I think this is an important issue that deserves its own thread.

I will try to summarize what I have found out about it, and even include my wild speculations...

"Eradication of Helicobacter pylori may be beneficial in the management of Alzheimer’s disease"
Abstract: Infectious agents have been proposed as potential causes of Alzheimer’s disease (AD). Recently, we documented a high prevalence of Helicobacter pylori (Hp) infection in patients with AD. We aim to access the effect of Hp eradication on the AD cognitive (MMSE: Mini Mental State Examination and CAMCOG: Cambridge Cognitive Examination for the Elderly) and functional (FRSSD: Functional Rating Scale for Symptoms of Dementia) status parameters. In the first part of the study, a total of 50 consecutive patients with AD and 30 age-matched anaemic controls underwent an upper gastrointestinal endoscopy, and gastric mucosal biopsies were obtained to detect the presence of Hp infection by histologic analysis and rapid urease test. Serum anti-Hp-specific IgG level was analysed by enzyme-linked immunosorbent assay. In the second part, Hp-positive AD patients received a triple eradication regimen (omeprazole, clarithromycin and amoxicillin), and all patients were followed up for 2 years, while under the same treatment with cholinesterase inhibitors. Hp was detected in 88% of AD patients and in 46.7% of controls (P < 0.001). Hp eradication was successful in 84.8% of treated patients. At the 2-year clinical endpoint, cognitive and functional status parameters improved in the subgroup of patients where Hp eradication was successful (P < 0.001 and P = 0.049 for MMSE and CAMCOG, respectively; P < 0.001 for FRSSD), but not in the other patients. Hp eradication may positively influence AD manifestations, suggesting a possible common link between Hp and AD.
http://www.springerlink.com/co...ab4620921dcd1e6&pi=2

What caught my attention is this statement: "At the 2-year clinical endpoint, cognitive and functional status parameters improved in the subgroup of patients where Hp eradication was successful ..., but not in the other patients. Hp eradication may positively influence AD manifestations, suggesting a possible common link between Hp and AD."

I have to connect the links here to AD here.

We've recently read that corrupted tau proteins can have characteristics similar to the prions of "mad cow disease", scrapie, chronic wasting disease of deer, and CJD of humans:

"Rogue protein 'spreads in brain'"
BBC Sunday, 7 June 2009
Scientists have shown a rogue protein thought to cause Alzheimer's can spread through the brain, turning healthy tissue bad. They believe the tau protein may share characteristics with the prion proteins which cause vCJD. When injected into the brains of healthy mice it triggered formation of protein tangles linked to Alzheimer's. However, experts stressed the Nature Cell Biology study did not mean tau could be passed from person to person. Tau is a protein present in all nerve cells, where it plays a key role in keeping them functioning properly. But a rogue form of the protein can trigger the formation of protein clumps within nerve cells known as neurofibrillary tangles. It is thought that these tangles are likely to be a major cause of Alzheimer's disease... Tau is a protein present in all nerve cells, where it plays a key role in keeping them functioning properly. But a rogue form of the protein can trigger the formation of protein clumps within nerve cells known as neurofibrillary tangles. It is thought that these tangles are likely to be a major cause of Alzheimer's disease.
http://news.bbc.co.uk/2/hi/health/8084787.stm

It is interesting to note that the degeneration tends to follow the path of neural networks:

"Neuronal subpopulations and genetic background in tauopathies: a catch 22 story?"
L. Bue´e*, A. Delacourte
Neurobiology of Aging 22 (2001) 115–118
"...these vulnerable neurons degenerate following precise pathways. Regarding encephalopathy such as PEP, it is clear that a virus follows neural networks for its propagation. It is now well established that there is also a sequential degeneration of vulnerable networks of neurons in AD and PSP. In AD, both biochemical and neuropathological studies show that NFT formation starts in the hippocampal formation (from transentorhinal to entorhinal and then hippocampus), progresses sequentially as follows anterior, inferior and medium temporal cortex, and then spreads into polymodal association areas, unimodal areas and primary and/or sensory areas..."
http://www.alzheimer-adna.com/.../2001Bueecatch22.pdf

Can toxins produced by bacteria initiate the process?

"Profiling the culprit in Alzheimer's disease (AD): bacterial toxic proteins - Will they be significant for the aetio-pathogenesis of AD and the transmissible spongiform encephalopathies?" Schmitt HP. Institute of Pathology, Department for Neuropathology, University of Heidelberg, Germany
http://www.ncbi.nlm.nih.gov/pu...anel.Pubmed_RVDocSum

Can a Hp infection also explain the success some people have been experiencing with the "perispinal Enbrel injections"? Enbrel is thought to work by inhibiting the effects or the production (I don't remember which right now) of "tumor necrosis factor", TNF-alpha. And guess what substance a Helicobactor pylori infection in the stomach causes the body to produce? Yep, TNF-alpha. In the full text of the Heliobacter article, it says on page 8, "However, Hp, an extracellular bacterium, could affect the brain and other target organs, such as the heart, indirectly, through the release of numerous cytokines, including TNF-[alpha] acting at a distance."

To me, this gives a reason for why the perispinal injection of Enbrel should work, why reports of its success are not merely wishful thinking. It's the link to a cause that validates the idea. I think that the success of Enbrel also supports the theory for the mechanism by which Hp in the stomach affects the brain.

For those getting the Enbrel treatments, I think this says, check to see if there is also an H-pylori infection present. (There may be other bacteria or viruses involved, such as Herpes simplex virus type 1 (HSV1) and Chlamydophila (Chlamydia) pneumoniae.)

Here is the link to the full text of the paper. Even for us non-professionals, it is understandable enough to undestand the ideas:
http://www.springerlink.com/co...38x7031/fulltext.pdf

Wild speculation time:
If an Hp infection turns out to be the beginning of the AD disease process, then for those currently suffering with the disease, I would first stop the progression, then eradicate the infection(s). We appear to have two ways to stop the progression: Enbrel or the MCT oil regimen. They don't seem to conflict, targetting different steps of the disease process, so it would probably be wise to use both.

Obviously, if eliminating a chronic bacterial infection reduces the body's production of TNF-alpha to normal levels, there will be no need for TNF-alpha blocking drugs such as Enbrel. This news will not be greeted with enthusiasm by the pro-Tobinick faction, nor the "there's nothing we can do, we're powerless, everyone should just die now" crowd.

