interview with dale bredesen protocol alzheimers prevention

Does the Bredesen Protocol Work? Dr. Dale Bredesen on Alzheimer’s Prevention

By The Editors | July 21st, 2023

Being Patient sat down with Dr. Dale Bredesen in 2019. Since, credibility questions about Bredesen's protocols and research have come to light.* This Q&A is updated with our editorial staff's disclaimers and corrections.

About 44 million people are living with Alzheimer’s or another form of dementia. According to Dr. Dale Bredesen, the key to preventing Alzheimer’s is to look at each person as an individual and determine what lifestyle changes or treatments for conditions that may lead to Alzheimer’s could benefit them by reducing inflammation in the brain and preventing Alzheimer’s from progressing.

He is known for his “Bredesen Protocol,” an unproven, “intensive, costly regimen of dietary supplements” and other dietary and lifestyle-related measures Bredesen says improve cognition and reverse cognitive decline associated with early Alzheimer’s disease.

EDITOR’S NOTE ABOUT THE BREDESEN PROTOCOL: Trusted Alzheimer’s research experts have called Bredesen’s study metholodologies and findings into question, and it’s important to know that in addition to being expensive, experts say that, generally, brain health supplements — none of which have been evaluated by the Food and Drug Administration and which are sold without regulation — can be not only useless, but harmful.

Dr. Dale Bredesen is known for his beliefs that lifestyle changes and expensive supplements can modify the course of a person’s Alzheimer’s disease. While a large body of credible, peer-reviewed research links certain lifestyle-related factors to a reduction in Alzheimer’s risk on a population-wide scale, science is a practice of consensus, and many of Bredesen’s specific beliefs do not have a scientific consensus to support them: Bredesen’s claims are unproven.  

In 2019, Being Patient spoke to Bredesen about whether researchers know what’s actually causing Alzheimer’s, what future Alzheimer’s treatments may look like and how people who are worried they may develop Alzheimer’s or are in the early stages of the disease may be able to prevent Alzheimer’s or slow its progression. Since, credibility questions about Bredesen’s protocols and research have come to light. This Q&A is updated with our editorial staff’s disclaimers and corrections.

What Does The End of Alzheimer’s Mean?

Being Patient: Your book is called The End of Alzheimer’s. That’s quite a bold statement to make. What exactly do you mean when you say “the end of Alzheimer’s?”

Dr. Dale Bredesen: Let me first clarify, that is a title that came from the publisher, not from me. The book I wrote was called Wit’s End and that title reflected researchers being at our wits’ end trying to figure out what’s going on with Alzheimer’s, as well as what’s happening to your brain when you have Alzheimer’s.

My wife, Dr. Aida Lasheen Bredesen came up with that title, so I thanked her and said, “I love that title, I’m going to submit that.” I also submitted ten others. They were all declined and it became The End of Alzheimer’s. Having said that, I understand why they used that title. The reality is that Alzheimer’s, which is now the third leading cause of death in the United States, as Dr. Kristine Yaffe and her team pointed out a few years ago with epidemiological studies, should be a rare disease. Unfortunately, people haven’t picked up on that yet. Prevention and early reversal are the keys and we really could make this a rare disease. This should be a past scourge, just as polio, TB and leprosy are.

EDITOR’S CORRECTION: We took a closer look at the study Bredesen referenced here and found that it does not show that Alzheimer’s should be a rare disease. Instead, it goes through seven different modifiable risk factors and estimates that a 10 percent reduction in these factors (diabetes, midlife hypertension, midlife obesity, smoking, depression, cognitive inactivity or low educational attainment, and physical activity) would prevent 8.3 percent of Alzheimer’s cases.

Being Patient: Do researchers know what is actually causing Alzheimer’s disease since that’s being debated?

Dr. Dale Bredesen: Some experts will tell you that we don’t know the cause of Alzheimer’s. That’s an interesting statement because it’s a singular statement: “the cause.” Who said it’s going to be one cause? And I think that this is where there’s a big and fundamental point being missed.

Alzheimer’s is one of the complex, chronic illnesses. One hundred years ago, most of us died of simple illnesses like pneumococcal pneumonia and TB. Of course, the great success of twentieth century medicine was developing appropriate public health measures and appropriate antibiotics so we could effectively treat those simple diseases. However, in the twenty-first century, the vast majority of us are dying from complex chronic illnesses such as cardiovascular disease, Type 2 diabetes, Alzheimer’s disease, other neurodegenerative conditions and cancer. These are all multifactorial diseases. That’s a fundamental difference.

