Could M. Globosa Cause Rosacea?

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Could M. Globosa Cause Rosacea?

Postby Artist » Tue Feb 12, 2008 6:52 pm

The addition of Head and Shoulders as a face wash a few times a week has helped overall so much, I've considered the possibility that M. Globosa activity (the yeast that causes seborrheic dermatitis) brought on my rosacea.

It makes sense. M. Globosa likes sebum, and our T-zones have lots of that. And, conveniently, the T-Zone is where capillaries are close to the surface among all that inflammation. Perhaps the M. Globosa-Lipase-Oleic Acid low grade inflammation, over the years, could be the inflammtory source causing the capillary changes over time - in people who have low or no resistance to the yeast.

It would also explain why it's random - you don't have to be a blusher to get it. So, once the inflammatory capillary changes occur (new hypersensitive capillary growth), you are in the symptomatic rosacea stage. Treat the Yeast, get rid of the "fire", but still have those abnormal and abundant capillaries. Maybe IPL would be required then. Just speculation, but interesting nonetheless!

But, it may be more likely that the seb derm started at some point due to the rosacea (secondary to it) and just made it worse.

So, I don't feel that underlying "fire" anymore, I think due to removing my inflammatory trigger of seb derm (caused by the continual M. Globosa-Lipase-Oleic Acid irritation). I hope that makes sense.. Perhaps worth a try since results are seen quickly if it helps.

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Re: Could M. Globosa Cause Rosacea?

Postby Artist » Tue Feb 12, 2008 7:32 pm

.... Also, M. Globosa thrives on Lipase, and there is a study that showed Rosaceans produce more lipase when rosacea warm skin was compared to normal warmed skin - study below.

I also pasted below the explanation of how capillaries change when in an environment of chronic inflammation.

Artist

LIPASE:

(7) Influence of skin temperature on bacteria in rosacea

Dr. Mark V. Dahl, chairman of Dermatology, Mayo Clinic Scottsdale, and Dr. Patrick M. Schlievert, professor of Microbiology, University of Minnesota Medical School.

The greater warmth of the facial skin of rosacea sufferers may play a role in triggering the unsightly bumps and pimples that are common signs of this disorder, according to a new study funded by a grant from the National Rosacea Society and reported at the 2001 annual meeting of the Society for Investigative Dermatology.

In the completed study, Drs. Dahl and Schlievert found that at higher temperatures bacteria from the facial skin of both rosacea patients and people without rosacea released substantially more potentially toxic substances. The study noted that the surface temperature of facial skin in rosacea patients may be warmer than normal skin due to redness and flushing, and the resulting increase in toxic substances may lead to the bumps and pimples often associated with the disorder.

"Researchers have long wondered whether bacteria may be responsible for the inflammation, papules and pustules of rosacea, especially because these signs can be successfully treated with oral and topical antibiotics that destroy bacteria as well as reduce inflammation," Dr. Dahl said.

The researchers cultured samples of Staphylococcus bacteria from the pustules (pimples) of four untreated rosacea patients and the skin surface of four people without rosacea at both 86 and 99 degrees Fahrenheit. They found that, while the bacteria grew at the same rate in both the lower and higher temperatures, at the higher temperature the samples produced larger amounts of potentially toxic proteins.

In addition, some substances were secreted by the bacteria at the higher temperature that were not produced at the lower one. This included a type of enzyme known as a lipase -- a protein that acts to speed chemical reactions -- that may break down oils on the skin surface, potentially leading to blemishes and inflammation. Moreover, while all samples from rosacea patients produced the lipase, half of the samples from people without rosacea did not.

Dr. Dahl described several possible interpretations of these study results. Common bacteria may have a tendency to generate more of these irritating substances at the higher temperatures encountered on the faces of people with rosacea. Also, they may generate different harmful materials at these higher temperatures. The nature of these materials or the amounts produced could trigger papules and pustules.

Dr. Dahl further noted that other bacteria might also behave differently on the warmer skin of rosacea patients.

"Our findings suggest that temperature may change the toxicity of many types of common bacteria, opening a whole new avenue of research into this widespread but poorly understood disorder," Dr. Dahl said.

Publication of results: Dahl MV, Ross AJ, Schlievert PM. Temperature regulates bacterial protein production: possible role in rosacea. Journal of the American Academy of Dermatology 2004;50:266-272.


