> Preclinical data have indicated that microorganisms associated with periodontal disease may contribute to the pathology of Alzheimer's disease.
I read damage to the nasal epithelium can allow pathogens to reach the brain:
"New research from Griffith University has shown that damage to the lining inside the nose increases the risk of bacteria sneaking into the brain via nerves, potentially causing long-term health issues." ... "Bacteria and viruses, and resultant neuroinflammation, may even contribute to neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases"
Although rare, amoebas found in untreated water can cause fatal brain infections if they get in your nasal passage[0], via neti-pots or swimming, for example.
More is good, but the NIH alone is already spending $2.8 billion/year on Alzheimer's research https://www.alz.org/get-involved-now/advocate/research-fundi... and that's not including spending from other government agencies (both US and international), charities, or pharma companies.
$23.6 trillion plus whatever else this situation will cost. I would guess $5-7 trillion more, at a minimum, because it will cost $1.2 trillion a month for shelter-in-place UBI.. and then however much of many trillions in loans go into default or are forgiven.
>...and the millions that Bill Gates asked for pandemic research 5 years ago.
I for one really regret I haven't been chipped yet from Bills ID2020 program. I wish it could be funded. The only people who could be against it are the anti-science nutters.
I'm sure the EULA of the chip program will include both a robust privacy policy and a CoC.
I’m not able to access this content, but I’ve noticed several theories about specific chronic diseases being the effects of persistent infections that haven’t been widely recognized as such.
If any of the theories are true, it means that many research efforts have been unwitting attempts at turning symptomatic carriers into asymptomatic ones.
It's just sad that we've had this theory for over thirty years and continued to pursue the amyloid hypothesis in spite of overwhelming failure of treatments targeting amyloid.
My father has fairly late-stage Alzheimers and I can't help but think we'd have a treatment by now.
If this ends up being true, does it lead to any potential lifestyle changes or medical interventions that could help lower one's risk of Alzheimer's? Are these infections measurable and curable with antibiotics or something, and we just don't bother doing it because there are no noticeable short-term effects?
I have a strong belief that there definitely are lifestyle changes you can make in order to lower your chances of getting Alzheimer's, and there is some support for them, although they need more research in order to confirm the exact magnitude and effect. Some of the ones which I believe are worth taking a closer look at are listed below:
– Another interesting link: In India, people have a much lower incidence of Alzheimer’s, and one of the primary reason is usually attributed to Indians eating a lot of Turmeric. It turns out in fact that one of the primary compounds in Turmeric is Curcumin, and its shown to help against herpes: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2668156/
Our current issue today is the we wait for things to go wrong and then we attempt to address them instead of trying to find the root cause and proactively trying to tackle the problem early. At the same time, finding the root isn’t necessarily easy, and performing longitudinal studies that would confirm a lot of these hypothesis would also be extremely difficult to implement, so I don’t necessarily have the solution to addressing the problem.
Some factors which I may have already listed above and which I strongly suggest you implement if you do want to lead a healthier life and prevent dementia are provided below:
– Daily exercise (both aerobic intertwined with strength training).
– Daily fasting (eating in a 4 – 8 hour window along with periodic 2-3 day fasts).
– Healthy diet: Stick to a mostly plant based diet. Eliminate high-glycemic index simple carbohydrates and replace them with healthier low-glycemic index choices (i.e. include lots of high fiber foods along with low GI fruits and vegetables). Replace bad fats (artificial trans fats and saturated fats) with good ones (fish, nuts, olive oil, avocados). Avoid highly processed foods and foods with added sugar.
– Take a teaspoon of turmeric daily (with black pepper, which increases its absorption).
I remember reading how Japan went from producing products which were garbage when it comes to quality and transforming themselves into becoming the kings of quality within quite a small time frame. The way they did this is through simple focus on root cause analysis and transforming their manufacturing processes from being reactive to introducing proactive measures and always focusing in on finding and addressing the root cause. I really wonder when medicine will start taking the same approach. It wouldn’t be an easy transformation, and the incentives today also aren’t exactly aligned to make this viable yet, but hopefully we see some changes within the next century or so, since the evidence to me seems to indicate that we could get a lot further by taking a look at lifestyle factors rather than the reactive measures we employ today.
