Miniaturization and Inflammation

As the follicle shrinks, does the sebum gland follow suit?

First, let's assume it doesn't. The sebum gland continues normal production of sebum, the flow becomes bottlenecked, therefore clogging the follicle, resulting in subsequent inflammation.

Now, let's assume the gland shrinks along with the follicle. This raises a question -- does this necessarily attenuate the sebum production? The smaller gland now has to work overdrive which can result in inflammation, if I am not mistaken.


Both scenarios point to inflammation being a side effect of balding, rather than one of the mechanisms involved.

Usually when I go to the movies and see enough balding people in front of me, they are the ones with the greasy scalps.

Insulin producing foods trigger a rise in both IGF-1 and DHT, which almost always increase sebum production. Also a high Omega-6 intake with a simultaneous low intake of Omega-3 increase DHT/sebum and increase the release of MMP-9 (follicle death enzyme).

Inflammation can be either local or systemic. Insulin resistance is involved in systemic inflammation. Then there is problems with immune privilege (limited
to alopecia areata), and then there is the question of sebum dependent organisms.

This here is the most striking info on this theory:

Am J Clin Dermatol. 2006;7(4):263-6.
Increased hair shedding may be associated with the presence of Pityrosporum ovale.
Nematian J, Ravaghi M, Gholamrezanezhad A, Nematian E.

Department of Mycology, Faculty of Medicine, Azad University of Medical Sciences, Tehran, Iran.

BACKGROUND AND OBJECTIVE: Although the available data show that hair loss is an important cosmetic problem worldwide, the pathogenesis of common hair shedding is not fully understood. The aim of this study was to evaluate the association between hair shedding and cutaneous Malassezia infection. Malassezia fungi have been the suspected cause of dandruff for more than a century. Previously referred to as Pityrosporum ovale or P. orbiculare, these fungi are now known to consist of at least seven species. METHODS: Over a 4-year period, we obtained 300 hair samples from medical students. Based on the clinical history and a hair-pull test, the participants were divided into two groups: normal subjects and subjects with hair shedding. The students' scalp skin was gently scraped, smeared on a slide, colored by methylene blue, and observed under 10x magnification. RESULTS: All participants who had positive smears with >or=3 P. ovale organisms per low-power microscopic field (10x) were defined as 'carriers.' Seventy-six percent of students were Malassezia carriers. The prevalence of positive smears was significantly higher among subjects with hair shedding than among normal subjects (89.92% vs 9.52%, p<0.001). Furthermore, participants with positive smears had a significantly higher frequency of hair loss complaints and positive hair-pull tests. CONCLUSION: The proportion of subjects who were carriers of Malassezia yeasts was significantly higher in the group with hair shedding, and our results therefore raise the possibility of a relationship between this unicellular organism and hair loss. Our study findings should be explored in a larger series of patients.

Inflammation of the hair follicle itself (folliculitis) is definitley caused by Malessezia yeasts. Malessezia yeast also are implicated in seborrheic dermatitis

This study here shows that folliculitis caused by Malessezia are not by infection but ordinary cutaneous species.

Med Mycol. 2008 Oct 23:1-7.
Malassezia folliculitis is caused by cutaneous resident Malassezia species.
Akaza N, Akamatsu H, Sasaki Y, Kishi M, Mizutani H, Sano A, Hirokawa K, Nakata S, Nishijima S, Matsunaga K.

Department of Dermatology, Fujita Health University School of Medicine, Toyoake, Aichi.

Malassezia folliculitis [MF] is caused by the invasion of hair follicles by large numbers of Malassezia cells, but it remains unclear which Malassezia species are involved in the disease. To clarify this situation, Malassezia species isolated from lesions of MF patients were analyzed by both culture and non-culture methods. In addition, Malassezia species recovered from the non-lesion areas of the skin of MF patients and skin samples of healthy subjects were included in this study. The test population consisted of 32 MF patients and 40 healthy individuals. The lesions were obtained using a comedone extractor, while swabs were employed to obtain skin samples from non-lesion areas of the patients and healthy subjects. Malassezia DNA was analyzed using a real-time PCR technique. The detection limit of the culture method was 5 CFU/cm(2) as opposes 50 cells/cm(2) with non-culture procedures. The predominant species recovered from MF lesions were M. globosa and M. sympodialis by culture method analysis, and M. restricta, M. globosa, and M. sympodialis with non-culture methods. These results were in agreement with those found with samples from non-lesion skin areas of MF patients and healthy subjects. This study clarified that MF is caused by Malassezia species that are part of the cutaneous microflora and not by exogenous species.

CS,

I would imagine if you are suffering from hair-loss you have Malessezia? Putting the research together seems to conclude that while Malessezia exists on all scalps when combined with the over active Sebaceous glands the Malessezia goes into overdrive. Of course this is the end result of all the other root causes you have listed elsewhere.

isaac - Malassezia yeasts use lipase enzymes (Phospholipase A2), to break down the sebum, which contains polyunsaturated fatty acids. In turn, it releases Arachadonic acid.

The arachidonic acid released creates of chain of inflammatory enzymes such as COX-2 or possibly lipoxygenase (LOX), leading to leukotrienes, etc.

In a nutshell, inflammatory prostaglandins. It is definitely known that inhibiting these prostaglandins helps increase hair growth.

So if we buzz our hair short (or pull our hair apart down the center), and if we check the top of our scalp and if the scalp has that glossy look while our body isn't sweating at all, is that an indicator as to if the regimine we are on has stopped our hairloss or not?

Also, I think there's two types of male pattern baldness (senile and premature). And only the senile baldness has the glossy look because it is caused by insulin increase due to aging. Wheras premature baldness, which typically holds onto that tuft of hair in the front of the head (atleast for a few years, but sometimes they keep that tuft of hair into their old age), is from different causes which I don't know. Whenever I see a young man (20's and 30's) going bald they seem to keep that tuft of hair in the front and they don't have the glossy look. And when I see a man over 40 with the tuft of hair there, I ask him what age he started thinning and he always says the 20's.

The Malessezia articles are interesting, when my hair was rapidly thinning for a year, I had a lot of dandruff and stuff falling out of my hair, if I didn't shampoo every other day to get the stuff out, my head would itch like crazy. But if fungi was the cause, wouldn't it affect all the hair and not just the male pattern?

Espio - Sebum is loaded with DHT, so the association is there. Lithium/DMSO will significantly reduce the sebum, but
it does not completely halt the loss. Other factors just beneath the scalp are at play, TGF-beta, MMP-9, etc.

in terms of internals to combat the overproduction of sebum/oily scalp, I have read in various places that Borage oil is quite helpful, so I was curious whether it is just the EPA and DHA in Borage oil which the articles mention (and which can be found from other sources too) or whether it is something unique about borage oil?

since my scalp oiliness is quite severe, i need an internal...anyone have any luck with any internals for reducing scalp sebum (i feel this is also partially stress related).

edci - Borage oil is a very rich source of the "good" Omega-6 fatty acid, GLA (Gamma Linolenic Acid). It helps moisturize skin and it inhibits DHT.