AUTOIMMUNE DISEASES CAUSED BY AN INFECTION?

[Piscarian]

But I have this problem with memory and attention which concerns me. I wanted so much to advance in learning - there is so much information I went through and when I came back to it, I noticed that it is not fixed. I know that knowledge must be applied in order to gain awareness, so it's hard work. I have to return again and again to the sources. I spend most of my day studying, studying in order to get prepared for each client.

Hi Shared Joy,

You might look into a product called Prevagen, it's a little pricey though.

 

[Shared Joy]

Re: AUTOIMMUNE DISEASES CAUSED BY ANo paleo and INFECTION?

Okay, a memory problem. Yikes. Well, that's not terribly abnormal past a certain age but I know what you mean: darned unpleasant and a real concern.

All things considered, I don't think that a memory problem is necessarily something that would mandate this protocol. I think that if it was me, I'd look into other, less risky and less brutal therapies. For example, taking boron and other minerals including magnesium and potassium, the B vitamins, making sure you get plenty of proper fats including CLA, fish oil, phosphatidyl choline (eat egg yolks!) and so forth. Possibly adding colostrum/lactoferrin to your daily supplements and MOST OF ALL, do something to exercise the brain: like learn to play a musical instrument and practice daily. Sleeping in full darkness for the correct number of hours is also very therapeutic.

There are a number of products available that are specific to boosting brain power/memory and researching this area would be helpful for you. But it really doesn't seem that you have good justification for undertaking this protocol for autoimmune and related conditions!

Thank you Laura,
I still have to allow myself some time to figure out what to do. Your notes make sense, I'm already doing most of it.
I do wish to liberate myself to become my own master, to get free of manipulation from critters or other entities. Tall order wishes.

Joy

 

[Shared Joy]

But I have this problem with memory and attention which concerns me. I wanted so much to advance in learning - there is so much information I went through and when I came back to it, I noticed that it is not fixed. I know that knowledge must be applied in order to gain awareness, so it's hard work. I have to return again and again to the sources. I spend most of my day studying, studying in order to get prepared for each client.

Hi Shared Joy,

You might look into a product called Prevagen, it's a little pricey though.

Thank you Piscarian, this is just inaccessible for me both as price and location.
It has to do with more pedestrian products for me...
Joy

 

[RedFox]

A few more jigsaw pieces (I had a hunch that biofilms could prevent the absorption of nutrients).

http://articles.mercola.com/sites/articles/archive/2012/06/23/whole-food-supplement-dangers.aspx

Magnesium stearate is essentially a chalk-like substance, which prevents the supplements from sticking together and allows the machinery to run smoother and faster, which equates to cost savings during the manufacturing process. Magnesium stearate is not a source of magnesium and has no benefits, but may have a detrimental effect on your immune function as stearic acid has been linked to suppression of T cells. The filler also stimulates your gut to form a biofilm, which can prevent proper absorption of nutrients in your digestive tract

http://bodyecology.com/articles/biofilm-how-this-slimy-coating-is-causing-chronic-fatigue-fibromyalgia-irritable-bowel-and-more

[..]
The Slimy Goo That Ensures Microbial Survival

If you run your tongue along your teeth after a long day and feel a slimy coating, this stuff is the beginning of biofilm.

Little bugs, which are found everywhere inside and outside the body, create biological homes using a mixture of sugars and proteins.

These structures are pretty tough. For example, biofilm in the mouth is dental plaque. (1) You know - that hard stuff the dentist scrapes off your teeth with a special dental tool.

In a healthy gut that is filled with beneficial microflora, the biofilm that they create is thin mucus. This healthy biofilm allows the passage of nutrients through the intestinal wall. Healthy gut biofilm is moistening, lubricating, and anti-inflammatory.

The anti-inflammatory function of healthy biofilm is a big plus since these days, the gut is so prone to infection and inflammation from outside chemicals, drugs, and processed foods.

But what about an unhealthy gut biofilm? What is that like?

An unhealthy gut biofilm, as you might suspect, does all the wrong things. For example, an unhealthy gut biofilm:

Prevents the full absorption of nutrients across the intestinal wall.
Protects disease-causing microorganisms from the immune system.
Protects disease-causing microorganisms from antibiotics and antifungals (this means both herbal and pharmaceutical-grade).
Promotes inflammation.
Houses toxins like heavy metals.

The sturdy protection that biofilm provides from pathogenic bugs is one reason why some infections are so troublesome to resolve. Yeasts, parasites, and bacteria find shelter in the biofilm matrix, evading an onslaught of even the strongest of medications.

This applies to conditions like:

Chronic fatigue syndrome and fibromyalgia, which are often thought to have an infectious root.
Parasites.
Systemic Candida overgrowth.
Heartburn or GERD (gastroesophageal reflux).
Small intestine bacterial overgrowth (SIBO), which includes symptoms like heartburn, bloating, gas, abdominal cramping, brain fog, arthritis, acne, and other skin conditions.
Irritable bowel syndrome, ulcerative colitis, and Crohn’s disease. (2)

Unhealthy biofilm allows some infections to persist for years. This means that the body may become more susceptible to other infections, or co-infections, as well as other chronic degenerative diseases.
In short, unhealthy biofilms promote disease and accelerate aging.

How to Break Through Unhealthy Biofilm

Unhealthy gut biofilm is a hideout for many pathogenic, or disease-causing, microorganisms. This means yeasts like Candida. It also includes the more noxious varieties of bacteria that are related to things like diarrhea, constipation, weight gain, and bloating. (3) Parasites also seek refuge in a well-built biofilm.

Just like dental plaque that needs to be picked away at with a special dental tool, unhealthy gut biofilm is a slimy substance that adheres to the intestinal wall. And, as rigorous antibiotic therapy has shown, this slime is tough to break apart.

Unhealthy gut biofilm requires special care.

The goal of most antibiotic, antifungal, and anti-parasitic therapies is to get rid of the disease-causing microorganism. In the past, biofilms have made this near impossible. This was because we did not know about biofilms. Only recently have scientists discovered biofilms and their function in the body. (4)

First, Proteolytic enzymes can help to break apart the structure of unhealthy gut biofilm when taken on an empty stomach. Proteolytic enzymes are enzymes like protease, papain, and pepsidase FP. If you take these enzymes with food, they will only help with the digestion of food. Make sure the enzymes are high potency and in the right proportions, like Assist Full Spectrum Enzymes.

