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A report in my local newspaper, Newsday (1/17/2006; page A26), titled "Immune system may also help brain" is an excellent example of how so many "experts" misinterpret phenomena involving "inflammation." The reporter, Jamie Talan, claims that these scientists think that "boosting the immnune system may be one way to protect against age-associated learning and memory problems..."
However, as Talan notes, "T-lymphocytes normally enter the brain to patrol for signs of infection. But scientists have discovered that these immune cells recognize a normal brain protein as foreign and mount an immue response by pumping out activated microglia, cells that produce inflammation."
Now if you've read my other essays here, you might consider the possibility that the reason why the body would "attack itself" is becaue the "normal brain protein" was modified by oxidative stress/lipid peroxidation (and that a diet low in PUFAs and high in SFAs may be a good way to prevent it). And my interpretation is that this situation is very bad - the cause of various "diseases" that are much more common in "advanced" nations.
However, these "experts" think that it will somehow lead to a "cure" for the problem that was caused by it in the first place, as ludicrous as that may sound. For example:
"These microglia support the birth of new neurons in these brain regions."
This is the kind of "birth" that leads to cancer, at least in some situations, but my point here is that they seem to assume that everyone will have certain cognitive problems as they "age" and so anything that provokes growth is likely to be "good." If they had a better command of the literature, however, they might realize that they are likely to be enhancing the process that led to the cognitive problems in the first place (by considering generating what is often called an "autoimmune attack").
The ignorance demonstrated here is frightening enough, but the possibility that they would actually provoke inflammation in someone's brain to "cure" what was caused by "inflammation" in the first place is in a realm of its own. |
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In a new study, a new molecule was discovered for which it is claimed plays a key role in an "inflammatory" disease:
QUOTE: ...The key to maintaining this mucosal barrier, the scientists discovered, is the "peacekeeper" activity of T-bet in the dendritic cells of the intestine's immune system. When T-bet is at normal levels, the boundary - a kind of demilitarized zone - remains intact and prevents trouble from pathogenic bacteria. But if T-bet is insufficient, the dendritic cells overproduce a powerful chemical called TNF-alpha (tumor necrosis factor-alpha) that triggers inflammation and causes normal cells to die. In ulcerative colitis, the T-bet-related excess of TNF-alpha leads to the death of cells making up the epithelial barrier of the colon, enabling harmful bacteria to chronically inflame the intestinal wall.
The scientists bred strains of mice that lacked T-bet and showed that the resulting disease was virtually identical to human ulcerative colitis... UNQUOTE.
The problem is that they don't seem to realize that "germs" are not likely to be a problem if conditions are optimal, but instead there is this statement (made by the author of the report):
QUOTE ...Beneficial bacteria in the colon aid in digestion and extraction of nutrients from food. However, harmful microbes also reside in the intestine, so animals that harbor bacteria have evolved a boundary, or barrier, in the form of the intestinal lining to keep the dangerous bacteria from injuring the colon wall... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2007/10/071004121042.htm |
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An interesting document, I think ---> http://www.lef.org/news/LefDailyNews.htm?NewsID=5962&Section=DISEASE
QUOTE :
Inflammation a common risk among diseases: If immune system is amiss, heart attacks, strokes and other deadly consequences may follow, researchers say
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10-08-07
Oct. 7--Researchers call it the "unifying theory" behind the major killers of our time -- cardiovascular disease, cancer and diabetes -- as well as scores of other diseases.
It's inflammation, which most people know by the red, painful swelling that follows an injury, bug bite or other surface wound. But it also exists in tissue below the skin, and scientists are now convinced this unseen inflammation is the culprit that worsens many chronic diseases.
Inflammation is the immune system's response for beating back invaders in the body, but inflammation gone awry can lead to heart attacks and strokes, aid cancers in turning deadly, cause Alzheimer's disease by destroying brain cells and usher in diabetes.
Out-of-kilter inflammation also is linked to clinical depression, schizophrenia, Parkinson's disease, asthma, osteoarthritis, liver disease and hypertension, among other disorders.
"Retrospectively, it's what we should have been looking at," said Lisa Coussens, a cancer biologist at UC San Francisco. "It's a major area of research."
Coussens and several other medical experts spoke last week at a conference sponsored by UC San Francisco that gave its audience a snapshot of research on the connections between inflammation and chronic diseases.