When people have gone after Alzheimer’s in the same way they went after pneumococcal pneumonia, looking at “one drug, one drug, one drug,” as well as “the cause, the cause,” that’s like using a checkers strategy for a chess match. It doesn’t work and we’ve proven that with billions and billions of dollars in pharmaceutical trials for Alzheimer’s drugs. It’s not the same kind of disease. It’s not that there is one cause of Alzheimer’s, at least as far as we know today. What we see is that there are dozens of contributors: insulin resistance is an important contributor, specific oral bacteria such as P.gingivalis enter the brain and they are important contributors. Specific molds and their toxins are important contributors. Specific viruses like herpes-simplex 1, HIV, HHV6-A and others are important contributors. The idea that you’re searching for the one cause is a misunderstanding.

We spent 30 years in laboratory research looking at what actually drives the process of neurodegeneration and when you look at that, what you see is many different causes. We tell people, “Imagine you have a roof with 36 holes in it.” A drug is a really good patch for one hole, but you’re now going to want to use that drug on the backbone of other things. Lifestyle is one of those, but it’s far more than that. All we are saying is something very simple: We must target what is causing the problem in each individual. It’s no surprise that it’s a little different in each person. In one person, it may be specific inflammatory processes from a leaky gut.

When we evaluate this in people, we’ve never seen a single person in which there were fewer than ten contributors who had cognitive decline. We want to look early and identify all the different things. There are pathogens and we could talk about those. There are specific toxins. We can talk about those. There are specific changes in metabolism. We can talk about those. Of course, there are genetic changes. Everyone’s a little different genetically. You have to look at all these different things. So far at least, the best outcomes have been with targeting those things that are actually causing the decline.

EDITOR’S NOTE: There is no actual, medical condition called “leaky gut.” Bredesen’s answer here also suggests that multiple contributing factors are substantial causes for cognitive decline. While multiple modifiable risk factors, enumerated in the correction note above, have been found to influence the course of Alzheimer’s disease, it is not accurate to say that they are definitive causes, as these are not proven — nor is it accurate to say that targeting them will stop the cognitive decline. Researchers agree that these factors may only be responsible for about one third of Alzheimer’s cases.

How should researchers look at Alzheimer’s disease?

Being Patient: What do you think of the hypothesis that Alzheimer’s will be treated a lot like HIV, where it’s not just one magic pill, but many things that you’re treating at one time? Is that a good way to describe it?

Dr. Dale Bredesen: Yes, but remember that HIV is actually quite simple. It’s just one virus. But even with that, you needed three drugs to have a big impact. Imagine HIV times ten. We’re looking at various things that actually contribute to this problem. Ultimately, Alzheimer’s disease is a protective response of your brain to numerous insults. If we’re going to treat it and prevent it most effectively, we’re going to have to determine for each person, what are the insults that it’s protecting itself from? Then we need to look at what needs to be rebuilt that we’ve lost so far. That’s the approach we’ve taken and we’ve published unprecedented improvements with that approach.

Being Patient: In your book, you mention four things that contribute to the production of amyloid in the brain. Can you describe what contributes to that production and how we can stop the dangerous part of that process to our brains?

Dr. Dale Bredesen: In the book, we said that there are actually subtypes of Alzheimer’s. We see some people in which the predominant cause or contributor is inflammation. Then you have to find out from what? Oral bacteria, chronic viral infections and various molds or fungi may cause this. It may be from a poor American diet. All of these things are associated with chronic inflammation. You can literally trace the molecular pathways when you activate inflammation.

EDITOR’S NOTE: The link between oral bacteria and Alzheimer’s disease has not been definitively established. While there is an association between chronic infection and developing dementia later in life, any direct cause-and-effect in this relationship is not clear. Also of note: There is very little research on the relationship between fungi and Alzheimer’s. Establishing a definitive link between nutrition and Alzheimer’s is challenging, and there is no evidence that diet is linked to all Alzheimer’s cases. It is only linked to a small percentage of cases. And there are no foods that can stop or reverse dementia.

As a simple example, one of the things that gets activated is called NF-kappa B. It’s a transcription factor and this has effects on numerous genes, including the ones that produce amyloid. You can trace the pathway from inflammation to the production of amyloid. It’s turned out as you know that amyloid is turning out to be part of the innate immune system. It’s part of your response to an insult.

Being Patient: Is it correct to think that we need amyloid to a certain extent, but we just don’t want to reach a tipping point?