-----------------------------------------------
INFLAMMATION:

Commentary - Chronic Inflammation - Links with Angiogenesis and Wound Healing

http://ajp.amjpathol.org/cgi/content/fu ... /1035#SEC2

(American Journal of Pathology. 1998;153:1035-1039.) © 1998 American Society for Investigative Pathology

Commentary - Chronic Inflammation - Links with Angiogenesis and Wound Healing - Guido Majno

From the Department of Pathology, University of Massachusetts Medical School, Worcester, Massachusetts

The contribution of blood vessels to inflammation can be divided into two phases. In the first phase, which lasts roughly 24 hours,

functional changes prevail: dilatation, increase in permeability, activation of the endothelium, and diapedesis. In the second phase,

although some of the functional changes persist, structural changes occur. There is remodeling of vessels, mainly capillaries and venules,

with extensive mitotic activity of the endothelium and pericytes. These two phases are generally recognized as "acute" and "chronic,"

whereby it becomes apparent that biological and clinical notions of "acute" and "chronic" are somewhat out of phase, the biological events

being telescoped into a shorter time.4 The response of the microcirculation to a chronic stimulus is the

issue addressed by the San Francisco group. As a model they chose Mycoplasma pulmonis infection of the airways in mice, a model relevant

to human disease because M. pulmonis belongs to the same genus as the human pathogen M. pneumoniae. The authors studied the trachea between 1 and 8 weeks after infection; at each time interval the blood vessels were perfused with silver nitrate or treated by methods that

characterize the phenotype of the endothelium (perfusion with suitable lectins, immersion in anti-vW antibody), then the trachea was cut

open, flattened out, prepared as a whole mount, and transilluminated. The key feature of this preparation is that it shows the vascular

network in three dimensions rather than in cross sections, thus allowing the observer to distinguish capillaries from arterioles and

venules. This is important because it is well established that the pathophysiology of the three microvascular segments is very different.

Thurston et al find that the microcirculation responds to the chronic stimulus either by producing more capillaries or by dilating existing

ones. Surprisingly, the type of response depends on genes: by testing two strains of mice, characterized by high versus low resistance to

Mycoplasma infection, the authors found that the number of vessels doubled in mice of the resistant strain, whereas existing vessels in

susceptible mice became wider. It is not clear whether the difference in vascular response is related to the difference in resistance to

infection.

The observed capillary dilatation is more surprising than it may seem because it has been known since Cohnheim (1867)5 that capillaries in

acute inflammation do not dilate significantly despite the increased blood pressure. Something else must therefore be happening to the

capillary wall in chronic inflammation. Perhaps the tone of the endothelial cells is decreased; by growing endothelium on a pliable

substrate we have shown that endothelial cells do in fact maintain a normal state of contraction or "tone."6,7

With time, the endothelial cells in the dilated capillaries of the inflamed trachea multiply, as we had observed in the rat cremaster.8

At this point the dilated capillaries acquire functional properties of venules and a sort of metaplasia takes place. We hope to learn from

further studies by the San Francisco team whether this change is reversible.

For both new vessels and old ones made larger, Thurston et al report that permeability to Evans blue appears to be in the normal range;

however, both types of vessels are more susceptible to a permeability-increasing mediator, substance P. This finding is of interest for the

pathophysiology of chronic inflammation as it suggests that newly formed or remodeled vessels could be maintained in an activated and/or

leaky condition with doses of chemical mediators too small to affect normal vessels.
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Re: Could M. Globosa Cause Rosacea?

Postby Quiller » Tue Feb 12, 2008 8:20 pm

I think it's an excellent possibility. Whether it's a mite, a fungus, or whatever else, I think many rosaceans have microbes on their skin which, if eliminated, would relieve symptoms greatly.

Pyrithione zinc is available at any drugstore, so why not wash the face and see what happens... it sure works for seb derm.
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Re: Could M. Globosa Cause Rosacea?

Postby Aurelia » Tue Feb 12, 2008 10:27 pm

Hi Artist,

It certainly is an excellent possibility well worth testing.

The majority of rosaceans do not show signs of seborrheic dermatitis, however I note the following from your thread "Seb Derm & Rosacea Studies?" (my emphases):


"So, what happens, even with mild seb derm, is you have inflammation from the Oleic Acid, and any of the following (but not required): flakes or scaling, tight dry feeling, redness/inflammation, you may be oily or not], you may have "patches" or not, itching sometimes occurs. Also, the skin cells slough off much more quickly (2-3 times faster than normal), so you have clumping off of skin - not good for rosacea since we need that barrier. Again, it may not be obvious. You may not see big skin clumps but still have this going on.

