Why is anti-inflammatory of any help?

[HairMetal]

I posted it on another board but nobody could answer me.

First some quoted facts

Inflammation (Latin, inflammare, to set on fire) is part of the complex biological response of vascular tissues to harmful stimuli, such as pathogens, damaged cells, or irritants.[1] Inflammation is a protective attempt by the organism to remove the injurious stimuli and to initiate the healing process.

Anti-inflammatory refers to the property of a substance or treatment that reduces inflammation. Anti-inflammatory drugs make up about half of analgesics, remedying pain by reducing inflammation as opposed to opioids, which affect the central nervous system.

NSAIDs work on a chemical level. They block the effects of special enzymes -- specifically Cox-1 and Cox-2 enzymes. These enzymes play a key role in making prostaglandins. By blocking the Cox enzymes, NSAIDs stop your body from making as many prostaglandins. This means less swelling and less pain.

Anti-inflammatory reduces the inflamation, not the injurious stimuli that will continue regardless of inflamation.

DHT is the injurious stimuli.

I couldn only get it if inflamation itself kills the folicle instead of the injurious stimuli.

 

[ripple-effect]

Where did you read that DHT is the injurious stimuli? DHT itself isn't what is attacking your follicle. DHT simply triggers an immune response in genetically predisposed hair follicles that causes your hair follicles to be inflamed.

In this case, your hair follicle = the injurious stimuli. Your body falsely thinks that your hair follicles are a threat and it needs to get rid of it. That is why you start losing it over time, and it's important to have anti-inflammatory's in your regimen to combat this inflammatory action of the body. It's also why it's important to get rid of DHT in your hair follicle to stop it from falsely signaling your body to attack it.

 

[Bryan]

Where did you read that DHT is the injurious stimuli? DHT itself isn't what is attacking your follicle. DHT simply triggers an immune response in genetically predisposed hair follicles that causes your hair follicles to be inflamed.

In this case, your hair follicle = the injurious stimuli. Your body falsely thinks that your hair follicles are a threat and it needs to get rid of it. That is why you start losing it over time, and it's important to have anti-inflammatory's in your regimen to combat this inflammatory action of the body. It's also why it's important to get rid of DHT in your hair follicle to stop it from falsely signaling your body to attack it.

A lot of people on hairloss sites have talked about that idea over the years, but I don't really know of any direct scientific evidence to support that view. As more and more scientific studies are indicating nowadays, DHT and other androgens cause the dermal papillae of scalp hair follicles to release harmful chemicals which directly suppress their growth. This is starting to seem more and more clear, all the time.

 

[ripple-effect]

In either case, DHT isn't directly attacking the follicle. It initiates a signaling cascade once it attaches to the follicle that is not fully understood yet. The theory I gave out is what makes the most sense to me.

 

[Bryan]

I think it's unfortunate that people keep repeating the idea that they heard about on hairloss sites that the body "attacks" hair follicles, or even more specifically that it supposedly mounts an "immune response" to hair follicles. That sounds like a cool idea to people who first hear about it, but I don't know of any scientific evidence for it.

Yes, I think androgens (including DHT) "attack" hair follicles directly, by causing them to release harmful chemicals and hormones which spread to the rest of the follicle and cause serious damage. The TGF-beta family of chemicals (both 1 and 2) are excellent examples of such harmful chemicals. There are others, too! You can find studies on PubMed which talk about this stuff all the time. Go by what doctors and hairloss researchers say, not what you read on hairloss sites.

 

[ripple-effect]

I think it's unfortunate that people keep repeating the idea that they heard about on hairloss sites that the body "attacks" hair follicles, or even more specifically that it supposedly mounts an "immune response" to hair follicles. That sounds like a cool idea to people who first hear about it, but I don't know of any scientific evidence for it.

Yes, I think androgens (including DHT) "attack" hair follicles directly, by causing them to release harmful chemicals and hormones which spread to the rest of the follicle and cause serious damage. The TGF-beta family of chemicals (both 1 and 2) are excellent examples of such harmful chemicals. There are others, too! You can find studies on PubMed which talk about this stuff all the time. Go by what doctors and hairloss researchers say, not what you read on hairloss sites.