Some traditional herbal preparations break through tough biofilm. We now know that of anti-parasitic and antimicrobial herbs that are so effective because they naturally bust through and degrade biofilm. These are:

Clove, or Syzygium aromaticum
False black pepper, or Embelia ribes (5)

Apple cider vinegar, a popular all-purpose home remedy and household cleaning agent, is an acetic acid solution. Apple cider vinegar strips away important minerals from the biofilm matrix. It can be taken internally for this purpose. Start with two teaspoons mixed in 8 ounces of water.
Once you have restored the health of your gut, it is a good idea to promote the growth of a healthy biofilm to prevent a recurrence of an unhealthy biofilm.

On bacteria becoming resistant to antibiotics:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4046891/

Active starvation responses mediate antibiotic tolerance in biofilms and nutrient-limited bacteria

Bacteria become highly tolerant to antibiotics when nutrients are limited. The inactivity of antibiotic targets caused by starvation-induced growth arrest is thought to be a key mechanism producing tolerance (1). Here we show that the antibiotic tolerance of nutrient-limited and biofilm Pseudomonas aeruginosa is mediated by active responses to starvation, rather than by the passive effects of growth arrest. The protective mechanism is controlled by the starvation-signaling stringent response (SR), and our experiments link SR–mediated tolerance to reduced levels of oxidant stress in bacterial cells. Furthermore, inactivating this protective mechanism sensitized biofilms by several orders of magnitude to four different classes of antibiotics, and markedly enhanced the efficacy of antibiotic treatment in experimental infections.

So at the very least getting lots of nutrients/minerals is important. Intermittent fasting on the protocol may also not be advisable.

In the laboratory, marked antibiotic tolerance can be produced by starving bacteria for nutrients (2). Starvation also contributes to tolerance during infection, as nutrients become limited when they are sequestered by host defenses and consumed by proliferating bacteria (3, 4). One of the most important causes of starvation-induced tolerance in vivo is biofilm growth, which occurs in many chronic infections (5–7). Starvation in biofilms is due to nutrient consumption by cells located on the periphery of biofilm clusters, and reduced diffusion of substrates through the biofilm (8). Biofilm bacteria show extreme tolerance to almost all antibiotic classes, and supplying limiting substrates can restore sensitivity (9).

How does starvation produce such pronounced antibiotic tolerance? A leading hypothesis implicates the inactivity of antibiotic targets in growth-arrested cells as a central mechanism. Target inactivity could block antibiotic action because bactericidal agents subvert their targets to produce toxic products. Thus if targets are inactive, quinolones will likely generate fewer DNA breaks, aminoglycosides will produce less protein mistranslation, and β-lactams will cause lower levels of peptidoglycan accumulation that triggers cell lysis.

However, growth arrest during starvation occurs in the context of pervasive physiological changes induced by starvation responses. This fact raises the possibility that tolerance depends upon these adaptive responses, and that growth arrest and target inactivity per se are not sufficient. Identifying tolerance mechanisms is important to devising new therapeutic strategies. For example, if tolerance is inseparably linked to target inactivity, sensitizing cells could require stimulating bacterial growth, a worrisome approach during infection. Alternatively, if physiological adaptations are critical, disrupting starvation response mechanisms could enhance bacterial killing.

To investigate the relative contributions of growth arrest and starvation physiology to tolerance, we sought experimental conditions in which nutrient-limited cells could be studied in the presence and absence of starvation responses. Many bacterial species sense and respond to nutrient limitation using a regulatory mechanism known as the stringent response (SR). Carbon, amino acid, and iron starvation activate the SR by inducing the relA and spoT gene products to synthesize the alarmone (p)ppGpp. This signal regulates the expression of many genes and is also involved in virulence (10–12).
[..]
The fact that the SR mediates resistance to drugs that interact with different cellular targets suggested that it disrupts a killing mechanism common to diverse agents.
[..]
SR inactivation improves antibiotic efficacy in murine infections, and blocks the emergence of resistant mutants
[..]
Whether cells recognize it or not, starvation will eventually stop growth and the activity of antibiotic targets. However, the capacity to sense and respond to starvation allows bacteria to arrest growth in a regulated manner that maximizes chances for long-term survival. Our data show that interfering with this orderly process sensitizes experimentally starved, stationary phase, and biofilm bacteria to antibiotics, without stimulating their growth. Furthermore, our experiments suggest that starvation responses protect by curtailing the production of pro-oxidant metabolites and increasing anti-oxidant defenses. Thus, antibiotic-tolerant states may depend upon physiological adaptations without direct connections to antibiotic target activity; or drug uptake, efflux or inactivation. Identifying these adaptations, and targeting them to enhance the activity of existing drugs is a promising approach to mitigate the public health crisis caused by the scarcity of new antibiotics.

Can we find things that inhibit the bacteria's stringent response? Is that even needed if we break down the biofilm?

 

[sitting]

To Joy re memory problems/possible alzheimers - have you looked into coconut oil? Don't have the link handy of video, but doctor whose father was experiencing beginnings of alzheimers

I think you're referring to Dr. Mary Newport and her husband Steve. It's an extraordinary story.
Here's the link:

https://www.youtube.com/watch?v=_9INyTTXfR0

 

[Hesper]

Finally caught up with putting the information from the thread into the Google document. Now it's probably time to fine-tune the categories (you know, pretty much learning as we go here), better document the experiences that people have had on the protocol, keep up with the thread, and put more info in from the books.

A LOT of ground has been covered in this thread. Hopefully this document can be used like an evolving map, since so many of us are new to the territory.

Here it is, for those interested. If for some reason the "document navigator" doesn't pop up, then you can add it on through Google Add-Ons (thanks Persej!!). It's pretty laggy for me, so I just copied and pasted to have a back-up, and for personal reading. It's a lot easier to read that way.

https://docs.google.com/document/d/1uy2iTblKBKI162PkMe-lsdqUuLuiKBYYBMsebzfjk3Y/edit#

 

[l apprenti de forgeron]

One thing I know for certain is that cayenne pepper is highly inflammatory to anyone with any of the conditions being discussed in this thread. Sydney MacDonald Baker, in "Detoxification and Healing", says that, if you are dealing with any kind of inflammation, the ONLY pepper one should consume is black pepper. No other peppers allowed since ALL of them are inflammatory. That is all nightshades should be excluded entirely. That actually includes goji berries.

