by Dr.Harald Wiesendanger– Klartext
What the leading media are hiding
No disease dreads people more than Alzheimer’s, the most common form of dementia: a gradual mental decline at the tragic end of which nothing is left of what makes a body a person. The neurodegeneration in the brain that causes it is considered incurable. But recent studies give hope. They illustrate the key role of the intestine: in the development of the disease and possibly also in its healing. Accordingly, those affected do not suffer an unchangeable, supposedly “age-related” fate – they pay for decades of nutritional sins and other unhealthy habits.
I was all the more horrified when one day shocking news made the rounds on our street: Mr. Jäger had crashed his car into a tree without breaking. Intentionally. He survived the apparent suicide attempt almost unharmed.
He had recently been diagnosed with Alzheimer’s. The onset of mental decline had driven him to despair. The unfortunate man wanted to spare himself and his beloved wife from progressing.
As soon as he was released from the hospital, Jäger tried to steer his replacement car into a river. The crash barrier of a bridge prevented it.
Weeks later, his third attempt finally brought him to his goal: walkers found him hanging in the woods.
No suffering terrifies people more.
More than any statistic or textbook, this tragedy made me unforgettable how horrible it must be to have to live with the certainty that you have Alzheimer’s disease: the most common form of dementia, accounting for around two-thirds of all cases.
People are not even more afraid of cancer than of slowly dissolving while they are alive – gradually losing everything that defines them: their memories, their ability to think, their language and motor skills, their emotional and social skills, their essential characteristics, finally her consciousness, her ego, her identity.
In the final stages, all that remains of what they once were is a pitiful shell, the appearance of which is painfully reminiscent of their former selves. The person who animated this cluster of cells has disappeared irretrievably. What’s left is a disoriented, incontinent idiot needing 24-hour care, a nightmare for loved ones.
In Germany, 1.7 million people suffer from dementia; by 2050, it should be three million. According to the World Alzheimer Report (1), 55 million people worldwide were affected by dementia in 2019; 139 million are prognosticated by mid-century. (2) Hundreds of millions of people with Alzheimer’s will be added.
The risk increases exorbitantly with age. Hardly more than 25,000 have not yet reached the age of 65. Two percent of 65-year-olds are affected. Among 70-year-olds, it is already three percent; among 75-year-olds six percent. One in five people under the age of 85 shows symptoms of the disease, and one in three under the age of 90. (3) From the time a doctor diagnoses Alzheimer’s dementia, there remains an average life expectancy of 1.5 to 8.5 years. (4) In the United States, one in three seniors is already dying of Alzheimer’s or some other forms of dementia – more than breast and prostate cancer combined.
Despite a tremendous amount of research, Alzheimer’s is still considered incurable. That’s what Mr. Jäger must have heard from his doctors: Don’t do anything; accept it. At best, isolated symptoms can be temporarily relieved and progression slowed down a little. Conventional doctors may have prescribed Mr. Jaeger acetylcholinesterase and nonsteroidal anti-inflammatory drugs such as ibuprofen; thiethylperazine and its derivatives; or memantine, an NMDA receptor antagonist that affects the neurotransmitter glutamate.
Others may have pointed out the benefits of brain teasers, occupational therapy, and psychotherapy. But can the underlying neurodegeneration be stopped? Or even undo it? Apparently, my neighbor couldn’t find anyone who could give him credible hope. It seemed to him that disaster was as inevitable as the Last Judgment.
Resigned too soon?
But maybe Hans Jäger gave up too soon. How much did he really know – about his illness, about chances of recovery, about ways to help yourself?
Proteins are the building blocks of our body, including the 86 billion nerve cells (5) that make up our brain. Mistakes in their structure can lead to chaos. Two types of abnormal protein deposits in the brain appear to be primarily involved in Alzheimer’s. Some form in the interstitium, the space between nerve cells.
Under the microscope, they are clearly visible as spots, or “plaques” in French. These deposits are composed of the abnormally folded protein fragment beta-amyloid. They are broken down in the healthy brain. In Alzheimer’s, on the other hand, they remain as rigid, indissoluble structures.