Hp was detected in 88% of AD patients. Hp eradication was successful in 84.8% of treated patients, which is about normal for all cases of Hp infection.

If you multiply 88% by 84.8%, you get ~75%... which seems to be about the percentage of people that are helped by MCT/coconut oil.

Also, one does not need to have an ulcer to have an Hp infection.

I don' t know where they got this statistic, but I found...

"In countries with poor sanitation, 90% of the adult population can be infected. In the U.S., 30% of the adult population is infected."
http://www.medterms.com/script....asp?articlekey=3676

90% of the people with an Helicobacter pylori (Hp) infection do NOT have stomach trouble or ulcers. Or, only 10% of people with an Hp infection have stomach trouble.

"H. pylori gastritis produces no symptoms in 90 percent of infected persons. The prevalence of H. pylori infection varies geographically and has been demonstrated to be as high as 52 percent in the United States. Factors associated with higher infection rates are increasing age, African-American or Hispanic race, lower levels of education, and birth in a developing country."
http://www.aafp.org/afp/20020401/1327.html

I'm sure that the percentage of people with an Hp infection that will develop AD is similarly small.

I looked up the statistics for Aricept. It is only effective for 50% of the people who take it, and then, it is only effective for about 6 to 12 months.

If the statistics of this research hold true, then one could expect the eradication of an Hp infection to be effective for about 75% of those treated, and the effect should last at least 2 years (which was the limit of how long they tracked the test participants).

If I were in charge of an insurance company, I think I would consider the cost of treating an Hp infection followed by the stabilization of the patient as a discount when compared to six months worth of Aricept, followed by the cost of a nursing home.

There are some interesting charts in the full text .pdf file of the paper:
http://www.springerlink.com/co...38x7031/fulltext.pdf

The original article was from researchers in Greece, so the statistics given for the prevalence of Hp infection may be different in your country.

Another thought I had was that the treatment for Hp is a two or three week course of multiple antibiotics. This probably knocks out a whole bunch of other bacteria in all parts of the body. What if the culprit is NOT Hp, but gets killed off by the Hp antibiotics?

Whatever the case, I think there are some simple tests such as a blood test for Hp antibodies, or this "breath test" that could be done relatively easily. I think it's worth asking the phsyicians about.

From what I've read, this bug is particularly hard to treat. They seem to be using a cocktail of three drugs for something like 14 days. The antibiotics can have side effects, making the treatment unpleasant.

I started thinking, what substances, other than prescription antibiotics, inhibit or eliminate Hp bacteria? I've heard that Pepto-Bismol will (the bismuth in it). And then I remembered that in Chinese medicine, cinnamon had long been used to treat stomach problems. A quick search of the Internet found that yes, indeed, cinnamon has been and is being investigated for its anti-Hp potential. But, which component of cinnamon is it? I don't know. This may mean that using whole ground cinnamon may be more effective than using extracts.

Some foods or spices may also reduce the Hp infection, but I haven't found anything yet, other than prescription antibiotics, that will eliminate it. Broccoli srputs, dill, and cinnamon may be good candidates. "Probiotics", or "good bacteria" may help by crowding out the H-pylori. Others will have to be explored.

For broccoli sprouts, its the sulforaphane in them that seems to help...

"Broccoli Sprouts Good for the Gut"
Compound in Broccoli Sprouts May Protect Against Ulcers, Stomach Cancer
By Jennifer Warner
WebMD Health April 6, 2009
http://www.webmd.com/digestive...uts-good-for-the-gut

Of course, if you can get a physician to test for Hp, and then prescribe antibiotics, go for it!

There are probably several conditions that eventually lead to AD. This particular one would not address genetic causes or exposure to a toxin.

I doubt that this is the end of the story. Never the less, I think that the idea of Helicobacter pylori being involved should be aggresively researched. If eliminating a Helicobacter pylori infection worked for 3 out of 4 cases, that would be a good start!

I started thinking about other antibiotics. I read that methylene blue is used as an antibiotic to treat urinary tract infections, malaria, and even bacteria "infections" in fish aquariums. Does it also eliminate Hp? Could that be why it has helped people with AD (Rember study)? Well, maybe. I found this article, but I don't have the whole text. It is intriguing.

"Evaluation of methylene blue and triple therapy for eradication of Helicobacter pylori infection in the nude mouse model"
KARITA M. (1) ; TADA M. (1) ; OKITA K. (1) ; TSUDA M. ; NAKAZAWA T.
International symposium on Helicobacter pylori and its diseases No5, Tokyo , JAPON (04/04/1992)
1993, vol. 5, SUP1 (6 ref.), pp. S79-S83
European journal of gastroenterology & hepatology

Abstract: "Objective: To determine how far Helicobacter pylori infection can be eradicated with methylene blue and triple therapy (amoxicillin, metronidazole, bismuth subnitrate), using a nude mouse model. Methods: Four weeks after inoculation of H. pylori into the stomach, two groups of nude mice were administered methylene blue or triple therapy via the stomach for 1 week. A control group of nude mice was given culture fluid alone after the inoculation. The number of H. pylori and histological changes in the stomach were determined weekly for 5 weeks, starting from the completion of drug administration. Results: In the methylene blue treatment group, the concentration of H. pylori was significantly reduced for 1-3 weeks after treatment compared with the control group..."

A final thought on this topic, this concept may also apply to the other rare neurodegenerative diseases such as PSP, CBD, the FTD, etc.

I left off the link to the "Evaluation of methylene blue..." article.
http://cat.inist.fr/?aModele=afficheN&cpsidt=4893514

The feeling I'm getting is like when you are working on a jigsaw puzzle, and the pieces start clicking into place.

I was also able to find this citation, but I don't have access to an electronic version. What I have access to only goes back to 1995!

"Testing negative for Helicobacter pylori after methylene blue spraying of gastric mucosa."
Hack HM, Parsonnet J, Triadafilopoulos G.
Gastrointest Endosc. 1994 May-Jun;40(3):397-8.
PMID: 8056268

Here's another interesting article about this connection... for those interested...

