Systemic Alzheimer's Prevention and Treatment: A Success Story

A Refutation of the Criticism of My Alzheimer's Findings

Recently, my Wikipedia profile[1] reads, among other things:

„The German biochemist Christian Haass criticized Nehls' statements on Alzheimer's disease for the Alzheimer-Gesellschaft München (Munich Alzheimer Society) in 2015 as misleading and harmful for those affected. Behavior and preventive measures did have an influence on the onset and progression of the disease. In principle, however, Alzheimer's disease cannot be prevented in this way. “Preventing Alzheimer’s disease simply through a correct lifestyle” is “too nice a pipe dream” and “does not do justice to the 1.2 million people affected in Germany.” Such claims are “well suited for pseudo-scientific treatises, but they are... [sic!] On closer inspection, it only serves the author’s vanity.”[2]

But first, let's take a closer look at Christian Haass' review of my 2014 book The Alzheimer Lie (currently only available in German), which he wrote for the Alzheimer Society Munich in 2015. It is striking that the very first lines give the false impression that I would describe Alzheimer's disease itself as a lie, or claim that Alzheimer's disease does not exist as a disease:

„Well, is Alzheimer's a lie? If you look at the number of patients, 1.4 million people in Germany alone, it's hard to call it a lie.“[2, translation by me]

However, this is obviously not the case (see also my article Unified theory of Alzheimer’s disease (UTAD): implications for prevention and curative therapy[3] or the list of ATnN therapists that has been growing steadily for years) and so the question arises why Haass is constructing this straw man argument here and whom he thinks he can convince with it. It is clear from the subtitle of my book that I am convinced that Alzheimer's is a real but "preventable disease" - I also emphasize this in my article "The key to the Alzheimer's puzzle".

The Alzheimer's deception thus involves claiming that the disease is supposedly inevitable or that age is the primary cause, even when there is clear scientific evidence to the contrary, showing that prevention is possible. This has serious implications, making Haass's attempt to deflect his own culpability by projecting onto me the accusation that I would be doing a disservice to the '1.2 million people affected in Germany' by offering them scientifically grounded prospects for prevention and cure seem like sheer mockery.

Alzheimer's Therapists Network (ATnN)

By claiming that age is the cause, and not just the condition, of the full development of severe symptoms of slowly progressive and long compensable neuronal decline, the false impression is created that correcting lifestyle factors that favor Alzheimer's has no significant impact on avoiding the disease. As a result, many people develop Alzheimer's who could have avoided it: Instead of encouraging people to lead healthier lifestyles, the disproven thesis of an age-related disease suggests that only pharmaceutical research and its drugs can save people from Alzheimer's.

In an article published in the Süddeutsche Zeitung on December 13, 2015, Haass raises hopes for a vaccination against Alzheimer's.[5] The intention behind this is to create a de facto autoimmune reaction of the immune system against a protein produced naturally in the body, the so-called β-amyloid, which we actually need to memorize (I will go into this in more detail later). At the same time, the article mocks all efforts to ensure a healthy brain through a healthier lifestyle, quoting Dennis Selkoe, pharmaceutical consultant on Alzheimer's, when asked how to protect against Alzheimer's, with the words:

"Choose the right parents and die early."

In other words, there is nothing you can do except hope for a pharmaceutical miracle cure. One thing is certain: by doing nothing, you are ensuring that one day, when it is too late, you will actually need such a miracle cure - a perfidious reassurance tactic that over the years narrows the natural scope of action.

For those who still believe this to be true, I recommend reading my peer-reviewed scientific article Unified theory of Alzheimer’s disease (UTAD): implications for prevention and curative therapy.[6], which provides a comprehensive and robust argument for why a variety of brain-damaging lifestyle factors over an extended period of time (age as a condition, not a cause) lead to the development of Alzheimer's disease.

Evidence for my thesis

My findings have also been confirmed in many clinical studies since 2016. For example, a large US study in 2022 concluded: "Our findings support significant benefits of healthy lifestyles for ADRD [Alzheimer's disease and related dementias] prevention among socioeconomically disadvantaged Americans, suggesting that promoting healthy lifestyles and reducing barriers to lifestyle changes are crucial [...]. "[7] Another cohort study from the same year confirms: "A healthy lifestyle was associated with a longer life expectancy among men and women, and with a larger proportion of remaining years lived without Alzheimer’s dementia."[8] By 2020, an analysis of two longitudinal studies concluded that if only 4 to 5 Alzheimer's-causing lifestyle factors (for a large number of others, see my UTAD-article) are taken into account, a 60 percent reduction in the risk of developing Alzheimer's disease can be achieved.[9]

If almost all causal (lifestyle) risk factors are corrected, the Alzheimer's process can even be reversed in the early stages of the disease, as Dale E. Bredesen and many other Alzheimer's experts proved in 100 case studies by 2018.[10] This result was impressively confirmed by a controlled clinical trial in 2022.[11] In 2023, Bredesen et al. again presented their rationale for a multifactorial approach in detail, impressively supporting my thesis of a multicausal preventive and therapeutic approach published in 2016.[12] The reader should be aware of the following: If an already incipient disease can not only be stopped, but the disease process can even be reversed by eliminating all the lifestyle factors that cause the disease, then prevention by the same lifestyle changes of a (still) healthy person is as good as guaranteed. This not only refutes Haass' and Selkoe's statements, but also leads to the question of how many people have developed Alzheimer's in recent years despite these findings, simply because the mainstream media exclusively courted such "Alzheimer's experts" who are suspected of being used as mouthpieces for an unscrupulous, profit-driven industry.

