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Dale bredesen book

Indian girls massage in leicester. Hd sex videos com. Holding a door open for a woman sexist. Girl to fuck it now in Melbourne. Video Porno Free Black. African sex dance vids. Dale E. Bredesen, M. He has collaborated on the publication of more than academic research papers. Bredesen received his undergraduate degree from the California Institute of Technology and his medical degree from Duke University. In this episode, Dr. Although the subtypes vary in their causes Dale bredesen book manifestation and often overlap to some degree, Dr. Bredesen explains that the underlying pathological features — the accumulation of amyloid beta plaques and tau Dale bredesen book — Dale bredesen book unifying aspects of the disease. He adds that how these features play out in the somewhat fragile environment of the brain depends on a wide array of click here parameters, such as genetics and lifestyle factors, including diet, sleep, exercise, and environmental exposures. Click here to read Dr. It is a known neurotoxin that destroys nerve synapses and Dale bredesen book clumps into plaques that lead to nerve cell death. But in recent decades research has revealed interesting characteristics that suggest amyloid-beta can play a protective role against fungal, bacterial, and viral infections. Pov compilation pov facial free videos sex movies porn tube Best site for softcore porn.

Laura ashley vintage high collar blouse. Are you familiar with some of those? One is the through a free fatty acid and the other one's through an actual transporter called the Mfsd2a transporter, which is actually in a phospholipid form, DHA is in a phospholipid form.

Dale bredesen book so, it appears click to see more there may be different ways, you know, that DHA gets across the brain, and one of the ways is potentially not working quite as well in ApoE4 individuals, at least that's my writing theory. But once the paper's accepted I'll send you a copy.

So it's super, super interesting. Yeah, and of course, as you know, I mean, Professor Wurtman from MIT has spent years looking at what does it actually take nutritionally to make synapses? And his Dale bredesen book was you need the DHA and you need acetylcholine as well. And so again, if you're going to be helping people to change that balance toward the synaptoblastic you want to Dale bredesen book sure that they have plenty of those precursors as well as the appropriate signals, reduction of inflammation, all these other things Dale bredesen book are actually part of an overall orchestrated event.

The other interesting thing is that DHA, and I didn't know this previously until I had been digging into the literature, it also seems to be important for some of the glucose transporters on the blood-brain barrier. And so if you're DHA-deficient those glucose transporters aren't working as well and you're not getting glucose into the brain, which is another real hallmark of Alzheimer's disease.

So that's Dale bredesen book interesting thing. So, a couple of interesting things I wanted to ask you about were kind of off-topic but not particularly. You mentioned Dale bredesen book type 3 sub-type.

Would the herpes virus fall into that? So, yeah. So herpes virus could give you type 1 or type 3 depending on Dale bredesen book you're actually responding to.

Dale bredesen book

If it's just a Dale bredesen book inflammation then it would be a little bit more like a type 1 with chronic inflammatory, but you're right. You know, again, many groups have said, "Okay, it's about herpes.

Okay, it's about P. And the reality is, all of these are capable of inducing the signal, this change where you're making the amyloid as part of a protectant. As you know, it's essentially part of your innate immune system. So if you're responding in that way it can be any of those things, it's not just one every single time, as far as anyone knows. So, yes, you alluded to the recent work on Dale bredesen book and especially, of course, six and seven.

And so, yes, not surprisingly. The Dale bredesen book thing I kinda wanted to mention just because I wanted you to know about it in case you weren't aware of it, there's some really interesting research coming out of Finland. Are you familiar Free real swinger sex videos saunas and the protective Yeah, of course, dramatic effects, and fits very beautifully with everything we've been talking about.

And certainly, what happens when you have a sauna, yes, you may induce some heat shock protein, Dale bredesen book, that's important, and it can be important in folding of proteins, but what also happens, of course, is that you detox.

And these people who are doing this repeatedly Genuis from Canada who showed that if see more look at composition of sweat compared to the blood there Dale bredesen book certain toxins that are very high, cadmium being the big one, over 1, times increase in sweat, so a good way to get rid of cadmium, but a good way to get rid of other things as well.

BPA, especially the hydrophobic toxins, the non-hydrophilic stuff tends to be very good in the sweat, but others as well. And so that's why it is very helpful, and many of us don't do enough of that sort of thing. And as has been pointed out, whether you're doing it through sweat and exercise or whether you're doing it through saunas, whether you're doing it through other mechanisms, yes, it's good to get.

And then you want to use a non-emollient soap immediately thereafter, things like Castile soap or whatever you like that's Dale bredesen book and get rid of the stuff so that you don't get re-penetration. Yeah, the other thing is that cardiovascular effects with the sauna and that may also be related to dementia as well.

So, is that something that you'd consider using in your protocol? Now, we recommend that people But as a general rule, you know, part of this is, again, as my Dale bredesen book says, resilience, part of this erotic irekand resilience.

We're taking people who are sub-optimal in their metabolism, in their inflammation, in their toxic status, in their lifestyle status, in their sleep, in their stress levels, these are surprisingly important. One of the first people who came through was a very intelligent physician. Dale bredesen book as we went through each thing he said to me, "Well, you know, I don't believe that, you know, that's not a cure for Alzheimer's, that's not a cure for Alzheimer's.

And as we went through each thing, you know, he was telling "Dale bredesen book," "Well, I don't believe this. So, it is about changing signaling within your synaptobalstic Dale bredesen book synaptoclastic ratio, providing the right support for that, DHA, acetylcholine and Vitamin D, and appropriate hormones, and BDNF, and all these things, and making sure that you don't have chronic exposure. And as you mentioned, sauna is actually a very powerful way to help reduce overall Dale bredesen book burden.

It is surprising how much toxic burden most of us are living with. So talking about the importance of intervening in multiple ways Dale bredesen book there are so many different pathways that lead to inflammation, that can lead to insulin resistance, that can lead to toxic burden, one of the really And actually, we've had a number of people who have tried to remove their amyloid with antibodies who've actually gotten worse with that happening. So you have Dale bredesen book go back to, why is there?

And it's tough because yes, it is both part of the mediator, it's not the cause of Alzheimer's, it's a mediator, and I think that's been one of the problems. People want to say it's the cause, more info a mediator, and there are many upstream things contributing to that.