Potatoes that have been completely denatured by turning them into instant potatoes can be consumed in small quantities, occasionally, but other than that, I haven't found a way around this. One pinch of cayenne in a whole pot of sauce can put me in hurt city for days!

What about sweet potatoes, are relatively safe?

With the research going down the electromagnetism route (energy etc) I keep wondering whether this was part of the health - giving function of Stonehenge energies of the ancients. Perhaps our bodies were nowhere near as infested then, but the resonance idea seems to make a lot of sense.

I recall that Stonehenge is not in alignment/ not 'functioning' any longer etc. But it is worth checking out as another possible source of healing? Perhaps there ARE places that CAN function still, or immanent energies we can 'harness' somehow?

That is very interesting. And, correct me if I'm wrong, that's one of the things that have not remained in testimonies by Gurdjieff and friends, how they have dealt with the issue of parasites in the work.

 

[Shared Joy]

I had originally posted this video on the pyroluria thread last year, but I just watched it again and think it's relevant enough to this thread to repost again here:

http://<iframe width="560" height="...hA" frameborder="0" allowfullscreen></iframe>

I really like this video, because it ties together several things I've been trying to gain a better understanding of: infection, pyroluria, and methylation polymorphisms. I think that anyone who is looking seriously at the infection issue should watch the entire video carefully, but I'll mention a few of the highlights:

........
For those with a historical bent, he also has an interesting anecdote toward the end about how the Russian general Korzakov protected his troops with a homeopathic treatment during their battle against Napoleon -- he lost only 5% of his troops, while Napoleon's died in significant numbers.

Hi Shijing,

this video is really amazing not just because its content but also revealing an extraordinary man dr. Klinghardt. I highly recommend it now that I watched it twice.
At the end he presents a homeopathic remedy for immune modulation, which is so simple that one wouldn't believe it: just scrap your tongue, add a bit of water to make it more fluid, then add five times more water, so you have a 1-5 dilution, and this is your homeopathic dilution for the day to bust your immune system.
For children use their own tongue slime , made the same dilution , then use 4 drops six times a day for immune modulation. he talks about a saline solution to replace water which would keep this solution bacteria free to be used longer.
I shall try it, as is good to know how it works as is so handy!

Joy

 

[Shared Joy]

To Joy re memory problems/possible alzheimers - have you looked into coconut oil? Don't have the link handy of video, but doctor whose father was experiencing beginnings of alzheimers

I think you're referring to Dr. Mary Newport and her husband Steve. It's an extraordinary story.
Here's the link:

https://www.youtube.com/watch?v=_9INyTTXfR0

Thank you Jeep and sitting,

thanks Heavens I'm not that advanced :D. I know the story and I shall eat more coconut oil. I use it anyway for cooking.

 

[Laura]

One thing I know for certain is that cayenne pepper is highly inflammatory to anyone with any of the conditions being discussed in this thread. Sydney MacDonald Baker, in "Detoxification and Healing", says that, if you are dealing with any kind of inflammation, the ONLY pepper one should consume is black pepper. No other peppers allowed since ALL of them are inflammatory. That is all nightshades should be excluded entirely. That actually includes goji berries.

Potatoes that have been completely denatured by turning them into instant potatoes can be consumed in small quantities, occasionally, but other than that, I haven't found a way around this. One pinch of cayenne in a whole pot of sauce can put me in hurt city for days!

What about sweet potatoes, are relatively safe?

Sweet potatoes are safe because they are not a member of the NIGHTSHADE family as are potatoes, most types of peppers, and goji berries.

 

[Yas]

Can we find things that inhibit the bacteria's stringent response? Is that even needed if we break down the biofilm?

Very interesting RedFox.

I did a quick search and this is what I've found on the subject:

Influence of Growth Rate on Susceptibility to Antimicrobial Agents: Biofilms, Cell Cycle, Dormancy, and Stringent Response
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC171955/pdf/aac00066-0035.pdf

DORMANCY AND STRINGENT RESPONSE

The growth of heterotrophic bacteria in natural environments is inhibited by periods of insufficient levels of energy and nutrients (41). Such inhibition may reduce the growth rate of the bacteria to such an extent that they may be considered to have growth rates that approximate zero. Moyer and Morita (27) hypothesized that cell populations exhibiting very low growth rates or a growth rate of zero are most closely representative of cells found in oligotrophic marine environments and that it is cells in these environments and similar ones that exhibit the phenomena associated with starvation and dormancy. Such studies may well cast light on cell properties in chronic infections.

The survival strategies of bacteria in their natural environments under starvation conditions have been identified (39) and suggest that bacterial cultures undergo a series of physiological or phenotypic changes which enable the survival of some of the cells. Rapid multiple divisions of starved cells which lead to the formation of ultramicrobacteria (<0.3 ium in diameter) have been observed (29). The presence of large, "normal" marine bacterial cells has been observed only at interfaces at which nutrients were readily available (22); presumably the rest of the bacterial cells were starved and were therefore dormant ultramicrobacteria. It is assumed that such a reduction division (29) in response to starvation improves the chances of individual genomes surviving by the rapid formation of multiple copies. The reduction division is followed by a progressive reduction in the viability of the cultures until only 0.3% of the original cell number is found to be viable after 70 weeks of starvation (27, 30). Novitsky and Morita (31) showed that because of the initial multiplication of cell numbers, over 15 times the original cell number was viable, after starvation, as ultramicrobacteria. Roszak and Colwell (38) suggested that ultramicrobacteria were exogenously dormant forms, responding to unfavorable environmental conditions, and sporelike or "somnicell" stages of nonsporeforming bacteria. Morita (26) also suggested that ultramicrobacteria were the dominant or normal state of bacterial cells in marine, aquatic, and terrestrial environments.

The similarity in the responses to nutrient starvation or nutrient limitation conditions of both sporeforming and nonsporeforming bacterial species may be due to the possession by both groups of the stringent response (SR) gene, relA. The SR is a phenotypic adaptation to conditions of amino acid limitation (4). The gene product of relA is ATP:GTP 3'-pyrophosphotransferase [(p)ppGpp synthetase I], which phosphorylates GDP and GTP to the polyphosphorylated ppGpp and pppGpp forms [referred to together as (p)ppGpp]. It is thought that the decrease in available GDP and GTP is responsible for the SR effect of protein regulation, as opposed to the creation of (p)ppGpp. However, it has been suggested that (p)ppGpp acts as a suppressor of ribosome or protein activity by direct binding to the ribosome (24).

relA activity can also induce sporulation in endosporeforming bacterial species (16, 32), although it is unclear whether this gene can be considered the primary gene in the sporulation process. It is more generally accepted that the spoOA gene is the primary gene in sporulation. It has been shown that the spoOA gene is responsible for the formation of highly phosphorylated nucleotides, ppApp and pppApp [referred to together a (p)ppApp] (35, 37). The mechanisms of action and induction of these two genes appear to be very similar. Indeed, the activity of a single gene, abrB, has been shown to suppress partially the effects of both relA and spoOA activities (16).

