Martha, I briefly saw your post and really liked it...not sure why you want to delete it? You asked WHY butter is "bad," milk is "neutral," and cheese and fermented dairy are considered "better." Great questions. I agree that this information is confusing for our population and often contradictory. Gundry, for instance, is opposed to cheese for our population.
Dr. Krauss's recommendations are based upon HIS research results. He hinted that it may be the fermentation involved in cheese-making, yogurts, and kefirs that offers the benefit. As always, proceed cautiously. N=1 should always trump any advice.
LOL, Stavia. I completely agree that Dr. Krauss is adorable and certainly meant nothing disparaging by all of my descriptors. I have the highest respect for him, and all of our presenters. I'm just using the girl part of my brain to provide details for those members who couldn't attend
Oh gosh Julie you have been very complimentary about all our scientists. I wasn't thinking about anyone else's descriptions. I was just remembering his adorability in that particular interaction. I wanted to hug him.
I am going to shut down for today and return when I am in less of a party-spoiling mood. Glad so many people seem to have had such an excellent experience.
(((Martha))) I hear you, my friend. We still have many unanswered questions. I'll TRY to put some of your concerns in perspective.
-Dr. Krauss's dairy advice is based upon real research that he conducted. I'll try to dig up the paper. I don't think the results were stratified by ApoE genotype.
-There is much peer reviewed science (7 major papers or more) that links LDL-P to CAD/CVD. IMO, for that reason alone, we need to care...not to mention the established link between AD and CAD/CVD.
-Dr. Bredesen's approach is a meeting of Eastern and Western medicine. Dr. Rao may represent some of the Eastern perspective. He has gobs of neuroscience credentials; but is also trained as an Aryuvedic practitioner. His advice is corollary to Dr. Bredesen's. Take what feels useful to you; discard the rest. No one has your particular set of genes, hence my suggestion to focus on N=1.
You are absolutely right. We're just being giving advice because we're asking for it. Our job is to sort through it. I've been following the AD research for three years now. IMO, Dr. Bredesen's paper provides a blueprint for our population in terms of AD prevention. Check out George's link above in which Dr. Bredesen both synthesizes (and makes changes based on new evidence) some of the recommendations from his original paper. It's not easy; but I do see that we ARE making progress. We are way ahead of where we were three years ago when I began this search.
(EDIT: Oops, I see that I responded to another deleted post. Maybe others are feeling similarly and this may still be helpful.)
Stavia wrote:Fascinating. Bredesen postulated that the e4 evolved when we moved from an arboreal life to the savannah thus exposing us to cuts on our feet, carrion cos we were most likely scavangers, and fighting in competition. The gene is pro inflammatory thus helped kill pathogens. The negative effects would only kick in at later life which we would have been extremely unlikely to make. As we have evolved, e4 has slowly been selected out in favour of the newer e3. Evolution isnt an end game. Perhaps we were not well adapred for longevity as hunter gatherers. Perhaps the diet was optimal for reproduction only. We should not assume that the hunter gatherer lifestyle was well adapted for the e4 allele in terms of our modern purposes which is to prevent LOAD.. Remember the paradigm of the selfish gene.
Just saying. I guess we will never know
Fully agree that evolution primarily selects for reproduction and this may have been the inherent weakness overcome by later evolution of E3 (i.e. as part of the Grandma hypothesis that elders played an important role in the reproductive success of their children who were more free to hunt and scavenge).
But it also seems plausible that the E4 gene became mismatched to other social evolutions - i.e. whether agriculture (i.e. grains), fixed animal husbandry, or even the simple loss of variability in food accessibility. Just one of many potential hypothesis, but in the latter, the idea would be that E4 thriftiness actually became a disadvantage when new food came in before the last had cleared. Although not uniquely so, this seems to fit the limited data at least I am aware of. The implication is that one option to is create a social context that is more similar to that under which our gene was an advantage. Of course without data, that might turn out to be fully wrong, so wouldn't recommend taking it to the bank blindly, but I am not aware of any current evidence that would contradict it?
PS: Note that this hypothesis also seems consistent with other suggested recommendations... notably 1) eating in accordance with light cycles and 2) fermentation (which would have been one of the only food preservation techniques to early peoples).