"Helicobacter pylori: Neurological and Ophthalmological Disorders"
M. U. Farooq & A. Bhatt
The Internet Journal of Neurology.
2008 Volume 9 Number 2

Abstract: Helicobacter pylori infection has been associated with many intestinal and extraintestinal infections. It has been linked with many neurological and ophthalmological disorders including cerebrovascular diseases, migraine, Alzheimer's disease, epilepsy, Parkinson's disease, multiple sclerosis, peripheral neuropathies, glaucoma, and non-arteritic anterior ischemic optic neuropathy. The pathophysiological mechanisms could involve various immunological processes in response to an infectious agent or different antigens released during tissue destruction resulting in activation of cellular and humoral immunity; platelet activation and aggregation; different vasoactive and inflammatory substances; reactive oxygen species; and apoptotic processes. The long-term effects of H pylori eradication therapy on the course of these disorders still need to be explored and warrant further studies.
http://www.ispub.com/journal/t...gical_disorders.html

Fascinating...off on my own search. Keep the articles coming.

I got a copy of one of the papers I wrote about earlier.

"Evaluation of methylene blue and triple therapy for eradication of Helicobacter pylori infection in the nude mouse model"

Here are some excerpts:

"We have demonstrated that methylene blue is bactericidal for Helicobacter pylori in vitro..."

"Compared with the control group, methylene blue significantly reduced the number of bacteria in ulture for 3 weeks after the treatment. Differences between groups became non-significant 4 weeks afte treatment..."

"With the administration of triple therapy, the number of H. pylori was significantly reduced from the beginning of treatment until the end of the study (5th week) compared with the control group..."

This is what I got out of it. Methylene blue is an effective antibiotic for H. pylori, but it is not as good as the "triple antibiotic therapy". However, the treatment with both methylene blue and the antibiotics was done for one week. Further research would be needed to confirm that long-term methylene blue therapy would be effective in keeping an H. pylori infection in check.

So, if H. pylori is the root cause of some proportion of AD cases, then the mechanism by which methylene blue is effective in reducing symptoms is in question. It had been proposed that methylene blue acted directly on the tau protein aggregations, and perhaps even the amyloid beta plaques. It has also been attributed with being able to enhance mitochondrial function. But the real mechanism may have been to reduce the number of H. pylori, and therefore the quantity of TNF (tumor necrosis factor) in the body.

But hey, as long as it works!

Is anyone considering having your LO checked for an Hp infection? Keep in mind that if the results of this study hold true for people in other countries, then there is about a 90% chance that they do have the infection, and about another 85% chance that treating the infection would help their AD symptoms. That works out to about 3 out of 4. Good odds, I'd say.

If there is a genetic component to someone's problem, such as is likely the case with Down syndrome, this wouldn't help.

Swarfmaker:

I assume that to determine a specific bacterial infection would require a specific test, but would the first sign of the h.pylori infection be an elevated WBC – as in any infection? Or can an elevated h. pylori level be present without an elevated WBC?

Thanks.

P.S. h. pylori is one of the items I asked about at my Mom's last appointment with the GP. The doc never addressed the question. (Or much of anything for that matter, but that is a different post.)

Is h. pylori something that is not widely considered as a possible contributing factor to AD? Or just a close-minded doc?

I will keep an eye on the post.

Kit, a medical practitioner would not read journals like the ones swarfmaker has been citing. This is research, and nothing has been established yet. They do not waste their time on hypotheses, because the vast majority never pan out.

A "link" does *not* mean that anyone has shown a causal relationship. For example, there might be a higher number of AD patients with H. pylori infections because they're more prone to contract such infections.

Many pathogens have been found to have links with AD. There have been a number of clinical trials to evaluate the use of antibiotics for treating AD, with very mixed results. For each pathogen/treatment, in some trials, some patients appeared to be helped, others did not; while other trials showed no benefit for any patient.

And no, H. pylori is not widely considered to be a possible contributing factor. This is an hypothesis being studied primarily by a small group of scientists in Greece. I requested a copy of the full 2009 paper on the small clinical trial they ran, since abstracts can sometimes be very misleading (not necessarily intentionally). The researchers took pains to develop a solid approach, and the paper is well-written. However, they, themselves, note that there were not a sufficiently large number of patients in the trial for the statistical analysis of the data to be reliable:

"The results of this study suggest that eradication therapy may somehow improve the degenerative process in AD. It should be noted, however, that the number of patients in the groups, particularly in group C, was small, and it may not, therefore, be possible to draw definitive conclusions."

They also go on to note that, while there are many hypotheses as to how various pathogens might affect the neurodegenerative process in AD, they are all speculative at this point.

Then they discuss some serious shortcomings of their own studies/hypotheses. For example:

"In contrast to data presented for other intracellular infectants [Chlamydia pneumoniae, Herpes simplex virus (HSV)-1, Borrelia species] found in brain regions demonstrating considerable AD pathology, most of the aforementioned mechanisms of how Hp infection could influence the pathophysiology of AD are not necessarily specific to the regional pathology observed in the AD brain, nor is there a specific temporal sequence indicated by which Hp infection would directly injure the brain, at the present time. ...In addition, a Hp eradication regimen might have influenced other infections in the AD, particularly those of Chlamydia peneumoniae and Borrelia species, and could explain, at least partly, the positive improvement observed in our AD patients at the post-treatment period."

Also, please note, the benefit seen in AD patients whose H. pylori infection was eradicated was relatively modest. For example, the MMSE scores went from 17.46 ± 6.09 at baseline to 19.6 ± 6.08 at year 1 and 19.92 ± 5.94 at Year 2. This appears to be better than the control group, whose MMSE declined as expected. However, remember that the total number of patients in the study was too small for the statistical analysis to be reliable.

In short, it is a very intriguing study, and the researchers have been developing their hypotheses very carefully. But they, themselves, recognize they have a long way to go before they show either a causal relationship between H. pylori and AD, or a significant benefit to AD patients from H. pylori infection treatment.

From what I've read so far, the first test for H. pylori would be a blood test. This would tell them if someone had been exposed to the bacteria some time in their life, but not if there was a current infection. Keep in mind that 9 out of 10 people with an infection do not have have gastrointestinal symptoms. If this tests positive, then they could use a test where the person swallows a substance that the bacteria uses, releasing a form of carbon in their breath that is then measured. Another way to detect an infection for sure is to use an endoscope (down the throat) and take a sample of the stomach lining.

