Zero carb diet will help prevent Alzheimer’s

[andlewis]

the single most important thing our population can do is to avoid insulin resistance, which will ensure the maintenance of metabolic flexibility- the ability to burn both glucose and ketones to maximize fuel to our brains. Our diets should also enable us to avoid nutrient deficiencies, (especially those vital for our brains, like omega-3 & choline ) while minimizing inflammation.

Well said!

[xactly]

We always talk about how there is no ONE diet that will work for all of us. We are each a compilation of so much more than our shared ApoE4 allele(s). That said, evidence is strongly converging to demonstrate that the single most important thing our population can do is to avoid insulin resistance, which will ensure the maintenance of metabolic flexibility- the ability to burn both glucose and ketones to maximize fuel to our brains. Our diets should also enable us to avoid nutrient deficiencies, (especially those vital for our brains, like omega-3 & choline ) while minimizing inflammation.

Thanks, Julie. I'm heading in the direction of a plant-based ketogenic diet, and I am giving consideration as to how to meet my omega-3 and choline needs. After I ran Chris Masterjohn's Choline Calculator several months ago, I started supplementing with 600 mg of choline DL-bitartrate (split into two daily doses taken with meals). I don't know which form of choline is best, but I may increase my dose because I'm eliminating the two to three eggs a day I use to eat to make up the rest of my choline deficit. I also have FTO alleles that negatively affect saturated fat processing, so I'm likely to benefit from lower saturated fat intake..

I'm lucky to have a FADS2 allele that makes me a more efficient converter of ALA to EPA; however, DHA and EPA are my big concerns. I will try to choose the most efficient way to cover that need, and that may be continuing to eat salmon roe. I've read Rhonda Patrick's research summary, showing E4s don't move DHA in ethyl ester form across the blood/brain barrier very well. I haven't seen anything from her on how E4s handle algal DHA, and I'm actively looking for that information.

[xactly]

A worry I have is that the effect:
"It [natural selection] couldn't care less about genes and lifestyle choices that keep you physically and mentally healthy into old age"
validly made by xactly might be worse than "couldn't care".
It might be "antagonistic pleiotropy", and genes that were good up to reproductive age may actively kill us later!

Eek! I share that concern. Before, I thought I was battling entropy. I now think I may be battling "antagonistic pleiotropy"! (Hmmm... that might be a good name for the arch-villain in the next Avengers movie.)

[Julie G]

I'm lucky to have a FADS2 allele that makes me a more efficient converter of ALA to EPA; however, DHA and EPA are my big concerns. I will try to choose the most efficient way to cover that need, and that may be continuing to eat salmon roe. I've read Rhonda Patrick's research summary, showing E4s don't move DHA in ethyl ester form across the blood/brain barrier very well. I haven't seen anything from her on how E4s handle algal DHA, and I'm actively looking for that information.

Waves, xactly! I'm also looking for information on how algal DHA affects our levels too and have had zero luck on finding that information. My guess is that this will be another area in which n=1 rules. In our upcoming book, Dr. Bredesen adds an Omega-3 index goal of greater than 10% for E4 carriers. If you decide to experiment with using only plant sources (which feels a bit risky to me, but may work given your favorable genetics) you are in a perfect position to inform us all. Here's a link for an inexpensive test. Please share your results if you decide to trial it.

[Barry Pearson]

Waves, xactly! I'm also looking for information on how algal DHA affects our levels too and have had zero luck on finding that information. My guess is that this will be another area in which n=1 rules. In our upcoming book, Dr. Bredesen adds an Omega-3 index goal of greater than 10% for E4 carriers. If you decide to experiment with using only plant sources (which feels a bit risky to me, but may work given your favorable genetics) you are in a perfect position to inform us all. Here's a link for an inexpensive test. Please share your results if you decide to trial it.

I've used QUANT. (The top-end test).
My Omega-3 Index is 13.65%. Almost off (the good end of) the scale.
My Omega-6: Omega-3 ratio is 2.2:1. (Population average is probably closer to 10:1 or 20:1).

