The John Kender Yeast Hypothesis

I was able to dig into the literature a bit more recently, and here is some of
what I discovered relative to my hypothesis that TTM is an allergic response
to the bloom of a lipophilic yeast.

I found that cholesterol is indeed an agent that makes Malassezia send out
hyphae into the skin. I found that Malassezia is responsible for dandruff and
for tinea versicolor, a skin disease; in the the latter disorder, the organism
is most prevalent within the stratum corneum, the inner layers of the skin,
which is naturally rich in cholesterol. I found that there is some evidence
that yeasts are not terribly picky about their lipids (as might be imagined,
they have had to be pretty adaptable since people's skin lipids vary). My
guess, then, is that any kind of sterols causes the yeast to "bloom": that is,
to grow in size, to send out hyphae which become spores, and to create more
yeasts.

I found that the yeast grows in the laboratory with a spurt that reaches it
maximum in about four days, then levels off. This is similar to what I and at
least two others have noticed as the delay of onset of symptoms after the
ingestion of certain foods (eggs and peanuts, mainly).

If found that one of the growth factors of Malassezia is glucose (basically,
sugar), and another is asparagine, an amino acid heavily present in legumes
and (I found) in some nuts. I found that caffeine is not so much a growth
factor as something that causes yeasts to skip the "resting phase" they
usually go through, so that it has something of the same effect.

My own experience and my reading suggest that the good effect I was
attributing to yogurt is probably due instead to the pineapple that I added to
it. I found that pineapple and kiwi fruit, as well as some other tropicals
(papaya, guava) contain a proteolytic enzyme called bromelain, which may have
anti-allergic properties. I suspect that this enzyme may help break up the
other enzymes that the yeasts themselves use to obtain food from their hosts.

In summary, my current guess of what is behind TTM is the following:

0) People with TTM suffer from an allergy. Period. They are allergic to
a normal yeast that is found in the skin and gut of virtually everyone,
but they react to it with itching and irritation and a need to remove the
allergen. Pulling is like sneezing, nothing more.

1) Certain growth factors cause the yeast to wax and wane and send out
"roots", which cause irritation in the sebaceous glands of the hair, and
sometimes of the face and other areas. Growth factors include
environmental ones such as heat, moisture, and carbon dioxide (which hair
itself, and wigs provide). Growth factors also include nutritional ones
such as sugar, caffeine, sterols (in eggs especially, but also butterfat,
shellfish, legumes, and yams), and asparagine (in peanuts especially, but
legumes and some nuts: all of which also have some sterols).

2) Hot spots are local yeast blooms which are aggravated and spread by
hair play. The pre-menstrual upsurge is due to the upswing of
progesterone, a sterol. There is delay of several days from cause
to maximal irritation, due to the growth of the yeast.

3) Ways to help the disorder include the antifungal (zinc pyrithione
shampoos, and others), the antinutritional (abstinence from offending
foods, plus ingestion of tannins in tea and red wine, of allycins in
garlic, and of bromelains in pineapple), and the antienvironmental (short
hair).

If this is all true, then there is a short cut to the above. The acid test
for the hypothesis is the following prediction:

TTM should respond to standard antifungal treatment such as the
administration, systemically or topically (i.e. orally or upon the skin),
of the customary antifungal drugs.

These include the imidazole family (ketoconazole and others), the polyene
family (nystatin and others), or topical applications of zinc pyrithione,
selenium sulfide, propylene glycol, and others. (Most of the systemic
drugs are by prescription only.) Positive effects should appear, as with
other fungal diseases, within two to four weeks.

However, it should also be the case that the disorder should relapse
quickly. This is because the course of the disease should be chronic, as
it is based on a congenital immunological defect (i.e. an allergy)--which
first becomes apparent at the puberty, when the sebaceous glands begin
secreting in earnest. Therefore, unless the recommended prophylactic
measures of periodic (monthly) retreatment are taken, as they have to be
with certain other fungal diseases such as tinea versicolor, the disorder
will continue to reappear.   

One thing that occurred to me after rereading my most recent yeast speculation was something about this anaesthetic aspect of the pulling phenomenon. Pulling doesn't hurt, and my guess is that it is due to a anaesthetising long chain alcohol. If the yeast hypothesis is correct, this suggests the following.  It is known that Malassezia inhabits the gut as well. (This is why acidophilus should work: by competition, acidophilus bacteria would reduce the yeast population.) Then, this anaesthetising alcohol may be picked up by the blood stream, circulating to the brain. Could it then also be the agent for the hair-pulling "trance"? 