Relationships between sporulation and the SR and between antibiotic production and susceptibility have been elucidated (23, 33, 35, 40). For example, the SR appears to be essential for self-resistance antibiotics produced by Bacillus subtilis (34). Chloramphenicol (1 ,ug/ml) was used to inhibit bacterial synthesis of (p)ppGpp, and the subsequent antibiotic production was demonstrably reduced (34). It was determined that the SR was indispensable for the initiation of antibiotic production by B. subtilis and that this antibiotic production led in turn to self-resistance. It was also shown that antibiotic-proficient mutants lacking the SR (relA) could also become self-resistant, indicating that the SR is essential for antibiotic production in B. subtilis but not for subsequent self-resistance.

Tuomanen and Tomasz (43) observed that unless the SR was relaxed, all nongrowing bacteria rapidly developed resistance to autolysis induced by a variety of agents, including various types of cell wall synthesis inhibitors. Cozens et al. (10) also remarked on the lack of susceptibility of slowly growing or nongrowing bacteria to p-lactam antibiotics and subsequent autolysis. The latter did, however, find that a novel carbapenem antibiotic, imipenem, could induce autolysis in E. coli. Matin et al (24) also suggested that nutrient-deprived cells were more resistant to disinfectant agents and to osmotic stress.

Stenstrom et al. (41) examined the effects of several antibiotics on bacterial cultures undergoing starvation. They found that some inhibitors significantly reduced the viability of long-term-starved cells. They also observed, however, that Salmonella typhimurium exhibited reduced susceptibility to tetracycline (an inhibitor of protein synthesis) after 20 days of starvation, as compared with its susceptibility at 12 days. Starved S. typhimurium also exhibited little or no susceptibility to inhibitors of cell wall or DNA synthesis. It was suggested that long-term-starved cells may express different phenotypes which may include changes in surface structures and binding and uptake of antibiotics (41). It is apparent that relA-competent cells possess unusual antibiotic susceptibilities and relationships in that they appear, in general, to have an enhanced resistance to many antibiotics. This resistance may be due solely to reduced rates of anabolism, which could explain the lack of susceptibility to cell wall- and DNA-active antibiotics observed by Stenstrom et al. (41). Alternatively, some product or products of the SR process may serve to protect intracellular targets from the action of antibiotics. In particular, the known binding affinity of (p)ppGpp for ribosomes may prevent the action of aminoglycoside antibiotics.

Tuomanen (42) observed that the metabolic state of bacteria subjected to conditions of amino acid limitation differed from that of growing cells by a pronounced and rapid decrease in the rates of protein, RNA, and cell wall syntheses. Tuomanen (42) posed the following question: is phenotypic tolerance obligatory in dormant cells? She hypothesized that if this were so, then two criteria must be met: (i) relA mutants should not be phenotypically tolerant and (ii) in the presence of the SR of all wild-type bacteria, antibiotics should fail to overcome phenotypic tolerance. The first case was found to be true (42), but the second proved false. Phenotypic tolerance of antibiotics is not absolute in all relA+ cells (41), indicating that relAU cells are susceptible to antibiotics which act as "relaxing" agents or that some other relA-related process may be inhibited with lethal effect. The observed reduction in susceptibility to some antibiotics, such as cell wall and DNA synthesis inhibitors, of viable but nongrowing cells raises the issue of the effectiveness of accepted MICs in both natural ecosystems (41) and chronic infections.

---

Relacin, a Novel Antibacterial Agent Targeting the Stringent Response
http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1002925

Abstract

Finding bacterial cellular targets for developing novel antibiotics has become a major challenge in fighting resistant pathogenic bacteria. We present a novel compound, Relacin, designed to inhibit (p)ppGpp production by the ubiquitous bacterial enzyme RelA that triggers the Stringent Response. Relacin inhibits RelA in vitro and reduces (p)ppGpp production in vivo. Moreover, Relacin affects entry into stationary phase in Gram positive bacteria, leading to a dramatic reduction in cell viability. When Relacin is added to sporulating Bacillus subtilis cells, it strongly perturbs spore formation regardless of the time of addition. Spore formation is also impeded in the pathogenic bacterium Bacillus anthracis that causes the acute anthrax disease. Finally, the formation of multicellular biofilms is markedly disrupted by Relacin. Thus, we establish that Relacin, a novel ppGpp analogue, interferes with bacterial long term survival strategies, placing it as an attractive new antibacterial agent.

---

Wile I was searching about this, I've found some article on EDTA and biofilms:

Metal Chelation and Inhibition of Bacterial Growth in Tissue Abscesses
http://www.sciencemag.org/content/319/5865/962.short

ABSTRACT
Bacterial infection often results in the formation of tissue abscesses, which represent the primary site of interaction between invading bacteria and the innate immune system. We identify the host protein calprotectin as a neutrophil-dependent factor expressed inside Staphylococcus aureus abscesses. Neutrophil-derived calprotectin inhibited S. aureus growth through chelation of nutrient Mn2+ and Zn2+: an activity that results in reprogramming of the bacterial transcriptome. The abscesses of mice lacking calprotectin were enriched in metal, and staphylococcal proliferation was enhanced in these metal-rich abscesses. These results demonstrate that calprotectin is a critical factor in the innate immune response to infection and define metal chelation as a strategy for inhibiting microbial growth inside abscessed tissue.