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So these have often been called cortical presentations, which have been noted for years by people like Professor Mario Mendez, to be typical in younger presentations of Alzheimer's and often in ApoE4 negative individuals. I think I also read one in your papers where you did this metabolic profiling there was a very prominent zinc deficiency in that. Yes, so for reasons that we don't entirely understand yet, many of the people with the type 3, the toxic sub-type have low serum zinc, high copper-zinc ratios, and low triglycerides. The low triglycerides may turn out to be related to malabsorption, we don't know for sure yet, but we don't really understand why the people often have these low copper-zinc ratios. Yeah, so as, you know, copper and zinc actually are competitive, for example, in their absorption. And so, too much of one actually is often associated with too little of another. And then typically in our society, as you know, most of us are deficient in zinc. There are actually about a billion people on Earth is the estimate for zinc deficiency. It's a very common problem because if you have poor gastric acidity, which is common as we age, if you're taking PPIs for GERD, if you're taking something for reflux, you won't absorb the zinc very well, if you have copper piping which most of us do, the copper will often compete with the zinc. And so many people have a little too much copper and a little bit too little zinc. And in fact, it was noted over 30 years ago that people with high copper-zinc ratios tended to have dementia more than those with normal copper-zinc ratios. So does this have something to do with it? I know there's like over to different enzymes in the body that require zinc. So does copper then bind to those enzymes and then sort of mess up the function or is that like the theory? So, no. The theory is that, as you know, copper is a generator of free radicals. You know, copper can act like iron in that sense. It has a free electron in the D orbital which does not occur with zinc. So in general, as you indicated, in these various enzymes, and it's hundreds, just as you said, it is an important structural component and it has a very specific architecture with the enzymes that it serves, so it is a structural thing in general. And copper, to my knowledge, doesn't actually replace that. But for example, zinc is important in many things that are related to cognitive decline, it's important in diabetes, it's important in functioning of insulin, it's important, of course, in the trophic activity of insulin and, you know, on and on. It's important in immune responses. So, it actually has many effects that are related to cognition. So it may even just be a biomarker for something underlying going on right in the toxic insult type of Alzheimer's disease you're talking about. It something to keep in mind when you see that, and especially if the person presents, and these people tend to be very distinctive, the people who have type 3. So, they tend to be young, and we see them in their late 40s, mid 50s very commonly. We've seen them as late as starting their first symptoms in the mids, but typically, their first symptoms are currying in the 40s and 50s. They are often women, they are often ApoE4 negative although not always. There are certainly people who are ApoE4 positive to have this. As you mentioned, they often have the low zinc, and then they typically present in a non-amnestic way. Interestingly, unless they are homozygous for E4, in which case they do present typically with an amnestic presentation, but the ones who are E4 negative typically present with problems, as I mentioned earlier, executive dysfunction problems. And so I always ask people, are you having trouble organizing things? We had one person, for example, who was known for her tremendous organizing capability and as she started to get the problem she just lost it. She could not organize things that she could do before, it's a very common complaint. Or as I said, people will say, "Oh, I can't calculate a tip anymore, or I can't pay the bills anymore," anything that is math-related or visual perception or word finding, things like that. You mentioned the ApoE4 a few times. Can you talk a little bit about just for people listening and watching, you know, what ApoE4 is, and it's a gene, and so why it plays a major role in Alzheimer's disease. Yeah, so, Apolipoprotein E is a really fascinating story, and of course, Professor Robert Mahley discovered this decades ago, and it has turned out to be the most important genetic risk factor for Alzheimer's disease. Seventy-five million Americans have a single copy of ApoE4. And when I say that what I mean by that is, everybody has two copies of either 2, 3, or 4, and the most common one is ApoE3. So it's common for people to be a 3,3 as an example. However, about a quarter of the population, so about 75 million Americans have one copy of ApoE4, and that's actually the primordial one. Then about seven million Americans have two copies, so they're homozygous for ApoE4. So most likely you will get it. And of course, the vast majority of people don't know. Now, in the past people said, "Don't check because there's nothing you can do about it," and that has completely changed. So there is a tremendous amount, and the reality is Alzheimer's should be a rare disease. It should essentially decrease to a very low level with the current generation. If everybody gets checked, we recommend that everybody 45 or over get a cognoscopy, it's a silly term but it's easy to remember. Everybody knows when you hit 50 you should get a colonoscopy, and if you hit 45 or over you should be getting a cognoscopy. You should be doing some testing and see where you stand, what are your risk factors, are you ApoE4 positive, do you have high homocysteine, methylation issues, inflammatory issues, nutrient issues, toxin issues, all these things, because they can all be addressed, and we can decrease the overall global burden of dementia. So there's a variety of biomarkers that you are suggesting people can go and get measured? Cognoscopy, yes. That's a nice term. So, including the genetic factor, ApoE4, seeing the ApoE4 and then you have a variety of biomarkers that you kind of just mentioned. Some of those, I think you also have published on before, talking about the insulin sensitivity as well, looking at insulin sensitivity and glycated hemoglobin. So maybe we can talk a little bit about some of those biomarkers and how But as we have made 2. And we now have over 3, people who are on this protocol with unprecedented, and we've published a number of the results. We actually have another thing that's just finishing up that reports another 50 people who have shown improvement. Fifty, wow. So the publications that I had read you had shown, I think it was about 10 patients. Right, and you showed that you were able to basically take a person that had Alzheimer's disease, some of them had to leave work because of their issues, and you put them on a protocol and they were not only were able to some of them return to work but they also seem to have brain mass returning and just so it was really phenomenal. Yeah, and I should say, you know, it goes back to one very simple principle. We've been trying to treat this disease without knowing what causes it. So I usually tell people it's as if you took your car into the mechanic because it wasn't working well, and the mechanic said, "Oh, Rhonda, no problem. This is called car not working syndrome and your car is going to die. I mean, shouldn't you figure out why, why something, what went wrong with it? People say, "We don't know what causes it, there's nothing you do about it. There's nothing we can do, and you're going to die. It is becoming less about mono-therapeutics and more about programmatics. And at the center of this is to understand why complex chronic illnesses occur. When you have something like there's a simple illness like pneumococcal pneumonia, you find the pneumococcus, you treat the pneumococcus, and all the other underlying things, alcohol, diabetes, anything that could have been contributing is less important because you've got at the pneumococcal pneumonia, that's not the case with complex chronic illnesses. With Alzheimer's there are dozens of things that can be contributing. And so what we want to do is address all of those. Yes, if you have pathogens, many people have, for example, Borrelia from Lyme disease or a Lyme co-infection like Bartonella or Babesia or Ehrlichia, things like that, then those need to be addressed. And of course, you need to change the underlying biochemistry. So as you indicated, there are specific biomarkers. So we want to know you are hsCRP, it's a marker of inflammation, of course, we want to know your homocysteine, the marker of methylation. If you're not methylated appropriately and your homocysteine is high, then you are at increased risk for neurodegeneration. And of course, it's been published that you have a more rapid decline in your cerebral grey matter volume and hippocampal volume if you have a high homocysteine. Is that because of vascular reasons or what's the homocysteine mean? Well, the publication did not distinguish. It just simply followed people over years and looked at the rapidity of the decline in volume and could show that not only was it more But then if you improve the homocysteine and brought it back to normal and they're looking at less than seven as being normal not less than 13, which is often used in the labs. Seven as being normal, then in fact what happened was people actually stopped their decline and leveled off. So it suggested that this is a causal relationship, that it is a mediator of cognitive, well, of change in cerebral volume as well as cognitive decline. Independent of other biomarkers, yes. So we want to know that. We want to know whether you have glycotoxicity. So we want to know what is your fasting insulin. And again, people will accept it way off the scale. We have an unfortunate situation where classically we have accepted laboratory values as within normal limits, WNL, very arbitrarily as being within two standard deviations of the mean. That actually makes no sense physiologically, it just says that there's a distribution there, it doesn't say that that's optimal for your health. So we'd like to know what your fasting insulin is, and optimally, it would be less than five or less than five, although again, within normal limits goes much higher than that. We'd like to know your hemoglobin A1C, which again, is a marker of, essentially over the last two months, your serum glucose. We'd like to know your fasting glucose. And then the atrophic, as you can imagine, there are lots of things. We want to know your vitamin D, and again, we want to see that it's optimal, not sub-optimal but within normal limits. We want to know your pregnenolone, progesterone, estradiol, testosterone, free T3. And we'd like to know your brain-derived neurotrophic factor in your NGF. There's no simple way on a clinical lab test today to get those, so you have to infer them from other things, you know, what is your hippocampal volume? You know, what have you been doing? If you change these various things we've been talking about, you're likely to have a decrease. Have you been exercising? If you're not exercising your BDNF is likely to be lower. So we want to look at all of the trophic support for your brain because these are critical things if you're going to make and keep a large network of synapses, you need to have that support. And then again, that balance changes for many of us as we age, especially if we are ApoE4 positive. ApoE4 gives you an advantage in that you have a hair trigger, essentially, for inflammation. You are responding But if you're not living in a pro-inflammatory, in an environment that's parasitic, then in fact you have this chronic inflammation that, again, good for when you're fighting things, good for if you step on a nail, good for situations that should be pro-inflammatory, but in the long run counterproductive. So, you know, as you know, this is so-called antagonistic pleiotropy. This is something that can help you when you're young but actually can put you at risk for diseases that will shorten your lifespan. And typically, cerebrovascular disease, of course, Alzheimer's disease and as you know, ApoE4 is actually underrepresented in centenarians. So it has been a short-gevity gene as it were. Again, that is changing and can change by understanding what's actually being driven by this. So we want to know all those markers and those for the type 2, and then of course, we want to know the markers for type 3. So we want to know if there are specific toxins and especially mycotoxins. So the toxins can be metalotoxins like mercury, relatively common one, they can be organic toxins like DDE, things like that, they can be biotoxins like trichothecene, ochratoxin A, aflatoxin, gliotoxin, these are toxins produced by various molds species like Stachybotrys and Aspergillus, and Penicillium, which are literally fighting us. I mean, they're literally saying, "Okay, I'm fighting back. So these are things where just as we're seeing increasingly bacteria that are antibiotic-resistant as Professor Shoemaker has pointed out, Dr. As we've had fungicides, as we've had, you know, buildings with leaks where we haven't recognized the danger from these. In fact, we've had more and more of this mold-related illness. So we want to know all those things for the types 3s. And of course, we also want to know have you had a history of head trauma, we want to know if you have vascular compromise, all of those things are critical. Now, you mentioned the diet. So, yes, we want to start with the basics, but again, ultimately, it's a program that is customized to you based on what's actually causing your cognitive decline or your risk for cognitive decline. So keto, so we want people to be in mild ketosis because that actually turns out to work better for cognition, and many people do better with their cognitive decline, just as Mary Newport showed, of course, with using coconut oil then that may or may not be the best way to do it for some people, other people like caprylic acid, MCT oil, other people are very good at generating endogenous ketones, which if you can do it, it's the best way to do it. I did have an issue with some of the connections drawn, which seem a little iffy, not to mention trendy. I have a bigger issue with the contradictions, like the book saying that the This is a harsh rating, but feels appropriate. I have a bigger issue with the contradictions, like the book saying that there is no backup for metals being a cause of dementia, but you should try having mercury fillings removed. Okay, mercury can have toxicity issues not necessarily for fillings, but fine , but then it is further specified that aluminum doesn't seem to contribute, yet one of the sample routines includes the elimination of aluminum from her deodorant. In a way that makes sense, because the people who are most likely to jump on bandwagons of clean eating and pure living are the people who will be most drawn to this book. I also do not doubt that when people improve their nutrition and sleep that they do better in many ways. I do doubt that adding all of these supplements as you eliminate some pretty good foods is helpful. I can almost excuse that everyone cheating on their diet - as determined by visiting health coaches - does not automatically rule out the connection between the protocol and their improvements, given that you might not have an issue with all 36 factors. However, that level of unverifiability, and the scare tactics that are used regarding stopping, and other factors feel like they are adding up to someone not improving just not having found the right essential oil yet, and if it doesn't work you just didn't try hard enough. I might have given it two stars if it were just kind of scientifically shoddy, but the way it ended up being angered me. A much better book along similar lines would be The Brain Fog Fix by Mike Dow, which covers similar ground with less pretension. Aug 30, Robert Luebke rated it it was amazing. This is a must read for anyone who fears the threat of getting Alzheimer's. Bredesen is a neurologist and researcher who lays out a plan called RECODE for preventing and even reversing some of the symptoms of Alzheimers. Nutrition plays a big role in his program, but the stories of patients who have improved from Dementia after being on this program is very promising. Oct 26, Peter McCluskey rated it it was amazing. Alzheimer's can be at least postponed for years in most people, and maybe fully cured. The main catches: It only works if started early enough and Bredesen only has crude guesses about what's early enough , the evidence is less rigorous than I'd like, and it's not a medical treatment, it's a quantified self approach on steroids ketones. If so, that's an enormous advance. The protocol involves more tests than I want to count. These are almost entire Alzheimer's can be at least postponed for years in most people, and maybe fully cured. These are almost entirely tests that are standard for some health-related reason. Bredesen suggests small changes to how to interpret those tests, and large changes to how much we should value optimizing the things they measure. It's a strategy that says "normal" health is unacceptable, we need to do better. This part of the protocol seems to be backed by decent research indicating that we should expect some sort of health benefits from it. Most biomarkers are less reliable than is commonly reported, but as long as they point in the right general direction, it's better than not to improve them. The protocol also includes an even larger set of ideas about how to optimize those biomarkers via lifestyle changes, vitamins, supplements, and maybe prescription drugs for a few people. Here, Bredesen appears to be using a much wider mix of science and fads. But for bone broth, he cites an article from mercola. As these examples suggest, the protocol is probably safer overall than the average American lifestyle, even if a few parts do a little harm. And we only need to trust him a tiny bit about the interventions he recommends, because he advises us to check carefully whether those interventions improve the biomarkers. How plausible is it that a complex set of interventions work where single interventions have consistently failed? My understanding of Bredesen's model implies that careful tests of individual interventions should show small benefits. Wait a minute! Bredesen didn't actually say that single interventions have failed! He said that single drugs have failed. So I did a little research. Wikipedia pointed me to evidence about exercise , including a small RCT which shows important benefits but needs many caveats. A bit more searching, and I find an RCT of B-vitamins showed some benefit, and this paper says that benefit happened mainly in people with adequate Omega-3s. I've already blogged about zinc and copper , where a small RCT showed weak evidence of benefits. Overall, single interventions seem to have better evidence than Bredesen led me to believe. Where are the large-scale trials that would be prompted by this evidence if we had a medical community that cared about preventing Alzheimer's? My initial impression of the book was that it's too good to be true. So, how could its most important claims could be wrong? There's no foolproof way to discredit this hypothesis, but also little reason to think it's more likely than with typical research. He's virtually guaranteed to attract more scrutiny than most - that would be a strange strategy to pursue if he had something to hide. If true, this would imply that he has some pretty unusual skills, and that there are serious problems with how some other doctors diagnose dementia. I can't rule out this hypothesis. I can see how he might be overstating the benefits this way, but I don't see how it could explain his results if there were no benefits. There's a weak sense in which most of the measurements are subjective. Maybe a professional poker player with a diagnosis of mild cognitive impairment could be mistaken about whether his poker improved. But his case studies include some pretty strong claims, including one report of a big increase in hippocampal volume measured by MRI, and one patient whose neuropsychologist advised him to "wind down his business and plan for the full-time care he would soon need". Two years later that neuropsychologist measured the patient's memory as having improved from the 3rd, 13th, and 24th percentile on three tests to the 84th, 79th, and 74th percentile, and the patient expanded his business. Those seem to be stretching the limits of what I can believe for measurement error. Many people have strong priors about Alzheimer's which lead them to find Bredesen's claims less plausible than these hypotheses, based on past experiences with Alzheimer's "cures", plus stereotypes about what approaches to disease work. Those priors might make some sense if researchers had tried many independent approaches. But it looks to me like the failure of most Alzheimer's research can be explained by a small set of problems: The inadequate exploration of different paradigms can be explained by an ordinary amount of groupthink plus bias toward approaches that support continued funding of areas that existing experts know best. So it's not wildly implausible that someone could find the equivalent of a trillion dollar bill or maybe a ten billion dollar bill if he has overstated the benefits a lot. It's not as if the bill was in plain sight - it's more like it was torn into dozens of pieces, and hidden in leaves. What causes the widespread reluctance to adopt the kind of functional medicine that Bredesen advocates? I don't expect doctors to like detecting suboptimal health and then watching helplessly as patients continue the lifestyle that caused the problem. Why would patients fail to follow the protocol? Partly because things like pizza and cookies are somewhat addictive. Partly because there are important social costs to admitting that we're not healthy enough to eat at a typical restaurant or party. Mainstream doctors are sometimes reckless - not washing their hands, or saying that patients can't do anything about Alzheimer's, when they could say something like "regular exercise may improve your odds". Somehow those mistakes stay less conspicuous than functional medicine's recklessness. I'm unclear what the current reaction is from mainstream Alzheimer's researchers. Bredesen seems to have gotten a mix of help and hostility in the past from mainstream institutions. The Buck Institute of which Bredesen is the founding president gets a good deal of NIH grant money, and he doesn't appear to have trouble publishing peer-reviewed papers related to his Alzheimer's ideas. But IRBs denied him permission to conduct a trial that involved an early version of his protocol because it would have tested too many things at once. That mainly seems like additional evidence that IRBs are unethical. It's quite possible that his protocol hasn't been stated clearly enough to qualify as a set of scientific hypotheses, and that it might end up testing some mix of articulated hypotheses and also the skills of the people involved [2]. If that was the IRB reasoning, it seems like a really awful reason for rejecting a trial. Even if it mostly ended up testing doctor's skill at giving advice, a positive result would falsify the claim that Alzheimer's cannot be prevented, cured or even slowed. Bredesen presents a nonstandard biochemical model of Alzheimer's. I'm not sure what to make of it. It doesn't seem particularly helpful for understanding why the protocol works. It does explain why the simple amyloid-beta hypothesis is wrong, but it's hardly the only hypothesis to explain that. He classifies Alzheimer's into three semi-distinct subtypes. I'm fairly convinced that Alzheimer's refers to more than one disease, but I don't get the impression that anyone knows how many subtypes can be usefully identified. Bredesen seems confused about the diet that humans evolved to eat. We don't have good evidence about human diet over that period, but it looks pretty likely that humans relied mainly on fruit during the early part of that period, and relied on high-carb roots during some parts of that period. Some modern hunter-gatherers Hadza eat way more honey than that 15 gram limit would allow. Maybe American lifestyles create a need for that strict limit, but that need isn't inherent in our biology. While evidence from hunter-gatherers weakens some of Bredesen's specific advice, it strengthens his claim that Alzheimer's depends on lifestyle choices: The book has somewhat inadequate warnings for people who want to wait until they get more severe symptoms: The protocol is already pushing the limits of what we have the mental capacity to implement in some people; the difficulty will vary unpredictably from person to person. Delaying until the symptoms become noticeable makes it harder to learn new habits, harder to track whether you've taken the right pills, harder to prepare new recipes, etc. What do I expect if he's right? I expect an expanded number of doctors using his protocol over the next few years to reach something like 10, people who are at risk of Alzheimer's. I expect a similar number of patients to see doctors who doctors who try to follow the protocol without being trained by a Bredesen-approved teacher. I expect these doctors to report widespread improvement in these patients, and I expect those reports to be controversial due to risks such as selective reporting. I recommend that the trial be evaluated in two separate steps: My hope is that will distinguish problems with patient compliance from issues of how improved biomarkers affect dementia. I'm unclear how the average doctor will react after those trial results are released. But among doctors that are relatively open to new ideas, I expect a profusion of competing protocols, with poorly documented claims about how well patients comply with the protocol. I expect that by around to , at least half a million patients will use one of these protocols, and that will be sufficient to a decline in the overall number of people developing Alzheimer's. Conclusion The book seems slightly careless about details such as citing good references, as if it were rushed to print rushing does seem appropriate. I suspect he exaggerates the benefits. He errs slightly in the direction of allying too much with alternative medicine. Mainstream medicine has some major flaws, but it's still important to persuade mainstream institutions to listen to the book's ideas. But it's good enough to persuade me to experiment with significant changes to my diet and supplements, and maybe enough to convince me to donate to the Buck Institute. Footnotes [1] - the book won't tell you directly whether it's safe for you to eat at restaurants and parties. It will tell you how to get evidence about whether those are safe for you. But the book did get me to look at apoe4. That page has an automated? These two showed up on the same alz. Healthier living could reduce worldwide dementia by a third, report says — The Washington Post One in three dementia cases 'could be prevented by lifestyle changes' — London Evening Standard I hope this is a sign that cognitive dissonance on the subject has reached a maximum. There are important limits to how reliable this evidence is, but the researchers were able to get decent evidence that some hunter-gatherers lived into their 80s, that hunter-gatherers did have people whose cognitive ability was impaired from childhood, and consistently did not know of late-onset cognitive decline. Beware that "it's due to modern lifestyles" doesn't guarantee there's a reasonable strategy to avoid Alzheimer's. Modern population densities support infectious diseases that hunter-gatherers don't get. Jun 29, Ron Frampton rated it it was amazing. These findings point to novel therapeutic strategies for AD and aging, resulting in an extension of human healthspan, the disease-free and functional period of life. We would love to hear from you. Contact us with any questions or call us at 1. Terms of Service Privacy Statement. The ideal of using triple therapy for HIV, of course, is the first approach that actually showed a real benefit and has been the standard of care since that time. I think that it is, perhaps, not surprising that we are seeing the same sort of thing with cognitive decline. I think that some of the drugs that have failed in clinical trials could actually succeed on the right foundation of additional therapeutics. How did you get interested in pursuing a different therapeutic approach toward cognitive decline? Our laboratory has been interested for many years in investigating the molecular underpinnings of neurodegeneration. Why is it so common? What are the drivers of this process? The idea is that if you could get at those specific molecular details, you could potentially work out therapeutics that would be effective. The first drug that we identified is currently in a clinical trial in Australia for early-stage mild, cognitive impairment. However, when we then looked at what all of the inputs to that specific critical balance were—a plasticity balance if you want to think about it that way—we found that the drug alone addressed only some of these but did not address all of them. Therefore, it actually made much more sense to try to address additional input to that same balance. The first was placebo and the second was the drug. A third arm, then, included an entire system of therapeutics. This is the same one that we ultimately published last year as MEND, or metabolic enhancement for neurodegeneration. The fourth arm was the system with the drug. The hope was that the drug would actually work much better on the backbone of the entire system. This was turned down by both the public and the private institutional review board, or IRB, as being too complicated. The IRB argued that we must not know how to do clinical trials because we were proposing something that had more than 1 variable. Our argument, of course, was that this is not a 1-variable disease. I think that has been borne out. That perspective will be helpful going forward in terms of using different approaches, both polypharmacy and monotherapeutic. Would you please describe your ideas and how they are different from the mainstream view? Two of these are actually not illnesses. Think about it a little bit like a company. Imagine that you have a bunch of accountants; each one specializes in a different area and they all report to a CFO. APP is the molecule that is integrating many different inputs to determine whether a strategic downsizing must occur. If it is required, then you are going to have to activate the compliance officer and you have to send out the appropriate memos. What you end up with is a very programmatic and well-orchestrated downsizing of the synaptic density..

So, on the one hand, it's a mediator of the pathophysiology. On the other hand, it's also a protectant, it's a response to things like pathogens. And so there's a double-edged sword there. It's fine, Dale bredesen book think, in the long run, it'll be fine to remove the amyloid, but you've got to remove the cause of it first. Now, of course, people have just tried to go earlier, earlier, article source and can we actually see some improvement?

So I think it won't be surprising if you can get a little improvement early on, but again, it's a little bit like saying if we fire the CFO we can all spend a little more for a while. Well, if we're Dale bredesen book going to go into the red, we want to make sure that we're spending for the right things. We want to know why your amyloid is there to begin with, we want to remove all those things, then remove the amyloid as opposed to just blindly removing this mediator and leaving the various inducers.