Another factor is that people have varying resistances to M. Globosa. Some are able to naturally inhibit the yeast, while others are not - some are just more resistant. Also, resistance changes over the course of one's life. So that, for example, during times of stress, you may be less resistant to this organism and have a flare of seb derm.
"

viewtopic.php?f=5&t=383


Some people are naturally resistant to yeast-type infections. For example, I took antibiotics daily for many years, including one 7-year stretch, and never once had any yeast or candida-like infections. I wonder if some of the rosaceans who fall into that lucky category and don't appear to have any seb derm might perhaps still have some involvement and it just isn't obvious?

Kind regards,

Aurelia
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Re: Could M. Globosa Cause Rosacea?

Postby Artist » Wed Feb 13, 2008 1:22 am

I find it hard to believe that anyone's face has absolutely no M. Globosa on it. My thinking is that, even in small numbers, M. Globosa could cause irritation. It was found to have very high lipase activity, and therefore produces a lot of the irritating oleic acid. So, I think it's possible that a lot of us have irritation from M. Globosa, whether or not it manifests as seborrheic dermatitis. If you have any M. Globosa on your face, it will use lipase and create irritating oleic acid in order to survive. If some of us have less lipase, we'd have less M. Globosa. Less sebum = Less Globosa. Higher resistance, less Globosa. I could be wrong. I'm just thinking here based on what I learned.

If it were me and I had inflammation or irritation, or rosacea that seems resistant to other therapies, I'd give the Head & Shoulders a try, simply because it only takes a few times to see results, and any potential irritation would be minimal if it didn't work.

Also, I noticed that there is a version of Head & Shoulders that uses an active ingredient other than Pyrithione Zinc. So, I'd double check to be sure the only active ingredient is Pyrithione Zinc. I got a shampoo only version that says "smooth and silky". I've read reports from a few that have had success trying the head and shoulders. I think they did have seb derm. I'm not sure if anyone without flakes has tried it.

All that said, please don't overdo it if you try it. Once a day for two days would probably be all that was needed to determine if it helps you. I would be mortified if anyone tried it and broke out terribly :(

Cheers!

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Re: Could M. Globosa Cause Rosacea?

Postby Artist » Wed Feb 13, 2008 2:46 am

This might help shed some light:

http://www.pgbeautyscience.com/dandruff ... ed-by.html
(Pasted below)

I think what they are saying means that oleic acid doesn't cause flaking in everyone. "Topical application of oleic acid (OA) induces a dandruff-like desquamation in the absence of Malassezia fungi, but interestingly only in dandruff-susceptible individuals. " So, I wonder if oleic acid still causes irritation in those individuals?

Artist



-----------------------------------
Dandruff and Seborrheic Dermatitis Result from Scalp Barrier Breach and Irritation

Christina M. Gemmer, BS; Yvonne M. DeAngelis, CVT; Joseph R. Kaczvinsky, Ph.D.; James R. Schwartz, Ph.D.; Thomas L. Dawson, Jr, Ph.D.;
Introduction

The etiology of dandruff and seborrheic dermatitis (D/SD) have become clearer over the last decade1. The skin physiology of D/SD is much more complex than a superficial flaking2. In this study, we define the role of Malassezia metabolism on scalp, investigating the role of irritating free fatty acids released by sebum digestion. We have also shown that removal of Malassezia, and hence the irritating metabolite, both corrects the pathophysiology (as demonstrated by electron microscopy) and improves the skin's barrier function (as demonstrated by a reduction in TEWL).


Objective

The objective of this study was to investigate the effect of oleic acid (OA), a sebum component3, on scalp condition as measured by ultrastructure, flaking, and barrier function. Comparison was also made between dandruff-susceptible and dandruff nonsusceptible individuals, to investigate the role of basal barrier function on the effect of OA.


Results

Figure 1. Dandruff and seborrheic dermatitis (D/SD) are more than just superficial disorders of the stratum corneum, including parakeratosis, intracellular lipid droplets, decreased desmosomes, membrane inter-digitation, and excess intercellular lipid. The abnormality is normalized by pyrithione zinc (PtZ) shampoo2.



Figure 2. Topical application of oleic acid (OA) induces a dandruff-like desquamation in the absence of Malassezia fungi, but interestingly only in dandruff-susceptible individuals.



Figure 3. Removal of Malassezia (and hence their free fatty acid metabolites) with a PtZ containing shampoo improves barrier function as evidenced by decreasing TEWL.