There are also strange tangles of fibrils: twisted fibers composed of tau proteins. This protein is an important component of transport structures within the nerve cells: the microtubules. These tiny tubes transport important nutrients, among other things. Tau proteins stabilize their outer shell like clamps.
In Alzheimer’s, they detach from it, bind to other tau molecules, and clump together to form fibrous bundles. They emerge from the cell body and attach themselves to the axons, the nerve cell extensions that transmit electrical impulses.
Both fatal protein accumulations, the “senile plaques” and the “clumps of tau,” block the transport system of the nerve cells and disrupt the communication between them. Gradually they die off.
No healthy brain without a healthy gut
How does this happen? It is becoming increasingly clear how the health of our brain is connected to the microbiome of our gut. Recent research suggests that gut bacteria can affect brain functions and even promote neurodegeneration.
A team of scientists from Switzerland and Italy has been investigating this connection for years. In their most recent study, they included 89 people between the ages of 65 and 85. (6) Some of them suffered from Alzheimer’s and other neurodegenerative diseases; the rest were mentally healthy and had no memory problems.
The researchers used PET imaging to detect amyloid deposits in their brains. In blood samples, they measured inflammatory markers and proteins produced by intestinal bacteria.
They found that large amyloid plaques in the brain were associated with high blood levels of lipopolysaccharides (LPS). LPS are cell walls of dead bacteria. However, the immune system treats them as active pathogens and initiates defensive measures against the supposed invaders. This is how LPS promotes inflammation. They are also found in amyloid plaques in the brains of Alzheimer’s patients.
In addition, short-chain fatty acids (SCFAs), namely acetate and valerate, were found in the blood samples of people affected by Alzheimer’s, as well as in their brain plaques. They also come from intestinal bacteria.
However, other short-chain fatty acids, namely butyrate, appeared to be protective. High butyrate levels were associated with less amyloid. Butyrate is produced by gut bacteria when they ferment fiber. In the brain, it activates the neurotrophic factor (BDNF) secretion, which stimulates nerve growth. In Alzheimer’s, its concentration is reduced.
“Our results are indisputable,” explains one of the scientists involved, Moira Marizzoni, from the Fatebenefratelli Center in Brescia: “Certain bacterial products of the gut microbiome correlate with the amount of amyloid plaques in the brain.”
With this, the team builds on earlier research, in which they found that the gut microbiota of people with and without Alzheimer’s differ significantly. In those affected, their diversity is severely limited; certain bacteria are overrepresented, and others are absent.
“In addition,” says neurologist Giovanni Frisoni, co-author and director of the Memory Center of the University Hospitals of Geneva (HUG) in Switzerland, “we have also discovered a link between an inflammatory phenomenon detected in the blood, certain gut bacteria, and Alzheimer’s disease. So we wanted to test the hypothesis: Could the inflammation in the blood be an intermediary between the Microbiota and the brain?”
Lessons from the Mouse Cage
Animal experiments confirm how closely a bacterial imbalance in the digestive tract is linked to Alzheimer’s disease. A 12-strong research group from Bern, Geneva, Lausanne, and Tübingen used breeding lines of mice that were specially developed for Alzheimer’s research: At an advanced age of twelve months, they form an Alzheimer’s-like disease, which also causes the typical amyloid deposits in the brain to appear.
As the scientists determined, these animals have a different intestinal flora than healthy conspecifics. What happens if you transfer intestinal bacteria from diseased animals to mice whose intestines have been sterilized beforehand? The microbe transfer means that plaques also form in the brains of those “vaccinated” in this way. (7)
The hope for a probiotic cocktail
As this suspicion grows, the team is planning further research to find out which specific bacteria or strains of bacteria could be responsible for the suspected effects. This could ultimately result in the formulation of a probiotic cocktail – with a neuroprotective effect at least at an early stage of the disease, even in presumed high-risk individuals long before any noticeable symptoms appear.
