From Dr. Dale Bredesen

[circular]

I'm with you thumperama, complicated not contradictory, at the same time probably no one knows whether it's a good idea to reduce it without addressing the unknown it may be protecting us from?

[GenePoole0304]

even curcumin can be a negative for some unfortunate people...like me.. I knew about this but this guy was able to work it out and explain the links.

http://emediahealth.com/2012/01/17/curc ... ertension/

and notice how many people admitted here they had a reaction to grape seed extract...good see the thread on resversatrol...

its all woo if it don't do you no good.. they have to start somewhere...but I like the de Longo connection.. its baby steps..

maybe we don't need much exercise, if you exercise and then sit the rest of the day couch potato-ing then the exercise is negated.. just keep moving and use a sauna regularly as the burn is the same there as exercise ...
http://www.eurekalert.org/pub_releases/ ... 090315.php

time to get up and drain fluid... ... ... ... ... .. . --- --- ---

[MarcR]

I have started a new topic, Community Guidelines and Moderation - Discussion, and I have moved a collection of posts over there from this topic to initiate the discussion and allow us to continue to "sift" through them in a dedicated spot.

[ApropoE4]

@ApropoE4, Ben

I really have no idea, but what if the BA views are not contradictory but are complicated? What if BA is both protective and its presence indicative of something undesirable--kind of like a scab on a cut? We can agree that it's not wise to pick the scab, but we do want to see it go away.

It seems that instead of assigning fraud labels to statements we don't understand, it's easy enough to ask for an explanation from the professionals in question.

To that objective, there are more upcoming ApoE4.info-sponsored interviews with professionals in the AD/ApoE4 community--like the original we had with Dr Dayspring. We should be sure to include a question about this to bring clarity to the topic.

The issue here isn't facts. Of course we're dealing with complex systems, and perhaps the best evidence of that is that even the disease processes themselves are far from fully understood after years of research. Are plaques somehow protective? is a little bit good but a lot not good? who knows. I don't and and I'm sure Bredesen doesn't know either.

The issue is how we relate to a group of people who describe themselves as researchers, but who do not follow the common conventions of scientific research and who appear to generally suggest courses of treatment that closely match current diet or alternative medicine fads.

Furthermore, it's hard so see why we would ignore a simple fact - if any of these proposed treatments were as effective as their promoters claim, medical journals would be lighting up like veritable Christmas trees of citations - contrary to the claims often repeated here that this is "emerging" science and therefore controversial, the scientific community is incredibly fast to jump on any ship that appears to be sailing towards the island where the fountain of youth, or the source of eternal energy are to be found.

https://en.wikipedia.org/wiki/Cold_fusi ... experiment

[Julie G]

Interesting and entertaining analogy with cold fusion, ApropoE4. Thanks to you, I've put a few new movies on my watch list. I love plots like these. The best recent movie IMO- The Imitation Game, similar feel.

Of course, Dr. Bredesen has never claimed to have found definitive proof, right? His work is all based upon published case studies and his work with patients. We are all very well aware of that. Given the individualized and multifactorial nature of his approach, I'm guessing it will be very difficult to get it past a review board for rigorous analysis. His strategies have helped me and others here. For how long- who knows? I'm hopeful that he'll find a way to build evidence that combining strategies specifically geared to a patient's unique needs improves cognition. I'm no scientist, like you, but it seems like a pretty common sense approach to me. Even Dr. Longo (mainstream enough?) concedes that it will most likely end up being combinations of strategies that make a dent in this disease.

You've previously stated that you don't find the protocol harmful and agree that it MAY be helpful. What specific aspect has suddenly begun to ring alarm bells for you? Thanks for helping us understand.

[MarcR]

ApropoE4, since the topic of this thread is Dale Bredesen, please let's agree to stop talking here about "a group of people who describe themselves as researchers". If you want to paint with a broad brush, you might consider visiting the new thread in the Site Feedback forum.