If the eradication of an H.pylori infection arrests the decline in even 1 out of 10 AD victims, not the 3 out 4 in the Greek study, I think this worth pursuing. Another way to look at it is, is it good to leave an H.pylori infection untreated? Even if it turns out that it is not involved in AD, Helicobacter pylori seems to be the weird guy hanging around the scene of many stomach-related crimes, such as some forms of stomach cancer. Look it up on Wikipedia for starters, and then do a Google search.

http://en.wikipedia.org/wiki/Helicobacter_pylori

Here's what Wikipedia says about diagnosis:

"Diagnosis of infection is usually made by checking for dyspeptic symptoms and by tests which can indicate H. pylori infection. One can test noninvasively for H. pylori infection with a blood antibody test, stool antigen test, or with the carbon urea breath test (in which the patient drinks 14C- or 13C-labelled urea, which the bacterium metabolizes, producing labelled carbon dioxide that can be detected in the breath).[33] However, the most reliable method for detecting H. pylori infection is a biopsy check during endoscopy with a rapid urease test, histological examination, and microbial culture. None of the test methods is completely failsafe. Even biopsy is dependent on the location of the biopsy. Blood antibody tests, for example, range from 76% to 84% sensitivity. Some drugs can affect H. pylori urease activity and give false negatives with the urea-based tests."

(Wikipedia is writen by "contributors" from all over the world. They are not necessarily "experts". The information is often correct, but can be absolutely wrong; so take what you read as a starting point for more research.)

I think this is the link to the full text of the paper.
http://www.springerlink.com/co...38x7031/fulltext.pdf

Swarfmaker, you might be better able to interpret experimental data if you learned a bit about statistical analysis. The standard deviations in the test results were very large, and the number of test subjects very small. One can produce what appears to be statistically significant results when they are, in fact, very misleading.

The authors of this paper that you keep citing *said*, quite clearly, that the total number of patients was too small for the statistical analysis to be reliable.

They did *not* find that "3 out of 4" AD patients benefitted from treatment.

Thank you both for the replies.

I am so new to this, but I think it is important for me to keep current with everything to do with a disease that is such a mystery. And I know I am dreaming, but I think the docs should too.

I am spoiled rotten by own doc, who is not only a big brain and considered a top diagnostician, but is always interested in anything new. And – hold on to your hats – will actually admit when he doesn't know something, still take it seriously and check into the new info.

If he accepted Medicare, I would have my Mom sitting on his lap in an instant.

Thanks, again. I will keep my eye on the posts for new information.

I will copy what I wrote in my June 21 post:

"Hp was detected in 88% of AD patients. Hp eradication was successful in 84.8% of treated patients, which is about normal for all cases of Hp infection. If you multiply 88% by 84.8%, you get ~75%... If the statistics of this research hold true, then one could expect the eradication of an Hp infection to be effective for about 75% of those treated, and the effect should last at least 2 years (which was the limit of how long they tracked the test participants)."

What is there to gain by discouraging people from pursuing this?

I posted the following info to the Rember thread, but I thought it belonged here too:

It is also interesting to note that in this article "ICAD: Tau-Targeted Therapy Slows Alzheimer's Progression for 19 Months"
http://www.medpagetoday.com/Me...gCoverage/ICAD/10320
it says, "In the trial reported here, 321 patients were randomized to 30 mg, 50 mg, 100 mg or placebo. The drug, Dr. Wischik said, was effective when it dissolved in the stomach, but was not effective when the drug was absorbed through the intestines. This was an issue for the 100-mg dose, which had 'absolutely no activity because it didn't dissolve in the stomach.'"

As I wrote in an early post, the Helicobacter pylori bacteria finds methylene blue to be rather toxic. This tends to support the idea that the dominant effect may not have been as a "Tau aggregation inhibitor (TAI)", but rather as an antibiotic. This would explain why the 100mg dose was not effective when it dissolved in the intestines, whereas the 30 and 60mg doses, which dissolved in the stomach, were effective. The antibiotic effect of the rember (which is basically methylene blue) reduced the H.pylori infection, thereby reducing the TNF levels.

**************

While researching this, I found some statements that H.pylori infections-- in the stomach-- may affect heart rhythms. The specific conditions mentioned were atrial fibrillation and PSVT. I don't have references to any publications yet.

quote:

What is there to gain by discouraging people from pursuing this?

Well, let's see.


(1) The patient should undergo endoscopy to get a reliable diagnosis. I don't know about you, but I've had one of those and I did not like it. I can't imagine asking an ADLO to undergo one unless I had much more reliable indications that it might be for a good cause.

(2) The eradication regimen involves long-term dosing with three antibiotics (omeprazole, clarithromycin and amoxicillin). I do wonder what this dosing regimen would do for bowel movements ... and what if the ADLO were already incontinent?

(3) Amoxicillin is a penicillin. Lots of people are severely allergic to this class of antibiotics.

(4) Each of these antibiotics can cause some pretty serious side effects, and each of them can affect kidney function, and each of them can interfere with a number of other drugs. Put together, quite a few people can't stay on the regime, even otherwise healthy ones. None of these medicines has been adequately tested in older patients, who are likely to be much more sensitive to them due to decreased kidney function - each drug may become very toxic under such conditions. None has been tested for safety/toxicity in older AD patients, who are even more likely to be more sensitive to them. And of course, the triple dose regimen has not been tested for safety/toxicity in older and/or AD patients, either.

On another forum, a caregiver reported having her ADLO put on only two of these antibiotics for simultaneous ear and urinary tract infections: "Until two days ago she was mobile, verbal, alert, continent by day, and healthy. ...Once she started on the drugs she went into a complete stupor. She is not responding to language, has a blank unknowing stare, is peeing all over the place, is unsteady on her feet, and is highly fatigued. She understands little, talks less, and hasn't even smiled at the cats in days."

Back in March, we had a caregiver report that her ADLO was put on the triple regimen for a "stomach infection", and within short order, was having to go to the bathroom at least once an hour, around the clock. We never heard what happened after that.