It has long been known that beneficial bacteria promote brain health in dementia patients. A 2016 study of 60 Alzheimer’s patients looked at how probiotic supplements affect cognitive function — with promising results. In those participants who drank milk containing probiotics, mental performance improved significantly – measured with the Mini-Mental State Examination (MMSE). In contrast, the MMSE score dropped in the control group that consumed regular milk.
What could account for the improvements seen? The researchers tap into several positive metabolic changes they found in the probiotic group, including lower triglycerides, very low-density lipoprotein, and C-reactive protein, a measure of inflammation, and lower markers of insulin resistance.
Walter Lukiw, a professor at Louisiana State University, explained to the online specialist service Medical News Today how closely the gut and brain are connected: The findings of the Italian-Swiss research group “are consistent with some of our recent studies, which suggest that that the composition of the microbiome of the gastrointestinal tract in Alzheimer’s is significantly altered compared to controls of the same age (…) and that both the gastrointestinal tract and the blood-brain barrier become significantly leakier with increasing age, so that microbial exudates”, i.e., secretions, “of the gastrointestinal tract – e.g., B. amyloids, lipopolysaccharides, endotoxins, and small non-coding RNAs – can get into the compartments of the central nervous system.” Biologists refer to a compartment as a reaction space within a cell that is delimited by membranes.
Probiotics can inhibit neurodegeneration.
Apparently, probiotics—preparations of living microorganisms, such as bifidobacteria and lactobacilli—influence the central nervous system and behavior via the microbiota-gut-brain axis. They could thus become a powerful weapon against Alzheimer’s both preventively and therapeutically by, among other things, modulating the inflammatory process and counteracting oxidative stress. (8th)
This was confirmed in a meta-analysis of five studies with 297 subjects. It turned out that cognitive abilities improved significantly in probiotic groups; malondialdehyde and highly sensitive C-reactive protein, two biomarkers for inflammatory processes and oxidative stress, also decreased significantly.
Further research will have to clarify which bacteria are most beneficial for preventing and treating Alzheimer’s. However, it is already becoming apparent that strain A1 of Bifidobacterium breve could be of particular use. In mice, the researchers confirmed that the cognitive dysfunctions usually triggered by amyloid beta are significantly reduced when the animals are given B. breve A1 orally daily. The intake appeared to suppress amyloid beta-induced changes in gene expression in the hippocampus. Hence the protective effect could come from. (9)
In spring 2018, the Japanese dairy company Morinaga Milk presented a new probiotic with Bifidobacterium breve A1. Study results appear to show that it improves spatial awareness, learning, and memory in mice with cognitive deficits. (10) Is this the future of Alzheimer’s prevention?
“We shouldn’t celebrate too soon,” says Giovanni Frisoni from Geneva University Hospital, dampening exaggerated expectations. “First, we need to identify the strains of the cocktail.” (11)
The “gut-brain axis”: what controls it?
In their search for the many factors and processes that are at work along the “gut-brain axis,” researchers are still poking around in the fog. But gradually, it clears up.
At Emory University in Atlanta, Georgia, a team led by Dr. Chun Chen in neurons from Alzheimer’s patients on a signaling pathway that may be one of the decisive factors. (12) The starting point is a transcription factor called C/EBPβ – a protein that binds to specific sections of DNA and regulates how much messenger RNA – mRNA – is made from it.
In doing so, it controls the expression of the gene so that the encoded proteins are produced in the right amount and at the right time. What does C/EBPβ do? It stimulates the production of asparagine endopeptidase (AEP) – an enzyme that promotes deposits typical of Alzheimer’s. A series of tests with mice confirmed that a changed intestinal flora under Alzheimer’s is accompanied by increased activity of the C/EBP/AEP signaling pathway.
Frida Fåk from Lund University suspects the solution to the riddle lies in the immune system. “90 percent of all its defense cells are located in the intestine. The processes there, therefore, influence immunological processes throughout the body, including in the brain.” (13). Metabolic products from the microbes could also trigger inflammatory processes there.
