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Does our immune system hold the key to beating Alzheimer’s disease?

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Incurable and increasingly prevalent, Alzheimer’s has long puzzled the research community. Now scientists believe the human body may be the best line of defence



Philip Ball

Sun 3 Mar 2019 12.00 GMT


For many years Alzheimer’s was regarded purely as a result of age-related wear and tear; no one thought it had anything to do with the immune system
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I have read many times on different sites that eating virgin coconut oil can keep you from getting Alzheimers  and CAN REVERSE having Alzheimers!! I eat 2 Tablespoons a day, 2 tsp of Redmond clay (Bentonite clay in a glass of water, don't use metal to measure or stir the clay, it has magnetic properties that attract the metals out of your body) that can cause Alzheimers.

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Anyone here have knowledge about natural healing for psoriasis??

My hubby suffers terribly, we will not do the Western medicine treatments such as Humira (sp) been there... 

Thanks in advance. I have done much online reading already. Certain vitamins may be appropriate, I've heard CBD may help ( he won't do it) also Cod liver oil ( organic, Jamaican). WH


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12 minutes ago, wealthhound said:

Anyone here have knowledge about natural healing for psoriasis??

My hubby suffers terribly, we will not do the Western medicine treatments such as Humira (sp) been there... 

Thanks in advance. I have done much online reading already. Certain vitamins may be appropriate, I've heard CBD may help ( he won't do it) also Cod liver oil ( organic, Jamaican). WH


So sorry about that. I knew someone that had savear psoriasis. She tryed all the natural stuff, plus the other non US approved stuff in Mexico. None of it helped. 

Good luck.

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It's been a while since I've posted so bear with me. Like most of mother other posts in here - this one could be a little long. I will give links to support my information - as usual. 


Both Alzheimer’s  and psoriasis have links to a common base - oxidative stress.  Quick primer on oxidative stress. As some of you know - I have a keen interest in this area as I have found it to have a role in almost all diseases.  


"Oxidative stress occurs when excess oxygen radicals are produced in cells, which could overwhelm the normal antioxidant capacity. When the concentration of reactive species is not controlled by internal defense mechanisms such as antioxidants (tocopherols, ascorbic acid, and glutathione) or enzymes involved in oxygen radical scavenging (catalase, peroxidase, and superoxide dismutase, SOD), oxidative damage occurs to proteins, lipids, and DNA, which could lead to cytotoxicity, genotoxicity, and even carcinogenesis when damaged (mutated) cells can proliferate. Oxidative stress could results from the following: (1) the presence of xenobiotics, (2) the activation of the immune system in response to invading microorganisms (inflammation), and (3) radiation, which makes oxidative stress a common denominator of toxicity or stress. In this chapter, the reader will find a variety of assays to measure oxidative stress and damage."


More simply put - Oxidative stress is essentially an imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects through neutralization by antioxidants. Essentially - the body is out of cellular homeostasis.  


If you will indulge me - let's look at Alzheimer's first.  Doing search on Google Scholar with "Alzheimer's and oxidative stress" will pull up over 640,000 articles.  These are citations from a few.


"Oxidative balance is emerging as an important issue in understanding the pathogenesis of Alzheimer’s disease. Examination of Alzheimer’s disease brain has demonstrated a great deal of oxidative damage, associated with both hallmark pathologies (senile plaques and neurofibrillary tangles) as well as in normal appearing pyramidal neurons. While this suggests that oxidative stress is a proximal event in Alzheimer’s disease pathogenesis, the mechanisms by which redox balance is altered in the disease remains elusive. Determining which of the proposed sources of free radicals, which include mitochondrial dysfunction, amyloid-β-mediated processes, transition metal accumulation and genetic factors like apolipoprotein E and presenilins, is responsible for redox imbalance will lead to a better understanding of Alzheimer’s disease pathogenesis and novel therapeutic approaches."