I can't access the full article.
---

Chelator-Induced Dispersal and Killing of Pseudomonas aeruginosa Cells in a Biofilm†
http://aem.asm.org/content/72/3/2064.full

ABSTRACT

Biofilms consist of groups of bacteria attached to surfaces and encased in a hydrated polymeric matrix. Bacteria in biofilms are more resistant to the immune system and to antibiotics than their free-living planktonic counterparts. Thus, biofilm-related infections are persistent and often show recurrent symptoms. The metal chelator EDTA is known to have activity against biofilms of gram-positive bacteria such as Staphylococcus aureus. EDTA can also kill planktonic cells of Proteobacteria like Pseudomonas aeruginosa. In this study we demonstrate that EDTA is a potent P. aeruginosa biofilm disrupter. In Tris buffer, EDTA treatment of P. aeruginosa biofilms results in 1,000-fold greater killing than treatment with the P. aeruginosa antibiotic gentamicin. Furthermore, a combination of EDTA and gentamicin results in complete killing of biofilm cells. P. aeruginosa biofilms can form structured mushroom-like entities when grown under flow on a glass surface. Time lapse confocal scanning laser microscopy shows that EDTA causes a dispersal of P. aeruginosa cells from biofilms and killing of biofilm cells within the mushroom-like structures. An examination of the influence of several divalent cations on the antibiofilm activity of EDTA indicates that magnesium, calcium, and iron protect P. aeruginosa biofilms against EDTA treatment. Our results are consistent with a mechanism whereby EDTA causes detachment and killing of biofilm cells.

----

The metal chelator EDTA has been shown to cause lysis, loss of viability, and increased sensitivity of planktonic Proteobacteria to a variety of antibacterial agents (reference 13; reviewed in references 25, 29, and 40). This has led to the use of EDTA as a preservative in many products. Little is known about the influence of EDTA on biofilms of Proteobacteria. Raad et al. (32, 33) have shown that EDTA combined with minocycline is an effective treatment for microorganisms embedded in biofilms on catheter surfaces. Their studies focused on Staphylococcus epidermidis, Staphylococcus aureus, and Candida albicans; however, they also reported two cases of P. aeruginosa-infected catheters where the EDTA-minocycline treatment caused a large decrease in the number of viable biofilm cells (32). Recently, Kite et al. (23) reported that tetrasodium EDTA could be used to eradicate biofilms on catheters. Ayres et al. (3) have examined the effects of permeabilizing agents on antibacterial activity against a P. aeruginosa biofilm grown on a metal disk. Their results further suggest increased anti-P. aeruginosa biofilm activity for several antibiotics when combined with EDTA (3).

We have further characterized the activity of EDTA against P. aeruginosa biofilms. We show that EDTA treatment of Pseudomonas biofilms results in 1,000-fold greater killing than treatment with gentamicin, an antibiotic commonly used to treat P. aeruginosa infections. Furthermore, a combination of EDTA and gentamicin can result in eradication of P. aeruginosa in our model biofilms. We present evidence that, in addition to killing, EDTA causes a rapid dispersion of P. aeruginosa cells from biofilms. Our data suggest that magnesium, calcium, and iron are involved in P. aeruginosa biofilm maintenance.

RESULTS

EDTA enhances loss of P. aeruginosa biofilm-associated cells.We examined the reduction in biofilm cells in response to EDTA treatment. Biofilms grown in a spinning disk reactor were exposed to various concentrations of EDTA, gentamicin, or both, and cell viability was measured (Fig. 1). In PBS, 50 mM EDTA reduced the number of biofilm-associated cells by >99%, while gentamicin (50 μg per ml, a concentration well over 10 times higher than the MIC for planktonic P. aeruginosa PAO1) caused a reduction of <10% in the number of biofilm cells. Furthermore, treatment with EDTA (50 mM) and gentamicin (50 μg per ml) together was more effective than EDTA alone (Fig. 1). Because Tris and EDTA can work synergistically to permeabilize planktonic Proteobacteria (25), we examined the effect of EDTA on P. aeruginosa biofilms in Tris buffer and found that all treatments were more effective in Tris buffer than in PBS (Fig. 1). In fact, the combination of EDTA (50 mM) and gentamicin (50 μg/ml) in Tris buffer completely eradicated biofilm-associated cells.

Effect of EDTA on P. aeruginosa biofilm structure.To examine the effect EDTA has on P. aeruginosa biofilm architecture, we used a flow cell system. As expected, P. aeruginosa biofilms developed mushroom-like structures in our experiments (Fig. 2). Addition of 50 mM EDTA resulted in preferential killing of cells inside the mushroom-like structures. The structures remained intact, as indicated by a shell of green fluorescent cells around the edge. Dead cells stained with propidium iodide (red) within the shell (Fig. 2). We chose 50 mM EDTA based on previous experiments (Fig. 1), which indicate that this is close to the minimal EDTA concentration for maximal killing of P. aeruginosa.

EDTA induces dispersal of cells from biofilms. Imaging of bacteria in flow cell biofilms over time suggested that EDTA caused not only killing but also dispersal of cells from the biofilm. To further examine the EDTA effect, we collected time lapse images by CSLM (see movies S1 to S3 in the supplemental material), and we determined total and viable cell numbers in the flow cell effluent at 10-min intervals (Fig. 3). Whereas an untreated flow cell showed a constant level of viable, dispersed cells in the effluent, an increase in the number of cells in the effluent was detected 50 min after addition of EDTA to the medium reservoir, corresponding to the time at which EDTA reached the flow cell (Fig. 3, top). This increase in the number of cells in the effluent correlated with a dispersion of green fluorescence (i.e., cells) in the flow cell as observed by CSLM (Fig. 3, green channel, 50 to 90 min). After 90 min, the cell numbers in the effluent decreased. We believe this decrease is due to washout of detached cells from the flow cell and EDTA killing of cells, as can be seen by a difference of approximately 100-fold between the direct and viable counts (Fig. 3, top). The interior of the biofilm is affected at this time as dying cells lose their GFP and the propidium iodide staining is exposed. Here we used a low concentration of propidium iodide (4 μM versus 30 μM for the dead-cell staining) that stains the extracellular matrix but not P. aeruginosa cells (4, 37). With further incubation in the presence of EDTA, the decrease in cell numbers progresses and the internal regions of the mushroom-like biofilm structures become devoid of viable cells (Fig. 3, 150 min).