The Italian-Swiss team of scientists led by Moira Marizzoni assumes that the gut microbiome can contribute to the risk of Alzheimer’s in several other ways, including influencing blood sugar, sleep, and daily biorhythms.
In addition, the blood-brain barrier could be disrupted: a physiological barrier that usually prevents harmful substances and pathogens from entering the brain. Once there, they can trigger a neuroinflammatory reaction.
In fact, it has since been shown that this barrier is more permeable in Alzheimer’s patients than in healthy people. But how does this happen?
A microbiologist from the Keck School of Medicine in Los Angeles, Berislav Zlokovic, suspects a disorder of the pericytes: connective tissue cells surrounding the blood vessels like an insulating layer. (14) They shield the central nervous system from toxic influences. In mice whose pericyte function is disturbed due to a genetic defect, beta amyloids are increasingly deposited – the animals become demented. (15)
What does this disorder convey?
The blood-brain barrier forms relatively early in the womb – usually around day 17 of development in mice. After that, Viorica Braniste from the Karolinska Institute in Stockholm could no longer label the fetal brain with Raclopid, a drug used in PET scans to image specific receptors. However, if the dams were raised sterile during pregnancy, with no bacteria in their intestines, Raclopid continued to penetrate the brains of the fetuses. Braniste sees this as a clear indication that the animals did not have an intact blood-brain barrier. This disorder continued even after the animals were born if the litter was kept sterile. (16)
Further investigation revealed that the disorder was probably due to reduced production of the proteins occludin and claudin 5. These two proteins usually are part of the so-called tight junctions, which, among other things, hold endothelial cells together like a belt. These compounds are also found in the gut. Braniste suspects that it takes a stimulus during prenatal development to close the gaps in the gut and brain with tight junctions. It is still unclear which signals from the intestine play a role in this. For example, it could be short-chain fatty acids produced by intestinal bacteria and absorbed through the mucous membrane.
If these findings can be transferred to humans, they shed new light on the fatal consequences of using antibiotics during pregnancy and early childhood. Could they contribute to a permanent disruption of the blood-brain barrier, which then promotes the development of neurological diseases?
“From forgotten organ to the main player.”
In any case, “there is growing evidence that the gut microbiome interacts with Alzheimer’s pathogenesis by promoting neuroinflammation and disrupting metabolic homeostasis,” the researchers said -pathology developed.” (17)
In every fifth case, Alzheimer’s is accompanied by another form of dementia: vascular dementia, caused by circulatory disorders in the brain. There are also nutritional sins behind this, as well as an unhealthy lifestyle in general, which conjures up obesity, high blood pressure, diabetes, and other risk factors. (18)
The sensational recovery of an 85-year-old English woman, Sylvia Hatzer, recently suggested that Alzheimer’s can literally be eaten away. A radical change in diet and regular exercise and cognitive exercises apparently caused her spirit to reawaken. The British Alzheimer’s Society now recommends them as a role model for fellow sufferers. (See PLAIN TEXT “Eat away dementia?”.)
A global comparison is also encouraging. If seniors were to contract Alzheimer’s disease “age-related,” it would be about the same in all age groups – everywhere, increasing evenly with increasing life expectancy, whether in the USA, the Persian Gulf, or the Far East. In fact, however, there are enormous differences: the USA, Qatar, and the United Arab Emirates, among others, recorded exceptionally high growth rates; Japan (19), on the other hand, reports a remarkably low increase – despite one of the oldest populations in the world. Different dietary habits explain this, at least in part.
Multiple causes require more than one countermeasure.
Causal thinking, in one way, is always foolish, especially in medicine. On the one hand, the importance of the bacterial community that colonizes the surface of the intestinal mucosa can hardly be overestimated: not only for our digestion but also for our immune system, for the aging process, for the development of many diseases, from Parkinson’s (20) to psychiatric disorders to stress-related behavior (21), moods and feelings (22), autism (23) and multiple sclerosis (24) On the other hand, the recent hype about the gut slightly narrows the view; it tempts us to attribute too much solely or primarily to the condition of our digestive tract.
