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Tooth paste, aluminium oxide and Crohn's Disease.

It's 3 articles that I chose to put in one thread.


Toothpaste and Crohn’s disease

SIR,-Professor Sullivan’s paper (Nov 3, p 1096) and subsequent correspondence (Dec 1, p 1382) raise important questions about the impermeability or otherwise of the gastrointestinal tract to ingested
particles. We cannot comment on the connection between insoluble
particle uptake and the pathogenesis of Crohn’s disease, but we have
investigated the uptake and fate of sub-micron particles from the
gastrointestinal tract in the rat. Our aim was to fmd out the extent of
uptake, if any, in view of the assumption that the mammalian
gastrointestinal tract is impenetrable to particles. Knowledge of the
uptake of bacterial and viral particles2 via the M-cells of Peyer’s
patches has been accompanied by periodic reports of particulate
"persorption",3-5 but controversy has persisted.
Insoluble polystyrene particles of well-defined diameters in the
range 50 nm to 3 um fed to rats were found to be taken up mainly via
the Peyer’s patches and subsequently transported to the serosa
(figure, a) and thence by the mesenteric lymphatic vessels to lymph
nodes. Particles up to 300 nm are transported into the venous
circulation and reach the liver in small amounts.6 Polystyrene was
chosen because it is non-biodegradable and completely insoluble,
but the work does demonstrate the size dependency of uptake of
Perhaps we should be more concerned about the fate of insoluble
materials in toothpaste and pharmaceuticals which might be taken
chronically, especially since the intestinal permeability patterns in
some disease states such as Crohn’s disease are abnormally high.7

Particle absorption in rat gastrointestinal tract.
(a) (top). frozen section of Peyer’s patch showing 500 nm polystyrene
fluorescent particles traversing from lumen to serosal side after oral dosing.
(b) (middle). mesenteric lymph vessel and connective tissue with 500
nm titanium dioxide particles (as aggregates, arrowed) after oral dosing.
x about 40.)
(c) (bottom) mesenteric lymph node showing lymphatic vessel with
titanium dioxide aggregates (arrowed). ( x about 75.)

SIR,-As Professor Sullivan points out, toothpaste contains a great
variety of inorganic metals and salts, many of which have been
shown in animal experiments to produce granulomatous lesions in
the intestine. However, the claim that these substances have not
been positively identified in human intestine is incorrect. Scanning
electronmicroscopy and X-ray energy spectroscopyl have revealed
aluminium, silicon, and titanium in Peyer’s patch macrophages in
the terminal ileum of patients with Crohn’s disease and controls; it
has been suggested that since both aluminium and titanium produce
granulomatous lesions in the human lung, these metals may be
involved in the pathogenesis of Crohn’s disease.2 The macrophage,
as the major cell type in intestinal granulomas, has been strongly
implicated in the pathogenesis of Crohn’s disease.3 It seems likely
that metal-containing macrophages will not function normally;
toxic metals such as lead, chromium, and nickel disturb a variety of
macrophage functions, including phagocytosis and enzyme
secretion.4 While Coffey was probably correct in assuming that
these substances are most commonly derived from the diets many of
these metals are on the surface of suture materials. Perhaps the
biological activity of these substances at surgical suture lines
contributes to the high rate of anastomotic recurrence after
operative treatment of Crohn’s disease that we had found

SIR,-Professor Sullivan invites us to revisit the hypothesis that
toothpaste caused Crohn’s disease. He suggests several possible
explanations for epidemiological findings in Crohn’s disease that
might be explained by toothpaste consumption. Crohn’s disease is
commoner among smokers than non-smokers and he suggests that
smokers consume more toothpaste by brushing more often.