Characterization of inflammatory infiltrates in male pattern alopecia: implications for pathogenesis.
Immunohistochemically, control biopsies were devoid of follicular inflammation (n = 3), while transitional regions consistently showed the presence of activated T-cell infiltrates about the lower portions of follicular infundibula. These infiltrates were associated with the induction of class II antigens on the endothelial linings of venules within follicular adventitia and with apparent hyperplasia of follicular dendritic cells displaying the CD1 epitope. Inflammatory cells infiltrated the region of the follicular bulge, the putative source of stem cells in cycling follicles.
http://www.ncbi.nlm.nih.gov/pubmed/1390168

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DHT seems to induce class-II antigens within the follicle. The immune system then perceives the follicle as a "foreign body," and targets it for destruction.
http://www.renewman.com/the-effects-of- ... -baldness/
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According to Houston researcher Dr. Peter Proctor DHT fouls up the "grow hair" and "shed hair" mechanisms in follicle cells. The good guys, Proctor postulates, are nitric oxide (NO) molecules that are secreted from nearby blood-vessel walls. They trip the cellular "grow hair" switch. The villain is superoxide--a highly reactive chemical produced by immune cells that accumulates around hair follicles. Superoxide throws the "shed" switch.

Even healthy follicles release their hair about every four years, but balding men shed more often. Their follicles, when DHT attaches to them, may excrete a protein that is not recognized by the body. The immune system then sends in the cavalry, triggering the release of more superoxide. "It's like when a transplanted organ is rejected," says Proctor. It's bad enough that superoxide throws every shed switch in sight, but it seems to react with nitric oxide to form toxic chemicals that irritate the follicles the way a strong bleach burns the skin.

Beavan, Colin New strategies to save your scalp.(male baldness) Esquire v127,n4 (April, 1997):108 (2 pages).COPYRIGHT 1997 Hearst Corporation.

Yes, I think androgens (including DHT) "attack" hair follicles directly, by causing them to release harmful chemicals and hormones which spread to the rest of the follicle and cause serious damage.

That means DHT is indirectly attacking the follicle. That is not direct.

You might want to also address how according to the reasoning you gave that inflammation is a bad thing and not a good thing. If the immune system is not responsible then inflammation could be a good thing because it means your immune system is trying to get rid of the "injurious stimuli" or the harmful chemicals that are being released from the DP.

 

[Bryan]

Characterization of inflammatory infiltrates in male pattern alopecia: implications for pathogenesis.
Immunohistochemically, control biopsies were devoid of follicular inflammation (n = 3), while transitional regions consistently showed the presence of activated T-cell infiltrates about the lower portions of follicular infundibula. These infiltrates were associated with the induction of class II antigens on the endothelial linings of venules within follicular adventitia and with apparent hyperplasia of follicular dendritic cells displaying the CD1 epitope. Inflammatory cells infiltrated the region of the follicular bulge, the putative source of stem cells in cycling follicles.
http://www.ncbi.nlm.nih.gov/pubmed/1390168

For a probably better, more involved and more technical paper on the same subject as the one you cited above, I recommend the following: "Androgenetic Alopecia and Microinflammation", Yann F. Mahe et al. International Journal of Dermatology 2000, 39, 576-583. That's a very technical, complex, and thorough work. At no time do the authors ever even hint or suggest that the immune system is "targeting" hair follicles for destruction; their main thrust seems to be that androgens stimulate the production of sebum around hair follicles, which appears to generate the main interest of the immune system and the inflammation that develops as a result.

DHT seems to induce class-II antigens within the follicle. The immune system then perceives the follicle as a "foreign body," and targets it for destruction.
http://www.renewman.com/the-effects-of- ... -baldness/

Again, that just seems to be some silly theory that became popular on hairloss sites on the Internet. I have yet to find any real medical study or source which talks about that idea seriously.

[...]
Even healthy follicles release their hair about every four years, but balding men shed more often. Their follicles, when DHT attaches to them, may excrete a protein that is not recognized by the body. The immune system then sends in the cavalry, triggering the release of more superoxide. "It's like when a transplanted organ is rejected," says Proctor. It's bad enough that superoxide throws every shed switch in sight, but it seems to react with nitric oxide to form toxic chemicals that irritate the follicles the way a strong bleach burns the skin.