Most autoimmune disorders are either infections or gut dysbiosis, which is actually pretty close to an infection too.
It's sad the establishment is taking so long to accept this. There are papers in Nature / Science showing really strong evidence for some autoimmune disorders.
Have the establishment really been pushing against these ideas that hard? Molecular mimicry seems to be a rather old idea, but I'm thinking that the push back is maybe more about what to do with this idea treatment wise. You've definitely done more research and reading in this area, so perhaps you could expound on how the establishment is being slow?
The theory of infectious origin of the Alzheimer's disease
The hypothesis that Alzheimer's disease has an infectious origin, has a long and controversial history. The data at the origin of this hypothesis are contradictory and mainly associative in nature, without it being possible to demonstrate a causal link. Interest in this theory has been renewed, however, by several recently published observations. In the section Viewpoint de la revue Nature Reviews Neurology, Ben Readhead, a researcher at the Biodesign Institute's ASU-Banner Center for Research on Neurodegenerative Diseases, joined several distinguished colleagues to discuss the idea that bacteria, viruses or other infectious pathogens can play a role in Alzheimer's disease.
First, it has been shown that the amyloid β can act as an antimicrobial peptide and that selected microorganisms can seed the deposition of Aβ in mouse models.
Second, genetic data has rekindled interest in the role of herpesviruses, in particular the human Herpes 6 virus (HHV6), in Alzheimer's disease.
Third, the epidemiological data from Taiwan suggests that antiherpetic drugs reduce the risk of dementia.
Preclinical data have indicated that microorganisms associated with periodontal disease may contribute to the pathology of Alzheimer's disease.
Finally, genetic, pathological and modeling studies of Alzheimer's disease have shown that the immune system plays an important role in Alzheimer's disease.
A hypothesis that has never been favored by researchers
This hypothesis may have been rejected too quickly. For example, microorganisms do not only cause acute illnesses, in fact certain microorganisms can hide in the body for decades in latent form, causing damage intermittently or after long periods of silence.
In addition, being infected does not necessarily mean being symptomatic. For example, out of the millions of people infected with Mycobacterium tuberculosis, only about a tenth of them will develop tuberculosis. Likewise, most people infected with HSV1 do not develop cold sores so it is possible that asymptomatic carriers of this virus were often mistakenly included in the control groups. It should also be noted that many viruses of the Herpes family (HSV1, HSV2, VZV) live preferentially in neurons.
A role for an infectious agent - in particular the herpes simplex 1 virus (HSV1) - in Alzheimer's disease (Alzheimer's disease) was proposed about 30 years ago based discovery of HSV1 DNA in the brain tissue of a large proportion of the elderly, followed by evidence that e the virus confers a high risk of disease to carriers of the ε4 allele of the gene apolipoprotein E (APOE * ε4).
Shortly after the detection of HSV1 DNA, two different species of bacteria, Borrelia burgdorferi and Chlamydia pneumoniae, were implicated in Alzheimer's disease, and a third species, Porphyromonas gingivalis, was recently added to the list.
Doubts remain, however
Nevertheless, it is known that an acute end-of-life infection, such as pneumonia, can cause a dramatic increase in the amount of microorganisms in the brain. They will then be detected post-mortem but that does not mean that these microorganisms are at the origin of the Alzheimer's disease. In addition, the issue of reverse causation is never really addressed: For example, clinical Alzheimer's disease can lead to poor dental hygiene and, therefore, damage to the oral microbiome.
Indeed, there are many challenges to prove the theory of microbial origin of Alzheimer's disease. A potential challenge is that each drug has a relatively narrow spectrum of antimicrobial activity. However, since a large number of microorganisms have been associated with Alzheimer's disease by a range of researchers, it would be difficult to interpret what a negative result in a clinical trial would mean, which would necessarily use a specific antimicrobial.