Regarding Dr. Bredesen's MEND protocol, I think the initial paper describing it was clear about what was done. One year later, I still have not heard anyone dispute the words in the paper. Instead, I have heard only vague critiques like your remark about not following "common conventions of scientific research". (Incidentally, I perceive some weaknesses in how those common conventions have been functioning. It's clear now that for 20+ years the scientific establishment has prioritized the amyloid beta hypothesis excessively and thereby starved any nonconforming research. Like Martha, I'm skeptical of everyone.)

Regarding what the paper actually says, here's my lay summary:

1. Hypothesis: AD is caused by biochemical imbalances that stress a broad range of body subsystems and thereby reduce the body's overall ability to maintain health.

2. Hypothesis: If we measure body subsystem functionality broadly and take steps to move the measured biomarkers into optimal ranges, we can change patients' cognitive decline trajectories.

3. Result: using a comprehensive approach, nine out of ten patients experienced obvious symptom remission.

So I see two hypotheses - a science word that I think means "educated guess" - and some results. Do you dispute this summary? For example, do you believe the paper is misrepresenting the two educated guesses as facts or full-fledged theories? Do you believe the paper is misstating the patient experiences? If so, what is your basis?

Currently, we have no solid scientific reason to believe that the hypotheses are true, and because of a lack of controls and the large variation in treatment from one patient to another, it's difficult to see how that will change anytime soon. General acceptance of this approach will require a large number - hundreds if not thousands - of equally surprising successful results. And even then I would expect Dr. Bredesen's peers to continue to express appropriate and rational concerns about the experimental design weaknesses.

All that said, as a lay person with a three-generation personal stake in AD treatment, I see promise in MEND for me and my family because I don't think Dr. Bredesen misstated the results, and I don't think nine out of ten patients improved as a result of random variation. I believe that one or more elements of the shotgun treatment plans used by these patients caused them to improve.

When I read through the footnoted papers explaining why Dr. Bredesen included each element in Therapeutic System 1.0 from the paper, I concluded that the strength of evidence for the MEND elements varies widely. I am skeptical of the benefits for some of the items. I think the treatment elements likely vary widely in their effects. And even though it may make professional scientists cringe, I am happy to see that MEND is continuing to evolve as per February's Therapeutic System 2.0.

I care about practical clinical benefits right now. With every day that goes by my father continues to decline. That decline has been occurring for years, and I have no reason to believe that it can reverse in the absence of a significant change like beginning to follow the MEND protocol.

So with all that in mind, I'm mystified by the harsh criticism of Dr. Bredesen and the dire warnings about trying MEND. What program out there offers a better option?

[GenePoole0304]

Course Change Everyone, the ship is splitting up..main the lifeboats and get your life jackets everyone!!


Finding could mean that each variation would need to be treated differently

UNIVERSITY OF CALIFORNIA - LOS ANGELES HEALTH SCIENCES


Alzheimer's disease, long thought to be a single disease, really consists of three distinct subtypes, according to a UCLA study.

The finding could lead to more highly targeted research and, eventually, new treatments for the debilitating neurological disorder, which robs people of their memories.

The study further found that one of the three variations, the cortical subtype, appears to be fundamentally a different condition than the other two, said Dr. Dale Bredesen, the study's author, a UCLA professor of neurology and member of the Easton Laboratory for Neurodegenerative Disease Research.

"Because the presentation varies from person to person, there has been suspicion for years that Alzheimer's represents more than one illness," said Bredesen, who also is the founding president of the Buck Institute for Research on Aging. "When laboratory tests go beyond the usual tests, we find these three distinct subtypes.

"The important implications of this are that the optimal treatment may be different for each group, there may be different causes, and, for future clinical trials, it may be helpful to study specific groups separately."