This, in turn, leads to hasty, one-sided measures. Despite the most comprehensive intestinal cleansing, the intestinal flora only improves in the short term as long as the diet is not changed consistently and over the long term. Some swear by probiotics (25) made from beneficial strains of bacteria; so-called prebiotics (26) with dietary fibers, which serve as food for intestinal bacteria, is also a hot tip. But both only work optimally (27) if the overall daily food intake is right:
- As little industrial sugar, table salt, and inferior fats as possible, no highly processed ready meals, no sweeteners, preservatives, and emulsifiers.
- Less meat, more plants, more organic.
- More pre-and probiotic foods.
- More fiber (28).
- Smaller meals, if possible freshly prepared, plenty of pure water.
Just eating differently is not enough, either. No disease has a single cause, and the same is true of Alzheimer’s. Accordingly, many influencing factors must be considered in diagnostics, prevention, and therapy. They range from inflammation, infection, and prions to risk factors such as vitamin deficiencies, cholesterol, trauma, diabetes, stress, and high blood pressure to exposure to smoking, alcohol, and drugs; pesticides and other environmental toxins, by chlorine and fluoride in tap water, by fine dust, aluminum, and heavy metals.
Couch potatoes are prone to dementia.
Esthete Jäger was a brain worker, a passionate couch potato. If I had known early on that he was threatened with Alzheimer’s, I could have recommended plenty of exercise to him. I would have told him about experiments at the University of Colorado in Boulder, where older lab rats were encouraged to use the exercise bike regularly. The daily fitness exercise activated her brain, particularly that area of the hippocampus involved in learning processes and memory. (29)
Medicines can cause dementia.
I should have looked in Hans Jäger’s medicine cabinet as well. It has long been known that several medicines limit mental performance; permanently used, they increase the risk of dementia considerably. These include hormone preparations, cholesterol-lowering drugs (statins) (30), acid blockers – so-called proton pump inhibitors (31) – and antibiotics.
Psychotropic drugs, which are routinely used in many old people’s homes and nursing homes, cause mass brain damage – scandalously often without medical indication to calm restless, confused seniors. In a 17-year study, antidepressants increased the risk of dementia by around 50 percent. (32) Benzodiazepines in particular — tried-and-tested anxiety suppressants, sedatives, and sleep inducers — doubled it. (33) Senile dementia is largely an iatrogenic phenomenon – caused by doctors willing to prescribe it.
Remedying mental decline pharmaceutically remains an unfulfilled promise. So far, no anti-dementia drug has come close to keeping what manufacturer-financed studies have given hope. The most recent example of this is the controversial Alzheimer’s drug aducanumab: With annual treatment costs of $100,000, it causes cerebral edema in one in three patients and cerebral hemorrhage in one in five. (34)
Restful sleep also protects
In addition, I would have taken more seriously what Hans Jäger once casually mentioned: he is a night owl, particularly productive well after midnight – out of necessity because he hardly gets any sleep at night.
Animal experiments by neurologists at Washington University in St. Louis suggest that sleep disorders put a strain on the brain and could cause long-term damage. Amyloid-beta accumulated in the brains of laboratory mice during prolonged sleep deprivation; at the same time, the rodents developed dementia-like symptoms. (35)
A study published in the specialist journal Neurology in 2019 (37) also gives an idea of how closely sleep hygiene and Alzheimer’s could be related (36): after a single sleepless night, the tau protein content in the blood plasma increases by 17% even in young adults. Previous studies have shown that sleep deprivation in older people leads to an increase in tau proteins in the cerebrospinal fluid. (38)
In 298 older women in the sleep laboratory, it was found that those suffering from sleep apnea – with at least 15 breathing interruptions per hour of sleep – were more likely to have memory gaps and other mild cognitive disorders; the likelihood of dementia increased. (39)
What could be the reason?