Surveys of oral cleanliness and periodontal disease, however,
indicate that smokers have far worse disease and oral hygiene and
more debris and calculus than non-smokers. Secondly although
people with Crohn’s consume more sugar, sugar consumption is
associated with less regular toothbrushing rather than more.2 The
finding of more Crohn’s disease among white-collar workers is supported by increased brushing activity in this social group, but is
such a non-specific marker of affluence, education, diet, and social
behaviour as to provide little useful insight into the true causal

SIR,-Professor Sullivan postulates involvement of inorganic
particles from toothpaste in Crohn’s disease. Intestinal mucosal
infiltration by phagocytes, polymorphs, and macrophages1 and the
generation of free radical and related oxygen-derived reactive
metabolites in inflammatory bowel disease2 are associated with an
enhanced blood neutrophil chemiluminescent response.3 The
success of elemental diets in Crohn’s disease, thought to be due to
the elimination of dietary antigens is consistent with the removal of
inorganic particulate toxins from the diet. Various inorganic
particulates that include model aluminosilicates are capable of
stimulating the production of polymorph-derived free radical
oxidants.5 Soluble components of toothpaste could exert a similar
effect. Fluoride may promote the inappropriate and chronic cellular
activation of NADPH oxidase 6leading to the enhanced production
of superoxide and other oxidant tissue-injurious chemical species;
and foaming agents may also contribute to cell membrane
perturbations and activation of the phagocyte respiratory burst.7
Further investigation of the therapeutic use of antioxidant agents,
micronutrient vitamins, and trace elements, as has been suggested
for the pneumoconioses,8 may be of value in Crohn’s disease too.


Bacterial-Metal Interactions: The Potential Role of Aluminum
and Other Trace Elements in the Etiology of Chrohn’s Disease

Despite the recent burst of excitement about the genomics of Crohn’s disease, the critical importance of environmental factors in this condition has been recognized ever since the disease was described. The chief suspects for this role have always been microorganisms and dietary constituents. any candidate microorganisms have been proposed, evaluated and discarded over the decades, but the most persistent theories have revolved around mycobacterial infection.

In sum, we propose that the iron-related trace element uptake and/or regulatory system of either the putative mycobacteria or of the human host, or both, are involved in the pathogenesis of Crohn’s disease. We further propose that the iron-uptake/regulatory system allows access to mycobacteria of metal ions other than iron (especially aluminum) resulting in
an alteration in the organism’s virulence and/or the host’s ability to contain it.

Once the aluminum-loaded organism is incorporated into the host, aluminum enhances the organism’s ability to induce a prominent granulomatous immune response, thus giving rise to the pathologic features of the disease. The implications of such a hypothesis, of course, extend well beyond Crohn’s disease alone.

Over the past twenty years, it has been demonstrated that microbial organisms can sur-vive—indeed, in some instances flourish—under extreme environmental conditions, such as extremes of temperature, high
and low pH, or high concentrations of trace metals and other
potentially toxic substances. Bacterial organisms have a remarkable
capacity to evolve and adapt successfully to such
harsh conditions.

Our hypothesis is testable in both human specimens and
analogous naturally occurring animal disorders as well as in
experimental animals. For example, this concept could be explored
in Johne’s disease, a focally endemic disorder of sheep
with many similarities to Crohn’s disease. Further, experimental
infection by aluminum-enhanced microbial species might
be employed as means for developing new animal models of
Crohn’s disease. Finally, genetic testing in Crohn’s disease patients
for host-related metal ion-dependent functions might
also prove a fruitful avenue of research.

To examine the hypothesis further we have correlated estimated
toothpaste consumption per person in 19854 with mortality data
from 1950-84 (fourteen countries) and incidence from published
studies for 1970-79 (eleven countries).5 The Spearman correlation
coefficient was 0-19 (p=0-52) with mortality and 0-33 (p=0’33)
with incidence. The incidence figure is artifactually raised due to the
clustering of three countries (Italy, France, and Canada, with both
low consumption of toothpaste and low incidence rates of Crohn’s
disease, see figure). If these countries are excluded the correlation
with incidence is, paradoxically - 0-69 (p = 0-06). We were unable
to obtain consumption data for an earlier time period or data on time
trends in consumption, which would have been more appropriate
for examining the association, but it is reasonable to suppose that the
rank ordering for each country has not changed too much over the
past 20-30 years. Although one must be cautious when interpreting
ecological data, our results, as well as the other above-mentioned
studies, do not seem to support the relation between toothpaste
consumption and Crohn’s disease.