Role of divalent cations in detachment and lysis of biofilms.Previous work on EDTA-treated planktonic P. aeruginosa focused on cell lysis. Our results suggest that treatment of biofilms with EDTA facilitates two processes: cell detachment and killing (Fig. 2 and 3). To gain insight into which divalent cations are involved in cell detachment and lysis, we utilized the difference in the stability constant [log(Kc)] that EDTA has for various divalent cations (barium [Kc = 7.78], magnesium [Kc = 8.83], calcium [Kc = 10.61], and iron [Kc = 25.0]) (35). We reasoned that any EDTA effect blocked by the addition of a specific cation (at a concentration that will completely saturate EDTA) is due to the role that cation (or a cation for which EDTA has lower affinity) plays in stabilizing the biofilm. In flow cell experiments, the addition of barium had no effect on EDTA-mediated killing and detachment. Addition of magnesium appears to block killing (GFP is not lost in the internal region of the mushroom), but some detachment is evident (Fig. 4). When calcium or iron is added, killing and detachment are completely blocked (Fig. 4). Similar results were obtained in spinning disk reactor experiments (Fig. 5), although in this system addition of calcium led to some detachment (40% of the cells detached and were in the planktonic state [Fig. 5, bottom]). Detachment was effectively blocked by addition of iron. This suggests that both calcium and iron may be important in stabilizing biofilms.

{...}

DISCUSSION

EDTA has a detrimental effect on the outer membrane permeability of free-living planktonic Proteobacteria (15, 25, 29, 40). By chelating divalent cations from their binding sites in lipopolysaccharide (LPS), EDTA facilitates the release of a significant proportion of LPS from the cell (26). Although prolonged treatments with EDTA are lethal, short treatments increase the permeability of the outer membrane to hydrophobic molecules (25, 29). Thus, there can be synergy between EDTA and other antibacterial agents (2, 8, 24). In this study we report that EDTA not only kills P. aeruginosa planktonic cells but also affects P. aeruginosa biofilms (Fig. 1 and 2).

Exposure of P. aeruginosa biofilms to EDTA killed P. aeruginosa cells and triggered detachment of cells from biofilms (Fig. 3 to 5). CSLM revealed that the majority of the cell population affected by the EDTA treatment resides in the inner regions of the mushroom-like structures. This type of killing or detachment pattern has been observed in P. aeruginosa biofilms exposed to various conditions (6, 34, 41). We note that sloughing of cells from the outer regions of the biofilms might also contribute to the detachment process. Chen and Stewart (9) have previously tested the abilities of various chemical treatments to remove mixed P. aeruginosa-Klebsiella pneumoniae biofilms. They reported that EDTA treatment (10 mM) resulted in a 49% reduction in cell counts, and they presented some evidence that this was due to dispersal of biofilm bacteria. The authors hypothesized that calcium was important for stabilizing the biofilm matrix (9). Other studies have also suggested a role for calcium in stabilizing biofilms of bacteria (18, 22, 39).

To better understand how P. aeruginosa biofilms are affected by EDTA treatment, we examined the abilities of different divalent cations to block EDTA-induced detachment and killing. Barium addition did not block killing, but the addition of magnesium, calcium, or iron did (Fig. 4 and 5). The relative stability constants of EDTA for the divalent cations may be ranked in ascending order as follows: barium, magnesium, calcium, and iron. Thus, our data support previous conclusions that magnesium can block lysis of planktonic P. aeruginosa by EDTA (1, 7). EDTA is thought to chelate stabilizing magnesium ions from the LPS, causing release of LPS from the outer membrane (5, 26). Magnesium did not completely block EDTA-induced detachment, but the addition of either calcium or iron did (Fig. 4 and 5). Based on previous work, one might have anticipated an involvement of iron and calcium in biofilm maintenance. In P. aeruginosa, addition of calcium to growth media increased biofilm cohesiveness, resulting in decreased detachment (38). Turakhia et al. (39) demonstrated that addition of EGTA (a calcium-specific chelator) to a mixed aerobic sewage sludge biofilm resulted in immediate detachment of cells from the biofilm. We found similar EGTA effects on detachment from the biofilm, but killing was fivefold lower than that found with EDTA (data not shown). Chen and Stewart (10) have tested the viscosity of a mixed P. aeruginosa-Klebsiella pneumoniae biofilm suspension following addition of various cations. They report that addition of iron salts significantly increased biofilm viscosity. The authors concluded that electrostatic interactions contribute to biofilm cohesion and that iron cations are potent cross-linkers of the biofilm matrix (10).

The use of EDTA to treat biofilm-related infections is being evaluated by several groups, with promising results (23, 32, 33); however, little is known about how EDTA causes increased killing of biofilm cells. The results of this study suggest that the activity of EDTA against biofilm cells is mediated by chelation of several divalent cations that are required to stabilize the biofilm matrix. Future work will be required to determine their specific role in this process. Our results imply that EDTA chelation of magnesium, calcium, and iron can enhance detachment of cells from the biofilm. EDTA also facilitates the killing of biofilm cells by chelating magnesium associated with the LPS. This dispersal process and the increased cell permeability facilitated by EDTA may also explain the enhanced killing observed in combined EDTA and gentamicin treatment (Fig. 1). This combination may have therapeutic utility.

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Suppression of bacterial biofilm formation by iron limitation
http://www.sciencedirect.com/science/article/pii/S030698770400283X

Abstract
The concentration of iron that permits bacterial differentiation generally differs from that needed for vegetative cell growth. An undesirable manifestation of differentiation is biofilm formation. The process in some, but not all, bacterial systems requires a higher level of iron than is needed for growth and it is suppressed by specific iron chelators. Human transferrin and lactoferrin, as well as at least six low molecular mass iron chelators, are now available for possible screening and clinical development as inhibitors of bacterial biofilm formation.

I can't access the full article.

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EDTA as a potential agent preventing formation of Staphylococcus epidermidis biofilm on polichloride vinyl biomaterials
http://www.researchgate.net/profile/Pawel_Rybojad/publication/23715633_EDTA_as_a_potential_agent_preventing_formation_of_Staphylococcus_epidermidis_biofilm_on_polichloride_vinyl_biomaterials/links/0deec51adf0bf52138000000.pdf


DISSCUSION

{...}

Several studies were undertaken to manage with microbial biofi lm on the biomaterials, including the incorporation of antibiotic or non-antibiotic agents (e.g. usnic acid, surfactin, epigallocatechin-gallate, ovotransferin, protamine sulfate) into biomaterials [15, 29]. The impregnation of catheters by antibiotics seems to be an inappropriate way of prevention of biofi lm formation, since in contrast to non-antibiotic agents, it can lead to an increase of bacterial resistance to antimicrobial drugs [15]. In this paper, we assessed the infl uence of EDTA in vitro on formation and eradication of S. epidermidis biofi lm formed on the PCV biomaterials (Nelaton and Thorax catheters). EDTA, a widely known chelating agent with anticoagulant activity is used for some medical purposes, such as the treatment of hypercalcemia [10, 15]. It is also used in dentistry to remove inorganic debris of the root canal and prepare it for obturation [14, 20].

