinflammatory nature of HDL in the acute phase

https://www.ncbi.nlm.nih.gov/pubmed/15166781

Low serum PON1 is associated with many diseases with a large inflammatory component including diabetes mellitus, rheumatoid arthritis, systemic lupus erythromatosis, and various hepatic and renal diseases including renal failure, psoriasis and macular degeneration [reviewed in 35]. These diseases are also characterised by having dysfunctional HDL believed to be (but not proven to be) caused by the low PON1 activity [56] and increased rates of CHD.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4458450/

[Verax]

Pomegranate juice (PJ) polyphenols have a specific transcriptional role in hepatocyte PON1 expression upregulation, and its secretion to the medium. We conclude that the anti-atherogenic characteristics of PJ polyphenols are modulated, at least in part, via hepatocyte PON1 upregulation and its subsequent release to the medium.

https://www.ncbi.nlm.nih.gov/pubmed/19783251

Residential exposure to OPs (mainly diazinon and CP) was associated with an increase in Parkinson's disease risk in PON1-55M carriers and to an increased risk of brain tumours in children with low PON1 activity

https://www.ncbi.nlm.nih.gov/pubmed/19907334/ https://www.ncbi.nlm.nih.gov/pubmed/16002382/

Epidemiological studies also suggest that occupational exposure to OPs might increase the risk of Parkinson's disease [118].

https://www.ncbi.nlm.nih.gov/pubmed/25460623/

Recently it has been suggested that PON1 has a role in healthy aging, however, the mechanism is currently unknown[25]

https://www.ncbi.nlm.nih.gov/pubmed/22897574