Absence of skin sensitivity to oxides of aluminium,
Silicon, titanium or zirconium in patients with
Crohn's disease

As the alimentary tract is exposed continually
to ingested substances, the possibility
that one or more of these is responsible for CD
is plausible. Dark pigment containing metal
particles in the bowel wall are found in
macrophages within Peyer's patches, which
mediate sampling and processing of inert
particles from the lumen of the bowel.
Experiments in animals have shown that insoluble
polystyrene particles of 50 nm to 3 ,um
are taken up mainly by Peyer's patches, transported
to the serosa, and thence by mesenteric
lymphatic vessels to lymph nodes14; particles of
titanium 500 nm in diameter are handled
similarly. There is some evidence to suggest
that intestinal permeability is increased among
CD patients and their healthy relatives,
suggesting this could be an important initiating
factor in the pathogenesis of CD.15

The results of our study do not suggest that
specific skin sensitivity to the three metals
compounds tested or to silica is present in CD
patients. As skin biopsy is invasive we did not
test further patients in this pilot study.
The presence of metallic particles within
diseased bowel wall most probably results from
intestinal absorption, but without pathological
consequence, as it also occurs in health.


Staff member
What's your feeling here kiny, that toothpaste causes Crohn's Disease?
Dunno yet, I started looking into it when I saw some slide from the hospital meant for students that showed tooth paste as a factor, it's an old slide.

So I started digging for articles. I didn't know titanium dioxide could penetrate, and if it can happen in a rat, alumina (tooth paste) can surely penetrate the guts of people with crohn if they are inflamed.

The second study shows bacteria need iron to survive, but they suspect bacteria might be able to adapt and live of aluminium..so why not tooth paste with aluminium oxide then if it can penetrate?

There's also the fact that in the West we use tooth paste and in places where people don't have crohn they do not (but they also don't use refridgerators, eat differently, have no contaminated MAP live stock, are less hygenic, etc).

My dad had crohn, I have crohn, and we both used very high amounts of tooth paste, so I was interested.

If you ask me if it causes crohn....hm...I still think it's mostly MAP and E. Coli. But I don't think tooth paste is so far fetched. Tooth paste also doesn't rule out MAP or E. Coli., there's another study I wanted to show but I have to look for it, it shows that MAP and E. Coli can adapt and live of extremely low amount of iron, reducing the iron intake in animals did nothing to kill off the bacteria, they just adapt and "steal" iron whenever needed from the body, so I don't know if changing tooth paste to one without aluminium oxide would help, but I'm looking at alternatives, or if the alternatives are not good, I will try to limit the amount of tooth paste if it isn't needed, I tend to just overuse tooth paste to the extreme, I used to eat it as a kid.


Staff member
One of the common ingredients in household items (including some toothpaste) I've been looking at is Triclosan. The FDA is doing a review as well. My wife and I have made sure to cut out all items that use it including dish soap, detergents, deodorant, etc.
But animals that countries, other than Western ones,use for transport, sport, food and dairy also carry MAP and Johnes disease too, don't they, so they do have MAP infected livestock, right?
David- I also try not to use Triclosan in my house. I read an article not related to IBD in this instance but allergies which my son also has. It is in relation to obsessive germ destruction by man made products not allowing his immune system to develop enough to do the job itself.
But animals that countries, other than Western ones,use for transport, sport, food and dairy also carry MAP and Johnes disease too, don't they, so they do have MAP infected livestock, right?
Some yeah, not all. The amount of infected animals differs greatly too.