During their talks, the speakers emphasized the promise inherent in the realization that one condition links so many diseases: Fundamentally similar treatments could be used to control them.
Some of the best evidence of inflammation's crucial role in exacerbating chronic diseases comes from studies on cancer rates in patients who were counseled to lower their risk for a heart attack by regularly taking anti-inflammatory medicines such as aspirin. That population has a significantly lower rate of cancer, compared with a similar population not taking anti-inflammatory medicines, Coussens pointed out.
"They were compelling," Coussens said.
As another example of the beneficial effect of controlling inflammation with over-the-counter medicines, regular use of ibuprofen is associated with lowered rates of Alzheimer's disease, said Cynthia Lemere, a professor of neurology at Harvard Medical School, who spoke at the San Francisco conference.
Coussens emphasized, however, that long-term use of aspirin and other anti-inflammatory drugs may cause other severe health complications or dangerous drug interactions, and a physician should be consulted before taking any medicine on a regular basis.
Deficits in nutrition and sleep are linked to increased inflammation, as is excess stress. Weight gain also can trigger chronic inflammation.
And once a disease reaches a serious stage, there is far less optimism among scientists that controlling inflammation can undo the damage.
"We're all talking about prevention, not reversal," said Lemere.
But there is excitement among researchers who suggest that if a disease is caught early enough, then taming inflammation could provide an effective tool for stopping the advance of the disease.
Chronic inflammation is caused by the persistent presence of pathogens and environmental pollutants, lifestyle and genetics, among others factors.
When the immune system is functioning normally, its front-line fighters swiftly respond to any injury, such as a splinter puncturing the skin or an invasion of microbes from a scrape or bug bite. These thuglike warriors, which go by names such as natural killer cells and macrophages, shoot out an arsenal of chemicals, rip holes into cell walls of invaders or even consume them whole.
But these fighters, part of the more primitive "innate immune system," lack the discriminate nature of their more sophisticated immune system counterparts, called the adaptive immune system. The latter takes longer to mobilize before sending out its more targeted arsenal.
In the meantime, these brutish cellular warriors sometimes take out healthy cells, a form of collateral damage. (The more sophisticated fighters aren't without their flaws -- they, too, can damage healthy cells.)
An immune system that is off kilter is rarely the direct cause of a chronic disease, researchers say. Instead, it can perform a devastating secondary role.
In the case of Alzheimer's disease, said Lemere, the Harvard neurologist, an innate immune cell works to ingest a type of plaque outside brain cells of people with the disease.
Sometimes, these immune cells ineffectively resort to chemical warfare against the plaque, which then destroys nearby brain cells. It is this brain cell death that causes the symptoms of Alzheimer's disease, including severe memory loss and mood swings. "I don't consider inflammation the cause of the disease," said Lemere. "But it certainly drives it forward."
"(The immune cells) are initially trying to help, but they get disregulated. They get revved up," she said. "It's sort of this big, vicious feedback loop."
Innate immune cells can cause cardiovascular disease by ingesting "bad cholesterol" that has begun literally to go rancid. These immune cells can then get trapped in arterial walls and contribute to plaque buildup. They may also stay on the attack, causing chronic inflammation. The plaque can then break off because of inflammation and form a blood clot that triggers a heart attack or stroke.
With type 2 diabetes, molecules released by innate immune cells and fat cells are implicated in interfering with the normal function of insulin, which regulates blood sugar levels.
When immune cells drop their armor after detecting danger has passed, they take on a healing role by secreting substances that promote blood vessel and tissue growth. But tumor cells can send signals that confuse these immune cells, causing them to switch allegiance and abet tumor growth instead of normal tissue growth. Tumors, like any other tissue, need a supply of oxygen and nutrients provided by blood.
Most cancers don't become deadly until they spread, or metastasize. Researchers say these hijacked immune cells foster the spread of cancer. But, if caught before the tumor has spread, anti-inflammatory treatment may be able to contain the tumor, creating the prospect of cancer becoming a manageable disease.