(Insert figures here)

Methods

Images were prepared as described2. Briefly, scalp tape strips were collected before and after treatment. Mid-sized flakes were placed in RuO4, rinsed, dehydrated, and Epon embedded. Thin sections were counter-stained with uranyl acetate and lead citrate, and analyzed in a Philips CM12 TEM at 100KeV. Clinical subjects used a non-antidandruff shampoo for 3 wks, were graded for dandruff, and grouped as dandruff or non-dandruff. Subjects then used a PtZ containing shampoo for 3 wks. Subjects were dosed with a 7.5% OA solution in propylene glycol 50%4 and placebo for 8 days and graded on days 3, 5, 6, 7 and 8. Days 5, 7 and 8 were significant, day 5 presented. Clinical subjects used a non-antidandruff shampoo for 3 wks and were then graded for dandruff. All subjects then used a PtZ containing shampoo for 4 wks. TEWL was measured by a VapoMeter.


Conclusions

Here we report evidence for differences in the skin barrier's ability to prevent flaking induced by fatty acid application between dandruff-susceptible and nonsusceptible individuals.

* Oleic acid, a fatty acid component of human sebum3, is shown to induce a dandruff-like desquamation which is ultrastructurally identical to dandruff.
* The same dose of oleic acid does not induce flaking in subjects who are not predisposed dandruff.
* Removal of the insult significantly improves scalp health as measured by TEWL. The presence of abnormal SC across the scalp of D/SD sufferers1, along with the lower susceptibility to oleic acid induced flaking are further indication of an innate susceptibility in the skin of D/SD sufferers.


References
1. AK Gupta, et al., Skin diseases associated with Malassezia species. JAAD 51:785-98. 2004
2. R. Warner et al.: Dandruff has an altered stratum corneum ultrastructure that is improved with zinc pyrithione shampoo. JAAD 45:897-903, 2001
3. VR Wheatley: The chemistry of sebum. in The physiology and pathophysiology of the skin, Volume 9, The sebaceous glands, A. Jarrett, ed., Academic Press, NY, NY, 1986
4. G Imokawa et al.: Decreased level of ceramides in stratum corneum of atopic dermatitis: An etiologic factor in atopic dry skin? JID 96:523-526, 1991
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Re: Could M. Globosa Cause Rosacea?

Postby David Pascoe » Wed Feb 13, 2008 3:14 am

One thing that will be interesting to see, is if people can eliminate M. Globosa and see some relief from any symptoms.

If there is some scientific basis to this (and it seems there is), and the shampoos/creams containing Pyrithione Zinc aren't too irritating we might see some good results.

Go for it all you rosacea experimenters out there !!

ok, go for it carefully and wisely, of course.
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Re: Could M. Globosa Cause Rosacea?

Postby marpusbean » Wed Feb 13, 2008 11:39 am

I agree, with many years of hindsight a pattern emerges.
Whe I was about 30, I caught Chickenpox from my daughter, for an adult this is nasty, I had spots on my scalp which took some time to go1
This seemed to weaken my scalp and I had perssistent flaking and dandruff, something I had not had before.
Some years later I found myself with redness in the creases of my forehead, and around the eyebrows with itching, clearly S.D.
This was kept under control, later I began to notice, that in hot rooms, I tended to get a red face, and my skin was a little warmer than before.
Later the full blown rosacea flareups came.
The big question is chicken or egg?
Did these slight setbacks to my skin cause it weaken, and then allow the vascular rosacea element to take over?
Or was that vascular weakness always there which made the scalp respond badly to the chickenpox and allow dandruff and SD to take hold before the rosacea developed,
It is a complex situation because we meet many young people on these boards who have rosacea at a very early age, this argues that there is a strong genetic, or hereditary, or skin type influence.
Then someone like me with a dark comlexion , who did not have acne, or any redness, blushing/flushing or signs of rosacea as a young man.
Who then develped rosacea well into middle-age seemingly associated with the SD and dandruff, maybe there are different roots to rosacea ,and even different versions of rosacea.
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Re: Could M. Globosa Cause Rosacea?

Postby Aurelia » Wed Feb 13, 2008 12:07 pm

Hi, Mr Marp.

Interesting to have your history there.

It does seem quite likely that there are "different roots to rosacea, and even different versions of rosacea". Hence the growing feeling that we are more likely to need a range of cures, rather than just one super-cure.

Kind regards,

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Re: Could M. Globosa Cause Rosacea?

Postby Aurelia » Wed Feb 13, 2008 12:17 pm

BTW Interesting to find this thread under "Success Stories". I hope people interested in seb derm will think to look for good news in this section of the board.

Mind you, a lot of members click to display "view active topics" or else log in so they can use the "view new posts" button, so never miss any of the discussions. Or perhaps only mods do that. :lol:

Kind regards,

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