In countries of the African continent, testing for M. paratuberculosis runs the gamut from never being done to gene probe confirmation of BACTEC cultures. We were able to find information about 12% or 6 of the continent's 49 countries: Kenya, Nigeria, Sudan, Tunisia, Zambia and South Africa. (Only the Sudan and Kenya are contiguous, and that minimally: Kenya shares only 1/20th of Sudan's border.) In this case, "finding information" meant discovering that at least one case had been reported in recent years. In South Africa the disease has been reported in both sheep and cattle with a focus of isolated herds in the wetter regions of the country (Natal, E. Transvaal). The disease is believed to be neither highly prevalent nor of major significance in this country. In Zambia paratuberculosis is reported to be a greater problem in sheep than in cattle and Tunisia's reports dealt only with camels. No information has been found to date on the other 43 African countries, and therefore no conclusions can be drawn about Johne's disease prevalence in those areas.


New Zealand reports that paratuberculosis is widespread in dairy cattle and goats plus is of concern in sheep and beef cattle as well. The number of recorded infected dairy properties has jumped dramatically over the last 4 years, and it is believed that this registry of infected premises understates actual prevalence. In concert with an increase in the extent of the disease (also evidenced by a doubling in vaccine sales in a year), all research was stopped.


China, Japan, India, Korea, Kazakhstan, Nepal and the Philippines are countries in Asia with contemporary, albeit infrequent, reports of Johne's disease. Japan's information was the most extensive for the region, reporting an annual average of 212 cases of clinical bovine paratuberculosis over the last five years. These cases were confirmed at slaughter. As the United States government continues its efforts through USAID to develop dairy industries in Pacific Rim countries, the need for Johne's disease testing for the new industries should provide a sense of the prevalence in this region.


Incidence of Johne's disease is reported to be increasing in the Netherlands, Finland, Italy and Scotland. In other parts of the European continent, no change in incidence has been noted over recent years. Countries belonging to the constant incidence category are Norway, Denmark, Portugal and Belgium, France, Cyprus, the Czech Republic, Greece, Hungary, Iceland, Slovakia, Spain, Switzerland and Turkey report that cases of paratuberculosis have been found within their borders but offer no guess about the direction in which incidence is moving.

Central and South America

We found information about only three countries in this region - Mexico and Brazil which report test positive cases and Argentina which believes incidence is increasing. "
Kiny: do you know anything about the MAP vaccine that's being worked on? I'm sure I read somewhere that some scientists at imperial uni London are developing one?
Kiny: do you know anything about the MAP vaccine that's being worked on? I'm sure I read somewhere that some scientists at imperial uni London are developing one?
Just what everyone knows, that's he's hard at work for one, John Hermon Taylor: http://www.youtube.com/watch?v=GPO63UWZgy4

There's myaconda (sp?) the triple TB cocktail from Borody who talked to John Hermon Taylor, and there's Naser who is studying nano sensor techniques to idtentify MAP faster than PCR 900 can do atm. (He is doing the trials in Florida that targets MAP)
Camel were exactly what I had in mind in my above comment, so many nomadic tribes of different countries consume camel milk as a staple. I just wondered what the prevalence of MAP is among the camel livestock. But if testing is scant in areas that have large camel populations I guess the information wouldn't be a full picture. Thanks Kiny.
Thanks for that.

I'm still rooting for the Plantains to be the answer. I found some fantastic plantain crisps and insist on 30g a day :)
Thanks for that.

I'm still rooting for the Plantains to be the answer. I found some fantastic plantain crisps and insist on 30g a day :)
Yup, I eat plantain bananas, but it's just hard to get them here. They should make a way to concentrate it in a tablet or something, some company was working on it. (the study that did it actually had concentraited plantain, some UK company made it specifically for that study, I contacted them, and they told me another company is working on a concentrated commercial solution, but I haven't heard about it since)

I saw you asked about naimals with MAP in some other thread. I was interested in MAP and eventually ended up talking to veterinairians and biologists, this site and the documents (all free) are written by the biologists who deal with Johne's disease, but they often talk about crohn too.