A number of times in the past on hairloss sites like this, I've mentioned Dr. Proctor as being the main source of the idea that the immune system "attacks" hair follicles; I've also mentioned that I've never found any actual medical studies or journal articles to back it up!

Yes, I think androgens (including DHT) "attack" hair follicles directly, by causing them to release harmful chemicals and hormones which spread to the rest of the follicle and cause serious damage.

[...]
You might want to also address how according to the reasoning you gave that inflammation is a bad thing and not a good thing. If the immune system is not responsible then inflammation could be a good thing because it means your immune system is trying to get rid of the "injurious stimuli" or the harmful chemicals that are being released from the DP.

The immune system doesn't try to "get rid" of the harmful chemicals being released from the DP.

 

[ripple-effect]

Again, that just seems to be some silly theory that became popular on hairloss sites on the Internet. I have yet to find any real medical study or source which talks about that idea seriously.

I just posted a study backing that "silly theory" up. Did you not read it?

These infiltrates were associated with the induction of class II antigens on the endothelial linings of venules within follicular adventitia and with apparent hyperplasia of follicular dendritic cells displaying the CD1 epitope.

The immune system doesn't try to "get rid" of the harmful chemicals being released from the DP.

Explanation?

I recommend the following: "Androgenetic Alopecia and Microinflammation", Yann F. Mahe et al. International Journal of Dermatology 2000, 39, 576-583.

If you have a link to full article I will try to read it. I was only able to access the Introduction, but I noticed that in the Intro it mentioned the study I posted earlier + another study showing a link between the immune system and hair loss. So it just seems silly to me how you apparently have never seen anything in medical literature about this when the Intro of the study mentions this connection.

http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract

 

[squeegee]

This thread is good stuff! unk:

 

[Bryan]

Again, that just seems to be some silly theory that became popular on hairloss sites on the Internet. I have yet to find any real medical study or source which talks about that idea seriously.

I just posted a study backing that "silly theory" up. Did you not read it?

These infiltrates were associated with the induction of class II antigens on the endothelial linings of venules within follicular adventitia and with apparent hyperplasia of follicular dendritic cells displaying the CD1 epitope.

That doesn't really say anything about the idea you're suggesting (that hair follicles are "attacked" by the immune system, in the same way that a transplanted human heart is "attacked"). Merely to talk about inflammatory "infiltrates" in and around hair follicles doesn't go NEARLY far enough.

As I've already said before, the Yann F. Mahe et al paper discusses hair follicle inflammation very thoroughly (it mentions and cites the earlier Jaworsky paper numerous times, I might add), yet never gives even the slightest hint or suggestion that the immune system "attacks" hair follicles. Their basic idea is that inflammatory substances are generated by the immune system to help fight the harmful effects of bacteria, mold, etc. Here is part of a brief statement they make near the end of the study:

Working hypotheses
We propose here working hypotheses which do not invalidate the contribution of a hereditary genetic androgen imbalance in Androgenetic Alopecia [they mean androgenetic alopecia], but rather attempt to integrate the neglected microinflammatory aspects of alopecia into the complex etiology of Androgenetic Alopecia. On the one hand, excessive local and/or endocrine, genetically exacerbated 5-DHT synthesis results in sebaceous gland enlargement; as a consequence, some scalps might offer more comfortable niches to harbor the previously mentioned pro-inflammatory microorganisms...

I recommend the following: "Androgenetic Alopecia and Microinflammation", Yann F. Mahe et al. International Journal of Dermatology 2000, 39, 576-583.

If you have a link to full article I will try to read it.

I don't have a link to the full paper. Sorry. I only have a paper copy of it.

I was only able to access the Introduction, but I noticed that in the Intro it mentioned the study I posted earlier + another study showing a link between the immune system and hair loss. So it just seems silly to me how you apparently have never seen anything in medical literature about this when the Intro of the study mentions this connection.

You're reading too much into these studies; as I've already said more than once, I haven't seen any published study or theory claiming that the immune system "attacks" human hair follicles in androgenetic alopecia, the same way that transplanted organs are "attacked". All I've seen is people talking about it on hairloss sites, and that includes what Dr. Proctor has said about it.

