INFLAMMATION - the solution?

Xenon wrote:Admin, I'd take your reply seriously if you could present an argument as to why I'm wrong. But you have not done so. You have labeled me contradictory, yet everything I have said in my post is consistent with lowering body heat to reduce inflammation.

Inflammation surely is the cause of hairloss, I would never deny something that grounded, and elevated body temperature does have a correlation with it, but so does low body temperature, have you done a basal body temperature test on yourself? this is very often depressed in people experiencing MPB.

If you bothered doing the research, you will discover that:

1) DHT clogs the capillaries of the galea.

Androgens interrupt wound healing, DHT in particular, stimulate the constriction of blood vessels and capillaries, in certain individuals inhibits WNT signalling, etc, essentially making anything that's trying to get to the scalp have a reduced flow, DHT doesn't clog anything, it's too small to do so, if this were the case people would be dropping dead on the street like flies.

2) It is a fact that 30% of body heat is released from the scalp

3) Heat escapes from sweat glands in the scalp. They are called eccrine glands.

4) The eccrine glands are located directly next to the follicle, and DHT spreads into them because they are located along the same capillary network.

5) When the capillaries of these sweat glands become clogged, then it doesn't take rocket scientist to work out that they will have difficulty in releasing body heat -- especially considering the fact that a third of our body heat is released from the head, hence it being the warmest part of the body.

The assertions here from what you wrote above are actually assumptions, I'm not saying you are entirely wrong, but you are very much not correct.

6) Go do a work out with some clothes on and observe how much body heat you generate. Then go take a hot shower. When you are dry, put on some thick clothes and then go have a hot drink. See how much body heat you generate when you do this and how much rushes to the scalp. Wash, rinse, repeat enough times and you will experience inflammation in your scalp. Now report back to me and tell me I'm wrong.

I do this everyday and I can definitely tell you that you're wrong about it causing hairloss for me, I take advantage of heat. A good day for me is laying in the sun for hours in the heat, then going inside to do a workout, then get a warm bath, then drink hot tea with the ladyfriend while watching a movie, and my hair thanks me for it, why? because I've found ways to remove many of the causes of my inflammation. As goes the Zeppelin song, I "Come from the land of the ice and snow", if anything the cooling down the scalp for prolonged periods is just as stressful or more on bloodflow than heat.

7) Recent studies discovered that a high amount of prostaglandin d were found in the follicles of bald men. Prostaglandins cause pain and inflammation, and they are produced by the enzyme Cyclooxygenase (COX). So the fact that a high number of prostaglandin d is found in the follicles of balding men, and the fact that they cause inflammation, suggests that hairloss is largely caused through inflammation.

Again I firmly believe hair loss is a result of inflammation, I've seen all the studies reporting it to be a factor, and have personally stopped my loss of hair by cutting down systemic inflammation in my own body. Heat just ends up not being the type of factor your theory says it is, if it were the case metabolic syndrome would increase the closer you get to the equator, but its exactly the opposite.

And on a side note: why are you just attacking me over this issue? I was merely responding to the OP's thread. Why have you not questioned him over the same things? He said that inflammation is the cause. I agree with him. So why did you only target me over this issue? ...Because of what I said to Ferox in that thread, no doubt. If this is the case, then you're using passive aggression to get back at me, yet you don't take into account that I was pointing out an important issue, so that other people wouldn't lose anymore hair. Did you bother questioning the detrimental effects of Ferox's methods and the heat inflammation (not to mention skin damage) vigorous boar brushing could cause to the boards members? No. Yet I did, and I'm being singled out for this.

The OP is Mastery, haha, me and him go way back to the point of me having spent time doing some research with him in person, he knows my stance very well, right 007?

Reason I signalled you out was because your understanding of hairloss is missing many pieces and users who are newer to hair loss should see opposing sides to every topic. I couldn't care less about anything else, if you want to poke Ferox that's really up to you, all things should be scrutinized.

The role of inflammation and immunity in the pathogenesis of
androgenetic alopecia.
Magro CM, Rossi A, Poe J, Manhas-Bhutani S, Sadick N.
Department of Pathology and Laboratory Medicine, Weill Medical College
of Cornell University, New York, NY, USA.