But: I've been doing some digging on the original guess, that the yeast produces something that causes grease production to increase. I have found that some micro-organisms are known to be able to cleave the side chains of sterols, producing hormones. In particular, some micro-organisms can take plant sterols like sitosterol (found in legumes, I seem to remember), and make androstenedione, which has as one of its effects increased sebum production. The drug companies are into this line of research for producing things like birth control pills more cheaply using, roughly speaking, fermentation techniques.  So, it "might not be impossible" (I can't avoid the double negative, as I cannot find anything saying so explicitly) that something like Malassezia does use local sterols to locally produce a local grease-enhancing effect.  This would mean that the "fat roots" are the deliberate results of a yeast bloom. Now suppose in addition, the yeast also produces a long chain alcohol that, due to an allergy in some people, is irritating to the pressure nerves. Further suppose that, since some shorter chain alcohols are known to have anaesthetic properties, this long chain alcohol is also generally soothing to pain nerves. What would happen then is that a yeast colony would cause a local glob of grease to grow that is itchy but not painful, causing the host to want to remove it--and to be able to do so without hurt and with relief.  In short, if there is a yeast at work, it would be self-perpetuating, as it would be able to make what it needed. And, one curious fact I also found was that androstenedione at higher percentages actually is a growth inhibitor for Malassezia. So what we may have here is a feedback loop: Malassezai finds a home, makes a grease glob through converting sterols to an androgen, and then stops growing at the right point. It is happy, and what actually messes this up this cosy arrangement is that those someones who have an allergy to one of the by-products feel compelled to remove the irritation. The poor yeast has to start all over nearby.  (One thing that this scenario would imply is that nearly all people have some fat roots here and there, but for most people it doesn't bother them. I don't know if this is true, although most people do carry Malassezia. I do know that now that my pulling is in remission, I do find an occasional hard small white plug or two in my skin, which doesn't bother me terribly, and which I find almost accidentally.)  Sorry if this grosses anybody out. Maybe I should have just answered Mike's question: yes, I believe a yeast is involved in some pulling, and possibly also in some alopecia, psoriasis, and giant hives.

Some more updates (Dec 1998)

1) The relation of yeast, sugar, and insulin. It appears that the yeast I
suspect, Malssezia, lives both in the gut (where it has access to the fats it
needs directly from foods) and in and on the skin (where, again, it can get
the grease it can't--or no longer needs to--make for itself, from sebum). My
guess is that what sugar does is directly stimulate the growth of the gut
yeast, before the sugar enters the blood stream where glucose levels are
controlled by insulin. This guess is supported by many people's observation
that the response to sugar is faster than the response to beans or egg yolk.
That is, the "brain itch" part (the raw "urge" independent of any skin
sensations) seems to come on faster than the "skin itch" part (the "burn" in
the skin) of TTM behaviors. So, no, it is not necessary for TTM to be then
related to diabetes: the yeast in the gut gets the sugar before its regulated.
This apparent two-site preference of M., and their different response times,
also is consistent with the fact that different people notice different
relative amounts of "urge" versus "burn".

2) Scalp samples of Malassezia: It is considered to be part of the normal skin
flora, so virtually all older adults test positive for M. Newborns don't,
young kids rarely do, and it is only after early adolescence that the
numberstake off. It is not my hypothesis that M. is a germ that causes a
disease; M. is supposed to be harmless. Instead, my guess is that TTM is an
allergic reaction (more properly, a response of the immune system) by only
some people to M., or to M.'s digestive enzymes (which are proteins that
yeasts excrete into the surrounding fluid to break down foodstuffs for uptake
in smaller pieces, some of which are known allergens), or possibly to the
byproducts of M.'s action on the foods themselves.

3) Relation to Candida: A separate yeast, with possibly separate effects.
More to the point, I think, is that research into OCD indicates that there may
be a link to the bacteria Streptococcus. The mechanisms postulated for some
OCD, going under the name of "Pandas", are that the immune system attacks
strep, but in the process, the same antibodies attack part of the central
nervous system, resulting in obsessions and compulsions. It seems to me that
a similar mechanism, in which the immune system attacks M yeasts, could also
trigger the "brain itch" part of TTM by a similarly mistaken attack on a
related part of the central nervous system.