Oh, wanted to add about the plantain, I asked some biologists how hard the extraction process was. The extraction process they used for plantain is called "polysaccharide NSP extraction", in essence you can do this at home, but it will take a long time before you can find the right parameters if you don't know what you're doing I think (and I don't) since you need the exact temperature and PH levels to get th emost out of it.
Kiny: thanks again :)

Wouldn't it be great for something, MAP vaccine, those qubiologics ones or something to just -work-. Think how many lives would be transformed. David would have to register excrohnsforum.com. Hah.

Last years's medical Nobel was for immune system work, wasn't it? Maybe a cure is on the horizon?


I switched over to natural toothpaste and mouthwash but I'll need to check the ingredients. I know many multi vitamins also have titanium dioxide which I have been trying to avoid.
I realised over a year ago that toothpastes containing artificial sweeneners were upsetting my gut. I switched to a natural toothpaste and I coud feel the difference.
I might also add that besides all the particles in toothpaste,
some brands also have carrageenan,most brands have sls.
Also read my thread on persorption
Old Mike
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Capsules from medication has microparticles too often, if you take something try taking it without the capsule (unless you really need it, like enteric coated ones).
Wow, I never knew about the Triclosan, not just in reference to the gut, but also heart, thyroid, etc. Thank you, I learned A LOT today after researching quite a bit today thanks to the articles posted.
sort of a cross reference, I already posted that article a while ago, but it was more about diet, but they mention dietary particles (microparticles that are undigested) too

Nutritional modulation of the inflammatory response in inflammatory bowel disease- From the molecular to the integrative to the clinical.

Gary E Wild, Laurie Drozdowski, Carmela Tartaglia, M Tom Clandinin, Alan BR Thomson

Gary E Wild, Department of Medicine, Division of Gastroenterology, McGill University, Montreal, Quebec; Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec, Canada

Just what everyone knows, that's he's hard at work for one, John Hermon Taylor: http://www.youtube.com/watch?v=GPO63UWZgy4

There's myaconda (sp?) the triple TB cocktail from Borody who talked to John Hermon Taylor, and there's Naser who is studying nano sensor techniques to idtentify MAP faster than PCR 900 can do atm. (He is doing the trials in Florida that targets MAP)

Any update on this? According to Wiki, Pfizer shelved Myaconda but is available in Australia?


Talks about the guy John-Hermon Taylor working on a Vaccine. Any update on this? Or is this project dead now?


Staff member
Titanium dioxide is contained in some drugs such as the omeprazole series nexium etc.
All of this is a bit concerning for those of us needing these drugs.
Also silica is used in some preparations and health store products.
Where does it all end?


Staff member
I literally could not find a toothpaste, even at the health store, without all this crap. I'm now brushing with baking soda, salt, and peppermint.


I use Tom's of maine antiplaque and whitening fluoride free tooth paste. The only thing bad in the ingredients is sodium lauryl sulfate which i've read is a mild poison.

David has the write idea. It's not like we need all this crap in our tooth paste anyways as long as we eat healthy.

my little penguin

Staff member
Thanks kiny many things to ponder.
Just harder to factor in when my son was only seven at dx and even younger at the first signs of the disease .
I could even see a teenager from a touth paste stand point .
Again lots to ponder
they removed some PDF, I'm just posting this so it's saved

I should save some old articles from BMJ too, not sure how easy they will be to find a in the future, it is a real pain to find some

AIEC causes granuloma, that is where you can actually isolate the bacteria, in the inflamed lesion. Granuloma are almost all macrophages with a few exceptions. AIEC resides in the macrophages, so it is not surprising you find them there.

Mycobacteria, yes they cause granuloma, MAP too.

Can't answer your question, I don't know. I think not every crohn's disease diagnosis is the same. Granuloma or not is a big difference. Granuloma are "typical" crohn's disease, easy to spot, easy to take biopsy.

Some people go into remission and get completely clear scopes, the granuloma can "disappear"...when the immune response is less active, T cell activate less macrophages, and there's no granuloma. It's possible that someone has an these bacteria and they are dorment, if they do, I don't know.