Conversely, however, these results also mean that a preventive or therapeutic approach to a multi-causal disease that is based on only one factor (such as a vaccination against an endogenous protein like β-amyloid, as propagated by Haass and Co.) must be doomed to failure a priori. I have explained this in detail in my 2016 scientific UTAD article. While I can understand the desire to identify a single cause for a problem and address it with modern precision (and of course economic interest), such simplifications obviously do not do justice to the reality that our modern science must reflect as comprehensively as possible. Of course, this also applies to Haass' emphasis on a single factor, the so-called amyloid thesis, on which a large part of the very profitable pharmaceutical research is based. Compare the criticism of Christian Haass: "... but each of us has the predisposition to develop this disease, because each of us produces the toxic [β-]amyloid that triggers Alzheimer's, and does so throughout our lives." This is convenient in the way it is described, but it is fundamentally and demonstrably wrong.

Unscrupulous Pharmaceutical Interests and Falsified Studies - Another Chapter in the Crime Story of Medical History

In fact, β-amyloid is not toxic at all, but as a monomeric endogenous protein is even indispensable for memory formation, as gene knockouts (the targeted switching off of certain genes and corresponding endogenous processes) in mice have already shown in 2007.[13] Here again, the reality is more complex than some "experts" would like to admit: β-amyloid as an oligomer (which can form from the monomer in the case of an unhealthy lifestyle, as I explain in detail in my UTAD article) is possibly a concomitant risk factor for the development of Alzheimer's, which is also attributable to lifestyle factors.

In fact, it has already been shown that the entire β-amyloid thesis is based on a large number of falsified studies from 2006 and the following years, as reported by none other than the prestigious scientific journal Science in 2022.[14] E. Bredesen and colleagues can stop or even reverse the disease process in Alzheimer's patients in the early stages of the disease on the basis of a multi-causal, systemic approach, as I called for in 2016 (see also my article The Key to the Alzheimer's Puzzle).

It puzzles me why scientists such as Christian Haass and his colleagues remain unimpressed by alternative approaches, despite their mono-therapeutic β-amyloid hypothesis having yet to significantly halt, much less reverse, the Alzheimer's process—a feat achievable through a species-appropriate lifestyle, as discussed earlier. As the German newspaper Frankfurter Rundschau wrote about the falsification of the β-amyloid thesis in August 2022, this "scientific scandal could now set research back considerably and make a number of approaches, including the development of new drugs, obsolete."[15] Instead of hoping for future drugs or constantly holding out the prospect of them, the general public would be better served by advising them to adopt a healthier lifestyle. This, however, would go against economic interests.

Interest-driven scholarship and research

But there is another point of criticism on my Wikipedia page that I do not want to withhold from you, as it is not without a certain humor:

„In 2021, the bioethiciane Silke Schicktanz described Nehls as a “popular science author”, whose content is more or less ignored by the scientific mainstream, with his focus on prediction and preventing dementia (as opposed to curing it) is illustrative of the contemporary discourse in Germany on the topic.“[16]

As described, I have successfully subjected my multi-causality thesis on the development of Alzheimer's disease to a scientific peer review process. The accusation that my work is pure "popular science" is therefore also far-fetched. So far, my UTAD article has been cited 23 times in other scientific papers (as of November 12, 2023). Whether this is a lot or a little is a matter of judgement. I would certainly be happy if it got even more attention. There are probably several reasons why this has not been the case so far:

1) Alzheimer's research, which is largely funded by pharmaceutical companies and therefore driven by their interests, is challenged by my multi-causality thesis. Therefore, my work cannot be cited to produce results that ensure future funding of studies by the pharmaceutical industry.

2) Only in July 2022 did it become generally known that the monocausal β-amyloid theory is based on fraudulent research results (see above).

Since the multi-causality theory of the development of Alzheimer's by Bredesen et al. and myself is so far the only theory on the basis of which the Alzheimer's process can be demonstrably prevented and even stopped and reversed in the early stages, it would be ethical to disseminate these findings. Anyone who opposes this with untenable claims, as I have discussed here, not only makes a fool of himself, but also lacks credibility, because he is recklessly gambling with the lives and suffering of countless people. After all, the goal should be to protect human life - and in the absence of support from the "mainstream media" (see the above quote from bioethicist Silke Schicktanz), this can be achieved by addressing those very people in a "popular-scientific" way, but with well-sourced essays and books.