Right, and with Alzheimer's disease it's so And things are always much more complex. Like it seems like, well, amyloid plaques in your brain, of Dale bredesen book you want to get rid of those. They're destroying synapses, and well, as you mentioned, it has a function, it has a really important function. And for the longest time, I remember I was trying to Why is it in there? Obviously, we have this whole elaborate system, we have these enzymes that cleave it in this right position, and it forms this 42 amino acid Dale bredesen book, I mean, that's all happening for a reason.

It doesn't seem like it Dale bredesen book be programmed into our biology to cause dementia. And so I think it really is Dale bredesen book to understand what the normal function is of the amyloid beta. And also with the tau, phosphorylated tau, and tau protein as well, is that something that you find quite often in the people that have the amyloid burden and are affected, they often also have tau tangles in? Dale bredesen book yeah. Check this out, tau imaging is still kind of in its infancy, so most people, we don't know.

So, they may have an amyloid-positive scan but they haven't have a tau scan. However, they are clearly in Alzheimer's, and as I say, we do know that many of them do from cerebral spinal fluid. So these people Dale bredesen book we've reported, I mean, these people have the low ATI that is associated, you know, amyloid tau index, so they have a low a-beta 42s in the Https://airplane.comando.pro/num5599-hufomuvaz.php and they have the high phospho-tau and total tau in the CSF, the ones that have been evaluated.

So, indirectly from that, we can say they definitely had tau, they're likely Dale bredesen book have phospho-tau tangles. And again, if you look at what this is doing, it makes a lot of sense. When you are trying to pull back on a connection then you need to collapse the superstructure.

And what is the phosphorylation of tau do? It allows it to Dale bredesen book off the microtubules so you have a rapid collapse of the structure.

The End of Alzheimer's: The First Program to Prevent and Reverse Cognitive Decline

So no surprise when you're Dale bredesen book this mode of you're trying to fight this off, you're trying to change, you're trying to pull back on your structure, you're going to phosphorylate your tau, pop it off, the microtubules, and you're going to die back, and that's exactly what you see.

So again, it's not, you know, that the tau is not the cause of the problem, it is a mediator based on what's going on genetically with pathogens, with toxins, with metabolic changes, with innate immune system, and you know, with trauma. So the things that are driving this are the here that we want to target.

What percentage of people would you say is more common Dale bredesen book have your sub-type 1, 1. Are those the most common would you say types of Alzheimer's disease?

And so this is a really good point. So, initially, what we saw was Dale bredesen book many people had this type 1. In fact, again, Professor Getzel from Https://pussypump.comando.pro/pub5852-rokam.php had a nice paper a few years ago showing that everyone he evaluated using exosomal analysis had the signature of insulin resistance in the nervous system, whether they had it peripherally or not.

It Dale bredesen book really striking. This was this change in phosphorylation of IRS So clearly that's a very common thing. But what we're finding is rarely do people have purely type 1. So please click for source fact, most people have some sort of Dale bredesen book exposure, pathogen exposure, that sort of thing.

So what it's turning out is that it's more about what's your mixture. Are you predominantly the type 3 with a little mixture of 1. And by the way, the easiest to deal with, type 1 and 1. You can improve with diet, exercise, sleep, stress, stuff like that. Improving the atrophic is a little harder. You've got to get all the right things, you've gotta And then the hardest Dale bredesen book all is the type 3 because you're having to find out If you've got mycootoxins being produced and you're living in them, you need to get out of there.

Or if you're working in them, you Dale bredesen book to get out of there. And until you do that you've Dale bredesen book this chronic exposure. Is there a test people can do to see if they've got this type of mold in their house? There's an easy test. In fact, you can go on I think the government has set up this so-called EPA Relative Mold Index, and you want to get a score that's less than two, again, as Dr.

Shoemaker recommended years ago. And you can easily get it, go on mycometrics.

Dale bredesen book

They literally Dale bredesen book you some little cloths and you can go around and take x. And if you've Dale bredesen book species that happen to produce a lot of toxins, it's a concern. Then you can actually measure the toxins in urine tests. So you can get an Dale bredesen book, and then again, you Dale bredesen book actually see with your detox Yeah, so you can get.

There are a couple of companies now that do make urinary mycotoxins tests. Okay, and Dale bredesen book for people that don't, let's say, you know, they don't have Dale bredesen book toxin exposure, or they don't think they do, but they don't if they've done this test, Dale bredesen book things that they can do in their diet and lifestyle to prevent the Alzheimer's disease would be the major things to reduce inflammation, which are a lot of things, diet, lifestyle, exercise, sleep, and then again, a lot of overlap there with improving insulin sensitivity and fasting glucose levels and all that.

Getting your hemoglobin A1C down, all those things, getting on a plant-based Terry Wahls has published a lot, and actually has done a lot of studies now on https://shorts.comando.pro/page11870-jepegote.php a similar sort of approach for multiple sclerosis, and has seen excellent results including in herself with taking this sort of an Dale bredesen book. So, again, looking at the drivers, and looking at what are we actually responding to, and are we having more of an auto-immune response, like with MS,or are we having more of an innate immune system response with Alzheimer's, these are critical for dealing with these complex chronic diseases.

Do you look at markers for gut health, because you were talking about What How to know if someone read your email the major Oh absolutely, oh yeah.

So, there Dale bredesen book a couple of ways to go. There is Genova test, a doctor's data test, there are different tests, there's like stool analysis sort of thing, but you can also do Cyrex, for example.

So Cyrex array 2, Cyrex has a whole set of different markers for different antibodies. So, if you have a leaky gut you're often going to respond to things like LPS coming from Dale bredesen book gut.

Then there's a Cyrex array 3 that looks at various of the domains of gluten and gliadin and so who Dale bredesen book can look at that. And then there are various auto-antibodies, etc. So yeah, these are very helpful to know. I haven't have heard of that one. In other words, when you start going down one side or the other, it is like a snowball rolling downhill.

You gather momentum on one side or the other. You have to get to the point of changing that. You have to get to a certain threshold, but once you do that, it will begin to gather momentum going down the good side instead of the bad side.

At the beginning, we do not know how many, but when you start to get results, you can limit the program to those things that Dale bredesen book you on the other side of the plasticity network, of the balance. For example, the first woman we reported on did 12 of the Nobody has managed to do every single one so far, but when you get to enough, then you get over the threshold. By the pics Shaved mature, this Dale bredesen book no different than what Dean Ornish, mdhas Dale bredesen book for years in atherosclerosis.

Dale bredesen book do enough of the right things, enough of his program, and he has documented the reversal Dale bredesen book atherosclerosis. What we are doing here is a little bit like synaptoporosis.

You get to the point where you are now able to support the production of new synapses and you start seeing improvement. Would you describe some of the results you have observed from use of the protocol? There have been about 70 people who have come through now. For Dale bredesen book, I just got a call this morning from a man who started a year ago and had a hippocampal volume, before he started the program, quantified at less Dale bredesen book the 20th percentile. It is now greater than the 75th percentile.

He actually could not believe that his own hippocampus had gotten larger. This patient, by the way, was at a point where he was going to have to quit his job. He is doing very well at his job now, continuing to do his job very effectively. We have another person who is over 3 years out now, still back to work full-time and doing very, very well. We have had a couple of people now who have gone on and off the program a couple of times, either because of traveling, stressful things in their lives, running out of some of the components, or getting ill and not being able to take some of the components.

They have shown very clearly that when they get Dale bredesen book the program, they get worse; then when they go back on the program, they get better again. That supports the idea that the program is actually helping them. Do you know how long it takes to observe the symptoms to start to resume going in the wrong direction when people go off the protocol?

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The return of symptoms Dale bredesen book the program is discontinued has varied somewhat, but typically people have reported noticing some decline within 2 Dale bredesen book. On the other side of the coin, symptom resolution on the program begins to be noticable in 3 to 6 months, but there are a couple of important modifiers there: Number 1, it depends on which subtype you have. Certain subtypes respond sooner and certain subtypes take longer. The second thing is that this is not something you start and then you do not change it.

Relevance to Alzheimer's Disease. These findings point to novel therapeutic strategies for AD and aging, resulting in an extension of human healthspan, the disease-free and functional period of life. We would love to hear Dale bredesen book you.

Contact us with any questions or call us at 1. Eat, Live, Thrive Diet. Robyn Thomson and Danna Demetre. Lisa Butterworth. Outsmarting Autism, Dale bredesen book and Expanded.

Patricia S. The Expert Guide to Sleeping Dale bredesen book. Chris Idzikowski. The Natural Apothecary: Penny Stanway. Apple Cider Vinegar. Baking Soda. Salt in My Soul. Mallory Smith. Feeding My Mother. The Healing Magic of Forest Bathing. Julia Plevin. Rachna Patel. Cook to Thrive. Natalie Coughlin. Michele Lent Hirsch. The rea Have utmost respect for Dr. The reader has to discern the actual test name from with in the text. I believe that in order to follow the ReCode protocol I would need the help of my doctor to order the tests and understand the results.

I certainly hope that more doctors and practioners read this book and make the approach more mainstream. That is what is needed for this to take hold and help so many people in need. View 1 comment. I listened to the audio book and this is one case where I definitely recommend getting the actual paper version and read it since it would be a reference volume. This is far too technical for listening as there are long lists of supplements and their recommended doses Dale bredesen book read out.

So, my 3 stars is referring only to the audio version. Will change it when I get the hard copy. Jul 19, Designlover rated it it was amazing. Actually I had received the uncorrected proofs from the publisher, but that Dale bredesen book did not have an all important index or some of click at this page graphics.

I ordered and received 5 copies of the hardback version of Dale bredesen book book, which I have distributed to friends. Bredesen has written the first comprehensive guide to preventing, halting, and reversing Alzheimer's Disease. It is a must read as it provides you with the tools necessary to understand what Alzheimer's disease is, how to prevent it, and how to treat it.

I am a clinician who has been using these Dale bredesen book for more than 2 decades and I know the methods work. This book gives you the blue print you need. Since nearly all of us will be affected directly or indirectly by dementia, this book is required reading if you care about your health, or the health of your loved ones. April Dale bredesen book, Bredesen's outstanding resume: Bredesen is the real deal, an unparalleled example of steadfast research and dedicated determination to find the contributing causes of this insidious disease.

I am happy to report L. County already has 30 copies on it's shelves. LAPL is currently processing it into their system. You can put a hold on it now. Please ask you local library to purchase it. It is available in different formats: Dale bredesen book your review after your read it. Pass it on to a friend. Dale E. Bredesen CV http: Hughes Associate, Laboratory of Dr.

Elizabeth R. Director, Mary S. Gray, Inorg. Wrighton, Inorg. In vivo oxidative stress in brain of Alzheimer Dale bredesen book transgenic mice: Requirement Dale bredesen book methionine 35 in amyloid beta- peptide of APP. Free Radic Biol Med ; Many neuronal and behavioral impairments in transgenic mouse models of Alzheimer's disease are independent of caspase cleavage of Dale bredesen book amyloid precursor protein.

J Neurosci ; Inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's disease. PLoS One ;5: Reversal of learning deficits in hAPP transgenic mice carrying a mutation at Asp Behav Brain Res ; Identification of new modulators and protein alterations in non-apoptotic programmed cell death. Sexy movie full Free Dale bredesen book Biochem Dec 15; 6: Dale bredesen book Alzheimers Disease ;22 1: J Alzheimers Dis ;25 1: Dependence receptors: Sci Sign Jan 25;4 Valosin-containing protein gene mutations: J Alzheimers Dis Differential expression and redox proteomics analyses of an Alzheimer disease transgenic mouse model: Neuroscience ; J Mol Neurosci ; Aging Dis ;2: PLoS One ;6, e, Cellular effects of APOE4: Implications for Alzheimer's disease.

The Journal of the Alzheimer's Association ;7: Altering APP proteolysis: PLoS One. No consistent bioenergetic defects in presynaptic nerve terminals isolated from mouse models of Alzheimer's disease. Journal of Neuroscience ;32 Dale bredesen book Ayurvedic medicinal plants for Alzheimer's disease: Alzheimers Res Ther Jun 29;4 3: Moonlighting peptides with emerging function.

PLoS One ;8 Do proteomics analyses provide insights into reduced oxidative stress in the brain of an Alzheimer disease transgenic mouse model with an ML amyloid precursor protein substitution and thereby the importance of amyloid-beta-resident methionine 35 in Alzheimer disease pathogenesis?

Antioxid Dale bredesen book Signal ;17 The small chaperone protein p23 and its cleaved product p19 in cellular stress.