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| I can see how some people can call it a "unifying theory" - there is certainly more than a small amount of truth value to it. However, they are being held back from taking the next, and very obvious step, of suggesting that people rid their bodies of arachidonic acid (because the "nutritional science" people of today keep insisting it's essential, despite the experiments of the 1940s that directly refuted this claim). |
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| | (1 recommendation so far) | Message 51 of 62 in Discussion |
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Here's a passage from a new report:
QUOTE: "We study airway inflammation, and mostly we think about that in a negative context - how to stop inflammation, as in the allergic inflammation that causes asthma," says Dickey. "But surely the ability of airways to become inflamed is there for a good reason... UNQUOTE.
What this person doesn't seem to realize is that harmful inflammatory responses appear to be controllable with diet, so to say that there is a "good reason" for it is misleading. It is likely that "modern" diets are responsible for the dangerous inflammation, and that "good inflammation" is not very common any more (other than cuts and minor insults that won't become chronic or won't be potentially life-threatening in the short term). "Nature" did not design it that way, because few if any humans had AA in their cells until the last several decades or so.
Source: http://www.sciencedaily.com/releases/2007/12/071203103414.htm |
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Here's interesting information that I have yet to hear in the "mainstream media," despite how many news stories there have been on anthrax since this was published:
Abstract: Anthrax causes profound inflammation and systemic shock. A recent study has shown that anthrax lethal toxin represses the transcriptional activity of the glucocorticoid receptor, which is a crucial component of the body's defenses against inflammation. The study reports evidence that lethal toxin blocks the glucocorticoid receptor by inhibiting the p38 mitogen-activated protein kinase pathway. Thus, these findings suggest that glucocorticoid receptor inactivation contributes to anthrax toxicity and raise the possibility of developing new strategies to combat this deadly disease.
Source: Trends in Pharmacological Sciences;
Volume 24, Issue 11, November 2003, Pages 558-559. |
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A new report contains information from "experts" who seem to understand inflammation:
QUOTE: ...the alarm-ringing death of a potentially dangerous cell, such as a cell infected with Salmonella, they added. These dying cells spill chemical signals and get a protective response. The resulting inflammation, which the body launches in self-defense, can at times backfire and damage vital tissues.
A research team lead by Dr. Brad T. Cookson, an associate professor of microbiology and laboratory medicine, named this type of cell death "pyroptosis," Greek for going down in flames. Cell death that doesn't cause inflammation is called "apoptosis": to drop gently like leaves from a tree...
"In addition to its protective role in fighting infection," Cookson added, "caspase-1 also plays a role in many medical conditions characterized by cell death and inflammation." These conditions include organ damage in the heart, brain, lungs, nerves, and kidneys. Understanding pro-inflammatory cell death pathways may lead to new therapies against fatal or disabling diseases, such as serious infections, heart attack, cancer and stroke... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2008/03/080310171453.htm |
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The experts still cannot get it right. You don't have to be genetically predisposed to produce high levels of anti-inflammatory cytokines or beat the inflammation with NSAIDs/Omega-3s. A simple dietary change to reduce the amount of PUFAs ingested would naturally and painlessly blunt any "chronic" inflammatory response.
QUOTE: emerging evidence suggests that polymorphic alleles of inflammatory cytokines, involved in high cytokine production, are related to 'unsuccessful' ageing as noted previously with respect to atherosclerosis and AD. On the other hand, controlling inflammatory status may enhance individual chance of achieving 'successful' ageing. So, major findings reporting a relationship between cytokine polymorphisms and longevity suggest that those individuals who are genetically predisposed to produce low levels of inflammatory cytokines or high levels of anti-inflammatory cytokines may have an increased capacity to reach the extreme limit of human life-span UNQUOTE.
From: Innate immunity and inflammation in ageing: a key for understanding age-related diseases
Immun Ageing. 2005; 2:8
SOURCE: http://belobog.si.umich.edu:8080/gin/viewArticle?pmcid=1166571 |
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| | (1 recommendation so far) | Message 55 of 62 in Discussion |
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Here is more support for my point about "diseases" being caused by the "immune system" (which is hypersensitive when you have arachidonic acid in your cells), rather than by a "germ:"
QUOTE: ...Macrophages are defined as white blood cells that are key players in the immune response to foreign invaders. In the study mice were intravenously injected with drug-loaded liposomes to deliberately deplete their spleens and stomachs of macrophages and then infected with H. pylori. Results showed that elimination of macrophages reduced the gastric pathology induced by H. pylori, however it did not affect bacterial presence in the stomach... UNQUOTE.