Sources:

[1] https://en.wikipedia.org/wiki/Michael_Nehls (last accessed on February 22, 2024)

[2] „Ist Alzheimer eine Lüge? Eine Stellungnahme“ – Alzheimer Gesellschaft München e.V., accessed on November 13, 2023)

[3] Michael Nehls: Unified theory of Alzheimer’s disease (UTAD): implications for prevention and curative therapy. In: Journal of Molecular Psychiatry. Juli 15, 2016, doi:10.1186/s40303-016-0018-8.

[4] https://michaelnehls.substack.com/p/the-key-to-the-alzheimers-puzzle(last accessed on February 22, 2024)

[5] Stephan Handel: Volkskrankheit Demenz: Allianz gegen das Vergessen. (December 13, 2015, last accessed on February 22, 2024)

[6] Michael Nehls: Unified theory of Alzheimer’s disease (UTAD): implications for prevention and curative therapy. In: Journal of Molecular Psychiatry. 15. Juli 2016, doi:10.1186/s40303-016-0018-8.

[7] Jae Jeong Yang, Laura M Keohane, Xiong-Fei Pan, Ruiqi Qu, Xiao-Ou Shu, Loren Lipworth, Kyle Braun, Mark D Steinwandel, Qi Dai, Martha Shrubsole, Wei Zheng, William J Blot, Danxia Yu. Association of Healthy Lifestyles With Risk of Alzheimer Disease and Related Dementias in Low-Income Black and White Americans. In: Neurology. Vol. 99, Aug 30, 2022, p. e944-e953. doi: 10.1212/WNL.0000000000200774.

[8] Klodian Dhana, Oscar H Franco, Ethan M Ritz, Christopher N Ford, Pankaja Desai, Kristin R Krueger, Thomas M Holland, Anisa Dhana, Xiaoran Liu, Neelum T Aggarwal, Denis A Evans, Kumar B Rajan. Healthy lifestyle and life expectancy with and without Alzheimer’s dementia: population based cohort study. In: BMJ. Apr 13, 2022, doi: 10.1136/bmj-2021-068390

[9] Klodian Dhana, Denis A Evans, Kumar B Rajan, David A Bennett, Martha C Morris. Healthy lifestyle and the risk of Alzheimer dementia: Findings from 2 longitudinal studies. In: Neurology. Jul 28, 2020, Vol. 9, p.: e374-e383. doi: 10.1212/WNL.0000000000009816

[10] Dale Bredesen, Kenneth Sharlin, David Jenkins, Miki Okuno, Wes Youngberg, Sharon Cohen, Anne Stefani, Ronald Brown, Seth Conger, Craig Tanio, Ann Hathaway, Mikhail Kogan, David, Hagedorn, Edwin Amos, Amylee Amos, Nathaniel Bergman, Carol Diamond, Jean Lawrence, Ilene Rusk, Mary Braud. Reversal of Cognitive Decline: 100 Patients. In: Journal of Alzheimer’s Disease & Parkinsonism. 2018, doi: 10.4172/2161-0460.1000450.

[11] Kat Toups, Ann Hathaway, Deborah Gordon, Henrianna Chung, Cyrus Raji, Alan Boyd, Benjamin D. Hill, Sharon Hausman-Cohen, Mouna Attarha, Won Jong Chwa, Michael Jarrett, and Dale E. Bredesen. Precision Medicine Approach to Alzheimer’s Disease: Successful Pilot Project. In: J Alzheimers Dis. 2022 Vol. 88, p: 1411-1421, doi: 10.3233/JAD-215707.

[12] Rammohan V. Rao, Kaavya G. Subramaniam, Julie Gregory, Aida L. Bredesen, Christine Coward, Sho Okada, Lance Kelly, and Dale E. Bredesen. Rationale for a Multi-Factorial Approach for the Reversal of Cognitive Decline in Alzheimer’s Disease and MCI: A Review. In: Int J Mol Sci. 14. Jan 2023, doi: 10.3390/ijms24021659.

[13] Yann Senechal, Peter H Kelly, Kumlesh K Dev. Amyloid precursor protein knockout mice show age-dependent deficits in passive avoidance learning. In: Behav Brain Res. Jan 10, 2008, Vol. 186, p: 126-132. doi: 10.1016/j.bbr.2007.08.003.

[14] Charles Piller. Research backing experimental Alzheimer’s drug was first target of suspicion. In: Science. Jul 22, 2022, doi: 10.1126/science.ade0350.; see also: https://www.science.org/content/article/potential-fabrication-research-images-threatens-key-theory-alzheimers-disease

[15] Pamela Dörhöfer. Waren wichtige Studien zu Alzheimer gefälscht? In: Frankfurter Rundschau. August 1, 2022

[16] Silke Schicktanz: If Dementia Prevention Is the Answer, What Was the Question? In: Annette Leibing, Silke Schicktanz (Hrsg.): Preventing Dementia? Critical Perspectives on a New Paradigm of Preparing for Old Age. 2021, p. 65–66