Itching Inflammation sebum and Hair loss

We contacted Dr. Kevin McElwee, owner of Keratin.com and asked him to write an article for us on how detrimental inflammation and sebum production is to the hair loss and hair loss treatment process. Here was his reply, and his very elaborate article:

"Well you opened a real can of worms with that article suggestion. It is a complex situation and you will find different dermatologists saying different things about the significance of inflammation in AGA (Androgenetic Alopecia, or Male and Female Pattern Baldness). I have spent a few hours trying to knock it into shape and as a result it has gotten rather long. Feel free to hack the article down to size."

The technical stuff...

When looking at tissue biopsies from human scalp skin it is fairly common to see inflammatory cells. Inflammatory cells are part of our immune system. They should always be there. We need them to protect against viruses and bacteria that can get into our body through wounds. Healthy skin should contain a lot of what are called dendritic cells and Langerhan’s cells. These cells form part of our primary immune defense. They are involved in what is called “immunosurveilance”. In other words, these cells migrate through the skin constantly checking our cells and other material they find to make sure there are no foreign proteins present, particularly foreign proteins from bacteria and viruses. There are even some inflammatory cells inside the upper regions of the hair follicle. They probably look for pathogens that might try to take up residence in the hair follicle canal.

Scalp skin contains more clusters of inflammatory cells than you would see in non-scalp skin. These cell clusters are often very close to follicles, and they contain other immune cell types that would not normally be seen in healthy skin. Many times they contain things like mast cells, lymphocytes, and sometimes neutrophils. While there are always a few of these cells in healthy skin, seeing them in greater numbers on the scalp is a rather worrisome sign. When inflammatory cells increase in number they are usually responding to something. The cause of the greater clustering on the scalp isn't totally understood. It could be a response to some change in the skin or hair follicles, or it could be from an outside factor entering the skin.

Not many studies have been done to look at these cell clusters. Three are mentioned in the footnotes of this article. These small studies generally involved taking biopsies and looking at the numbers of inflammatory cells around hair follicles. By comparing the frequencies of cell numbers in alopecia affected and normal scalp skin, most of the authors concluded that inflammation might contribute towards the hair loss. However, there is a flaw in this reasoning. These studies always look at the inflammation after hair loss had developed. They didn't take into account the possibility that changes in the hair follicle DURING hair loss may attract the cells, and an inflammatory response. So there is a lot of argument among dermatologists over whether scalp inflammation in AGA actually contributes to AGA. Some well respected dermatologists believe that it does, while others say that scalp inflammation is common and seen even when AGA is not present.

Many people who experience Androgenetic Alopecia (male and female pattern baldness) express concern about a tingling and itching that can vary in severity from a slight tingling to an extremely annoying inflammation. It has been hypothesized that this itching, which almost always seem to appear at the onset of MPB, is a response to the hormonal changes going on in the scalp. Even in the absence of MPB, dermatitis on its own will result in a mild telogen effluvium type hair loss, so in the presence of MBP, dermatitis can significantly speed up the speed of your loss and inhibit the effectiveness of your treatments. Both AGA and dermatitis are quite common and it is quite possible to have both conditions together. Many people do. In fact, it has been hypothesized that even in the absence of any noticeable itching, this same inflammation can exist on a smaller scale and should be treated with a shampoo like TGel or Nizoral.

If you have a combination of both AGA and a the itch of dermatitis, then successfully treating the dermatitis will not only slow down the speed of your loss, but it will help with your hair growth. It would not stop progression of the underlying AGA, but it would give some degree of hair growth improvement. There are two main kinds of dermatitis to consider, seborrheic dermatitis and contact dermatitis. Seborrheic dermatitis involves an inflammatory response to the oils produced by the sebaceous glands while contact dermatitis is the result of exposure to some allergic factor – most often a chemical in a shampoo or conditioner. Both types of dermatitis can cause a fungal infection that makes things worse.

Anti Inflammatory in the Propecia Trials

When studies on Propecia were conducted, the drug users were all asked to wash their scalps with Tgel shampoo. The reasoning behind this was two fold. First, cosmetic hair products do affect the look or hair and the trial investigators were going to take global photographs so they wanted the volunteers to all be using the same shampoo product throughout the study. Second, the issue of whether dermatitis could influence the hair growth response to Propecia needed to be minimized. Tgel is a reasonably effective treatment for dermatitis (seborrheic or contact) while at the same time it has no known direct stimulation or inhibition of hair growth. By using Tgel the investigators could remove the question of whether scalp dermatitis was influencing any hair growth response to the Propecia use from the clinical trial. Some think the investigators were worried that Propecia might stimulate dermatitis itself hence the use of Tgel, but there has never been any official word to confirm or deny this, and at least to my knowledge there has been no reporting of dermatitis exacerbation with the use of Propecia.

Continued in part two...