Only some literature data suggest that EDTA possesses potential activity against microbial biofilm [3, 10, 11, 15, 19]. Moreover, the literature data indicate that the inhibitory effect of EDTA against staphylococcal biofilm was increased in combination with minocycline, ovotransferin and protamine sulfate [16, 17, 18, 29]. Our results showed that the adhesion and formation of the S. epidermidis biofilm on the PCV Nelaton and Thorax catheters was inhibited by EDTA at low concentrations (between 1–2 mmol/l). In contrast, the eradication of mature S. epidermidis biofi lm required, in most cases, much higher concentrations of this agent (>32 mmol/l); only in the case of two strains was the biofi lm disrupted in low concentrations of EDTA – 2–4 mmol/l. Our data indicate also that there was no correlation between the ability of slime production by staphylococcal strains and the concentrations of EDTA needed for inhibition of adhesion or biofilm formation and eradication of the mature structure. This observation may suggest that slime is not the effective agent protecting staphylococcal cell against EDTA.

Root et al. [19] studied the effect of EDTA in vitro on the eradication of biofi lm formed by S. epidermidis on a Hickman catheter made from silicone. According to their data, high concentration of EDTA (108 mmol/l) was required to eradicate the staphylococcal biofi lm. However, other authors have shown that concentrations of EDTA, higher than 2 mmol/l expressed a toxic effect in vitro on the viability of cell cultures [3]. The mechanism most possibly responsible for the inhibitory effect of EDTA on staphylococcal biofilm formation is the chelation of metal ions. It is well-known that the PIA (Polysaccharide Intracellular Antygen) in S. epidermidis is a necessary factor involved in the fi rst step of biofilm formation. The appropriate cell surface properties determined by the presence of PIA antigen depends on the level of Mg2+ ions [28]. Therefore, the decreased level of Mg2+ ions is due to chelation by EDTA, and may inhibit the adhesion procces and, as a result, also the formation of biofilm [15].

CONCLUSIONS

Our data indicate that EDTA may be regarded as a useful agent in the prevention of staphylococcal biofilm formation on PCV medical devices, but not for the disruption of mature biofilm, due to its cytotoxicity at higher concentrations.

Unfortunately, I have to leave now, so I can't add my impression on all this. In summary, it seems that the EDTA protocol could be REALLY important before the antibiotic one, so the critters are at least weaker.

I'm sorry if I posted something that was already posted... I'm always catching up with the thread but maybe I missed something.

FWIW...

 

[goyacobol]

To Joy re memory problems/possible alzheimers - have you looked into coconut oil? Don't have the link handy of video, but doctor whose father was experiencing beginnings of alzheimers

I think you're referring to Dr. Mary Newport and her husband Steve. It's an extraordinary story.
Here's the link:

https://www.youtube.com/watch?v=_9INyTTXfR0

My mother is showing some signs of early alzheimers and this would be a great way to slow or reverse the symptoms. Coconut oil sounds very promising for many problems.

Thanks

 

[Lilou]

You might look into a product called Prevagen, it's a little pricey though.

I don’t think I’d waste my money on Prevagen. The reviews are split on its effectiveness. Some say the protein it contains, apoaequorin, is neurtralized by stomach acid, so it cannot even get to the brain to help with memory. Some say it works, which could simply be placebo effect. What is for sure, is the FDA has issued warnings, and the company is having some legal troubles.

[quote author= http://www.highya.com/prevagen-reviews]
“Prevagen contains a synthetic version of the jellyfish-derived protein apoaequorin. The warning letter states that because this ingredient is not a vitamin, mineral, amino acid, herb, botanical or an extract or metabolite thereof, it cannot be a dietary supplement ingredient.” In addition, the FDA claimed that the company failed “to report adverse events and product complaints associated with Prevagen, including heart arrhythmias, chest pain, vertigo, tremors, and fainting, seizures and strokes.” [/quote]

The only ingredient contained in Prevagen is apoaequorin, which is a calcium binding protein that helps regulate calcium levels within your body. As a result, this calcium can be used (at least in part) by your body to improve brain function. I’m no expert on this, but I’d be wary of a calcium blocker – this could have similar effects as calcium channel blocker medications used for heart disease, which could explain the symptoms some people reported.

Overall, it looks like its days on the market as a supplement are numbered.

 

[nicklebleu]

I had a look if turpentine was any help in resolving the biofilm issue - and apparently there is. However there is very little in the medical literature about turpentine, for obvious reasons. But some alternative health providers advertise the ingestion of turpentine as part of a candida protocol (this has been talked about here on the forum before). So it might be work including turpentine on the protocol in view of disrupting biofilms.

While sifting through the data I ran across a paper describing hepcidine, which is quite fascinating. Hepcidine has been talked about in this thread earlier on as well.

Hepcidin: inflammation's iron curtain

H. McGrath Jr and P. G. Rigby 1

Rheumatologists and their patients are the beneficiaries of a recently identified peptide, hepcidin (Table 1). Isolated from human urine and plasma in the year 2000 [1, 2], hepcidin appears to be the long-sought iron-regulatory hormone responsible for the anaemia of chronic disease [3, 4]. It is more than that: it is an acute-phase reactant, responding to infection and inflammation [5]; it is an antimicrobial peptide that disrupts microbial membranes [1, 6]; and it provides an iron-restricted internal milieu inhospitable to microbes [7, 8].

Hepcidin is a 25 amino acid, 2–3 kDa, cationic peptide that has broad antibacterial and antifungal actions [1]. In concert with other antimicrobial peptides, known as defensins and cathelicidins [9], it provides a first line of defence at mucosal barriers [1, 2]. However, more germane for rheumatologists is its control of iron kinetics. Produced by hepatocytes, hepcidin inhibits the intestinal absorption [1, 10], macrophage release [3, 7] and placental passage [10] of iron. Hepcidin mRNA moves with the body's iron levels, increasing as they increase and decreasing as they decrease [11]. More pertinently, hepcidin rises with infection or inflammation and falls with hypoxia or anaemia [12].