Wexxx Videocom Watch Video Jesus porn. I expect an expanded number of doctors using his protocol over the next few years to reach something like 10, people who are at risk of Alzheimer's. I expect a similar number of patients to see doctors who doctors who try to follow the protocol without being trained by a Bredesen-approved teacher. I expect these doctors to report widespread improvement in these patients, and I expect those reports to be controversial due to risks such as selective reporting. I recommend that the trial be evaluated in two separate steps: My hope is that will distinguish problems with patient compliance from issues of how improved biomarkers affect dementia. I'm unclear how the average doctor will react after those trial results are released. But among doctors that are relatively open to new ideas, I expect a profusion of competing protocols, with poorly documented claims about how well patients comply with the protocol. I expect that by around to , at least half a million patients will use one of these protocols, and that will be sufficient to a decline in the overall number of people developing Alzheimer's. Conclusion The book seems slightly careless about details such as citing good references, as if it were rushed to print rushing does seem appropriate. I suspect he exaggerates the benefits. He errs slightly in the direction of allying too much with alternative medicine. Mainstream medicine has some major flaws, but it's still important to persuade mainstream institutions to listen to the book's ideas. But it's good enough to persuade me to experiment with significant changes to my diet and supplements, and maybe enough to convince me to donate to the Buck Institute. Footnotes [1] - the book won't tell you directly whether it's safe for you to eat at restaurants and parties. It will tell you how to get evidence about whether those are safe for you. But the book did get me to look at apoe4. That page has an automated? These two showed up on the same alz. Healthier living could reduce worldwide dementia by a third, report says — The Washington Post One in three dementia cases 'could be prevented by lifestyle changes' — London Evening Standard I hope this is a sign that cognitive dissonance on the subject has reached a maximum. There are important limits to how reliable this evidence is, but the researchers were able to get decent evidence that some hunter-gatherers lived into their 80s, that hunter-gatherers did have people whose cognitive ability was impaired from childhood, and consistently did not know of late-onset cognitive decline. Beware that "it's due to modern lifestyles" doesn't guarantee there's a reasonable strategy to avoid Alzheimer's. Modern population densities support infectious diseases that hunter-gatherers don't get. Jun 29, Ron Frampton rated it it was amazing. Mar 24, Tatiana Shorokhova rated it it was amazing. Nov 28, Ro Laberee rated it it was amazing Recommended to Ro by: Before summarizing Dr. There is no treatment for it. After a diagnosis, there is a clear message conveyed — You are not going to get better Before summarizing Dr. After a diagnosis, there is a clear message conveyed — You are not going to get better. This is the beginning of the end. It will probably be awful. Everything else offered is a knock-out pill of one kind or another. We are making great strides in cancer and in molecular biology, generally. Meanwhile, death by dementia is rapidly increasing. It robs victims of their humanity — sometimes over decades — it terrorizes and bankrupts their families, and we have no effective treatment. While the technology industry makes startling advances in Artificial Intelligence almost weekly, we have stood by and watched the human intelligence of our seniors wither away appallingly. This situation seems ghoulish to me. You have likely heard neuro-specialists parroting the amyloid plaque hypothesis. In fact, only those toeing the amyloid line can get funding for their research. Meanwhile, amyloid plaque is also found in the brains of perfectly healthy individuals. Amyloid is only one piece of a very complicated puzzle. Scientists and doctors investigating the root causes of cognitive decline and braving the icy waters of non-amyloid based research are mostly ignored. In this book, Dr. Bredesen addresses the other pieces of the dementia puzzle and lays out his protocol, which has helped many hundreds of people reverse their cognitive decline. There were two chapters I had to read twice and, yes, I took notes. My best take-aways: Exercise almost every day. Make it count. This stimulates BDNF brain-derived neurotrophic factor which supports new neuron growth. Stop eating sugar. It is poison for neurons. Protect your sleep. Vitamin D3!!! Take it. Or, be outside in the sun without sunblock every day, if possible. No, not for hours. Fresh, organic vegetables with every single meal, and lots of them. Lots of good fat — coconut oil, avocados, fatty fish like salmon , nuts, and grass fed beef or chicken, but in small servings 7. Eliminate gluten. Get your BMI in a good range. Exercise your brain by challenging yourself, move around throughout the day, and get out and socialize. The supplementation he recommends is rather extensive and it is keyed to your health blueprint. You need to follow through on extensive bloodwork in order to know exactly how much inflammation your body hence your brain is dealing with and where you stand with insulin sensitivity. These two things — inflammation and insulin senstitivity — are dire enemies of cognitive health. And environmental toxins…. He urges those with cognitive decline to try to maintain a mild state of ketosis by eating lots of fat, some protein, but very little carbs. This makes the brain use fat as its main source of energy, which optimizes cognitive health. This is a widely-accepted practice and many people without any cognitive decline at all eat a ketogenic diet for better performance in life. His results, which he details in the book, have been astounding. I have personally joined some of the online groups using his protocol — it is the real deal. It does not look easy. It looks like a big commitment. It looks like work. In chatting with one of my kids about this, he said: Hard choices — easy life. If someone you love is battling cognitive decline, read this book. Take action. Take control of the situation for him or her. Do all that you can. Do not wait for a new drug because anything new is going to be targeting only ONE of the many things which cause cognitive decline. You want a solution with addresses the whole mess. Sep 07, Beth Haynes rated it it was amazing Shelves: Just finished the first read through. Planning to read a second time to look more carefully at his references. Bredesen proposes a new take on the causes of Alzheimer's arguing that beta amyloid is not the primary problem but is instead the protective response of the brain to a variety of insults. He has found there are a least 36 potential contributing factors which he lumps into three basic cause-related subtypes - inflammatory, lack of sufficient supportive nutrients, and toxic. His report of r Just finished the first read through. His report of reversing the dementia of Alzheimer's through diet and lifestyle modifications is very intriguing, and the success he has had with over patients makes it worth careful consideration. Feb 16, Heather rated it really liked it. I have to be honest, I skimmed a lot of the science part of this because I knew it would go over my head, but I wanted to read about the tests and results for patients who have actually tried Dr. Bredesen argues that hundreds of years ago, people died of a single disease that had a single cure. Nowadays, people are living longer lives and most of the time are dying from complications or several things. Alzheimer's isn't a single disease with a single cure, but is like I have to be honest, I skimmed a lot of the science part of this because I knew it would go over my head, but I wanted to read about the tests and results for patients who have actually tried Dr. Alzheimer's isn't a single disease with a single cure, but is like a roof with 36 holes on it where you have to patch as many holes as possible to restore a balance in the brain to stay or become healthy. I was really impressed with the book when I first read it, although after reading "Do You Believe in Magic? If this is really working, why isn't it being used for everyone? I picked this up for extra research for a project I was working on and I am so glad that I did! If this doesn't inspire you to a healthier lifestyle, I just don't know what will! This doctor's research is fascinating and refreshingly holistic. It is very east-meets-west - western medicine meets eastern healing. I hope that this catches on so that we can arm people with the tools to avoid this painful disease, which has claimed two of grandparents' lives. The doctor introduces the word "dementoge I picked this up for extra research for a project I was working on and I am so glad that I did! The doctor introduces the word "dementogens," which is like a "carcinogen" for brain health. It refers to things that lead to cognitive decline such as a diet full of gluten and sugar, high exposure to toxins, chronic inflammation, and head trauma. These are things we have a measure of control over. I do encourage reading this book so that you can commit to the best health that you possibly can and help reverse any cognitive decline you may be suffering in your own family. The first time I was exposed to AD was in a biotechnology course in university, where the professor briefly touched on the current biomedicine approach. In this strategy, some researchers used antibodies specific to the amyloid-beta protein to destroy the plaques that kill off synapses in the brain this is the hallmark pathology of AD. Back then, I just filed it along with the rest of my notes as a potential exam question. Six months later, I stumble upon Dr. Dale Bredesen on AD. I was instantly hooked by his research and his protocol that not only aims to prevent AD but also to reverse it. Bredesen goes into extensive details on defining the disease, the science behind his approach, and a step-by-step guide for those struggling with cognition issues. Inflammatory hot: Reversal of cognitive decline in Alzheimer's disease. Transcriptional Effects of ApoE4: Relevance to Alzheimer's Disease. These findings point to novel therapeutic strategies for AD and aging, resulting in an extension of human healthspan, the disease-free and functional period of life. But now, this comprehensive approach offers solid results, bringing hope to so many. If you have a brain, read this book. This is the book to transmute fear into action. Bredesen translates the knowledge of science to the wisdom that helps to heal our people. A must read for anyone wondering what can be done for this dread disease, whether for themselves, a loved one, or a patient. Join Reader Rewards and earn your way to a free book! Join Reader Rewards and earn points when you purchase this book from your favorite retailer. Read An Excerpt. Hardcover —. Add to Cart Add to Cart. Product Details. Inspired by Your Browsing History. How to Shine a Shoe. Potter Gift. Complete Physique. Hollis Lance Liebman. Plant Power Bowls. Sapana Chandra. The Kripalu Kitchen. Jeremy Rock Smith and David Joachim. Click here to read Dr. It is a known neurotoxin that destroys nerve synapses and then clumps into plaques that lead to nerve cell death. But in recent decades research has revealed interesting characteristics that suggest amyloid-beta can play a protective role against fungal, bacterial, and viral infections. One example is seen in the herpes virus, which upregulates the production of amyloid-beta protein in vitro. In turn, the protein binds to and agglutinates the viral particles. There may be good reason for this antimicrobial property too: Animal experiments demonstrate that chelating agents can even reduce deposition of amyloid-beta. These interactions with metals become important in the discussion of Dr. Click here for a FoundMyFitness episode featuring guest Dr. Gordon Lithgow discussing metals in the context of aging, protein aggregation, and neurodegenerative disease. A key element in the acquisition of knowledge about our risks factors and what can be done to manage our risks is what Dr. Bredesen proposes a pretty radical idea: The key to doing this? However, a recurring theme a recurring theme throughout our discussion with Dr. Bredesen is that what most labs and clinicians call normal may actually be different than what is optimal. Whether a person is at risk of developing the disease versus actively manifesting symptoms is often reflective of the number of their suboptimal biomarkers: View a more comprehensive list at popular APOE4 community site apoe4. Hello everyone. I'm really excited to be sitting here with Dr. Dale Bredesen, who is internationally recognized for his understanding of the mechanisms of neurodegenerative disease, particularly Alzheimer's disease. In fact, he was the founding president and CEO of the Buck Institute back in , so that's really kind of cool. And he also is an author of a "New York Times" best-selling book called "The End of Alzheimer's Disease," which I'm sure we're going to talk quite a bit about today. It's got a really interesting multi-pronged protocol for preventing and also helping treat mild cognitive dementia and Alzheimer's disease. So thank you so much, Dale, for having me here at your place. So maybe we can start a little bit by just talking about some of the characteristics and pathological distinguishing features of Alzheimer's disease and maybe what your thoughts are on what can cause Alzheimer's disease or leads to it. Right, so it's a good point because cognitive decline, very common, and Alzheimer's is the most common cause of cognitive decline, ultimately dementia. And by definition, this means that you have amyloid plaques in the brain and phosphorylated tau tangles. So those are the two main pathological hallmarks of Alzheimer's. But as you can see, that doesn't tell you why you got it, it just is something you look at the brain, and of course, you can get something that looks virtually identical without the amyloid and you can get amyloid without the cognitive decline. So, it's a marker but it's an imperfect one. Yeah, that's a really good point you brought up. And do you have any thoughts on why there are some people that do have amyloid plaques in their brain that aren't demented and then some others that just don't seem to handle it? Yeah, it's a great point. So, here's the thing, the whole world is turning upside down now when it comes to our understanding of Alzheimer's. It's been over years, of course, going back to Alois Alzheimer's publications back in and , and there hasn't been a good understanding of this disease. And of course, amyloid has been for years vilified and there's no question, it is a neurotoxin. It does have toxic effects. The surprise has been that this is also a protectant. It's actually something that is made by your brain when you have specific insults. It also, as Professor Ashley Bush showed a number of years ago, it's actually quite a good binder of divalent metals like copper and zinc, and things like that, iron. And we showed a number of years ago, it is also a response to a reduction in trophic support, so you actually get a change in signaling. So, there are multiple different insults and metabolic changes that lead the brain to produce this stuff. And so I think there's been confusion because it's clear that when you produce it you're at this increased risk for having a degenerative process, but as you indicated, there are many people that produce it and they successfully are protecting themselves, they don't actually have the downsizing. What's often been stated is those who then have inflammation on top of that seem to be the ones that do worse, and that's a very general idea, but really it is a set of things. And we identified and published, a number of years ago, 36 different factors that all contribute to this, but they actually break down into just a couple of categories. So, any sort of pathogens, anything that's giving you inflammation, whether you have it because you have a leaky gut or because you have P. And in fact, we think more and more of amyloid as being like napalm. You got the bad guys coming across the border, so you're now going to put down stuff that kills the bad guys, the napalm but in so doing you're now going to reduce your arable soil. You're now living in a smaller country, and that's exactly what's going on in the brain, you are downsizing the overall network. So, that's what we call type 1 or inflammatory or hot Alzheimer's. And I should mention, it turns out ayurvedic physicians from thousands of years ago who recognized dementia that was related to something that was hot, that was abnormal and ultimately inflammatory, as well as that was related to dryness, which is what we call type 2, where you have decreased trophic support. It can be nerve growth factor, brain-derived neurotrophic factor, estradiol, testosterone, pregnenolone, progesterone, thyroid, vitamin D, all of these things are critical to support of synaptogenesis. So we think of the signaling as being a ratio of synaptoblastic activity where you're actually sending signals to make and store synapses just like you think of osteoblastic activity versus synaptoclastic activity where you're actively pulling back and you're reorganizing. And of course, this is going on all the time. You're actively forgetting the seventh song that played on the radio on the way to work yesterday and you're actively forgetting a lot but you're remembering the key things, like where your keys are and where your son is and all that sort of stuff. And so, there is a change in that ratio in Alzheimer's disease because of type 1 with inflammation or type 2, which we call atrophic or cold, because you don't have the support for those synapses, so you're literally I can either watch all five starve slowly or I can put one in a foster home and feed four," and that's basically the downsizing that's happening when you cannot support the neural network that you have. And then we have a type that's actually type 1. And we named it that because it has features of both type 1, inflammatory, and type 2, atrophic. So what happens is you develop insulin resistance, so you now have a change in signaling that actually occurs because of this chronic high insulin. But of course, you're also glycating proteins with But you're glycating many proteins, so you get now a response to that as well. So you have an inflammation in an atrophic and so that's why it's 1. And then type 3 turns out to be completely different, and that is a response to toxins. So there is a toxic form, which we call toxic or vile Alzheimer's disease. In addition, there are people we called type 4 who have more of a vascular component and then type 5, which is more of a traumatic component, but they're really both related to these other ones. It's really about, do you have inflammation? Are you fighting something off? Do you have trophic support, and are you exposed to specific toxins? Wow, and so in all of these different subtypes of Alzheimer's disease they all sort of have some of the same distinguishing pathological features like amyloid beta plaques, tau tangles between all of them. So they all have amyloid plaques, they all have, by definition, tau tangles, but the presentation can be different. Now there are some overlaps, the type 1s and the type 2s are typically amnestic presentations more common with ApoE4, and that's true for the type 1. The type 3s, the toxic ones are quite different. They often present with a non-amnestic presentation. It's executive dysfunction, problems with calculation, problems with visual perception, problems with word finding, so-called primary progressive aphasia, all of these things, they are really bi-parietal presentations as opposed to bi-temporal presentations, essentially. So these have often been called cortical presentations, which have been noted for years by people like Professor Mario Mendez, to be typical in younger presentations of Alzheimer's and often in ApoE4 negative individuals. I think I also read one in your papers where you did this metabolic profiling there was a very prominent zinc deficiency in that. Yes, so for reasons that we don't entirely understand yet, many of the people with the type 3, the toxic sub-type have low serum zinc, high copper-zinc ratios, and low triglycerides. The low triglycerides may turn out to be related to malabsorption, we don't know for sure yet, but we don't really understand why the people often have these low copper-zinc ratios. Yeah, so as, you know, copper and zinc actually are competitive, for example, in their absorption. And so, too much of one actually is often associated with too little of another. And then typically in our society, as you know, most of us are deficient in zinc. There are actually about a billion people on Earth is the estimate for zinc deficiency. It's a very common problem because if you have poor gastric acidity, which is common as we age, if you're taking PPIs for GERD, if you're taking something for reflux, you won't absorb the zinc very well, if you have copper piping which most of us do, the copper will often compete with the zinc. And so many people have a little too much copper and a little bit too little zinc. And in fact, it was noted over 30 years ago that people with high copper-zinc ratios tended to have dementia more than those with normal copper-zinc ratios. So does this have something to do with it? I know there's like over to different enzymes in the body that require zinc. So does copper then bind to those enzymes and then sort of mess up the function or is that like the theory? So, no. The theory is that, as you know, copper is a generator of free radicals. You know, copper can act like iron in that sense. It has a free electron in the D orbital which does not occur with zinc. So in general, as you indicated, in these various enzymes, and it's hundreds, just as you said, it is an important structural component and it has a very specific architecture with the enzymes that it serves, so it is a structural thing in general. And copper, to my knowledge, doesn't actually replace that. But for example, zinc is important in many things that are related to cognitive decline, it's important in diabetes, it's important in functioning of insulin, it's important, of course, in the trophic activity of insulin and, you know, on and on. It's important in immune responses. So, it actually has many effects that are related to cognition. So it may even just be a biomarker for something underlying going on right in the toxic insult type of Alzheimer's disease you're talking about. It something to keep in mind when you see that, and especially if the person presents, and these people tend to be very distinctive, the people who have type 3. So, they tend to be young, and we see them in their late 40s, mid 50s very commonly. We've seen them as late as starting their first symptoms in the mids, but typically, their first symptoms are currying in the 40s and 50s. They are often women, they are often ApoE4 negative although not always. There are certainly people who are ApoE4 positive to have this. As you mentioned, they often have the low zinc, and then they typically present in a non-amnestic way. Interestingly, unless they are homozygous for E4, in which case they do present typically with an amnestic presentation, but the ones who are E4 negative typically present with problems, as I mentioned earlier, executive dysfunction problems. And so I always ask people, are you having trouble organizing things? We had one person, for example, who was known for her tremendous organizing capability and as she started to get the problem she just lost it. She could not organize things that she could do before, it's a very common complaint. Or as I said, people will say, "Oh, I can't calculate a tip anymore, or I can't pay the bills anymore," anything that is math-related or visual perception or word finding, things like that. You mentioned the ApoE4 a few times. Can you talk a little bit about just for people listening and watching, you know, what ApoE4 is, and it's a gene, and so why it plays a major role in Alzheimer's disease. Yeah, so, Apolipoprotein E is a really fascinating story, and of course, Professor Robert Mahley discovered this decades ago, and it has turned out to be the most important genetic risk factor for Alzheimer's disease. Seventy-five million Americans have a single copy of ApoE4. And when I say that what I mean by that is, everybody has two copies of either 2, 3, or 4, and the most common one is ApoE3. So it's common for people to be a 3,3 as an example. However, about a quarter of the population, so about 75 million Americans have one copy of ApoE4, and that's actually the primordial one. Then about seven million Americans have two copies, so they're homozygous for ApoE4. So most likely you will get it. And of course, the vast majority of people don't know. Now, in the past people said, "Don't check because there's nothing you can do about it," and that has completely changed. So there is a tremendous amount, and the reality is Alzheimer's should be a rare disease. It should essentially decrease to a very low level with the current generation. If everybody gets checked, we recommend that everybody 45 or over get a cognoscopy, it's a silly term but it's easy to remember. Everybody knows when you hit 50 you should get a colonoscopy, and if you hit 45 or over you should be getting a cognoscopy. You should be doing some testing and see where you stand, what are your risk factors, are you ApoE4 positive, do you have high homocysteine, methylation issues, inflammatory issues, nutrient issues, toxin issues, all these things, because they can all be addressed, and we can decrease the overall global burden of dementia. So there's a variety of biomarkers that you are suggesting people can go and get measured? Cognoscopy, yes. I think that has been borne out. That perspective will be helpful going forward in terms of using different approaches, both polypharmacy and monotherapeutic. Would you please describe your ideas and how they are different from the mainstream view? Two of these are actually not illnesses. Think about it a little bit like a company. Imagine that you have a bunch of accountants; each one specializes in a different area and they all report to a CFO. APP is the molecule that is integrating many different inputs to determine whether a strategic downsizing must occur. If it is required, then you are going to have to activate the compliance officer and you have to send out the appropriate memos. What you end up with is a very programmatic and well-orchestrated downsizing of the synaptic density. That is exactly what is seen in this illness. We say we do not understand where it comes from and that there is nothing you can do about it. If you look at the molecular mechanistics, what you will see is that this is actually a well-orchestrated, nondisease, strategic downsizing based on many different inputs and a mismatch of those with what is actually required to maintain those synapses and to continue with the remodeling that goes on throughout life. From there, what led you in the direction of addressing this with a systemic protocol of lifestyle and nutritional interventions? This came directly from looking at the underlying molecules that mediate this change. For example, if you look at this model, then you will understand why simply reducing the amyloid-beta protein is helpful; it is something to think about, and it is certainly an important part of the overall plan. What you are really doing there is simply not sending out the memo. You are not telling people to downsize. You are ultimately going to fall short based on the mismatch between what is needed and what is coming in. Here is a simple example: There is a direct molecular link between estrogen, its receptor, its gene activation, the molecule that cleave APP at the alpha site, and pushing the APP in the direction of supporting growth and maintenance. That is 1 of 36 different contributors we initially identified. If there are all of these things that are playing on this same central mechanism and, ultimately, this central mechanism is taking these into account and either deciding that there is support there or that there is not support there and that there must be downsizing, then the most appropriate physiological approach would be to address all 36 of the members of that network. That is how we started. Your protocol was published in the September edition of the journal Aging. To be fair, given the page limitations, we published what we could. There are many new instances and, of course, we have the follow-up to that. What we published was system 1. We now have system 2..