A microcirculatory system in the brain and spinal cord that was only discovered in 2012 is active almost exclusively during sleep: the glymphatic system. It serves as a waste disposal system for the central nervous system: it flushes out excessive and harmful material – around seven grams of potentially toxic protein waste and cellular scrap that could disrupt brain functions daily. (40) It also removes beta-amyloids and tau proteins from the intercellular space (41) – in mice during sleep twice as fast as in waking phases, and in other animals, even 95% more. (42) With increasing age, this drainage system becomes less and less effective. (43) In Alzheimer’s patients, as in all neurodegenerative diseases, it seems to be significantly disturbed. (44)
Animal experiments at the Baylor College of Medicine in Houston, Texas, suggest that sleep disorders not only accompany Alzheimer’s disease but also contribute to and exacerbate its development. (45) They concentrated on a specific region in the diencephalon (thalamus), the nucleus reticularis. Its task could be to shield the brain at night from external sensory impressions that prevent restful sleep. It is less active in Alzheimer’s mice. As a constant EEG derivation shows, this is associated with sleep disturbances: the animals woke up 50% more often than healthy conspecifics.
The glymphatic system is involved in this. During sleep, the spaces between the nerve cells expand to form a “drainage” through which deposits and metabolic products are discharged into the cerebrospinal fluid, a fluid-filled cavity in the brain.
On the other hand, the sleep quantity is similar to medicines: more does not necessarily mean more, and an overdose turns medicines into poisons. This was illustrated by a three-year study by the 12 de Octubre University Hospital in Madrid on 3,300 men and women over 65. Those participants who slept more than nine hours a night and during the day were twice as likely to have dementia as those who slept for seven hours.
More than five percent of the late risers during the study period developed dementia. In contrast, less than two percent of the 7-hour sleepers fell ill; in the case of the 8-hour sleepers, four percent were ultimately affected. Study leader Julian Benito-Leon regards daytime sleepiness in seniors, as well as an excessively increased need for sleep, as a serious early indicator of dementia. (46) Both could point to a deeper common cause, such as depression or drug effects.
Cognitive resilience: mentally fit despite Alzheimer’s
Wouldn’t it have been comforting for Hans Jäger to know that knowledge workers like him can significantly delay the progression of dementia? Anyone who has been intellectually active all their lives at work and in their free time can retain their cognitive abilities for a long time in old age, even if their brain suffers from Alzheimer’s disease.
Above all, I could have encouraged my neighbor with the famous “nun study”: a longitudinal study in which the epidemiologist David Snowdon from the University of Kentucky in Lexington included 678 American nuns between the ages of 75 and 106. From 1986 it ran for almost 15 years. The researcher used laboratory values, psychological parameters, and histological sections of the brain. Through the archives of the monasteries, he gained insights into the biographies of the participants and their intellectual activities decades ago.
Many had Alzheimer’s disease. What Snowdon found is all the more astounding: the pathological finding in the brain – multiple plaques – was independent of the repeatedly assessed intellectual performance of the person concerned during their lifetime. This means that even people whose autopsy revealed severely altered brain findings could carry out mentally demanding tasks until their death. (47)
Recently, US researchers attribute this phenomenon to the transcription factor MEF 2: another protein that binds to specific DNA sequences to control the expression of a particular gene. Its formation protects mice from dementia. It is also increasingly formed in the brains of mentally active people as they age. (48)
Epidemiological studies such as the “Religious Orders Study” (49) from 1994 or the “Memory and Aging Project” (50) from 1979 had already noticed that older people suffered from dementia less often if they had attended university as young people than worked in intellectually demanding jobs and, in retirement, trained their brains with stimulating activities such as reading or doing crossword puzzles.
What is this “cognitive resilience” based on?
A team led by Li-Huei Tsai from the Picower Institute for Learning and Memory in Cambridge/Massachusetts investigated how a mentally stimulating environment affects the brain in mice. While some animals were raised in empty cages, others were given a running wheel and toys that were changed every few days. Subsequent examinations of the brains revealed that the stimulating activities affected the epigenome. It determines which genes can be activated in a cell. The MEF2C gene was one of them in the stimulated mice.