(5) Failure to adhere strictly to the dosage regimen can result in the development of resistant strains and possibly deadly infections. Due to the side effects of just two of these drugs, described above, the caregiver decided to take her ADLO off the antibiotics after six days -- it was a weekend and she couldn't contact the doctor -- and the side effects improved significantly. The doctor started a different antibiotic as soon as he was told, but it was too late. Eight days later: "The infection has now worsened to the point that medicated ear drops can not reach it due to swelling and pussy discharge. It is very deep in her ear, has worked through the skin layers, and is now infecting her skull bone. I didn't even know this was possible, but it's a condition called skull-based osteomyelitis. It is quite serious and could take months to heal. If untreated it can have severe consequences like deafness or even death, but we caught it early enough that we should be able to resolve the problem eventually. She has seen an ear, nose, and throat specialist 5 days in a row now and he is quite concerned, but we have seen some improvements since we switched from a GP to the ENT. We can anticipate months of interrupted sleep and painful throbbing in her inner ear."

I'd actually feel A LOT more comfortable with this than Axona.
A urease breath test can be done in lieu of endoscopy.
There are alternatives to penicillin for patients who are penicillin allergic.
And the side effects of the treatment are known. It's common sense not to discontinue any treatment regimen without consulting a doctor.

The urease test is done on a tissue sample, from the biopsy of the stomach lining, which is then cultured for the bacterium and tested for urease. So while the urease analysis itself is simple, getting the sample is not.

A breath test can sometimes be used instead of a biopsy. It involves drinking a special liquid that is radioactive. The breath test does not analyze for the bacterium itself; rather, it looks for rapid release of radiolabeled carbon dioxide, presumably released by an enzyme that the H. pylori produces. Since this is a very nonspecific test, there are many different sources of false positives and false negatives. And, of course, your particular healthcare provider has to be set up to run the test. A "stable-label" liquid can be used instead; it is more reliable, but requires mass spectroscopy for analysis, which most clinical labs don't have.

As for side effects, please pay attention to what the warnings and precautions for these meds state, very clearly: the side effects in older patients, let alone older AD patients, are unknown for any one of the three antibiotics, let alone all three together. All three are known to affect kidney function. Since kidney function often declines in older people, doses of any one of these antibiotics that would not harm younger patients may become very toxic to older patients. Put all three together, and you have a potentially serious problem.

One caregiver already found that giving just two of these antibiotics did horrible things to her loved one. I imagine she was similarly blase about antibiotics before that experience.

Others are finding that they cause severe urinary incontinence and frequent urination after just a day or two of administration. With severe incontinence and frequent urination comes the potential for dehydration, with all that dehydration can do to an ADLO. And taking the patients off these particular antibiotics after a day or two (or five, or even ten) can cause the development of drug-resistant bacteria that can be fatal.

You may think those are acceptable risks ... I would think twice about taking such risks for my loved one for a "treatment" that no one has yet shown will actually benefit an AD patient.

JAB,
I wasn't saying that I was planning to do this tomorrow or anything, but I think with the urease breath test, it's safer than something unknown like Axona or megadoses of cinammon or megadoses of various vitamins. Axona had some effects on the kidney and liver too and since it's so new, we don't know what the long term effects will be.
Serious side effects from antibiotics are pretty rare considering how often they are used. If my LO had a UTI, pneumonia, etc, I'd be heading to the PCP for an antibiotic.
I'm not sure where you are getting three antibiotics from. I read one proton pump inhibitior and two antibiotics as one of the choices for treatment.
IF something like this were widely available, I'd try it with a lot less worry than something that has so much more to be known about it. I was just kinda speculating, that's all

Jellybeans (I simply adore your name, have I told you that?), I'm pretty leery of giving anyone antibiotics unless there's a really, really good reason to do so. They've been abused so much that we are heading into very serious trouble with emerging new pathogens and re-emerging old ones that are very resistant to anything we have available in our drug arsenal. Infections that used to be easy to treat are now deadly.

The triple regimen I was talking about is the one used in the studies that swarfmaker is so enthusiastic about.

H. pylori eradication is not as simple as some people seem to think. E.g., according to

http://www.rxlist.com/helicobacter_pylori/article.htm

the types of combinations you're talking about (antibiotics plus PPIs etc) "...can be expected to cure 70%-90% of infections. However, studies have shown that resistance of H. pylori (failure of antibiotics to eradicate the bacteria) to clarithromycin is common among patients who have prior exposure to clarithromycin or other chemically similar macrolide antibiotics (such as erythromycin). Similarly, H. pylori resistance to metronidazole is common among patients who have had prior exposure to metronidazole. In these patients, doctors have to find other combinations of antibiotics to treat the H. pylori. Antibiotic resistance is another reason why antibiotics should be used carefully and judiciously for the right reasons, and indiscriminate use of antibiotics for improper reasons should be discouraged."

The PPIs do not kill the H pylori bacteria -- they treat the damage that is done to the stomach. Two antibiotics plus a PPI means you only have two drugs that target this bacterium, which is often resistant to antibiotics. Because of the known antibiotic resistance of H. pylori, some treatment regimens include at least three antibiotics -- or more.

Interestingly, H. pylori antibiotic regimens may differ across regions of the world because different areas have begun to show resistance to particular antibiotics. For example, I just tripped across a clinical trial you might find interesting:

http://clinicaltrials.gov/ct2/show/NCT00719420

Another comment of possible interest when it comes to treating ADLOs: even when the treatment is only for ulcers, otherwise healthy patients may find the triple therapy you mentioned "complicated because it involves taking as many as 20 pills a day. Also, the antibiotics used in triple therapy may cause mild side effects such as nausea, vomiting, diarrhea, dark stools, metallic taste in the mouth, dizziness, headache, and yeast infections in women."


As for Axona, there is a pretty big body of information on the health risks of MCT oils in healthy people. There is also a large body of information on the effects of ketogenic diets on people with serious health problems on which to predict possible side effects in AD patients.

And if you look at the prescribing information for Axona, you'll find that Accera has a "generally recognized as safe (GRAS)" report from the FDA on caprylic acid. I suspect you won't find any antibiotic with GRAS status ... !

JAB,
You were the first person to respond to my very first post here and you commented about my user name then.

H.Pylori can cause health issues. So, in my opinion, I don't think it would be a completely inappropriate use of an antibiotic if someone tested positive for H.Pylori. I know that it's not currently recommended, but it's not the worst use of antibiotics I can think of.