J Here Neurosci ;46 2: Next generation therapeutics for Alzheimer's disease. J Alzheimers Dis ;37 2: The small co-chaperone p23 overexpressing transgenic mouse. J Neurosci Dale bredesen book ; 2: Neuroprotective sirtuin ratio reversed by ApoE4.

PNAS ; The multi-functional drug tropisetron binds APP and normalizes cognition in a murine Dale bredesen book model. Brain Research ; Issue Cover.

J Alzheimers Dis ;40 3: Essential versus accessory aspects of cell death: Cell Death Differ ;22 1: Reversal of cognitive decline: A novel therapeutic program.

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Aging ;6 9: Journal of Alzheimer's Disease, May. John, V. Reed, J. Physiology and Pathology of Cell Death. Cambridge Dale bredesen book Press, New Dale bredesen book. Molecular and Cellular Biology of Aging in press. Feb 28, Gina rated it did not like it. This is a harsh rating, but feels appropriate.

Dale bredesen book

The idea is that there are 36 factors that can result in dementia, and so dealing with those factors can reverse it, especially if you catch it early. The 36 sounds Dale bredesen book a lot, and it is, but I don't automatically object to that. There can be a lot of complex interactions. I did have an issue with some of the connections drawn, which seem a little iffy, not to mention trendy.

I have a bigger issue with the contradictions, like the book saying that the This is a harsh rating, but feels appropriate. I have a bigger issue with the contradictions, like the book saying that there is no backup for metals being Dale bredesen book cause of dementia, but you should try having mercury Dale bredesen book removed. Okay, mercury can have toxicity issues not necessarily for fillings, Dale bredesen book finebut then it is further specified that aluminum doesn't seem to contribute, yet one of the sample routines includes the elimination of aluminum from her deodorant.

In a way that makes sense, because the people who are most likely to jump on bandwagons of clean eating and pure living are the people who will be most drawn to this book. I also do not Dale bredesen book that when people improve their nutrition and sleep that they do better in many Dale bredesen book.

I do doubt that adding all of these Dale bredesen book as you eliminate some pretty good foods is helpful.

I can almost excuse that everyone cheating on their diet - as determined by visiting Dale bredesen book coaches - does not automatically rule out the connection between the protocol Dale bredesen book their improvements, given that you might not have continue reading issue with all 36 factors.

However, that level of unverifiability, and the scare tactics that are used regarding stopping, and other factors feel like they are adding up to someone not improving just not having found the right essential oil yet, and if it doesn't work you just didn't try hard enough. I might have given it two stars if it were just kind of scientifically shoddy, but the way it ended up being angered me.

A much better book along similar lines would be The Brain Fog Fix by Mike Dow, which covers similar ground with less pretension. Aug 30, Robert Luebke rated it it was amazing. This is a must read for anyone who fears the threat of getting Alzheimer's. Bredesen is a neurologist and researcher who lays out Dale bredesen book plan called RECODE for preventing and even reversing some of the Dale bredesen book of Alzheimers. Nutrition plays a big role in his program, but the stories of patients who have improved from Dementia after being on this program is very promising.

Juicy Black Ass In Tights. Dale E. Integrative Medicine: Up to this point, cognitive decline, once identified, has been largely considered irreversible and unstoppable. Do you consider this the case now, and why? Dr Bredesen: I do not consider this the case now. There has been tremendous progress in the last several years, and this is a very exciting time for studies of neurodegenerative illness. We published the first paper to show that just last September with a small, anecdotal group.

In your paper, you talked about the monotherapeutic approach. Today, what are the drawbacks of a monotherapeutic approach? In other words, these are networks of molecular pathways that are out of balance, associated with a chronic disease process. The idea of going after these with a single drug, although it has been successful in some cases under some circumstances, is not the optimal approach—either from the standpoint of theory Dale bredesen book from the Dale bredesen book of practice.

The idea Dale bredesen book a Dale bredesen book approach to cancer has actually been in place since the s and is the standard approach now. The ideal of using triple therapy for HIV, of course, is the first approach that actually showed a real benefit and has been the standard of care since that click here. I think that it is, perhaps, not surprising that we are seeing the same sort of Dale bredesen book with cognitive decline.

I think that some of the drugs that have failed in clinical trials could actually succeed on the right foundation of additional therapeutics. How did you get interested in pursuing a different therapeutic approach toward cognitive decline?

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Our laboratory has been interested for many years in investigating the molecular underpinnings of neurodegeneration. Why is it so common? What are the drivers of this process?