How?
I've eliminated all "modern" seed oils (Omega-6 PUFAs) from my diet.
I've eaten oily-fish with Meal-1 (of my Two Meals A Day) every day for years.
(I eat a variant of the Carnivore Diet. It makes these things easier to achieve).

I suspect that this (obsessive?) approach to Omega-3 and Omega-6 has contributed to my HS-CRP = 0.28.
Very low inflammation. (Omega-6s tend to be inflammatory. Omega-3s anti-inflammatory).

What is this "upcoming book"? Sounds intriguing!

[Julie G]

What is this "upcoming book"? Sounds intriguing!

I'm helping Dr. Bredesen and his integrative physician wife, Dr. Aida LaSheen, write the sequel to "The End of Alzheimer's," available summer 2020. It will feature a deep dive into nutrition and all aspects of the protocol.

[Barry Pearson]

What is this "upcoming book"? Sounds intriguing!

I'm helping Dr. Bredesen and his integrative physician wife, Dr. Aida LaSheen, write the sequel to "The End of Alzheimer's," available summer 2020. It will feature a deep dive into nutrition and all aspects of the protocol.

I'll certainly buy that!

[DaleBru]

Also looking forward to that sequel.

[xactly]

In our upcoming book, Dr. Bredesen adds an Omega-3 index goal of greater than 10% for E4 carriers. If you decide to experiment with using only plant sources (which feels a bit risky to me, but may work given your favorable genetics) you are in a perfect position to inform us all. Here's a link for an inexpensive test. Please share your results if you decide to trial it.

Thanks for the link to the OmegaQuant test. I listened to Peter Attia's interview of Bill Harris, the president of OmegaQuant, and I learned a lot. Harris said it takes about four months for a dietary change to show up in the Omega-3 Index, so I will plan to take the test in about four months time. As mentioned in my previous post, I may continue to consume salmon roe as my source of Omega-3 fats, since they appear to offer the highest amount of DHA in phospholipid form.

When Peter Attia interviewed Rhonda Patrick, he told a story about one of his patients who was following a ketogenic diet. When he ran tests, the man's Lp(a) was off the charts at something like 3500 mg/dL. He tried to get the patient to discontinue the keto diet, but the man was unwilling to do so because he felt great otherwise. So, they changed his fat consumption to almost all mono- and polyunsaturated, sharply limiting saturated fat intake. When the man made this change, his Lp(a) test results improved dramatically.

Rhonda Patrick mentioned the FTO gene as a possible source for that kind of sensitivity to saturated fats. Since I have the FTO alleles, I think they may be the source of the spike in LDL-C I see when I consume animal products. Peter hazarded a guess, based on his patient population, that this sensitivity to saturated fats may affect about 10 - 20% of the population.

[circular]

My sister in law has familial hypercholesterolemia. Her LDL-C is well over 200, her doctor wanted to put her on statins. She's a vegan...so her diet is rich in carbohydrates/grains, probably has a fair amount of seed oils. She underwent a CAC and full lipid panel. Her crp was similar to mine @ .3, her triglycerides are great, oxLDL was 29, and CAC came back at zero. How does the IR hypothesis explain this?

I'm not sure about the IR hypothesis (is there just one?), but if she's eating a lot of high fiber grains/carbs her net carbs might not be that high relatively speaking (at least not beyond the capacity of her insulin sensitivity to handle them well). Her glucose absorption rate would be diminished by the fiber, keeping insulin under the curve lower. If she's getting good exercise too, then she could be burning through the blood sugar more efficiently, at least peripherally. I consider that it's probably true that such a whole foods diet could be healthy from a peripheral metabolic standpoint, but that there are going to be those whose inflammation is triggered by the lectins and/or who need more ketones for optimal brain/CNS metabolism. Do all E4s at least fall into the latter category? I'm not sure at the n=1 level, but I trust the research has shown that as a group we do.