MEF2, “Myocyte Enhancer Factor 2”, is a transcription factor that is not only involved in the embryonic growth of the heart muscle but is also involved in the development and function of nerve cells. The genes activated by MEF2 contain blueprints for ion channels in the cell membrane, which influence the excitability of a neuron and, thus, the nerve signals. In two biobanks that examined the brain cells of deceased people, the activity of MEF2 and the genes it controls correlated with cognitive resilience before death.
The researchers created “knockout mice” by eliminating individual genes from the genome. Without MEF2, the animals no longer benefited from the stimulating environment in their cage: they developed dementia just as quickly as the other animals.
In another experiment, the animals were genetically modified in such a way that they produced more of the tau protein. Usually, they quickly develop dementia. However, this prevented a second intervention, which led to an increased formation of MEF2.
This may result in new therapeutic approaches. Drugs that increase MEF2 activity may delay the development of dementia, even in people with no intellectual interests.
Fasting activates self-cleansing – also from Alzheimer’s plaques.
Biologists call the way in which the body disposes of biological waste and promotes the formation and reproduction of new, healthy cells “autophagy.” Fasting activates them. (51) This is a key reason why it is beneficial in neurodegenerative diseases such as Alzheimer’s to abstain from eating at daily intervals of at least 12, preferably 18 hours, or for a week or two.
According to the American doctor Dr. Steven R Gundry. “We have an amazing repair system that works when you fast,” Gundry said in a 2017 interview. “The intestine rests. It’s probably one of the smartest things any of us can do: let the gut wall rest, not have to absorb nutrients, and not have to deal with the constant influx of lectins or toxins. But I believe, more importantly, fasting gives the body a chance to finally do some serious brain cleaning. (…) Alzheimer’s and Parkinson’s have a common cause: the brain defends itself against a perceived threat. This also comes from LPS. If you quiet your bowels and don’t let LPS enter your system, and the longer you can keep that up, the better off you will be.”
Reverse Mental Decay?
How much a correspondingly complex approach can achieve is demonstrated by Dr. Dale Bredesen, Professor of Molecular and Medicinal Pharmacology at the University of California, Los Angeles School of Medicine, author of “The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline.” (More about Bredesen’s work in the KLARTEXT article “Neurologist proves: Alzheimer’s can be cured.”) Ensuring a healthy intestine is just one of many parameters that his ReCODE concept considers. It records and evaluates 150 factors that are known to contribute to Alzheimer’s disease.
In this way, he identifies the particular subtype of the disease – or a combination of subtypes – and creates a highly effective treatment protocol based on this. It includes fasting, avoiding gluten and processed foods, and reducing the intake of polyunsaturated fatty acids, too Called PUFAs, found in low-grade cooking oils and trans fats. A high-fat ketogenic diet, moderate protein, and low in carbohydrates, Bredesen believes it is ideal for preventing the degeneration that can lead to Alzheimer’s and contributes to a healthy gut. In addition, Bredesen focuses on better oral hygiene, vitamin D and B12, micronutrients, a balanced hormone level, detoxification, meditation, and more and better sleep.
Considering a total of 36 metabolic aspects that characterize a healthy lifestyle, Bredesen achieves impressive treatment results. Nine of the first ten patients who followed his ReCODE protocol made significant progress within three to six months. In isolated cases, the cognitive decline could not only be stopped or at least slowed down but even reversed. (52) Since then, similar results have been seen in hundreds of other patients.
In his sensational 2017 book The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline, Bredesen laid out a step-by-step program for preventing and curing Alzheimer’s for a broad audience of patients, caregivers, physicians, and treatment centers leaves.
The bottom line is simple: we can easily ensure that our brain stays healthy into old age: through a comprehensively healthy lifestyle. And that’s why we should always protest when we are told that “age” is a risk factor for everything and everything. A rhetorical trap is set to prevent us from taking control of our own health. “We cannot reduce our risk by changing our birth certificate;
That is why old age is not a risk factor that can be changed, but rather the inevitable consequence of continuing to live,” the Danish medical professor Peter C. Gøtzsche points out. “Those who insist on naming age as a risk factor should remember that birth is also a risk factor that will eventually lead to death with certainty.” (53)
But prevention is bad for business.