The anaemia of chronic disease has long confounded physicians. It is generally normocytic and normochromic, but may be hypochromic or microcytic [13]. The low serum iron and normal-to-low iron-binding capacity, in conjunction with a high-to-normal serum ferritin level in patients with inflammatory disease, has been perplexing. Also notable has been the shortened red blood cell survival and blunted erythropoietin-induced production of red blood cells. At one time known as the anaemia of infection, it became known, after man's entry into the age of antibiotics, as the anaemia of chronic disease, and now, perhaps more aptly, it is the anaemia of inflammation.

Iron can be toxic. It catalyses the generation of reactive free radicals [14] and activates NF-κB, the prototypic transcription factor for genes involved in inflammation [15]. At high levels, iron is damaging to tissues. Humans need little dietary iron, 1–2 mg a day sufficing for the average adult male [16]. However, mammals lack a regulated pathway for iron excretion [12], so iron absorption has to be tightly regulated. Hepcidin acts as a negative regulator of iron absorption: USF2 knockout mice lacking hepcidin mRNA become iron-overloaded [17]; transgenic mice with increased hepcidin expression die at birth with severe iron deficiency [10]; humans with hepcidin-producing adenomas develop an iron-refractory iron deficiency anaemia [4]; and gene mutations affecting hepcidin cause haemochromatosis in humans [18] and in mouse models [17].

In animals and man, the anaemia of inflammation is due primarily to hepcidin-induced sequestration of iron in the macrophage [18]. The link between inflammation/infection and liver production of hepcidin is attributed to IL-6, produced at sites of infection/inflammation [13]. Human hepatocytes increase hepcidin mRNA in the presence of IL-6 or lipopolysaccharide and in the presence of IL-6 produced by monocytes exposed to lipopolysaccharide [5]. Infection in one human subject reportedly increased excretion of hepcidin in the urine 100-fold [5]. Mice respond to the inflammation generated by an injection of turpentine with a six-fold increase in hepcidin mRNA and a two-fold decrease in serum iron [10]. Remarkably, the white bass responds to infection with Streptococcus iniae with a 4500-fold rise in hepcidin mRNA expression [19].

In addition to iron levels and inflammation/infection, there is another factor that affects hepcidin levels: it is anaemia. Along with hypoxia, anaemia overrides the effects of iron and inflammation/infection, reducing levels of hepcidin mRNA [4, 12]. Were this not the case, inflammation, by maintaining high hepcidin levels, would keep the haematocrit dropping. Instead, down-regulation of hepcidin mRNA expression by anaemia produces a new steady state, usually with haematocrits 3–5 points below normal.

In addition to disrupting bacterial membranes, hepcidin provides an inhospitable internal milieu for microbes that successfully enter the bloodstream. Micro-organisms need iron [14]. Bacteria require iron for the production of the superoxide dismutase that protects them from host oxygen radicals [20, 21]. Hepcidin, by inducing macrophage sequestration of iron, robs bacteria of this element. Blood and intracellular bacteria [22] may weaken; biofilms may not develop [7]. Pertinent here is the recent report of an inverse relationship between the incidence of tuberculosis and rheumatoid arthritis (RA) [23], raising the possibility that that the inaccessibility of iron in RA protects from tuberculosis [24].

Pallor, weakness and fatigue have been recognized as hallmarks of chronic disease for millennia. Anaemia obviously contributes to the pallor. Less obvious is whether the decrease in serum iron diminishes its availability to myoglobin and the enzymes catalysing the redox reactions required for the generation of energy (cytochromes) sufficiently to contribute to weakness and fatigue.

Defensins are antimicrobial peptides produced by cells of epithelial linings [9]. Hepcidin, like defensins, is an antimicrobial peptide that kills on contact. However, because it is produced by the liver, has not been found to have chemotactic properties, and differs structurally from defensins [25], it will likely be classified as an acute-phase reactant [5].

The identification of hepcidin opens the door to therapeutic approaches for several disorders and to proscriptions regarding the use of iron. Recombinant hepcidin may be the ideal therapeutic agent for those with some forms of juvenile haemochromatosis and with the less severe but more common form of haemochromatosis caused by mutations in the HFE gene [26]. Hepcidin-induced iron deprivation may prove helpful in preventing the development of resistant bacterial biofilms [10]. For the anaemia of inflammation, often resistant to erythropoietin therapy [27], inhibitors of hepcidin, by releasing sequestered iron, could restore haemoglobin levels and conceivably correct an iron lack in myoglobin and cytochromes as well. Finally, of related interest is a recent report that moderate alcohol intake reduces levels of C-reactive protein and IL-6 [28], the principle chemokine for the generation of hepcidin mRNA, extrapolating to a possible ameliorative role of alcohol in both inflammation and the anaemia of inflammation.

As to proscriptions, iron supplements should be monitored, not only because the resulting increase in hepcidin can fuel antimicrobial engines unnecessarily, but because hepcidin increases macrophage iron sequestration in the synovium as elsewhere. Synovial iron has the propensity to generate oxygen free radicals that have been linked to the chronicity and erosiveness of joint disease in RA [29]. In fact, intramuscular injections of iron have long ago been reported to cause acute flares of joint inflammation in RA [30]. A broader phlogistic potential of iron towards the joint comes from a recent report that iron depletion by serial phlebotomies diminishes recurrences of gouty arthritis [31]. If one adds all of the above to the reported links of iron sufficiency to colon cancer [32], diabetes mellitus [33], chronic hepatitis [34] and atherosclerosis [35], it would seem best to phase out gratuitous iron supplementation altogether.

The discovery of hepcidin provides a thread that ties together the perplexing triad of decreased serum iron, increased macrophage iron and chronic inflammation. In addition, it offers a unique opportunity for determining the effects of iron on disease, the usefulness of hepcidin inhibitors or promoters to control iron kinetics, and the proper means of iron administration. In the aggregate, these will represent a step forward in the treatment of a variety of diseases.

The authors have declared no conflicts of interest.

Source including free full-text

 

[shijing]

My mother is showing some signs of early alzheimers and this would be a great way to slow or reverse the symptoms. Coconut oil sounds very promising for many problems.

goyacobol, if you haven't found it already, there's a thread on coconut oil here that you may be interested in taking a look at:

Coconut Oil

There are also some books available on treating Alzheimer's with coconut oil:

Alzheimer's Disease: What If There Was a Cure?

Virgin Coconut Oil and Alzheimer's Disease: A Holistic Guide to Geriatric Care

Stop Alzheimer's Now!: How to Prevent & Reverse Dementia, Parkinson's, ALS, Multiple Sclerosis & Other Neurodegenerative Disorders