"Genetic and lifestyle-related risk factors for Alzheimer disease (AD) are associated with an increase in oxidative stress, suggesting that oxidative stress is involved at an early stage of the pathologic cascade. Moreover, oxidative stress is mechanistically and chronologically associated with other key features of AD, namely, metabolic, mitochondrial, metal, and cell-cycle abnormalities. Contrary to the commonly held notion that pathologic hallmarks of AD signify etiology, several lines of evidence now indicate that aggregation of amyloid-β and tau is a compensatory response to underlying oxidative stress. Therefore, removal of proteinaceous accumulations may treat the epiphenomenon rather than the disease and may actually enhance oxidative damage. Although some antioxidants have been shown to reduce the incidence of AD, the magnitude of the effect may be modified by individual factors such as genetic predisposition (e.g. apolipoprotein E genotype) and habitual behaviors. Because caloric restriction, exercise, and intellectual activity have been experimentally shown to promote neuronal survival through enhancement of endogenous antioxidant defenses, a combination of dietary regimen of low total calorie and rich antioxidant nutrients and maintaining physical and intellectual activities may ultimately prove to be one of the most efficacious strategies for AD prevention."


One of my favorite sites kind of rolls all the information up into a bit easier to read synopsis.


"Alzheimer’s disease, an age-associated dysfunction of brain cells that is degenerative in nature, is clearly connected to oxidative stress. Highly specialized brain cells are slower to replace themselves and warrant the body’s protection. The brain has mechanisms that aid this—the blood-brain barrier, for example, and the myelin sheath surrounding nerve fibers are protective of nerve cells.


Damaged mitochondria in combination with chronic oxidative stress often result in the body’s inability to correct imbalances of cellular waste and toxins. Glutathione (a potent antioxidant produced by the body) plays a role in cleaning up but is ineffective without the presence of certain REDOX signaling molecules to help neutralize oxidizing free radical toxins.


This deficiency, usually from sluggish, damaged mitochondria, can be genetically predisposed but may also (especially when manifest in the earlier years) result from habitual smoking, insufficient diet, and stress. Additionally, brain cells have naturally high levels of certain fatty acids, which are especially susceptible to oxidation. The vast blood supply that normally serves the brain is a key factor in the input of oxygen and nutrients and the outtake of waste. Any brief restriction of the blood supply to brain tissue is devastating, and even minor chronic deficiency of good circulation is equally debilitating to the ability of brain cells to maintain balance away from the oxidative zone."!


Let's do the same thing with psoriasis.  Google scholar search with "psoriasis and oxidative stress" will again yield over 52,000 results.  Again - here are a excerpts from a few of the articles. 


"Psoriasis is a chronic inflammatory, proliferative skin disease characterized by pathological skin lesions due to various exogenous and endogenous factors. It is associated with a number of biochemical and immunological disturbances. Recently, it has been suggested that increased reactive oxygen species (ROS) production and compromised function of antioxidant system may be involved in the pathogenesis of this disease. In the present study, 90 psoriasis patients were selected. Disease severity was assessed by psoriasis area severity index score and grouped as mild, moderate and severe (each group consists of 30 subjects) and compared with 30 healthy controls. Serum levels of malondialdehyde, nitric oxide end products and the activities of antioxidant enzymes such as erythrocyte-superoxide dismutase, catalase and total antioxidant status were investigated in these groups/subjects. As compared to controls, we found severitywise significantly increased serum malondialdehyde, nitric oxide end products with decrease in erythrocyte-superoxide dismutase activity, catalase activity and total antioxidant status in patients with psoriasis suggesting worsening of the disease. It seems to be linked with the enhancement of Reactive Oxygen Species production and decreased antioxidant potential in psoriasis."


"Psoriasis is a chronic immune-mediated hyperproliferative inflammatory skin disease in which a cytokine network concept is well established. Skin is a major target of oxidative stress mainly due to reactive oxygen species (ROS) originating from the environment and skin metabolism itself. Although endogenous antioxidants attenuate the harmful effects of ROS, increased or prolonged presence of free radicals can override ROS defense mechanisms and mediate numerous cellular responses that contribute to the development of a variety of skin disorders, including psoriasis. Regarding psoriasis, antioxidant strategies have proven to be beneficial therapeutics. The cellular signaling pathways such as mitogen-activated protein kinase/activator protein 1, nuclear factor κB, and Janus kinase–signal transducers and activators of transcription are known to be redox sensitive and proven to be involved in the progress of psoriasis."


Again - heading to The Redox Doc - he does give a good synopsis.


"Skin wraps the body in a protective shield, which itself is a living organ actively burning fuel, repairing, and replacing itself 24/7. Environmental factors such as UV light and airborne and topical toxins negatively impact skin health, prompting an adaptive response which is driven by REDOX chemistry. Oxidative damage varies by the degrees of REDOX potential of the tissue affected, since cellular repair is slowed by an imbalance of REDOX signaling molecules.