Of course, these researchers are probably ignorant of the evidence about macrophages containing omega 3s or omega 6s versus those that do not.
SOURCE: http://www.sciencedaily.com/releases/2008/05/080523071035.htm |
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| | (1 recommendation so far) | Message 56 of 62 in Discussion |
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Today I read a report that once again highlights how our great scientific minds are focusing on epiphenomena rather than the underlying causes. The title is: "Protein Linked To Alzheimer's Disease Also Has Role In HIV Progression." Similarly, one could say, "lack of oxygen linked to being dead." The question is, how helpful are such statements?
Here are the first two sentences from that report: "A protein related to heart disease and Alzheimer's is found to be a factor in HIV. The apolipoprotein (apo) E4 isoform has been implicated in neurodegeneration in Alzheimer's disease, cardiovascular disease, and stroke..."
Source: http://www.sciencedaily.com/releases/2008/06/080616170816.htm
I did an internet search for "apolipoprotein (apo) E4 inflammation" and one of the first few links returned was a study which contained the following statement:
"...apolipoprotein (apo) E4 is much more than a contributing factor to neurodegeneration. ApoE has critical functions in redistributing lipids among CNS cells for normal lipid homeostasis, repairing injured neurons, maintaining synapto-dendritic connections, and scavenging toxins. In multiple pathways affecting neuropathology, including Alzheimer's disease, apoE acts directly or in concert with age, head injury, oxidative stress, ischemia, inflammation, and excess amyloid {beta} peptide production to cause neurological disorders, accelerating progression, altering prognosis, or lowering age of onset..."
Source: http://www.pnas.org/cgi/content/abstract/0600549103v1
Though they make some good points, such as: "...In response to CNS stress or injury, neurons can synthesize apoE. ApoE4 uniquely undergoes neuron-specific proteolysis, resulting in bioactive toxic fragments that enter the cytosol, alter the cytoskeleton, disrupt mitochondrial energy balance, and cause cell death..." a key question involves what one might be able to do to prevent these kinds of "diseases."
Fortunately, one group of scientists do seem to be trying to get at the underlying cause of this particular phenomenon:
"...We showed previously that free radical damage to arachidonic acid (AA) and docosahexaenoic acid (DHA) in brain can be quantified by measuring isoprostanes (IsoPs) and neuroprostanes (NPs), respectively, highly accurate and specific markers of free radical-mediated damage (Roberts et al., 1998; Roberts, 2000). Additionally, because the major isomers of IsoPs and NPs, F-ring or D/E-ring compounds, derive from common endoperoxide intermediates by reduction or isomerization, respectively, the ratio of F- to D/E-ring compounds is a measure of the reducing environment in which oxidation occurred (Reich et al., 2000, 2001). Here we used these quantitative endpoints to test the hypothesis that there is a gene-environment interaction between apoE and alpha -tocopherol with respect to age-related oxidative damage to mouse cerebrum..."
Source: http://www.jneurosci.org/cgi/content/full/21/16/5993
Of course, it would be best is terms like "inflammation" were put aside and instead this kind of molecular-level evidence was viewed with the intention of determining exactly what the sequence of events is. If one does that, the obvious question is, what if we took arachidonic acid and DHA out of our cells, replacing it with the natural, and much less biochemically active, Mead acid? It would not be expensive or difficult (relatively-speaking) to do experiments to determine if ApoE4 is a problem under similar conditions, only with Mead acid in place of AA and/or DHA. My "educated guess" is that the incidence or the age of onset of these kinds of "diseases" would be lowered significantly and raised by many years (probably decades, in many cases, in humans), respectively. I'd even be willing to put up my own money to do such experiments, but only if it turns out that I am wrong here. Who else is willing to "put his money where his mouth is?" |
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| | (1 recommendation so far) | Message 57 of 62 in Discussion |
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There is so much misinformation even in the peer review scientific journals these days. E.g. the experts cannot comprehend or totaly ignore that the major PUFA found in helthy cartilage is the Mead acid:
SOURCE: http://www.newhope.com/nutritionsciencenews/nsn_backs/Mar_01/pufa_s1.cfm
QUOTE:
PUFAs and Cartilage
The process of resorption releases free radicals and enzymes in restricted locations to "hollow out" areas of the bone surface. Unlike bone, cartilage in these areas has little natural ability to protect itself from such free radical damage. Cartilage contains less total PUFAs than bone, with unusually low levels of n-6 PUFA. However, it apparently selectively incorporates n-3 LC-PUFA, which is considered to be a protective mechanism against oxidative stress.