I DO totally agree with you that antibiotic misuse is really running rampant. Too many stupid and/or lazy doctors prescribe it for every sneeze and sniffle and too many patients want them for infections that are clearly viral. I think that physicians who prescribe antibiotics inappropriately are the real culprits.
I thought of this more for my LO than the AD population in general. It boggles the mind to know that people with a healthy brain can't/don't/won't take medications as prescribed. But, I'm good at doling out my Grandma's pills(And she takes way more than 20 a day now- (lots of vitamins, just no megadoses)

I find the Axona threads a little daunting. It's not easy to google MCTs and get much information -so much of the information is about how it helps epilepsy in kids and a lot of articles require payment before reading. I know that today it's on the GRAS list, but that could change tomorrow especially with the relatively new population taking such a large amount of it indefinitely. My LO's pcp was too lazy to google "Axona" so I doubt that he'll know anything about how a ketogenic diet will impact her (and she doesn't fall into the totally healthy category
). Another nice thing about treating with knowns is that pcp's know the side effect profile well.

I do hope that I didn't in any way offend you by my posts about this. I think that you are a great source of knowledge and you are so very generous about sharing your knowledge. (Your tone didn't suggest that I irked you, just wanted to make sure ) I was just kinda thinking that it would be a good idea if they'd start screening and treating AD patients for H Pylori (or at least my Grandma), because they don't seem to be speeding along with this particular research.

"Offend" me? Good heavenly days, no! I am used to very lively "discussions" with scientific colleagues, most of whom are not nearly as diplomatic as you!

quote:

Originally posted by JAB:
"Offend" me? Good heavenly days, no! I am used to very lively "discussions" with scientific colleagues, most of whom are not nearly as diplomatic as you!

Just wanted to be sure this wasn't coming off like I was saying that I was right and you were wrong. It's hard to tell how things translate on a message board.

Just got this in one of my newsletters.

When any kind of drug might be questionable, I look for healthy alternatives. This might be one of them. Can't hurt, right?

Just for added info.

Better than Antibiotics in H. Pylori Battle: Broccoli Sprouts


Helicobacter pylori (H. pylori) bacteria presents a medical conundrum -- while the gut bacteria has been implicated in ulcers and stomach cancer, it also seems to confer protection against other health problems, including esophageal cancer. What’s a person to do? One helpful strategy might be to eat broccoli sprouts. It seems they are a natural way to help maintain H. pylori at a level that is helpful, not harmful.

Sitting right next to the much more popular alfalfa sprouts in groceries and health-food stores, these "baby broccoli plants" are even better for you than in their grown-up form. New research from Tokyo University of Science and Johns Hopkins University School of Medicine investigated how regular consumption of broccoli sprouts affected people with H. pylori infection, the frequent cause of peptic ulcers and stomach cancer. The study included 48 H. pylori-infected adults who were randomly assigned to consume 70 grams a day (about two and one-half ounces) of either broccoli sprouts or alfalfa sprouts. Researchers found that after eating broccoli sprouts for eight weeks, participants significantly lowered biomarkers for H. pylori while those who ate alfalfa sprouts did not show this benefit.

Jed W. Fahey, ScD, a faculty research associate in the department of pharmacology and molecular sciences, was a study coauthor. He told me that the active component against the bacterium is a phytochemical called sulforaphane. This natural substance induces and boosts some of the body’s protective anti-inflammatory enzymes and also has antibiotic properties particularly effective against some strains of H. pylori. Broccoli sprouts are a much more potent source of sulforaphane than is even the freshest broccoli, Dr. Fahey said.

A dietary source to combat H. pylori is excellent news for many people. Estimates are that as many as 50% of Americans harbor the bacteria, though they don’t always have symptoms. However, when the H. pylori runs rampant and causes infection, treatment can be tough -- typically it involves taking two different antibiotics simultaneously, often in addition to a bismuth preparation or an acid-suppressing protein-pump inhibitor. The end result of all this is, quite often, yet another ulcer -- and, in about 20% of patients, it doesn’t even solve the problem.

Broccoli sprouts offer a natural alternative and an easy and tasty way to combat H. pylori. Note, however, that the protective effect fades if you stop eating the sprouts, so you should eat broccoli sprouts regularly (two to three times a week). Dr. Fahey points out that they keep for several days in the refrigerator and are wonderful in salads, sandwiches and wraps.

Source(s):

Jed W. Fahey, ScD, faculty research associate, department of pharmacology and molecular sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland.

I was in the produce section of a grocery store the other day, and I saw a package of broccoli sprouts. It made me think of this post.

What was the news letter you got this from?

This meets all of my criteria for unproven wild ideas: relatively cheap, probably safe, and easy to try. Why not?

swarfmaker, I'll welcome you back here again also.

I always forget to post the link to these things, but fortunately I found it pretty quick.

It's here:

http://www.bottomlinesecrets.c...tml?article_id=49509

Infections May Lead To Faster Memory Loss In Alzheimer's Disease
ScienceDaily (Sep. 8, 2009) — Getting a cold, stomach bug or other infection may lead to increased memory loss in people with Alzheimer's disease, according to research published in the September 8, 2009, print issue of Neurology®, the medical journal of the American Academy of Neurology. The study found that people who had respiratory, gastrointestinal or other infections or even bumps and bruises from a fall were more likely to have high blood levels of tumor necrosis factor-α [TNF-α], a protein involved in the inflammatory process, and were also more likely to experience memory loss or other types of cognitive decline than people who did not have infections and who had low levels of the protein...
http://www.sciencedaily.com/re.../09/090907162306.htm

I would also suspect conditions like urinary tract infections, tooth infections, and toenail fungus.

Enbrel works by blocking TNF-α, doesn't it? Eliminating a chronic infection should have the same effect by reducing TNF-α levels as getting Enbrel treatments, and getting rid of an infection should be a whole lot less expensive.

Another note on this. In the Rember studies published last year, the higher doses of Rember were not effective. The researchers mentioned that the 100mg dose did not dissolve in the stomach, but rather the intestine. Methylene blue is an antibiotic. The effectiveness of Rember may have been due more to the methylene blue killing off the Helicobacter pylori than to its tau-tangle fighting properties.

Enbrel lowers TNF, this is true. Infections cause AD patients to have worse symptoms and raise TNF levels, this is true too. But, if you're theory means that most AD patients only have AD because of an infection, I think you are way off. My Mom gets worse when she has an infection, when the infection is gone, she would usually go back to how she was before the infection, with or without Enbrel Injections. When she went through a major trauma, like surgery, she lost abilities and nothing could bring them back, even our Enbrel injections.