Pakistansexx Xx Watch Video Samurai42 sex. They literally send you some little cloths and you can go around and take x. And if you've got species that happen to produce a lot of toxins, it's a concern. Then you can actually measure the toxins in urine tests. So you can get an idea, and then again, you can actually see with your detox Yeah, so you can get. There are a couple of companies now that do make urinary mycotoxins tests. Okay, and so for people that don't, let's say, you know, they don't have the toxin exposure, or they don't think they do, but they don't if they've done this test, the things that they can do in their diet and lifestyle to prevent the Alzheimer's disease would be the major things to reduce inflammation, which are a lot of things, diet, lifestyle, exercise, sleep, and then again, a lot of overlap there with improving insulin sensitivity and fasting glucose levels and all that. Getting your hemoglobin A1C down, all those things, getting on a plant-based Terry Wahls has published a lot, and actually has done a lot of studies now on using a similar sort of approach for multiple sclerosis, and has seen excellent results including in herself with taking this sort of an approach. So, again, looking at the drivers, and looking at what are we actually responding to, and are we having more of an auto-immune response, like with MS,or are we having more of an innate immune system response with Alzheimer's, these are critical for dealing with these complex chronic diseases. Do you look at markers for gut health, because you were talking about What are the major Oh absolutely, oh yeah. So, there are a couple of ways to go. There is Genova test, a doctor's data test, there are different tests, there's like stool analysis sort of thing, but you can also do Cyrex, for example. So Cyrex array 2, Cyrex has a whole set of different markers for different antibodies. So, if you have a leaky gut you're often going to respond to things like LPS coming from your gut. Then there's a Cyrex array 3 that looks at various of the domains of gluten and gliadin and so who you can look at that. And then there are various auto-antibodies, etc. So yeah, these are very helpful to know. I haven't have heard of that one. So for the Genova diagnostics, is that the metabolic metabolism test or is there a gut one? There's a gut health one specifically, GI effects. And then, so yes, so Dr. Aristo Vojdani, he's the one who developed these various assays for Cyrex that are now being used by the Cyrex company, an excellent immunologist. So the reality is, you know, it's an era in which just like I'm going to take an Uber, for example, you don't necessarily have to call the taxi anymore. In this era we can actually get a lot more data, the quantified self is becoming more and more popular and more and more common. And it's something to some extent of the responsibility for our longevity and for our health is resting more and more with us. If you want to learn more about the protocol, please go take a look at the book, and it's called "The End of Alzheimer's" from Random House. And the only thing you can do is, is you can go to the website, drbredesen. And we are responding too, there are a lot of comments on the first book that is coming out now in 26 different languages, a lot of comments saying, "We want more specifics about what URLs do we use? Where do we go? Well, thank you so much for this conversation, Dr. Bredesen, for your wonderful research. Characterized by amnesia. A toxic 42 amino acid peptide that aggregates and forms plaques in the brain with age. Amyloid-beta is associated with Alzheimer's disease, a progressive neurodegenerative disease that can occur in middle or old age and is the most common cause of dementia. Heat shock proteins have been shown to inhibit the early aggregation of amyloid beta 42 and reduce amyloid beta plaque toxicity [1]. A concept from evolutionary biology that suggests certain genes may influence fitness differently throughout the life cycle. Genes that exhibit antagonistic pleiotropy increase the odds of successful reproduction early in life but have deleterious effects later in life. For example, mutations causing overproduction of sex hormones may increase the sex drive and reproductive success but could, hypothetically, promote prostate cancer in males and ovarian cancer in females with aging. A lipoprotein produced in the liver and the brain. In the brain, ApoE transports fatty acids and cholesterol to neurons. In the bloodstream, it binds and transports cholesterol, bringing it to tissues and recycling it back to the liver. Involving both parietal lobes of the brain. The parietal lobes sit behind the frontal lobe, roughly to the back and top of the head. A person with parietal lobe damage may have difficulty carrying out normal activities of daily living, such as showering or eating. Biparietal damage or losses can produce significant changes in personality. Involving both temporal lobes of the brain. The temporal lobes sit on the lateral sides of the brain, just above the ears. They are involved in the organization of sensory input and the development of memories. A person with temporal lobe damage or losses will have difficulty placing words or pictures into categories and may have impaired memory. A term used in chemistry to describe one of the four orbitals surrounding an atom. The D orbital contains five electrons, each having defined energy levels. A range of cognitive, emotional, and behavioral difficulties that commonly occur after injury to or deterioration of the frontal lobes of the brain. A person who experiences loss of executive functions may have problems with planning, organization, flexible thinking, social behavior, decision making, emotional control, and concentration. A digestive disorder, also known as acid reflux. GERD is characterized by burning pain in the upper abdomen, chest, and back. Treatment of GERD usually focuses on dietary and lifestyle modifications and pharmaceutical measures to reduce stomach acid production, and includes proton pump inhibitors, histamine blockers, and over-the-counter antacids. A chemical process in which a sugar molecule bonds to a protein or lipid molecule. It differs from glycosylation, which is an enzymatic reaction. Glycation occurs in the bloodstream, primarily to the dietary sugars glucose, fructose, and galactose. Fructose is nearly 10 times more likely to be glycated than glucose. Pertaining to the toxic effect of excess blood sugars on nerve cells. Glycotoxic substances, or glycotoxins, include advanced glycation end products AGEs , which are produced when a sugar molecule bonds to a protein or lipid molecule. They can be consumed in the diet or produced by the body as normal byproducts of glucose metabolism. AGEs promote oxidative stress, trigger production of reactive oxygen species, and stimulate the release of proinflammatory cytokines. AGEs are elevated in people with chronic high blood glucose levels, such as those with diabetes. The hemoglobin A1c test is often used to assess long-term blood glucose control in people with diabetes. Glycation is a chemical process in which a sugar molecule bonds to a lipid or protein molecule, such as hemoglobin. As the average amount of plasma glucose increases, the fraction of glycated hemoglobin increases in a predictable way. In diabetes mellitus, higher amounts of glycated hemoglobin, indicating poorer control of blood glucose levels, have been associated with cardiovascular disease, nephropathy, neuropathy, and retinopathy. Also known as HbA1c. A type of signaling protein. Mutations in the IRS-1 protein are associated with type 2 diabetes and susceptibility to insulin resistance. A physiological condition in which cells fail to respond to the normal functions of the hormone insulin. During insulin resistance, the pancreas produces insulin, but the cells in the body become resistant to its actions and are unable to use it as effectively, leading to high blood sugar. Beta cells in the pancreas subsequently increase their production of insulin, further contributing to a high blood insulin level. Porphyromonas gingivalis, a gram-negative bacterium found in the oral cavity and throughout the digestive tract of humans. A class of drugs that reduce acid production in the stomach. PPIs are used to treat dyspepsia indigestion , peptic ulcer disease, gastrointestinal reflux disease also known as GERD , and other gastrointestinal diseases. Proton-pump inhibitors may alter absorption of dietary minerals, a potential mechanism for an association between consumption of PPI and poorer bone health. A complex developmental process during which synapses are formed synaptoblastic activity and eliminated synaptoclastic activity in the brain. If you enjoy the fruits of , you can participate in helping us to keep improving it. Creating a pay-what-you-can subscription does just that! Plus, we throw in occasional member perks and, more importantly, churn out the best possible content without concerning ourselves with the wishes of any dark overlords. The process of analyzing DNA by sequencing methods is subject to error and can be wrong, however. Although your report is based on conclusions drawn from published scientific studies about various SNPs, many of these studies explain only a small part of the heritability of a trait or disease risk, and they don't take into account how different polymorphisms may interact with each other. In addition, many published studies do not account for medical history or environmental, dietary, microbial, or lifestyle factors, which can alter the true risk for any trait or disease. It will also discuss optimal nutritional and lifestyle interventions that may be appropriate for your genotype based on evidence. The report, however, is not medical advice, and it is important that you discuss any dietary and lifestyle changes with your physician before you proceed. Please also refer to question: In order for us to generate your report, your DNA must be analyzed by a provider like 23andMe or Ancestry. If you use 23andme, you only need to get the basic ancestry service to receive FoundMyFitness genetic report. These are the only providers we support currently. The focus of the FMF report is on the genes that I believe have the greatest influence on healthspan. In this sense, it is a living report that might be worth re-running periodically to see my latest revisions and possible corrections! Whenever possible, I also try to state in your report the combined effect of multiple SNPs instead of merely the individual ones. Reports are valid for 30 days. In the event that your report is updated during that day period, you can re-run your report to get the latest version. If you register for an account, you can delete your report immediately after running it. If you skip registration, your report will be deleted after 30 days. We do not save data that are not used in the creation of reports. A type characterized by systemic inflammation, reflected in such laboratory results as a high hs-CRP high-sensitivity C-reactive protein , low albumin: The atrophic subtype of Alzheimer's disease — a reduction in support for synaptogenesis. A type characterized by an atrophic profile, with reduced support from molecules such as estradiol, progesterone, brain-derived neurotrophic factor BDNF , nerve growth factor NGF , testosterone, insulin, and vitamin D, often accompanied by increased homocysteine and insulin resistance, the last feature of which Dr. Bredesen refers to as type 1. The cortical subtype of Alzheimer's disease — an environmental toxin-related type associated with chronic Inflammatory response syndrome CIRS that presents with more general cerebral atrophy and frontal-temporal-parietal abnormalities, resulting in an emphasis on executive deficits, rather than the more amnestic quality of hippocampal impairment. The emergence of new properties of amyloid-beta. Click To Tweet Amyloid-beta as an antimicrobial response. The interaction of metals with amyloid-beta. If everybody gets checked, we recommend that everybody 45 or over get a cognoscopy. Click To Tweet In this episode, Dr. In this episode, we also discuss Herpes study. Metal-binding study. These subtypes include: Bredesen describes as a lack of proper cell signalling as a consequence of long-term reductions in nerve growth factor, brain-derived neurotrophic factor and other hormones that result in a fall in synaptoblastic-to-synaptoclastic ratio in other words, synapse-generationg versus synapse-destroying activities. Bredesen, such as environmental molds or metals. See also Bredesen also shares some details on his upcoming publication, namely, that it will include a more substantial 50 patient cohort. Some of these signaling factors, namely BDNF, are not amenable to being assayed, but are produced robustly in response to exercise. See the episodes with Dr. Panda for a great discussion of daily time-restricted eating. See the episode with Dr. Eric Verdin for a discussion on this research. Relevant study. Listen to this episode with Dr. Relevance to Alzheimer's Disease. These findings point to novel therapeutic strategies for AD and aging, resulting in an extension of human healthspan, the disease-free and functional period of life. We would love to hear from you. Contact us with any questions or call us at 1. So, how could its most important claims could be wrong? There's no foolproof way to discredit this hypothesis, but also little reason to think it's more likely than with typical research. He's virtually guaranteed to attract more scrutiny than most - that would be a strange strategy to pursue if he had something to hide. If true, this would imply that he has some pretty unusual skills, and that there are serious problems with how some other doctors diagnose dementia. I can't rule out this hypothesis. I can see how he might be overstating the benefits this way, but I don't see how it could explain his results if there were no benefits. There's a weak sense in which most of the measurements are subjective. Maybe a professional poker player with a diagnosis of mild cognitive impairment could be mistaken about whether his poker improved. But his case studies include some pretty strong claims, including one report of a big increase in hippocampal volume measured by MRI, and one patient whose neuropsychologist advised him to "wind down his business and plan for the full-time care he would soon need". Two years later that neuropsychologist measured the patient's memory as having improved from the 3rd, 13th, and 24th percentile on three tests to the 84th, 79th, and 74th percentile, and the patient expanded his business. Those seem to be stretching the limits of what I can believe for measurement error. Many people have strong priors about Alzheimer's which lead them to find Bredesen's claims less plausible than these hypotheses, based on past experiences with Alzheimer's "cures", plus stereotypes about what approaches to disease work. Those priors might make some sense if researchers had tried many independent approaches. But it looks to me like the failure of most Alzheimer's research can be explained by a small set of problems: The inadequate exploration of different paradigms can be explained by an ordinary amount of groupthink plus bias toward approaches that support continued funding of areas that existing experts know best. So it's not wildly implausible that someone could find the equivalent of a trillion dollar bill or maybe a ten billion dollar bill if he has overstated the benefits a lot. It's not as if the bill was in plain sight - it's more like it was torn into dozens of pieces, and hidden in leaves. What causes the widespread reluctance to adopt the kind of functional medicine that Bredesen advocates? I don't expect doctors to like detecting suboptimal health and then watching helplessly as patients continue the lifestyle that caused the problem. Why would patients fail to follow the protocol? Partly because things like pizza and cookies are somewhat addictive. Partly because there are important social costs to admitting that we're not healthy enough to eat at a typical restaurant or party. Mainstream doctors are sometimes reckless - not washing their hands, or saying that patients can't do anything about Alzheimer's, when they could say something like "regular exercise may improve your odds". Somehow those mistakes stay less conspicuous than functional medicine's recklessness. I'm unclear what the current reaction is from mainstream Alzheimer's researchers. Bredesen seems to have gotten a mix of help and hostility in the past from mainstream institutions. The Buck Institute of which Bredesen is the founding president gets a good deal of NIH grant money, and he doesn't appear to have trouble publishing peer-reviewed papers related to his Alzheimer's ideas. But IRBs denied him permission to conduct a trial that involved an early version of his protocol because it would have tested too many things at once. That mainly seems like additional evidence that IRBs are unethical. It's quite possible that his protocol hasn't been stated clearly enough to qualify as a set of scientific hypotheses, and that it might end up testing some mix of articulated hypotheses and also the skills of the people involved [2]. If that was the IRB reasoning, it seems like a really awful reason for rejecting a trial. Even if it mostly ended up testing doctor's skill at giving advice, a positive result would falsify the claim that Alzheimer's cannot be prevented, cured or even slowed. Bredesen presents a nonstandard biochemical model of Alzheimer's. I'm not sure what to make of it. It doesn't seem particularly helpful for understanding why the protocol works. It does explain why the simple amyloid-beta hypothesis is wrong, but it's hardly the only hypothesis to explain that. He classifies Alzheimer's into three semi-distinct subtypes. I'm fairly convinced that Alzheimer's refers to more than one disease, but I don't get the impression that anyone knows how many subtypes can be usefully identified. Bredesen seems confused about the diet that humans evolved to eat. We don't have good evidence about human diet over that period, but it looks pretty likely that humans relied mainly on fruit during the early part of that period, and relied on high-carb roots during some parts of that period. Some modern hunter-gatherers Hadza eat way more honey than that 15 gram limit would allow. Maybe American lifestyles create a need for that strict limit, but that need isn't inherent in our biology. While evidence from hunter-gatherers weakens some of Bredesen's specific advice, it strengthens his claim that Alzheimer's depends on lifestyle choices: The book has somewhat inadequate warnings for people who want to wait until they get more severe symptoms: The protocol is already pushing the limits of what we have the mental capacity to implement in some people; the difficulty will vary unpredictably from person to person. Delaying until the symptoms become noticeable makes it harder to learn new habits, harder to track whether you've taken the right pills, harder to prepare new recipes, etc. What do I expect if he's right? I expect an expanded number of doctors using his protocol over the next few years to reach something like 10, people who are at risk of Alzheimer's. I expect a similar number of patients to see doctors who doctors who try to follow the protocol without being trained by a Bredesen-approved teacher. I expect these doctors to report widespread improvement in these patients, and I expect those reports to be controversial due to risks such as selective reporting. I recommend that the trial be evaluated in two separate steps: My hope is that will distinguish problems with patient compliance from issues of how improved biomarkers affect dementia. I'm unclear how the average doctor will react after those trial results are released. But among doctors that are relatively open to new ideas, I expect a profusion of competing protocols, with poorly documented claims about how well patients comply with the protocol. I expect that by around to , at least half a million patients will use one of these protocols, and that will be sufficient to a decline in the overall number of people developing Alzheimer's. Conclusion The book seems slightly careless about details such as citing good references, as if it were rushed to print rushing does seem appropriate. I suspect he exaggerates the benefits. He errs slightly in the direction of allying too much with alternative medicine. Mainstream medicine has some major flaws, but it's still important to persuade mainstream institutions to listen to the book's ideas. But it's good enough to persuade me to experiment with significant changes to my diet and supplements, and maybe enough to convince me to donate to the Buck Institute. Footnotes [1] - the book won't tell you directly whether it's safe for you to eat at restaurants and parties. It will tell you how to get evidence about whether those are safe for you. But the book did get me to look at apoe4. That page has an automated? These two showed up on the same alz. Healthier living could reduce worldwide dementia by a third, report says — The Washington Post One in three dementia cases 'could be prevented by lifestyle changes' — London Evening Standard I hope this is a sign that cognitive dissonance on the subject has reached a maximum. There are important limits to how reliable this evidence is, but the researchers were able to get decent evidence that some hunter-gatherers lived into their 80s, that hunter-gatherers did have people whose cognitive ability was impaired from childhood, and consistently did not know of late-onset cognitive decline. Beware that "it's due to modern lifestyles" doesn't guarantee there's a reasonable strategy to avoid Alzheimer's. Modern population densities support infectious diseases that hunter-gatherers don't get. Jun 29, Ron Frampton rated it it was amazing. Mar 24, Tatiana Shorokhova rated it it was amazing. Nov 28, Ro Laberee rated it it was amazing Recommended to Ro by: Before summarizing Dr. There is no treatment for it. After a diagnosis, there is a clear message conveyed — You are not going to get better Before summarizing Dr. After a diagnosis, there is a clear message conveyed — You are not going to get better. This is the beginning of the end. It will probably be awful. Everything else offered is a knock-out pill of one kind or another. We are making great strides in cancer and in molecular biology, generally. Meanwhile, death by dementia is rapidly increasing. It robs victims of their humanity — sometimes over decades — it terrorizes and bankrupts their families, and we have no effective treatment. While the technology industry makes startling advances in Artificial Intelligence almost weekly, we have stood by and watched the human intelligence of our seniors wither away appallingly. This situation seems ghoulish to me. You have likely heard neuro-specialists parroting the amyloid plaque hypothesis. In fact, only those toeing the amyloid line can get funding for their research. Meanwhile, amyloid plaque is also found in the brains of perfectly healthy individuals. Amyloid is only one piece of a very complicated puzzle. Scientists and doctors investigating the root causes of cognitive decline and braving the icy waters of non-amyloid based research are mostly ignored. In this book, Dr. Bredesen addresses the other pieces of the dementia puzzle and lays out his protocol, which has helped many hundreds of people reverse their cognitive decline. There were two chapters I had to read twice and, yes, I took notes. My best take-aways: Exercise almost every day. Make it count. This stimulates BDNF brain-derived neurotrophic factor which supports new neuron growth. Stop eating sugar. It is poison for neurons. Protect your sleep. Vitamin D3!!! Take it. Or, be outside in the sun without sunblock every day, if possible. No, not for hours. Fresh, organic vegetables with every single meal, and lots of them. Lots of good fat — coconut oil, avocados, fatty fish like salmon , nuts, and grass fed beef or chicken, but in small servings 7. Eliminate gluten. Get your BMI in a good range. Exercise your brain by challenging yourself, move around throughout the day, and get out and socialize. The supplementation he recommends is rather extensive and it is keyed to your health blueprint. You need to follow through on extensive bloodwork in order to know exactly how much inflammation your body hence your brain is dealing with and where you stand with insulin sensitivity. These two things — inflammation and insulin senstitivity — are dire enemies of cognitive health. And environmental toxins…. He urges those with cognitive decline to try to maintain a mild state of ketosis by eating lots of fat, some protein, but very little carbs. This makes the brain use fat as its main source of energy, which optimizes cognitive health. Linda Lancaster. Tap, Taste, Heal. Marcella Friel. Michelle Lhooq. Alexia Brue and Melisse Gelula. The Sensory Herbal Handbook. Adam Gordon. Stuff Every Cannabisseur Should Know. The Pursuit of Endurance. Jennifer Pharr Davis. Healthier Together. Emily Winfield Martin. Dementia Reimagined. The Lyme Solution. Darin Ingels. The Complete Vegan Cookbook. Natural Gourmet. Yoga for Everyone. Dianne Bondy. The Cruise Control Diet. The ideal of using triple therapy for HIV, of course, is the first approach that actually showed a real benefit and has been the standard of care since that time. I think that it is, perhaps, not surprising that we are seeing the same sort of thing with cognitive decline. I think that some of the drugs that have failed in clinical trials could actually succeed on the right foundation of additional therapeutics. How did you get interested in pursuing a different therapeutic approach toward cognitive decline? Our laboratory has been interested for many years in investigating the molecular underpinnings of neurodegeneration. Why is it so common? What are the drivers of this process? The idea is that if you could get at those specific molecular details, you could potentially work out therapeutics that would be effective. The first drug that we identified is currently in a clinical trial in Australia for early-stage mild, cognitive impairment. However, when we then looked at what all of the inputs to that specific critical balance were—a plasticity balance if you want to think about it that way—we found that the drug alone addressed only some of these but did not address all of them. Therefore, it actually made much more sense to try to address additional input to that same balance. The first was placebo and the second was the drug. A third arm, then, included an entire system of therapeutics. This is the same one that we ultimately published last year as MEND, or metabolic enhancement for neurodegeneration. The fourth arm was the system with the drug. The hope was that the drug would actually work much better on the backbone of the entire system. This was turned down by both the public and the private institutional review board, or IRB, as being too complicated. The IRB argued that we must not know how to do clinical trials because we were proposing something that had more than 1 variable. Our argument, of course, was that this is not a 1-variable disease. I think that has been borne out. That perspective will be helpful going forward in terms of using different approaches, both polypharmacy and monotherapeutic. Would you please describe your ideas and how they are different from the mainstream view? Two of these are actually not illnesses. Think about it a little bit like a company. Imagine that you have a bunch of accountants; each one specializes in a different area and they all report to a CFO. APP is the molecule that is integrating many different inputs to determine whether a strategic downsizing must occur. If it is required, then you are going to have to activate the compliance officer and you have to send out the appropriate memos. What you end up with is a very programmatic and well-orchestrated downsizing of the synaptic density..