Cartilage may be particularly susceptible to degradation when dietary intakes of n-6 PUFAs are high and PGE2 levels are excessive, since resorption-related free radicals increase. With these increases, cartilage cannot maintain its preferred PUFA composition. Supporting this concept is research showing that oxidative stress impairs normal bone and joint function, and that vitamin E supplementation enhances bone growth and cartilage metabolism.1
References
1. Watkins B, et al. Importance of dietary fat in modulating PGE2 responses and influence of vitamin E on bone morphometry. World Rev Nutr Dietetics 1997;82:250-9.
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I came across a report today that underscores how unfortunate it is that our "experts" are so "specialized." If these people had a wider knowledge base, they'd realize that "chronic inflammation" is not a problem with Mead acid in your cells, and there would be no need to spend huge amounts of money on something that might never work in practice, when all that's needed is to tell people to avoid certain kinds of food, food preparation methods, and/or food combinations:
QUOTE: ...the absence of a single protein, called "ROCK1," profoundly reduces inflammation in the walls of blood vessels provoked by fatty deposits (atherosclerosis). In this study, scientists found that ROCK1 is necessary for immune cells, called macrophages, to "clean up" vascular walls when they come into contact with fatty deposits. Inflammation is a normal byproduct of the clean-up process and, when it goes unchecked, leads to clogging and hardening of the arteries.
When ROCK1 is absent, macrophages no longer contributed to these fatty deposits and mice showed significantly less inflammation and atherosclerosis. This discovery could lead to new treatments, such as ROCK1 inhibitors, that could dampen the inflammatory response to fatty deposits and slow the progression of atherosclerosis, and in so doing, reduce the incidence of heart attacks and strokes... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2008/06/080618114733.htm |
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This goes to the same point made in the last post to this thread:
QUOTE: ...The new study--a collaborative effort by researchers in Germany and the US--shows that an anti-inflammatory drug (called CNI-1493) may have the same effect. The drug--already tested in humans for the treatment of inflammatory diseases--protected nerve cells against amyloid beta --induced damage in culture. In mice prone to developing an Alzheimer's-like disease, the drug decreased brain inflammation and improved memory and cognitive function.
Other anti-inflammatory drugs, such as ibuprofen, have been shown to reduce Alzheimer's disease lesions in the brains of rodents, but CNI-1493 appears to be faster and more effective... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2008/06/080624110952.htm |
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This new report is a "mixed blessing." There is an understanding of how omega 6s fuel "chronic inflammation," but there is a notion that omega 3s are the "cure," though the reality is that it is very dangerous, but in a different way:
QUOTE: Farm-raised tilapia, one of the most highly consumed fish in America, has very low levels of beneficial omega-3 fatty acids and, perhaps worse, very high levels of omega-6 fatty acids, according to new research from Wake Forest University School of Medicine.
The researchers say the combination could be a potentially dangerous food source for some patients with heart disease, arthritis, asthma and other allergic and auto-immune diseases that are particularly vulnerable to an "exaggerated inflammatory response..." UNQUOTE.
Source: http://www.sciencedaily.com/releases/2008/07/080708092228.htm |
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I have a recent experience with hydrochloric acid on the skin. There is a cleaner that contains about 10 percent hydrochloric acid in some kind of gel. I used to use it to clean toilets. It got inside my gloves a couple of times. I got inflammation characterized by many many small blisters just under the skin, very painful blisters. Dosages of steroids, which are supposed to shut off cytokine production, made these blisters go away. I had another flare-up after I finished that course of steroids and I needed another. DMSO seems to help a lot.
So yes, the body attacks damaged cells. I presume that a stronger healthier body is more able to fine-tune such attacks. It's a vicious cycle when inflammation damages cells and causes them to send out more signals to trigger more autoimmune attacks.
Phosphoric acid is a viable suspect in autoimmune disease, too. It damages bones and proteins. People voluntarily drink the stuff. |
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| Keep reading my essays or posts on this site. If you do, you'll see that if you have Mead acid in your cells, you're much less likely to have that kind of nasty, prolonged inflammatory response (that you get with AA in your cells). |
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