Skin disorders like psoriasis, a chronic immune-mediated inflammatory condition, are also based in REDOX imbalance, since cellular signaling pathways like transcription factor Kappa B are known to rely on proper REDOX balance. While the ingestion of antioxidants has some value, it is widely known that REDOX signaling molecules provide the electron-rich REDOX molecules that endogenous antioxidants require to operate efficiently to eliminate the free-radical exposure that override cell defenses. Activate your REDOX potential with sleep, hydration, plant-based nutrition, and supplementing with REDOX molecules."!


While it may seem that simpy adding more antioxidants to the diet would help alleviate oxidative stress, it's not that simple. It's all about the body being in balance and homeostasis.  You actually need a certain amount of oxidants to actually make the bodies immune response work correctly.  This balance is accomplished with what are knows as REDOX signaling molecules. These little molecules are one of the primary ways our body communicates it's needs and reactions - sometimes even more quickly than our nervous system.


Here is a good discussion about those. 


Bottom line for me is the need for cellular homeostasis. Diet is a great first step - processed foods wreck havoc on the body. Whole grains, natural fats, fruits, vegetables - you've all heard it before.  I also take the stabilzed REDOX supplement they talk about in the above article.  I know it has helped me in many areas.


Disclaimer: I am affiliated with the company the makes the REDOX supplement - so I will not give any more information about that here in the forum. I understand and appreciate Mr. Montana's forum rules and will definitely abide by them.  

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Strangely enough - this was in the news today


Pfizer denies report it hid possible Alzheimer’s breakthrough


Pfizer is fighting back against a report that it hid the potential of a blockbuster drug to prevent Alzheimer’s disease in order to avoid shelling out for a “costly clinical trial.”


Researchers at Pfizer in 2015 found that Enbrel, an anti-inflammatory drug used to treat rheumatoid arthritis, seemed to reduce the risk of Alzheimer’s disease by 64 percent, the Washington Post reported Tuesday.


But a clinical trial on 3,000 to 4,000 patients to test the hypothesis would have cost about $80 million, according to research prepared by Pfizer’s inflammation and immunology department and seen by the Washington Post.


The Washington Post noted that Enbrel was near the end of its 20-year patent life and financial incentives for further research into the drug were “diminishing.”


But Pfizer contends that its decision not to pursue a study of Enbrel’s other possible uses was motivated by science and not money.


“Our decision not to pursue a broader clinical trial … [was] based first and foremost on scientific rationale and not on the basis of financial incentives as the story seems to imply,” Pfizer said in a statement after the Washington Post story ran.


The data was found from a review of 127,000 insurance claims completed by Pfizer employees. The group split the claims equally between people who had Alzheimer’s and those who did not. In the group of people who did not have Alzheimer’s, 302 were treated with Enbrel. Only 110 in the group with Alzheimer’s had used Enbrel, it was reported.


Members of the medical community the Washington Post spoke with argued that Pfizer should have done more to publicize the potential uses of Enbrel to spur other research even if the drugmaker didn’t plan to do its own study.


“Having acquired the knowledge, refusing to disclose it to those who might act upon it hides a potential benefit, and thereby wrongs and probably harms those at risk of developing Alzheimer’s by impeding research,’’ said Bobbie Farsides, professor of clinical and biomedical ethics at Brighton and Sussex Medical School in London.


But not all of the people the Washington Post spoke with agreed.


“I do think you have to draw some limits, and say that not every piece of information they have in their files has to be disclosed with others,’’ said Marc Rodwin, a professor at Suffolk University Law School in Boston.


A source close to Pfizer told the New York Post that the drug giant publishes findings that meet the “gold standard” of medical research versus “hunches.”


While researchers have been studying the role of brain inflammation in Alzheimer’s, Pfizer during a three-year internal review determined that a clinical trial was not likely to be successful because the drug doesn’t reach brain tissue.


A study of 41 patients published by the American Academy of Neurology in May 2015 about potential uses for Enbrel proved to be inconclusive.


“While there were some interesting trends that favored [Enbrel], there were no statistically significant changes in cognition, behavior, or global function,” according to an abstract of the researcher’s findings.

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