Attia Feldman podcast

(Todd Allen) #44

As Peter explained it, there is a tremendous amount of reputable science (unlike nutritional science) which shows there are 3 primary factors which all have to occur to drive atherosclerosis.

#1 endothelial quality. Basically how permeable are your artery linings. This can be seen surgically but otherwise we don’t have an accurate way to evaluate it. It can degrade with many factors such as age, diabetes, and infections. If you don’t know yours is good, safest to assume it isn’t.

#2 inflammation. Although we have clinical markers of inflammation such as hs-crp they aren’t specific enough, accurate enough or monitored closely enough to solidly judge risk.

#3 LDL particle count. This is a multiplier with the other two. If any of the 3 is very low your risk will be low. This is the one we can best measure. For the small minority of people where this goes sky high with keto (or fasting) you can bury your head in the sand and hope one of your other 2 factors is very low. Or you might look into why it is going so high and explore options to reduce it.

(Banting & Yudkin & Atkins & Eadeses & Cordain & Taubes & Volek & Naiman & Bikman ) #45

I mean, using Dave’s latest metaphor, LDL on a fast would be a shut down of the intestinal delivery service, and instead be the liver service doing all the delivery. Shocking, but maybe you need the LDL to move your energy source around.

Why is it shocking that when you are “fat fueled” you have more transport modules for energy, vitamins and such in your blood? Should that be remotely controversial? I would think not. And yet, here we are.

(CharleyD) #46

Don’t forget Insulin level to promote growth, especially of intima, the smooth muscle in the artery walls.

I think it should get it’s own bullet point in your list. I doubt you could have disease without it.

(CharleyD) #47

Autophagy should show that to be not the case. I’d predict fasting to be healing of atheromas.

(Adam Kirby) #48

This is the logical leap that has a missing step. The assumption is that independently lowering this factor has an effect on atherosclerosis, therefore reducing LDL-P is good. Problem is this causal relationship has never been established. It’s a theory that Attia and others have based on correlations, nothing more.

The Kitavans are a prime example of people with very low CVD but high ApoB. And when black swans clearly exist I get really skeptical about a theory. Mine is that either LDLs are being pathologically damaged or they aren’t, and if they’re not being damaged then your LDL-C and LDL-P reflects an appropriate level for your body and current diet.

(Banting & Yudkin & Atkins & Eadeses & Cordain & Taubes & Volek & Naiman & Bikman ) #49

Additionally, there are mortality studies that show, for most populations, you can lower your LDL with a statin, but you can’t really improve your all cause mortality numbers.

Statins do not decrease all-cause mortality in the vast majority of people. Long-term studies have never been able to demonstrate that women of any age or with any degree of heart disease live longer by taking statins. The same long-term studies show that men over the age of 65 live no longer by taking statins. Men under 65 who have never had heart disease – and were talking actual heart disease here, not just an elevated cholesterol level – gain no longevity benefit from taking statins. The only small group of people who have been shown to benefit from statins are men under 65 who have had a heart attack. But unfortunately that benefit is small.

But Attia can take his statin and tell himself the muscle weakness, brain fog, and increased incidence of diabetes is just keeping him alive longer (even though it doesn’t).

(Adam Kirby) #50

LDL-P is just another surrogate marker to fixate on in lieu of LDL-C, since even people like Attia realize how horrible a predictor LDL-C is. I’m interested in root cause of the modern chronic disease state, and LDL-P doesn’t tell me any more about that than LDL-C.

(Banting & Yudkin & Atkins & Eadeses & Cordain & Taubes & Volek & Naiman & Bikman ) #51

Exactly. As @DaveKeto has said, industry folks focus on LDL because they have a drug for it. If they develop a drug for Lp(A) or Apo(B), or whatever, you’ll see more testing for that, and more treatment for that, and more studies support the causal link between New Thing A and Specific Set of Death Conditions Y, and hooray, we have an allopathic medicine to improve New Thing A… even if it increases Total Set of Death Conditions.

(Adam Kirby) #52

Here’s a relevant study that recently came out. Higher LDL-P in low carb athletes than high carb ones. Although fewer small dense LDLs. Then is sdLDL the real key, or just another surrogate marker?

As an aside I think any usage of the word “paradox” means, “we’re still really ignorant about this”. Although maybe Phinney and Volek are being tongue-in-cheek? :stuck_out_tongue:

(Jeff Gilbertson) #53

LDL increase on a fast because the source of energy is stored fat, as opposed to dietary fat.

When fat comes from diet, chylomicrons are supplying the energy, and LDL is reduced.
When that source goes away (fasting), then stored fat is mobilized, and LDL increases.

This is the whole reason the Feldman Protocol works.

(Karen) #54

I think that is part of who he is…the arrogance. I saw on the TED talk when he first embraced keto and was healing his himself, he was humble and apologetic. Much more tolerable. You can’t fault who he is, but perhaps he may see it in himself someday. Hard to be humble when you’re strong, young, smart, skilled, educated, fit, etc.



(Boudewijn) #55

He evaluated the podcast with ivor cummins :

And added a response on his own website :

I don’t understand it unfortunate as the cholesterol, ldl, etc. is to complex for me

(Kirk Wolak) #56

Jamie, I know this is an older post…
But I agree 100% about Attia. He seemed petty because of his prefixing the conversation, and how he talked during the conversation. Without the prefix, it would not have been as bad, honestly (to me).

Next, LMHR with High A1C before LCHF… Then High LDL.

Dr. Nadir LCD2019 pointed out that making LDL and making Ketones are linked.

Imagine of LMHR are people with a natural SPORTS affinity. Body can really amp up energy easily to keep these people going. Now imagine the person is not doing crazy exercise. The excess ability to produce energy results in higher Glucose numbers (A1C), and when LCHF, higher Ketone levels, BUT at a certain point of not needing them, it starts spewing out LDL to move them around and store them elsewhere. (ie, tank is full here boss, send them on there way).

To me this implies the Feldman protocol (eat more fat to lower cholesterol) could also use EXERCISE in these people to lower Cholesterol (LDL). Because by consuming the Ketones with exercise, I HYPOTHESIZE that they will make LESS LDL…

It also makes me want to test his BMR/RMR before and after the Feldman protocol is used, or every morning for 5 days (normal, 3 days of extra fat, and morning of test). Both following the feldman and then the feldman + Exercise. My assumption is that the LDL will drop further.

And Dave is the perfect test person, because he can target his LDL so accurately. If he can’t do that, because he walked 5-10 miles more each day, or did 2-3 cycles of HIIT each day, then the direction it moves gives us some insight into what Dr. Nadir was talking about. Is it a COMPETITIVE process or a COOPERATIVE process (it makes more ketones AND more LDL, or the pathway competes with one pushing against the other).