The idea is that if you could get at those specific molecular details, you could potentially work out therapeutics that would be effective. The first drug that we identified is currently in a Dale bredesen book trial in Australia for early-stage mild, cognitive impairment. However, when we then looked at what all of the inputs to that specific critical balance were—a plasticity balance if you want to think about it that way—we found that the drug alone addressed only some of these but did not address all of them.

Therefore, it actually made much more sense to try to address additional input to that same balance. The first was placebo and the second was the drug. A third arm, then, included an entire system of therapeutics. This is the same one that we ultimately published last year as MEND, or metabolic enhancement for neurodegeneration. The fourth arm was the system with the drug. The hope was that the drug would actually work much better on the backbone of the entire system. This Dale bredesen book turned down by both the public and the private institutional review board, or IRB, as being too complicated.

The IRB argued that we must Dale bredesen book know how to do clinical trials because we were proposing something that had more than 1 variable. Our argument, of course, was that this is Dale bredesen book a 1-variable disease. I think that has been borne out. That perspective will be helpful Dale bredesen book forward in terms of using different approaches, both polypharmacy and monotherapeutic. Would you please describe your ideas and how they are different from the mainstream view?

Two of these are actually not illnesses. Think about it a little bit like a company. Imagine that you have a bunch of accountants; each Dale bredesen book specializes in a different area and they all report to a CFO.

APP is the molecule that is Dale bredesen book many different inputs to determine whether a strategic downsizing must occur. If it is required, then you are going to have to activate the compliance officer and you have Dale bredesen book send out the appropriate memos.

What you end up with is Dale bredesen book very programmatic and well-orchestrated downsizing Dale bredesen book the synaptic density. That is exactly what is seen in this illness. We say we do not understand where it comes from and that there is nothing you can do about it.

If you look at the molecular Dale bredesen book, what you will see is that this is actually a well-orchestrated, nondisease, strategic downsizing based on many different inputs and a mismatch of those with what is actually required to maintain those synapses "Dale bredesen book" to continue with the remodeling that goes on throughout life.

From there, what led you in the Dale bredesen book of addressing this with a systemic protocol of lifestyle and nutritional interventions? This came directly from looking at the underlying molecules that mediate this change. For example, if you look at this model, then you will understand why simply reducing the amyloid-beta protein is helpful; it is something to think about, and it is certainly an important part of the overall plan.

What you are really doing there is simply not sending out the memo. You are not telling people to downsize. You are ultimately going to fall short based on the mismatch between what is needed and what is coming in. Here is a simple example: There is a direct molecular link between estrogen, its receptor, its gene activation, the molecule that cleave APP at the alpha site, and Dale bredesen book the APP in the direction of supporting growth and maintenance.

That is 1 of 36 different contributors we initially identified. If there are all of these things that are playing on this same central mechanism Dale bredesen book, ultimately, this central mechanism is taking these into account and either deciding that there is support there or that there is not support there and that there must be downsizing, then the most appropriate physiological approach would be to address all 36 of the members of that network.

That is how we started. Your protocol was published in the September edition of the journal Aging. To be fair, given the page limitations, we published what we could. There are many new instances and, of course, we have the follow-up to that.

What we published was system 1. We now have system 2. As physicians, we have been hampered over the years by having to deal with very small data sets. We are dealing with extremely complicated organisms and yet we have very small data Dale bredesen book, such as what the sodium is or what the potassium is. In the field of oncology, sex Xxx xyz current excitement is in doing whole-genome analysis for the tumor and whole-genome analysis for the patient and comparing those to infer Dale bredesen book that what the drivers are for the actual tumor.

This is what has been read more to as Dale bredesen book medicine. We are looking at a large number of metabolic components and, of course, we also encourage people to get genome sequencing. Then we can infer from all those data what the most likely pathways are that contribute to this ongoing downsizing that is occurring in your brain. As you mentioned, this is fairly complex and there are Dale bredesen book variables, as well as many therapeutic targets in the system.

Is the result a protocol that is difficult for patients to adhere to? And as such, does it have to be followed to the letter?

This is a really important point. First of all, this is a different way to do medicine. Instead of therapeutics, this is programmatics. I believe that is the future of the treatment of chronic illness: Second, this is going to be personalized.

This is going to be a program for you based on Dale bredesen book is driving your particular problem. Third, of Dale bredesen book, now that we are seeing results, we are looking at article source we can make this simpler. You Dale bredesen book to remember, at the beginning, we did not know what was going to make people better and these were people dying of an untreatable Dale bredesen book illness.

Well no, it is not a Dale bredesen book approach, but Dale bredesen book is not a silver bullet approach. It is silver buckshot instead of silver bullets. We want to hit everything that is contributing to your illness if we are going to have hopes of getting it to stop and then Dale bredesen book itself. We are now working with health coaches who can help to make sure you do all the different parts of the program, because as you alluded to, it can be somewhat complicated.

It needs to be complicated enough to address the underlying pathogenesis, but if it is so complicated that no one can do it, then of course it is not going to be very practically beneficial.

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One positive note here: When you go back click here the molecular details and you look at how Dale bredesen book plasticity system actually works, what you find is that there are prionic loops. In other words, when you start going down one side or the other, it is like a snowball rolling downhill. You gather momentum on one side or the other. You have to get to the point of changing that. You have to get to a certain threshold, but once you do that, it will begin to gather momentum going down the good side instead of the bad side.

At the beginning, link do not know how many, but when you start to get results, you can limit the program to those things that put you on the other side of the plasticity network, of the balance.

For example, the first woman we reported on did 12 of the Nobody has managed to do every single one so far, but when you Dale bredesen book to enough, then you get over the threshold. By the way, this is no different than what Dean Ornish, mdhas Dale bredesen book for years in atherosclerosis. You do enough of the right things, enough of his program, and he has documented the reversal of atherosclerosis.

What we are doing here Dale bredesen book a little bit like Dale bredesen book. You get to the point where you are now able to support the production of new synapses and you start seeing improvement. Would you describe some of the results you have observed from use of the protocol?