Another problem is the duration of the disease. We know that the underlying pathology of Alzheimer's disease begins 20 years or more before the onset of symptoms. So, how to prove that an infectious process that occurred decades before the onset of symptoms, really contributed to the disease process?
One may also wonder why bacteria or viruses would escape the innate innate immune defense mechanisms, which are responsible for protecting the brain against such an invasion.
> One may also wonder why bacteria or viruses would escape the innate innate immune defense mechanisms, which are responsible for protecting the brain against such an invasion.
Well there is Subacute sclerosing panencephalitis. Which is a delayed complication of measles that happens from months to decades after infection.
> Preclinical data have indicated that microorganisms associated with periodontal disease may contribute to the pathology of Alzheimer's disease.
That shouldn't be too hard to test: is the proportion of dentists and dental hygienists with Alzheimer's significantly different from the general population? It's just a homework problem for a Biostatistics course.
There are a wide variety of ways to test this, yet no significant link has been found. I see this hypothesis come up a lot on HN. It’s a favorite around here.
Consider this: HN generally attracts the intelligent type of personality. What scares that type of personality most? Losing the gift of intelligence. What is the most common thing that can take that away? Dementia. How do you make yourself feel safer about such an unpredictable thing as dementia? Convince yourself that it’s caused by something that can easily be controlled with modern medicine - microbes. It’s not so scary anymore, is it?
[+] [-] clumsysmurf|6 years ago|reply
I read damage to the nasal epithelium can allow pathogens to reach the brain:
"New research from Griffith University has shown that damage to the lining inside the nose increases the risk of bacteria sneaking into the brain via nerves, potentially causing long-term health issues." ... "Bacteria and viruses, and resultant neuroinflammation, may even contribute to neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases"
https://medicalxpress.com/news/2020-03-injury-nose-bacteria-...
[+] [-] anonAndOn|6 years ago|reply
[0] https://www.ijidonline.com/article/S1201-9712(18)34525-9/pdf
[+] [-] softwaredoug|6 years ago|reply
[+] [-] e40|6 years ago|reply
[+] [-] arthurcolle|6 years ago|reply
[+] [-] jonny_eh|6 years ago|reply
[+] [-] melling|6 years ago|reply
After this one is over, perhaps we can add a few billion for research into diseases like Alzheimer’s, Parkinson’s, pancreatic cancer, etc ...
...and the millions that Bill Gates asked for pandemic research 5 years ago.
[+] [-] streptomycin|6 years ago|reply
[+] [-] snazz|6 years ago|reply
[+] [-] anonsubmit2671|6 years ago|reply
https://usdebtclock.org
[+] [-] omgwtfbyobbq|6 years ago|reply
[+] [-] sslayer|6 years ago|reply
[+] [-] _red|6 years ago|reply
I for one really regret I haven't been chipped yet from Bills ID2020 program. I wish it could be funded. The only people who could be against it are the anti-science nutters.
I'm sure the EULA of the chip program will include both a robust privacy policy and a CoC.
[+] [-] odyssey7|6 years ago|reply
If any of the theories are true, it means that many research efforts have been unwitting attempts at turning symptomatic carriers into asymptomatic ones.
[+] [-] arcticbull|6 years ago|reply
My father has fairly late-stage Alzheimers and I can't help but think we'd have a treatment by now.
[+] [-] cactus2093|6 years ago|reply
[+] [-] photon_lines|6 years ago|reply
– Regular exercise may delay Alzheimer's in those at high risk of disease: https://inews.co.uk/news/health/regular-exercise-delays-alzh...
– Dr. Dale Bredesen Protocol: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4712873/
– Control Hypertension: https://www.fightaging.org/archives/2020/01/controlling-hype...
– DASH diet: Healthy eating to lower your blood pressure: https://www.mayoclinic.org/healthy-lifestyle/nutrition-and-h...