I believe AD itself causes high TNF levels, which is why Enbrel works to improve some cognitive abilities, then sustains the patient for an indefinite amount of time, up to 4 1/2 years (and counting) for some.

I wish it was as simple as just getting rid of infections but from my past experience and after listening to others, it's just doesn't seem that simple. But, I definitely do think infections and understanding how they effect the mind will be a key issues in understanding how to stop TNF in the first place from causing AD, if indeed it does.

As always, just my opinion...just a caregiver.

Thanks, Felicia

I posted this on both threads, hope you all don't mind. I wanted to make sure Swarfmaker saw my apology!

--------------------
Swarfmaker,

I've been thinking and what I said about you being "Way Off" is "WAY OFF"! I'm sorry, I shouldn't of said that. Maybe your theory is correct, maybe certain infections or the amount of infections a person has had can trigger something in the body to "Kick-Off" Alzheimer's. Maybe AD can be considered an Infection of it's own that isn't curable by antibiotics, but can be controlled by TNF inhibitors such as Enbrel. Who knows!!!
I also think that it may have something to do with injuries to the body, which raise TNF levels such as Ruptured Discs, which is one of the clues that helped Dr. Tobinick came up with his treatment.

Thanks, Felicia

The report specifically says they looked at infections/injuries that could lead to inflammation and that resulted in high levels of TNF-alpha in the blood -- not just any old infection or bruise.

High levels of TNF-alpha in the blood is indicative of systemic inflammation, not just localized inflammation. Studies have shown that Helicobacter pylori does not typically cause systemic inflammation, e.g.:

Bayraktaroğlu T, Aras AS, Aydemir S, Davutoğlu C, Ustündağ Y, Atmaca H, Borazan A. Serum levels of tumor necrosis factor-alpha, interleukin-6 and interleukin-8 are not increased in dyspeptic patients with Helicobacter pylori-associated gastritis. Mediators Inflamm. 2004 Feb;13(1):25-8.

"Helicobacter pylori (H. pylori) is a non-invasive microorganism causing intense gastric mucosal inflammatory and immune reaction. H. pylori-induced gastric mucosal cytokine overproduction has been clearly documented previously. The stomach has a large surface area and continuous spill-over of locally produced cytokines into the blood stream is a possibility. ... We could not show elevated circulatory levels of IL-6, IL-8 and TNF-alpha in H. pylori-infected cases. We believe that H. pylori-related cytokine activation become concentrated on gastric mucosa and this pathogen-induced local inflammatory cascade does not cause changes in circulatory levels of these cytokines. Moreover, there is no correlation between the levels of serum cytokines and Sydney parameters."

What do you want to bet that toenail fungus doesn't normally cause systemic inflammation, either...

That was such an interesting paper, I just had to read the whole thing. Interesting stuff in the "Discussion" section.

"In the literature, some authors reported increased circulatory TNF-a levels while serum IL-8 levels remained normal in H. pylori- infected persons.7 Some others reported elevated serum TNF-a levels in patients with CagApositive H. pylori infection.8 IL-1, IL-6 and IL-8 were all also elevated in Cag A-positive cases.20,21 We did not determine the Cag A status of our patients. Thus, we do not know whether most or all of our patients were infected with a Cag A-negative strain. However, we know that our patients neither had endoscopic sign of gastroduodenal ulceration nor had severe gastritis on histopathology. Therefore we possibly had patients infected with less pathogenic strains of this bacterium such as with Cag A-negative H. pylori . The other possibility may be the inhibition of further inflammation by a gastric protective cytokine IL-10.22 Although we do not measure its levels on gastric mucosal extracts and circulation, we know that IL-10 secreted by gastric mucosa has inhibitory effects on gastric mucosal immune response associated with local proinflammatory cytokine activation. As a result of contradictory reports, including ours, we do not know whether the continuous spill-over of cytokines into the blood stream could be possible as a consequence of gastric mucosal cytokine activation and increased synthesis. If true, this may be a potential threat in patients with H. pylori infection for some ‘extra-gastric’ pathologies, such as coronary heart disease, primary Raynaud phenomenon, sideropenic refractory anemia and delayed growth in children. 23 28 We think that further studies are needed to make firm conclusions on H. pylori - induced changes in the circulatory cytokine levels."
http://www.pubmedcentral.nih.g...1781536&blobtype=pdf
(Anyone want to look into whether "further studies" have been performed?)

The age of those in the study was about 45. The greatest risk factor for AD is age. I have to wonder what a study like this would show for people over 60 years old. I mean, when someone gets AD under the age of 60, it's considered "early onset", and may be due to some other cause, like Downs syndrome, or some genetic problem.

Regarding toenail fungus...

Stimulation, inhibition and death of macrophages infected with Trichophyton rubrum.
Campos MR, Russo M, Gomes E, Almeida SR.
Departamento de Análises Clínicas e Toxicológicas, Faculdade de Ciências
Farmacêuticas, Universidade de São Paulo, Avenida Prof. Lineu Prestes, 580,
Bloco 17, CEP 05508-900, São Paulo, Brazil.

Trichophyton rubrum is the most common pathogen causing dermatophytosis, accounting for approximately 80% of the reported cases of onychomycosis. Since 90% of the chronic dermatophyte infections are caused by T. rubrum, it is likely that this pathogen must have evolved mechanisms that evade or suppress cell-mediated immunity. Several reports have highlighted the participation of phagocytes in the immune defense against fungi; however, few studies have addressed the role of these cells in dermatophytosis. In this study, we investigated the interactions of resident and peritoneal macrophages with T. rubrum. We show here that the interaction of T. rubrum conidia with resident macrophages results in the production of TNF-alpha and IL-10 but not IL-12 and nitric oxide...
PMID: 16293438
(... which I have not read in full. I bring up the point only for consideration.)

Through all this discussion, I hope people do not lose sight of the idea that if this is indeed the cause for many cases of AD, then it CAN be treated, either by attacking the infection, or inhibiting the TNF-alpha.

My vote would be to attack the infection, eliminate the TNF at the source. Heck, how dangerous and expensive is it to try adding broccoli sprouts to someone's diet?