The subtypes are:

Inflammatory, in which markers such as C-reactive protein and serum albumin to globulin ratios are increased.
Non-inflammatory, in which these markers are not increased but other metabolic abnormalities are present.
Cortical, which affects relatively young individuals and appears more widely distributed across the brain than the other subtypes of Alzheimer's. It typically does not seem to cause memory loss at first, but people with this subtype of the disease tend to lose language skills. It is often misdiagnosed, typically affects people who do not have an Alzheimer's-related gene and is associated with a significant zinc deficiency.
The findings of the two-year study, which involved metabolic testing of 50 people, appear in the current issue of the peer-reviewed journal Aging.

No effective therapy for Alzheimer's exists. And scientists have yet to completely identify the cause, although multiple studies have pointed to metabolic abnormalities such as insulin resistance, hormonal deficiencies and hyperhomocysteinemia, a condition characterized by an abnormally high level of an amino acid in the blood.

In a 2014 paper, Bredesen showed that making lifestyle, exercise and diet changes designed to improve the body's metabolism reversed cognitive decline in nine out of 10 patients with early Alzheimer's disease or its precursors.

The current finding grew out of an extensive evaluation of the data from last year's study, and it could eventually help scientists pinpoint more precise targets for treatments -- the same approach that has led to major advances in treating other diseases.

For example, Bredesen explained, researchers have recently been able to develop precise treatments for cancer by sequencing tumor genomes and comparing them to the patients' genomes to better understand what drives the formation and growth of tumors.

"However, in Alzheimer's disease, there is no tumor to biopsy," Bredesen said. "So how do we get an idea about what is driving the process? The approach we took was to use the underlying metabolic mechanisms of the disease process to guide the establishment of an extensive set of laboratory tests, such as fasting insulin, copper-to-zinc ratio and dozens of others."

Going forward, Bredesen and his team will seek to determine whether the subtypes have different underlying causes, and whether they respond differently to potential treatments.

The need for a new approach to treat Alzheimer's is urgent. It is the most common age-related dementia, and the number of people with the disease in the U.S. is expected to increase to 15 million in 2050, from nearly 6 million today. The cost to treat people in the U.S. with Alzheimer's and other dementias is expected to be $226 billion in 2015 alone, and could reach $1.1 trillion in 2050.

http://www.eurekalert.org/pub_releases/ ... 091615.php

[Harrison]

Full text is available: http://www.impactaging.com/papers/v7/n8/pdf/100801.pdf

First off, it should be noted that in his 3 sub-types of AD, the first two types are represented by single case studies. The third type, which he believes is related to low zinc, has 6 examples. It would be really great if some kind of data mining of databases for relationships between markers and AD diagnoses (Kaiser Permanente in California did this for A1c) could be used to confirm this on a larger scale. Until then we n=1 anecdotes.

That said, case 1 (inflammatory) scared me. Male ApoE 3/4 with MTHFR A1298C, 25 BMI, 96 mg/dl fasting glucose, 2.2 TSH. Check for me. My c-reactive protein, homocysteine, albumin:globulin ration, fasting insulin, testosterone, and vitamin B12 are all better than the case study though. This really brings home all the recent discussions about what to believe as far as small samples, supplements, etc. There is so little to go on, I think the only thing one can do is pick out the interventions that have little likelihood of doing harm and then going by what one's body (or lab results) tell it.

[Stavia]

Agreed Harrison. Much too little data to be anything but interesting at this stage. And I'm doing exactly the same - picking the interventions that are likely to be generally beneficial and unlikely to harm.

[Julie G]

Thanks for sharing Gene. Excellent insights as always, Harrison & Stavia. We heard about this at The Buck, right? I was under the impression that these subtypes emerged from a larger dataset...not sure how many though. The first two categories were most common & the third was atypical. I agree, it'll be interesting to see how these subtypes hold up with larger numbers. I love your idea of running the observation through data mining, Harrison, but I suspect very few docs are collecting all of this data. I see myself as a combo of the first two- SCARY

We've previously talked about this paper. Bear with me as I try to move your comments to that thread.