– Insulin Resistance and Alzheimer’s Disease: Bioenergetic Linkages: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5671587/
– Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/
Some good reading and support for the herpes / viral hypothesis is provided below:
– Alzheimer's risk 10 times lower with herpes medication: https://www.medicalnewstoday.com/articles/322463
– Alzheimer’s Disease-Associated β-Amyloid Is Rapidly Seeded by Herpesviridae to Protect against Brain Infection: https://www.cell.com/neuron/fulltext/S0896-6273(18)30526-9
– Another interesting link: In India, people have a much lower incidence of Alzheimer’s, and one of the primary reason is usually attributed to Indians eating a lot of Turmeric. It turns out in fact that one of the primary compounds in Turmeric is Curcumin, and its shown to help against herpes: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2668156/
Our current issue today is the we wait for things to go wrong and then we attempt to address them instead of trying to find the root cause and proactively trying to tackle the problem early. At the same time, finding the root isn’t necessarily easy, and performing longitudinal studies that would confirm a lot of these hypothesis would also be extremely difficult to implement, so I don’t necessarily have the solution to addressing the problem.
Some factors which I may have already listed above and which I strongly suggest you implement if you do want to lead a healthier life and prevent dementia are provided below:
– Daily exercise (both aerobic intertwined with strength training).
– Daily fasting (eating in a 4 – 8 hour window along with periodic 2-3 day fasts).
– Healthy diet: Stick to a mostly plant based diet. Eliminate high-glycemic index simple carbohydrates and replace them with healthier low-glycemic index choices (i.e. include lots of high fiber foods along with low GI fruits and vegetables). Replace bad fats (artificial trans fats and saturated fats) with good ones (fish, nuts, olive oil, avocados). Avoid highly processed foods and foods with added sugar.
– Take a teaspoon of turmeric daily (with black pepper, which increases its absorption).
I remember reading how Japan went from producing products which were garbage when it comes to quality and transforming themselves into becoming the kings of quality within quite a small time frame. The way they did this is through simple focus on root cause analysis and transforming their manufacturing processes from being reactive to introducing proactive measures and always focusing in on finding and addressing the root cause. I really wonder when medicine will start taking the same approach. It wouldn’t be an easy transformation, and the incentives today also aren’t exactly aligned to make this viable yet, but hopefully we see some changes within the next century or so, since the evidence to me seems to indicate that we could get a lot further by taking a look at lifestyle factors rather than the reactive measures we employ today.
[+] [-] nextos|6 years ago|reply
It's sad the establishment is taking so long to accept this. There are papers in Nature / Science showing really strong evidence for some autoimmune disorders.
See this previous thread for an extended discussion: https://news.ycombinator.com/item?id=21917884
[+] [-] JamesBarney|6 years ago|reply
The establishment also believes that gut dysbiosis and infections can trigger or play a role in this misclassification too.
The problem is that a lot of enthusiasts believe this insight is a lot more beneficial than it is.
[+] [-] James_Henry|6 years ago|reply
[+] [-] unknown|6 years ago|reply
[deleted]
[+] [-] bitwize|6 years ago|reply
[+] [-] narrator|6 years ago|reply
[+] [-] ink_13|6 years ago|reply
[0] https://www.alzforum.org/news/conference-coverage/first-phas...
[+] [-] jjtheblunt|6 years ago|reply
[+] [-] zackees|6 years ago|reply
https://web.archive.org/web/20200327181753/https://padiracin...
Full text:
The theory of infectious origin of the Alzheimer's disease The hypothesis that Alzheimer's disease has an infectious origin, has a long and controversial history. The data at the origin of this hypothesis are contradictory and mainly associative in nature, without it being possible to demonstrate a causal link. Interest in this theory has been renewed, however, by several recently published observations. In the section Viewpoint de la revue Nature Reviews Neurology, Ben Readhead, a researcher at the Biodesign Institute's ASU-Banner Center for Research on Neurodegenerative Diseases, joined several distinguished colleagues to discuss the idea that bacteria, viruses or other infectious pathogens can play a role in Alzheimer's disease.
First, it has been shown that the amyloid β can act as an antimicrobial peptide and that selected microorganisms can seed the deposition of Aβ in mouse models.