 

[Hoppi]

Your own immune system kills the follicle I believe...

 

[Bryan]

Your own immune system kills the follicle I believe...

Yeah, that's what a lot of lay people on hairloss forums believe, even if there isn't much of any indication that that's what doctors and hairloss researchers believe!

Below is yet another excerpt from the Yann Maher paper which I've been quoting lately. It shows that the authors of the paper seem to think that the inflammation from male pattern baldness is caused by the body's reaction to the microorganisms and sebum that's found in the skin, as at least a partial result of androgenic stimulation; it doesn't have anything to do with the immune system "attacking" hair follicles (I've included the reference numbers they've cited in this passage just to show that they know what they're talking about, and aren't just making this stuff up):

The cytokine/chemokine side of microinflammation
Why does microinflammation take place in the pilosebaceous unit and for what benefit and purpose? Figure 2 and Fig. 3 show, in a simplified sequence, that inflammation is a multistep process which may start from a primary event. Let us look at the clues at the "crime scene" of Androgenetic Alopecia: we observe a perifollilar infiltrate in the upper follicle near the infundibulum.(2-7) This suggests that the primary causal event for the triggering of inflammation might occur near the infundibulum.(2-7) Supporting this point of view, improvement of the inflammatory aspect of Androgenetic Alopecia has been reported in a pilot study with an antimicrobial lotion.(7) One could speculate that several inhabitants of the scalp, such as the "triad" (Propionibacterium sp.; Staphylococcus sp.; Malassezia ovalis) or other members of the transient flora, could be involved in this complex inflammatory process.(7) The presence of porphyrins (produced by Propionibacterium sp.) in the pilosebaceous duct of 58% of Androgenetic Alopecia patients (compared with 12% of control subjects), which are able to induce the production of complement (C5) chemotactic factor, is considered to be a possible cofactor of this initial pro-inflammatory stress.(6,7) Keratinocytes are also known to respond within minutes to chemical stress, pollutants, UV radiation or even mechanical stress.(37) Not only are radical oxygen species,(38) NO,(39) PGs, and histamine(40) produced, but also intracellularly stored IL-i(alpha) is released(37,41). By itself, this pro-inflammatory cytokine (as well as IL-i(beta) which binds to the same receptor) is able to inhibit the growth of isolated hair follicles in culture in vitro.(9-11) [...]

 

[purecontrol]

In the end the main point is that too much inflammation = bad. Too much inflammation does a lot of bad things such as autoimmune issues, to over production free radicals (oxidants), and out right hyper sensitizing the AR (androgen receptors).

If you want more hair you need to address too much inflammation as well and every thing that causes it.

Keep in mind though that alone is not going to save your hair, as with anything a total approach is best.

 

[Bryan]

In the end the main point is that too much inflammation = bad. Too much inflammation does a lot of bad things such as autoimmune issues, to over production free radicals (oxidants), and out right hyper sensitizing the AR (androgen receptors).

How do you suppose inflammation causes androgen receptors to become more "sensitive"? How exactly does that work? :dunno:

 

[purecontrol]

In the end the main point is that too much inflammation = bad. Too much inflammation does a lot of bad things such as autoimmune issues, to over production free radicals (oxidants), and out right hyper sensitizing the AR (androgen receptors).

How do you suppose inflammation causes androgen receptors to become more "sensitive"? How exactly does that work? :dunno:

Bryan have you even looked over anything concerning epigenetics at all?

If you or anyone else where has not, then I suggest you familiarize yourselves with this information.

You can't change your genetics, but you sure as hell can change it's expression.

Also on a final note, new studies show that the majority of illness is diet related. Meaning that people's lifestyle are causing them need medical care, but in reality you just need to stop being a pig.

 

[Bryan]

How do you suppose inflammation causes androgen receptors to become more "sensitive"? How exactly does that work? :dunno:

Bryan have you even looked over anything concerning epigenetics at all?

If you or anyone else where has not, then I suggest you familiarize yourselves with this information.

You can't change your genetics, but you sure as hell can change it's expression.

Please answer the question I asked you.