Oh, and for anyone wondering about the blood test for H.pylori, I had it myself the last time I had a cholesterol test. It won't tell you if you currently have an infection, but only if you have been exposed to the bacteria at some point. It's not 100% accurate either, but if I find out I have been exposed, I'm gonna start adding broccoli sprouts to my salads!

Oh, I like the idea of adding broccoli sprouts to the diet. I bet they're very good for you for a lot of different reasons. In fact, I think I'll put that on my shopping list, see whether we like the taste. Sooner or later, my husband is going to rebel against all the spinach and spring mix salads I feed him -- we need a bit more variety!

I just think that the Holmes study is way too vague and poorly designed to draw any reliable conclusions. For one thing, there were far too many variables to have a reasonable number of patients in any category. (If you look at all the variables they say they examined, it would average out to 18 patients each, which isn't nearly enough to do reliable statistical analysis on.) And as the papers you and I have been looking at show, inflammation is a very complex phenomenon, and is not defined by a single protein in the blood. Not to mention, it is my understanding that measurements of decline rates aren't reliable for any periods of time less than three years.

And then, of course, there's that recent study which concluded inflammation isn't a factor in AD...

I went to my local health food store at lunch today looking for broccoli sprout supplements. It's one of the better stores in my area. I didn't find the supplement mentioned by john1943 in another post , BroccoCaps, but I found another brand. I hope it works. I found broccoli seeds from Now Foods, so I bought a bottle and a glass "sprouting jar". I've also seen broccoli sprouts in some of the better grocery stores. The brand name was "BroccoSprouts". I figured I could grow my own. I wonder if I have to supply them with sulfur in the water for the sprouts to have sulfuraphane?

My plan is to start out with giving my mother the supplement. Then, I'm going to become a broccoli sprout farmer. The sprouts will go into the Magic Bullet blender with a cup of V-8 vegetable juice.

I'm experimenting. I plan to use 2.5 oz of broccoli sprouts 3 or 4 times per week.

As a side note, while I was in the health food store, I picked up some vitamin D supplements for myself. There is a rumor that vitamin D, either from supplements for from sunshine on your skin will keep the Pig flu (H1N1) virus at bay. It's going to be pretty gloomy here for the next 7 months, so depending on sunshine for vitamin D was out. I figured it was worth the experiment.

quote:

Originally posted by swarfmaker:
I found broccoli seeds from Now Foods, so I bought a bottle and a glass "sprouting jar".

Swarf, I tried growing my own sprouts a few years ago. I hope you are more patient with the process than I. No problems growing the sprouts. Separating the tiny little seed husks from the plants is another story (unless you don't mind eating them too). I got my setup from a website called "sprouthouse.com" (I think). The sprouts tasted a little bit like radishes to me--a little tangy.

John

A member of the Yahoo "tauopathies" group, coaster2314, posted this interesting article today:

"Susceptibility of Helicobacter pylori to bactericidal properties of medium-chain monoglycerides and free fatty acids"

BW Petschow, RP Batema and LL Ford
Mead Johnson Research Center, Bristol-Myers Squibb Co., Evansville, Indiana 47721, USA.

Antimicrobial Agents and Chemotherapy, Feb 1996, 302-306, Vol 40, No. 2
American Society for Microbiology

Previous studies have shown that various short- and medium-chain free fatty acids (FFAs) and their corresponding monoacylglycerol esters (MGs) have antibacterial activity in vitro against primarily gram- positive bacteria. More recent studies have also shown that the growth of Helicobacter spp. is inhibited by linoleic acid and arachidonic acid. The purpose of the present study was to evaluate the susceptibility of Helicobacter pylori to the in vitro bactericidal properties of medium-chain MGs and FFAs. Incubation of H. pylori with saturated MGs, ranging in carbon chain length from C10:0 to C14:0, at 1 mM caused a 4-log-unit or greater reduction in the number of viable bacteria after exposure for 1 h. Lower levels of bactericidal activity were observed with C9:0, C15:0, and C16:0 MGs. In contrast, lauric acid (C12:0) was the only medium-chain saturated FFA with bactericidal activity against H. pylori. The MGs and FFAs were bactericidal after incubation for as little as 15 min at neutral or acidic pHs. Higher levels of MGs and FFAs were required for bactericidal activity in the presence of higher amounts of protein in liquid diets. We also found that the frequency of spontaneous development of resistance by H. pylori was higher for metronidazole and tetracycline (10(-5) to 10(-6)) than for C10:0 MG, C12:0 MG, and C12:0 FFA (< 10(-8)). Collectively, our data demonstrate that H. pylori is rapidly inactivated by medium- chain MGs and lauric acid and exhibits a relatively low frequency of spontaneous development of resistance to the bactericidal activity of MGs. Further studies are needed to establish whether MGs may be useful either alone or with other known therapeutic agents in the management of H. pylori infections in humans.
http://aac.asm.org/cgi/content/abstract/40/2/302

swarfmaker,

I saw where you had the blood test for H-Pylori, I was wondering if you had any results back from it? If you don't want to answer that, that's okay because it is personal and I understand that. I'm going to ask the doctor for the blood test for all of us the next time we have labwork.

I'm very intrigued with the concept of a chronic inflammation/infection being the initial culprit in AD and maybe more diseases. When you think back on the history of the person, are there any signs of a small chronic infection that most of us don't pay attention to? In the case of my lady, she has a history of cold sores, boils, toenail fungus and common colds, nothing serious about any of them and none of them are sustained, just chronic things that pop up from time to time.

Her body temperature has always run at 97.6 where most people run at 98.6. Whether this makes a difference or not, I don't know. I know that when a person has a virus or infection they run a fever which is the body's way of fighting the infection. Maybe 98.6 fights minute infections/inflammations better than a body temp of 97.6. This is just a thought I had, and may have no bearing on anything. I wonder if any other people with AD have a lower body temp.? This is just one of the many things that are bouncing around in my mind right now and it just made me curious. Anyone else have any thoughts on this too?

Well, here's what happened with the results of the blood test. What I was actually doing was a 12-hr fasting cholesterol test. When they called to give me the results of that, which could have been better, I didn't think to ask about the H.pylori test! The way this office works is, if there isn't a problem, you don't hear about the test results. So, I figure they didn't find anything, and I'll ask about it again when I go in for a check up.