Providing medical care and nursing for a person with dementia currently costs payers an average of just under 21,000 euros per year, with a duration of the suffering of 1.5 to 8.5 years from diagnosis to the last breath – on average, five years – around 100,000 euros per person affected. (In the case of severe Alzheimer’s dementia, it is 45,000 euros per year.) (54) 34 billion euros in the Federal Republic alone in 2016. (55)
This amount will increase drastically – in Germany, by 2060, it is expected to reach 90 billion euros. (56) Because in a single individualized society, fewer relatives can and want to provide care, Paid professionals have to get involved earlier and more extensively. At the same time, diagnostics and therapeutics are becoming more and more complex and expensive.
Basic arithmetic is enough to discover what fabulous business these trends are opening up. If the number of people with dementia worldwide actually almost triples by 2050 to around 140 million (57), then they will ensure sales well in excess of the trillion mark.
From an economic point of view, healthy people are non-consumers who have yet to transform themselves from potential patients into actual patients. Anyone who wants to make money from Alzheimer’s – be it with diagnostics, drugs, therapies, or care services – cannot stand by and watchword of knowledge and successes like Bredesen’s spread.
He must prevent them from being included in medical training and further education, from finding their way into treatment guidelines from specialist societies, and from reaching an all too broad audience via the mass media. He must do everything in his power to ensure that as many people as possible continue to believe in the myth of “age-related” mental decline, which one can only wait and bravely endure until big pharma comes up with innovative drugs and vaccines.
Those who lack the patience and confidence to await such breakthroughs seem to have no choice but to see no one else – like the unfortunate Herr Jäger. I am sure that this man could still be alive fifteen years after his horrific end with a reasonably alert mind, which Japanese haikus would still not overwhelm. No unavoidable fate forced his final act of desperation with a rope in the forest.
But a hair-raising lack of information, deliberately created by those who profit from mass suffering, maintained by their lobbyists, favored by a chronically ill health care system that accumulates false financial incentives: instead of first and foremost rewarding those who support and restore health, it rewards most lavishly those who Managing loss of health is laborious – evidence-based, of course.
The parallels to the corona crisis are apparent. How many millions upon millions of people infected with SARS-CoV-2 could still be alive if they hadn’t let themselves be persuaded that they were “at the mercy” of a “new” killer virus as long as there were no vaccines? How many would have been spared severe illnesses, hospitalization, transfer to the intensive care unit, or premature rest in the grave if they had found out in good time what censored doctors and scientists, denigrated as “fake news” disseminators, were trying to point out from the beginning of the pandemic: that Covid-19 can be effectively prevented and treated at every stage using long-established, inexpensive medicines and dietary supplements? (See, e.g., here and here.)
For Covid, as well as for Alzheimer’s, cancer, diabetes, high blood pressure, cardiovascular diseases, and all other diseases of civilization applies: There is nothing to earn from healthy people. Neither of the dead. Those in between are interesting: the chronically ill. The more of them there are, the longer they remain, so the better for the sales of the healthcare industry, for the returns of their investors, for the fees of their academic tenants, and funding pots in the third-party brothel.
Opportunities for a cure are decided less in medical research facilities today than in the boardrooms of Big Pharma, Blackrock, and Vanguard. At least Hans Jäger no longer has an opportunity to become clear about it.
(Harald Wiesendanger)– Klartext
* pseudonym
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Remarks
2 DOI: 10.1016/S2468-2667(21)00249-8
3 Skript (Memento vom 21. September 2008 im Internet Archive) (PDF; 612 kB) der Sendung Quarks & Co zum Thema Alzheimer
4 https://www.stiftung-gesundheitswissen.de/wissen/alzheimer-demenz/hintergrund
5 https://www.helmholtz.de/newsroom/artikel/wie-viele-nervenzellen-hat-das-gehirn/
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