Milfs fucking Watch Video Xxx Unapaja. But this is the exact same thing we're seeing with people, and especially people with early cognitive decline. Now, as you go later and later, it's more and more difficult, but we have seen people even with MoCA scores of zero show improvement. So, yes, I think the work that you quoted supports that notion, that in fact, having ketones is actually quite helpful for cognition. Do you think, and here's a couple of questions related to that, and that is, you know, is that Also the ketones, as you mentioned, are used by the brain quite nicely. And interestingly, it actually spares But I'm wondering if people like myself, I don't really practice a ketogenic diet but I also don't I eat a very healthy diet. I definitely try to make sure I don't eat anything refined, no refined carbohydrates or processed food or things like that. But the thing is, is that my So, for me going on ketogenic diet, do you think there would still be more benefit even though the whole, you know, insulin sensitivity thing And you know, you can even do so all sorts of online evaluations for your own cognitive ability. And I do think that many of us are sub-optimal in our metabolism, and we know this. One of the problems, of course, is that there have been a lot of assumptions made during the 20th century. Yes, it's fine to have processed foods, it's just as good, you know, it's fine to have more sugar, on and on and on, which just simply have turned out to be wrong. And it has to do with sleep, it has to do with exercise, all sorts of things. We were built, as human creatures, to do certain things well and to do other things we weren't built for. If we all were jumping out of a third-story windows as something to do that would be fun that would not go over well for us. And to some extent, we're doing the same thing with the way we're living. So, obviously, you've managed to stay fit and to have a good fasting insulin and all these sorts of things. However, a little bit will depend on what you're actually doing, for example, where is your hemoglobin A1C? For example, is there some inflammation there or not? The bottom line is that we were not made as human organisms to consume the amount of simple carbs that we typically are exposed to. So to some extent, just as we're being exposed to all these other toxins, of course, sugar is one of them. And whether you try to be exposed to it or not often we are exposed to it from all sorts of different foods and things like that. Going out to eat So many people It does contribute to chronic inflammatory conditions like arthritis and like cognitive decline. So, I think that having a high-fat diet has been helpful for many people, but what you can suggest is, look, if you ever have any cognitive decline get in as early as possible and then consider this. In your case, of course, as you indicated, you're interested in prevention because you already know that you're ApoE4 positive, so it might be worth trying it just to see, but you know, obviously, you're doing a lot of other things right currently. And measuring a lot of different I think that's very important. So the diet and then exercise and the sleep is really important. You mentioned the glymphatic system, you know, there's Well, of course, there are multiple. There's the ratio of formation to clearance is critical. And of course, you're going to be forming more and keeping more if you actually have a state of inflammation or of responding to a pathogen. So actually, you know, there was a really interesting test developed by Professor Milan Fiala at UCLA, developed about almost 10 years ago now. And what he was looking at was taking peripheral blood mononuclear cells, so you're essentially taking the blood macrophages, and you're now simply challenging them. He would give them amyloid, and just look to see how good are they at phagocytosing, at eating and getting rid of the amyloid. And the surprise was, all the people who have Alzheimer's are very poor at eating and getting rid of this amyloid. It was as if they're literally trying to keep the amyloid around. Then we realized, yeah, this is a state. So, as you know, it's become clear that you change, your cells change states. You have the metabolic flexibility, you have burning this, burning that for fuel, one of the states you change back and forth between a pro-inflammatory state, essentially an NF-KappaB-mediated state, and on the other hand, an anti-inflammatory, a state that is involved more with SIRT1. These two actually have multiple sites of mutual inhibition. So you're literally flipping back between these different states, and the people who had cognitive decline are poor at getting rid, they're literally keeping this amyloid around. And he looked at their M1 to M2 ratios, essentially inflammation to resolution, he saw two patterns. The people who don't eat the amyloid and who have the cognitive decline either have a pro-inflammatory state where they have a lot of M1 and very little M2 or he found that they literally had an atrophic state, the same thing we saw as type 2, where they simply could not produce enough of this to resolve. So they literally had very low levels. And so in fact, getting the right levels, about two-and-a-half to one, was associated with the best outcomes. So, you do have this phenomenon, and so yes, as you know, you've got everything from insulin degrading enzyme, Neprilysin, macrophage clearance, glymphatic system, and on and on and on. There are multiple ways but as long as you're in that state where you're using multiple mechanisms to keep this stuff around, you're not going to be very good at metabolizing it. This paper that you are referring to, I do remember reading a paper that you had published a few years ago where you had taken this, essentially, I guess, you can use that as a biomarker if the people with Alzheimer's disease are not clearing amyloid beta plaques via phagocytosis with their monocytes effectively, that's sort of kind of a surrogate marker for what's going on in the brain potentially, right? Right, and you had done a small study where you had given people some omega-3 supplements along with some antioxidants and vitamin D, and it improved their phagocytosis of the amyloid plaques in the periphery, and also I think their cognition, some individuals had improved cognition, ApoE4 negative ones, I remember. Right, and so I was a co-author on that paper with Professor Fiala. So again, he invented the test and he's now doing, you know, the small number of things that you described there. What we're doing is a much larger set where we're doing more of a program but clearly that is an important part of it. You have the inflammatory part but then you have to have the resolution part. And if you don't have that resolution part, again, a change in mode, then you're stuck with this chronic inflammatory state. And so things like omega-3s and omega-3 derived maresins and things like that are actually involved with the resolution, resolvins, named for that very event. I remember in that paper, and I've also done some reading on this because I have a paper that hopefully will be published quite soon on ApoE4-related Alzheimer's disease and particularly with respect to omega So there's some evidence that for whatever reason, fish, when people that have ApoE4 are given fish or eaten fish they're protected against Alzheimer's disease, but DHA supplementation, it's not the same at least for ApoE-positive individuals. And it's kind of been mystery as to why that is. And by the way, Professor Paul Clayton from Oxford has discussed this numerous times and written about this. And his argument is that, of course, fish have much more than just DHA and EPA and things like that, so they have antioxidants, things like the secoiridoids and things like this, whether you find them in plants or animals that actually are protective, because you have to remember you're looking at something with multiple sites of desaturation so it's very sensitive to oxidation. And so you have to protect that, and you're absolutely right. Again, this idea that we had in the past that, you know, fish, hey, it's just as good just to get that oil out, it's not just as good. And although the oil can be helpful, you better make sure that it's not oxidized, and you know, better to get it in its appropriate setting. Very interesting, some interesting papers had come out from a few labs, one from Salem Norman. Norman Salem, sorry. He had shown in animals, if you take animals and give them a human ApoE 3, 4, 2, and then feed them DHA orally, there was a transport defect in DHA across the blood-brain barrier. And so I kind of review this work on a variety of other papers as well, you know, where there's a couple of major mechanisms by which DHA is transported across the brain. Are you familiar with some of those? One is the through a free fatty acid and the other one's through an actual transporter called the Mfsd2a transporter, which is actually in a phospholipid form, DHA is in a phospholipid form. And so, it appears that there may be different ways, you know, that DHA gets across the brain, and one of the ways is potentially not working quite as well in ApoE4 individuals, at least that's my writing theory. But once the paper's accepted I'll send you a copy. So it's super, super interesting. Yeah, and of course, as you know, I mean, Professor Wurtman from MIT has spent years looking at what does it actually take nutritionally to make synapses? And his point was you need the DHA and you need acetylcholine as well. And so again, if you're going to be helping people to change that balance toward the synaptoblastic you want to make sure that they have plenty of those precursors as well as the appropriate signals, reduction of inflammation, all these other things that are actually part of an overall orchestrated event. The other interesting thing is that DHA, and I didn't know this previously until I had been digging into the literature, it also seems to be important for some of the glucose transporters on the blood-brain barrier. And so if you're DHA-deficient those glucose transporters aren't working as well and you're not getting glucose into the brain, which is another real hallmark of Alzheimer's disease. So that's another interesting thing. So, a couple of interesting things I wanted to ask you about were kind of off-topic but not particularly. You mentioned this type 3 sub-type. Would the herpes virus fall into that? So, yeah. So herpes virus could give you type 1 or type 3 depending on what you're actually responding to. If it's just a chronic inflammation then it would be a little bit more like a type 1 with chronic inflammatory, but you're right. You know, again, many groups have said, "Okay, it's about herpes. Okay, it's about P. And the reality is, all of these are capable of inducing the signal, this change where you're making the amyloid as part of a protectant. As you know, it's essentially part of your innate immune system. So if you're responding in that way it can be any of those things, it's not just one every single time, as far as anyone knows. So, yes, you alluded to the recent work on herpes and especially, of course, six and seven. And so, yes, not surprisingly. The last thing I kinda wanted to mention just because I wanted you to know about it in case you weren't aware of it, there's some really interesting research coming out of Finland. Are you familiar with saunas and the protective Yeah, of course, dramatic effects, and fits very beautifully with everything we've been talking about. And certainly, what happens when you have a sauna, yes, you may induce some heat shock protein, great, that's important, and it can be important in folding of proteins, but what also happens, of course, is that you detox. And these people who are doing this repeatedly Genuis from Canada who showed that if you look at composition of sweat compared to the blood there are certain toxins that are very high, cadmium being the big one, over 1, times increase in sweat, so a good way to get rid of cadmium, but a good way to get rid of other things as well. BPA, especially the hydrophobic toxins, the non-hydrophilic stuff tends to be very good in the sweat, but others as well. And so that's why it is very helpful, and many of us don't do enough of that sort of thing. And as has been pointed out, whether you're doing it through sweat and exercise or whether you're doing it through saunas, whether you're doing it through other mechanisms, yes, it's good to get. And then you want to use a non-emollient soap immediately thereafter, things like Castile soap or whatever you like that's non-emollient and get rid of the stuff so that you don't get re-penetration. Yeah, the other thing is that cardiovascular effects with the sauna and that may also be related to dementia as well. So, is that something that you'd consider using in your protocol? Now, we recommend that people But as a general rule, you know, part of this is, again, as my wife says, resilience, part of this is resilience. We're taking people who are sub-optimal in their metabolism, in their inflammation, in their toxic status, in their lifestyle status, in their sleep, in their stress levels, these are surprisingly important. One of the first people who came through was a very intelligent physician. And as we went through each thing he said to me, "Well, you know, I don't believe that, you know, that's not a cure for Alzheimer's, that's not a cure for Alzheimer's. And as we went through each thing, you know, he was telling me, "Well, I don't believe this. So, it is about changing signaling within your synaptobalstic to synaptoclastic ratio, providing the right support for that, DHA, acetylcholine and Vitamin D, and appropriate hormones, and BDNF, and all these things, and making sure that you don't have chronic exposure. And as you mentioned, sauna is actually a very powerful way to help reduce overall toxic burden. It is surprising how much toxic burden most of us are living with. So talking about the importance of intervening in multiple ways because there are so many different pathways that lead to inflammation, that can lead to insulin resistance, that can lead to toxic burden, one of the really And actually, we've had a number of people who have tried to remove their amyloid with antibodies who've actually gotten worse with that happening. So you have to go back to, why is there? And it's tough because yes, it is both part of the mediator, it's not the cause of Alzheimer's, it's a mediator, and I think that's been one of the problems. People want to say it's the cause, it's a mediator, and there are many upstream things contributing to that. So, on the one hand, it's a mediator of the pathophysiology. On the other hand, it's also a protectant, it's a response to things like pathogens. And so there's a double-edged sword there. It's fine, I think, in the long run, it'll be fine to remove the amyloid, but you've got to remove the cause of it first. Now, of course, people have just tried to go earlier, earlier, earlier and can we actually see some improvement? So I don't have do buy and take a lot of pills. David Brown In my opinion, the supplements he lists are worthless. The effectiveness of his program is all in the "basic plan. His claim is that all these things need to be applied together -- the whole is greater than the sum of the parts. He laments that no one will authorize and sponsor serious research to prove his claim. I really found hope inside these pages for people who are suffering with Alzheimer or dementia or have loved ones fading before their very eyes. It definitely entails a complete lifestyle change for many. Are you ready to see a change? Noah Pikes Yes! Past being ready, as I began following Bredesen's protocol as laid out via a "cognoscopy" involving measurements of some different parameters …more Yes! Past being ready, as I began following Bredesen's protocol as laid out via a "cognoscopy" involving measurements of some different parameters of body and brain substances, 7 months ago. It is a gradual process but I sense it is having a positive effect. See all 3 questions about The End of Alzheimer's…. Lists with This Book. Community Reviews. Showing Rating details. Sort order. Oct 09, Maggie Stiefvater rated it it was amazing Shelves: Last year, I was diagnosed with adrenal insufficiency, autoimmune, and a hookworm infestation after losing the ability to stay awake, think, digest food, grow hair, or perform easy physical tasks like lifting a backpack. I couldn't remember my home address; I certainly couldn't write novels. I was failing as a human and as a creator. My functional physician put me on a dauntingly strict regimen of diet, supplements, and cortisol management, and slowly my physical health returned. More slowly, my Last year, I was diagnosed with adrenal insufficiency, autoimmune, and a hookworm infestation after losing the ability to stay awake, think, digest food, grow hair, or perform easy physical tasks like lifting a backpack. More slowly, my brain followed. When the brain fog still lingered, however, I picked up this book in hopes of understanding why I hadn't gotten my cognition back completely. Bredesen's protocol is strikingly similar to the autoimmune protocol my doctor put me on, and incorporating the differences into my own regime has given me even more functionality is just a few weeks. The incidence of autoimmune disease, Alzheimer's, and Parkinson's has skyrocketed in developed countries, and science gallops alongside it looking for answers. Old theories on lupus, depression, and hormone imbalances are rapidly changing as research increasingly points to how we're making ourselves sick as a society. Very cool, very exciting, and very daunting times. This book collects some of the newest stuff. I'm recommending it to everyone with any kind of autoimmune, brain fog, or dementia. View all 16 comments. Critically important reading My wife was diagnosed with mild cognitive impairment while a member of the Kaiser network. They did a few diagnostic tests ,get a MOCA score on my wife of 19, got her drivers license revoked, and essentially said, "this is a terrible disease, there is nothing tone done for it, good luck". None of the Bredesen Protocol is part of the Kaiser program, and the physicians we spoke with did not even know what a functional medicine physician is, but did not think that Kaiser Critically important reading My wife was diagnosed with mild cognitive impairment while a member of the Kaiser network. None of the Bredesen Protocol is part of the Kaiser program, and the physicians we spoke with did not even know what a functional medicine physician is, but did not think that Kaiser had one. Fortunately, we were able to qualify for a Bredesen Immersion program with Dr. Bredesen and a team he assembled of trained functional medicine physicians. Subsequently, we are " all in" with the Bredesen protocol. It is not a diet, bit a complete lifestyle change. My wife' symptoms have not progressed and in many area have improved, just sine April Yes, the program is challenging and has some expense associated with it, but compared to what? An Alzheimer's unit in a nursing home, not to mention the emotional toll on everyone - does this seem like an easier and cheaper alternative to anyone? This book and the ReCode protocol offers something that cannot be measured, real hope. I urge you to read the book and take the protocol seriously, it can change you and your loved ones lives. View all 3 comments. Apr 09, Doug Bradshaw rated it it was amazing. A friend brought this book to me and asked me to read it and then to help him incorporate the protocol into his life to fend off mild cognitive impairment symptoms. The book was recommended to him by a well known MD. He has been studying the disease for 20 plus years. MD's and pharmaceutical companies have been looking for a drug to help Alzheimer's patients for a long time. There A friend brought this book to me and asked me to read it and then to help him incorporate the protocol into his life to fend off mild cognitive impairment symptoms. There are a few drugs that help a little bit, but unfortunately, this type of one drug solution so common in medicine won't work because there are dozens of potential causes of the disease. He has identified 36 causes and that list is growing. He compares the causes to holes in the roof that need to be patched. Patching one or two holes won't do the trick. The three main categories of the causes of the disease are: Inflammation caused by a multitude of different factors including unhealthy foods, drug interactions, and many others. This inflammation triggers the immune system that can then cause an unhealthy brain environment. Metabolic issues, also caused by a multitude of factors, insulin resistance, lack of the vitamins needed to properly break down foods, unhealthy foods, lack of exercise, daylight, etc. Sometimes there are toxins that can cause serious problems such as mold and a list of others such as lead poisoning, etc. I have merely touched the surface of each category and the various components of each. Many of the holes are fairly simple to identify, low levels of certain vitamins, high A1C levels, high homocysteine level, BMI over 30, low testerone levels, low cholesterol levels surprised at that one , and many more. These can be identified with blood labs. There are also or toxin tests, pet scans, genetic testing and many more that will probably require help from a doctor. It seems to me that this book is excellent for anyone over the age of 45 to read and then to incorporate as much as possible into a healthier lifestyle and prevention, even if you show no signs of cognitive issues. I am excited to get my own blood labs done. I especially enjoyed reading about the many patients who started Recoding and then sometimes reversed the disease and stopped the progression in its tracks. I'm also planning to watch several YouTube videos that have been posted by the doctor himself and other doctors who are implementing the work into their practices. View all 13 comments. Jun 19, Maureen Smith rated it it was amazing. This is one of the most important books I have ever read; and I will read it over and over again in between loaning it out to others. It seems we all know someone who has been diagnosed with Alzheimer's Disease, so this should be a must-read for anyone who doesn't want to accept the current death sentence usually associated with it. This was an advanced reader's copy, and I expected to find many editing mistakes, but I was pleasantly surprised to find an extremely well written and edited book. I think it would be easy to understand for the average lay person, yet is not boring for someone with medical knowledge. Bredesen has been studying and documenting his amazing life work, that is no longer a theory; people have reversed their Alzheimer's Disease by changing their lifestyles. I already have a list of people who want to read my copy. I wish every medical person I know, every hospital and nursing home dietician, everyone who has a relative with Alzheimer's, and everyone over forty who cares about maintaining their optimal cognitive ability, would read this book. View 2 comments. Dec 13, Doris Jean rated it really liked it Shelves: As I read the book, I thought it read as though two authors were collaborating, then at the end he thanked his team of three editor-writers and I think that this team did not work closely enough since the writing was choppy and inconsistent. For example, one section said 50 mg. There were many diagrams and charts and some toward the beginning of the book were so confusing that they were incomprehensible. There were several parts in need of editing for clarity. Chapter 1 addresses metabolic imbalance of 36 factors affecting AD. Chapter 2 says that the plaques and tangles of AD are a defense for the brain against the factor imbalance. Chapter 3 relates symptoms of AD as recalled by patients who have improved enough to tell how they felt before they improved. Chapter 4 was how to give yourself AD — I would have omitted this chapter completely. Chapter 5 had diagrams of the neuron with plaques and tangles and explained "dependence receptors" and APP amyloid precursor protein. He explained that APP is a "dependence receptor" poor diagram, poor explanation which can be enzymatically cut into either two or four pieces. The two-piece cuts are healthy, the four-piece cuts are Alzheimer's. APP is a prion and with beta-amyloid one gets a self-replicating prionic loop cascade — and Alzheimer's. Chapter 5 was a good chapter. Chapter 6 was unclear, he is trying to define AD into four types: Chapter 7 talked of factors, supplements, advanced glycation end-products AGE's - from sugar! Chapter Eight is entitled "Reversing Cognitive Decline" - ReCode seems to be to take vitamin B 6,9, and 12 and trimethylglycine and avoid meat, nuts and beans which give the amino acid methionine which yields homocysteine which is inflammatory. This does not convince me. Next, he has "DESS" which is diet, exercise, sleep and lack of stress. The "12" part means that one waits at least twelve hours after the last meal of one day to eat breakfast the following day to help the body into the fat-burning stage of ketosis. I have been reading many of the newer books on health and it seems that epigenetics is gaining respect. Many now encourage using food in a ketogenic diet to influence genes to improve health. A ketogenic diet will lower insulin which is being identified as an enemy of longevity because it shortens telomeres. This author also explains that insulin is needed in the brain to clear out sugar but there is an insulin-clearing enzyme IDE which is also needed to clear out the beta-amyloid plaques and the insulin will always get the enzyme before clearing the plaques. So high sugar means high insulin which means no enzyme left to clear out the plaques, it will all be used up on the sugar. He demonizes gluten, but I think it's not the gluten that is a problem — it's the glyphosate RoundUp which is genetically inside the grain cell and sprayed on the outside of grains to dehydrate for a fast harvest. Glyphosate causes holes in body membranes leaky gut and leaky blood-brain barrier and molecules leak through these holes and go into places where they do not belong and cause inflammation and metabolic imbalances. He seems to be a vegetarian, he never recommends eating meat or butter. I do not think he means to recommend farmed fish which are not fit for food, they are fed poorly and dyed and genetically manipulated. He didn't say how to restore synapses specifically. Chapter 11 is crutches for cravings: So eat protein for glutamine and animal fat butter, etc. Chapter 12 gave brands of supplements and websites. Appendix A gave more websites. Rachna Patel. Cook to Thrive. Natalie Coughlin. Michele Lent Hirsch. The Hormone Fix. Everyday Yoga Meditation. Stephen Sturgess. Recipes for Your Perfectly Imperfect Life. Kimberly Snyder, C. Katherine Harmon Courage. The Essential Oils Hormone Solution. Mariza Snyder. Lesley Regan and Joe Leigh Simpson. Related Articles. Looking for More Great Reads? Download our Spring Fiction Sampler Now. Download Hi Res. LitFlash The eBooks you want at the lowest prices. Read it Forward Read it first. Pass it on! Detailed C. The End of Alzheimer's In this paradigm shifting book, Dr. View More. Get In Touch We would love to hear from you. There are many new instances and, of course, we have the follow-up to that. What we published was system 1. We now have system 2. As physicians, we have been hampered over the years by having to deal with very small data sets. We are dealing with extremely complicated organisms and yet we have very small data sets, such as what the sodium is or what the potassium is. In the field of oncology, the current excitement is in doing whole-genome analysis for the tumor and whole-genome analysis for the patient and comparing those to infer from that what the drivers are for the actual tumor. This is what has been referred to as 21st-century medicine. We are looking at a large number of metabolic components and, of course, we also encourage people to get genome sequencing. Then we can infer from all those data what the most likely pathways are that contribute to this ongoing downsizing that is occurring in your brain. As you mentioned, this is fairly complex and there are many variables, as well as many therapeutic targets in the system. Is the result a protocol that is difficult for patients to adhere to? And as such, does it have to be followed to the letter? This is a really important point. First of all, this is a different way to do medicine. Instead of therapeutics, this is programmatics. I believe that is the future of the treatment of chronic illness: Second, this is going to be personalized. This is going to be a program for you based on what is driving your particular problem. Third, of course, now that we are seeing results, we are looking at how we can make this simpler. You have to remember, at the beginning, we did not know what was going to make people better and these were people dying of an untreatable terminal illness. Well no, it is not a shotgun approach, but it is not a silver bullet approach. It is silver buckshot instead of silver bullets. We want to hit everything that is contributing to your illness if we are going to have hopes of getting it to stop and then reverse itself. We are now working with health coaches who can help to make sure you do all the different parts of the program, because as you alluded to, it can be somewhat complicated. It needs to be complicated enough to address the underlying pathogenesis, but if it is so complicated that no one can do it, then of course it is not going to be very practically beneficial. One positive note here: When you go back to the molecular details and you look at how this plasticity system actually works, what you find is that there are prionic loops. In other words, when you start going down one side or the other, it is like a snowball rolling downhill..

There have been about 70 people who have come through now. For example, I just got a call this morning from a man who started a year ago and had a hippocampal volume, before he started the program, quantified at less than the Dale bredesen book percentile.

It is now greater than the 75th Dale bredesen book. Asian with southern accent porn.

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