Dr. Dale Bredesen: Of course, we’ve always vilified amyloid and said, if we can just get rid of this “bad guy,” things will work. As you know, all of those trials have failed. With amyloid, it’s not that it’s good or bad — it’s both. It’s playing a role and yes, in a sense, as I said, it’s a response to an insult. You are essentially deciding, am I going to put my resources into growth and maintenance, which is what you do when you’re not being insulted, or am I going to put my resources into protection and defense? That’s of course what you’re doing when things are bad. In that sense, amyloid is a little bit like napalm. If someone’s coming across your borders and you’re trying to deal with them, you may use this, but in so doing, you are now living in a smaller country and downsizing. That’s what’s happening with this. It’s not that it’s good or bad. It’s a response.


Does the Bredesen Protocol work?

There isn’t strong evidence that the Bredesen protocol works. While there are a few published studies featuring the Bredesen protocol, the methods have been criticized by other researchers in the field. Dr. Joanna Helmuth, a neurologist at UCSF, pointed to problems with methods, incomplete information, undisclosed financial conflicts of interests and other potential issues in Lancet Neurology.

A group of Alzheimer’s experts argued in another paper that these types of protocols often overstate the evidence and fail to communicate weaknesses and uncertainties in their data: “Such unmeasured language may create false hope, cause financial harm, undermine informed consent, and frustrate the production of generalizable knowledge necessary to face the societal problems posed by this devastating disease,” they write.

These protocols also focus on using a variety of expensive diagnostic tests and supplements, which are not regulated by the FDA. Generally, experts say that many brain supplements can be not only useless, but harmful. Some don’t contain the ingredients they claim to and there isn’t strong evidence that any of these supplements help treat Alzheimer’s.

Can Alzheimer’s be reversed?

As of now, no, Alzheimer’s is not reversible. There are no known disease-modifying cures for Alzheimer’s disease. There is one FDA-approved disease-modifying drug so far that shows the potential to slow the disease by removing beta-amyloid from the brain. But to date, gold-standard research establishes that there is not yet a cure. In fact, scientists aren’t even sure what causes Alzheimer’s. Research is underway looking at everything from inflammation to viruses.

Can Alzheimer’s be prevented?

Worldwide, roughly 50 million people are currently living with dementia (including the leading cause of dementia, Alzheimer’s disease). That number is expected to more than triple within 30 years. Research shows that, on a population scale, as many as 40 percent of dementia cases may be preventable with certain, science-backed health and lifestyle modifications. Learn more about how to help prevent or delay dementia by addressing the disease’s leading lifestyle-based risk factors.

UPDATED 21 July 2023, 1:30 P.M. ET: This article was updated to give our readers the most accurate, science-backed information.

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Dale Bredesen

Dr. Dale Bredesen

Dr. Bredesen is a professor in the Department of Molecular and Medical Pharmacology, as well as the Founding President and CEO, Professor Emeritus at the Buck Institute for Research on Aging. He received his undergraduate degree from Caltech and his medical degree from Duke.  He served as Resident and Chief Resident in Neurology at UCSF, then was postdoctoral fellow in the laboratory of Nobel laureate Prof. Stanley Prusiner.  He was a faculty member at UCLA from 1989-1994, then was recruited by the Burnham Institute to direct the Program on Aging. In 1998 he became the Founding President and CEO of the Buck Institute for Research on Aging, and Adjunct Professor at UCSF; then in 2013 he returned to UCLA as the Director of the Easton Center for Alzheimer’s Disease Research.

The Bredesen Laboratory studies basic mechanisms underlying the neurodegenerative process, and the translation of this knowledge into effective therapeutics for Alzheimer’s disease and other neurodegenerative conditions, leading to the publication of over 220 research papers. He established the ADDN (Alzheimer’s Drug Development Network) with Dr. Varghese John in 2008, leading to the identification of new classes of therapeutics for Alzheimer’s disease.  He and his group developed a new approach to the treatment of Alzheimer’s disease, and this approach led to the discovery of subtypes of Alzheimer’s disease, followed by the first description of reversal of symptoms in patients with MCI and Alzheimer’s disease, with the ReCODE (reversal of cognitive decline) protocol, published in 2014, 2016, and 2018. His book, The End of Alzheimer’s, is a New York Times Bestseller.  

One thought on “Does the Bredesen Protocol Work? Dr. Dale Bredesen on Alzheimer’s Prevention

  1. In @2017 Dr Bredesen was interviewed on NBC Dr. Oz re the Protocol. At that time he indicated a test of the Protocol was underway at Cleveland Clinic and somewhere in Portland. Are those tests still underway? Are there any results available yet?

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