Second, genetic data has rekindled interest in the role of herpesviruses, in particular the human Herpes 6 virus (HHV6), in Alzheimer's disease.
Third, the epidemiological data from Taiwan suggests that antiherpetic drugs reduce the risk of dementia.
Preclinical data have indicated that microorganisms associated with periodontal disease may contribute to the pathology of Alzheimer's disease.
Finally, genetic, pathological and modeling studies of Alzheimer's disease have shown that the immune system plays an important role in Alzheimer's disease.
A hypothesis that has never been favored by researchers This hypothesis may have been rejected too quickly. For example, microorganisms do not only cause acute illnesses, in fact certain microorganisms can hide in the body for decades in latent form, causing damage intermittently or after long periods of silence.
In addition, being infected does not necessarily mean being symptomatic. For example, out of the millions of people infected with Mycobacterium tuberculosis, only about a tenth of them will develop tuberculosis. Likewise, most people infected with HSV1 do not develop cold sores so it is possible that asymptomatic carriers of this virus were often mistakenly included in the control groups. It should also be noted that many viruses of the Herpes family (HSV1, HSV2, VZV) live preferentially in neurons.
A role for an infectious agent - in particular the herpes simplex 1 virus (HSV1) - in Alzheimer's disease (Alzheimer's disease) was proposed about 30 years ago based discovery of HSV1 DNA in the brain tissue of a large proportion of the elderly, followed by evidence that e the virus confers a high risk of disease to carriers of the ε4 allele of the gene apolipoprotein E (APOE * ε4).
Shortly after the detection of HSV1 DNA, two different species of bacteria, Borrelia burgdorferi and Chlamydia pneumoniae, were implicated in Alzheimer's disease, and a third species, Porphyromonas gingivalis, was recently added to the list.
Doubts remain, however Nevertheless, it is known that an acute end-of-life infection, such as pneumonia, can cause a dramatic increase in the amount of microorganisms in the brain. They will then be detected post-mortem but that does not mean that these microorganisms are at the origin of the Alzheimer's disease. In addition, the issue of reverse causation is never really addressed: For example, clinical Alzheimer's disease can lead to poor dental hygiene and, therefore, damage to the oral microbiome.
Indeed, there are many challenges to prove the theory of microbial origin of Alzheimer's disease. A potential challenge is that each drug has a relatively narrow spectrum of antimicrobial activity. However, since a large number of microorganisms have been associated with Alzheimer's disease by a range of researchers, it would be difficult to interpret what a negative result in a clinical trial would mean, which would necessarily use a specific antimicrobial.
Another problem is the duration of the disease. We know that the underlying pathology of Alzheimer's disease begins 20 years or more before the onset of symptoms. So, how to prove that an infectious process that occurred decades before the onset of symptoms, really contributed to the disease process?
One may also wonder why bacteria or viruses would escape the innate innate immune defense mechanisms, which are responsible for protecting the brain against such an invasion.
[+] [-] Gibbon1|6 years ago|reply
Well there is Subacute sclerosing panencephalitis. Which is a delayed complication of measles that happens from months to decades after infection.
https://en.wikipedia.org/wiki/Subacute_sclerosing_panencepha...
[+] [-] litoE|6 years ago|reply
That shouldn't be too hard to test: is the proportion of dentists and dental hygienists with Alzheimer's significantly different from the general population? It's just a homework problem for a Biostatistics course.
[+] [-] IAmGraydon|6 years ago|reply
Consider this: HN generally attracts the intelligent type of personality. What scares that type of personality most? Losing the gift of intelligence. What is the most common thing that can take that away? Dementia. How do you make yourself feel safer about such an unpredictable thing as dementia? Convince yourself that it’s caused by something that can easily be controlled with modern medicine - microbes. It’s not so scary anymore, is it?
[+] [-] unknown|6 years ago|reply
[deleted]
[+] [-] andybaldwin|6 years ago|reply
[deleted]
[+] [-] hackermaster100|6 years ago|reply
[deleted]
[+] [-] untilHellbanned|6 years ago|reply
[+] [-] James_Henry|6 years ago|reply