Russ
E3/4 Eat whole, real, flavorful food - fresh and in season... and mix it up once in a while.
Russ you are very smart and I am loving this discussion. When you said social context I immediately saw feast-famine as one possibility. Life must have been very tough. I really like your approach. One must be careful not to assume the modern daily supermarket availability in any way substitutes for the real Paleolithic.
Again many thanks to Julie and everyone who attended the events with me. You are an inspiration and meeting you in peerson has been life changing for me.
A couple of comments that may have not been mentioned yet:
1. Dr. Bredesen said he is working on a "system 2.0" that will include additional supplements such as phosphatidyl serine, more specific measurement and dosing of choline and omega 3's, and something he called "resolvants," which help resolve inflammation. Anyone know what he means by "resolvants"? Are they drugs such as NSAIDS?
2. Dr. Bredesen said "Neuroview" the retinal amyloid scan, is expected to be available in 2016.
3. Dr. Krauss said there is a direct correlation of LDL-C and an inverse correlation of HDL-C, to cerebral beta amyloid. He said this is independent of APOE genotype. There are at least 7-9 forms of LDL, they decided to simplify this when they classified LDL as either small or large. In general the small LDL is more of a problem from cardiovascular disease and the med and large LDL are a problem for AD. APOE4's have more large and less small LDL. Diets low in fat (esp sat fat) will help lower large LDL. Niacin and low carb diets will lower small LDL. LPA variation is 90% genetic and unlikely to be affected by diet, but it can be lowered by niacin. Although he does advise statins to treat high LDL if diet is ineffective, he said "there is no evidence that lowering LDL by statins will help AD."
4. At Gladstone, Dr. Mahley said APOE4 has a direct effect on cognitive decline that is independent of its effects to increase deposition and decrease clearance of amyloid beta. He says E4 causes AD, and has a role in other dementias and Parkinson's and MS. Aging is a cause of nerve cell injury but when E4 is produced as a response to injury (the injury can be aging, oxidative stress, trauma, or amyloid deposition), the nerve cell sees the E4 as abnormal and tries to destroy it with proteolysis, which creates E4 fragments that are toxic.
This made me kind of question his hypotheses, even though I know he has been studying E4 for > 20 years. I just think it is maladaptive for a cell to produce a protein that it immediately needs to destroy in a way that is toxic to itself. I don't know of other examples in biologic systems where this occurs normally (not as a disease process), and up until 220,000 years ago everyone was E4/E4.
5. The structure corrector drug they are developing sounds promising based on the disease mechanism they propose. Dr. Mahley had a slide titled "Hope" and he hopes to be in clinical trials for safety in 2 years and have a drug available in 5 years. But they only have some preliminary mouse data from mice genetically altered to produce E3 and E4 (not normally part of the mouse genome). There was a short video he showed us of a poor E4 mouse swimming in circles in a water maze, unable to find the hidden platform, whereas the E3 mouse could swim pretty much directly to it. When they were both treated with the structure corrector APOE4 R6IT their results appeared to be much more similar. But the results slide was missing data on E3 mice that were untreated and I wonder why that was. The result they showed was how many times the mice crossed where the platform used to be (they removed it for that experiment) and not time to get to the platform which was what they showed us to show the difference between E3 and E4 mice. I think perhaps even for the mice not all the data is consistent so they are showing us the best results they have. However they are about to start a company and obtain lots of funding so hopefully they will have more opportunity and manpower to work on it. They said they are recruiting several senior level scientists with expertise in drug development.
Again, it was so great to meet everyone who came! I look forward to a lot more discussion with you about our meet up and everything E4!
K
Karlena et al - am I understanding this correctly: Mahey said, out and out, that e4 CAUSES AD?!?!
Are you kidding me?
So if we are able to effectively ward off oxidative stress, trauma, and excessive amyloid deposition, if we 4s live long enough, we'll still develop the disease? Much like Sartre - no friggin' exit?
Other than cooking up potions in his lab, did he have any other advice for us?
Lovely.
I'm just a oily slick in a windup world with a nervous tick.