BACKGROUND: Female pattern hair loss affects many women; its
pathogenetic basis has been held to be similar to men with common
baldness. OBJECTIVE: The objective of this study was to determine the
role of immunity and inflammation in androgenetic alopecia in women and
modulate therapy according to inflammatory and immunoreactant profiles.
MATERIALS AND METHODS: 52 women with androgenetic alopecia (AA)
underwent scalp biopsies for routine light microscopic assessment and
direct immunofluroescent studies. In 18 patients, serologic assessment
for antibodies to androgen receptor, estrogen receptor and cytokeratin
15 was conducted. RESULTS: A lymphocytic folliculitis targeting the
bulge epithelium was observed in many cases. Thirty-three of 52 female
patients had significant deposits of IgM within the epidermal basement
membrane zone typically accompanied by components of complement
activation. The severity of changes light microscopically were more
apparent in the positive immunoreactant group. Biopsies from men with
androgenetic alopecia showed a similar pattern of inflammation and
immunoreactant deposition. Serologic assessment for antibodies to
androgen receptor, estrogen receptor or cytokeratin 15 were negative.
Combined modality therapy with minocycline and topical steroids along
with red light produced consistent good results in the positive
immunoreactant group compared to the negative immunoreactant group.
CONCLUSION: A lymphocytic microfolliculitis targeting the bulge
epithelium along with deposits of epithelial basement membrane zone
immunoreactants are frequent findings in androgenetic alopecia and could
point toward an immunologically driven trigger. Cases showing a positive
immunoreactant profile respond well to combined modality therapy
compared to those with a negative result.
PMID: 22134564

Inflammation is a response of a tissue to injury, often injury caused by invading pathogens. It is characterized by

increased blood flow to the tissue causing
increased temperature,
redness,
swelling, and
pain.

A bacterial infection initiates inflammation through several interconnecting mechanisms:

The "nonself" surface of bacteria allows the complement system to be activated through the "alternative pathway".
Certain surface molecules of the bacteria, called Pathogen-Associated Molecular Patterns (PAMPs), bind to Toll-like receptors (TLRs) on or in a variety of leukocytes.
Link to discussion of PAMPs and TLRs.

Mast Cells

Mast cells are found in the tissues.

Their cytoplasm is loaded with granules containing mediators of inflammation.
Their surface is coated with a variety of receptors which, when engaged by the appropriate ligand, trigger exocytosis of the granules.

Mast cells appear to be key players in the initiation of inflammation.

Their Toll-like receptors trigger exocytosis when they interact with PAMPs like
the lipopolysaccharide (LPS or "endotoxin") of Gram-negative bacteria (TLR-4)
the peptidoglycan of Gram-positive bacteria (bind TLR-2)
Their receptors for complement fragments trigger exocytosis when they bind
C3a and C5a
bacteria coated with C3b

Activated mast cells release literally dozens of potent mediators;

some immediately as they discharge their granules
some later as they synthesize them by new gene transcription.

These mediators are active in either (or, in some cases, both)

recruiting all the types of white blood cell to the site
monocytes that become macrophages when they leave the blood and enter the tissue
neutrophils
antigen-presenting dendritic cells
all kinds of lymphocytes:
B cells and T cells, leading to an adaptive immune response;
NK cells (an effector cell in innate immunity).
eosinophils
activating many of these recruited cells to produce their own mediators of inflammation.

I shall not attempt to catalog all the players, but here are some of the major (and best understood) ones.
Tumor Necrosis Factor-alpha (TNF-α)

Large amounts of TNF-α are quickly released by stimulated mast cells. All the cells involved in inflammation have receptors for TNF-α and are activated by it to synthesize more on their own. This positive feedback quickly amplifies the response.
Link to a description of how the binding of TNF-α to its receptors on a responding cell initiates new gene transcription by the cell.
Tryptase
Tryptase is the most abundant protein released by mast cells. It is a serine protease. Like the mammalian enzyme trypsin, tryptase cleaves peptide bonds on the C-terminal side of arginines and lysines. It activates C3 of the complement system and probably supports inflammation in other ways as well.
Chemokines

These are chemotactic cytokines; that is, secreted proteins that attract other leukocytes into the area. Several have been identified.
Reactive Oxygen Species (ROS)

These are produced by activated phagocytes: macrophages and neutrophils. They are toxic for microorganisms but can also lead to tissue injury. ROS are described in detail on another page. Link to it.
Histamine

The granules of mast cells are loaded with histamine and their exocytosis releases this potent mediator. Histamine increases the blood flow to the area and the leakage of fluid and proteins from the blood into the tissue space. Thus the quick release of histamine produces the redness and swelling associated with inflammation.
Interleukin-1 (IL-1)
Macrophages, monocytes, and activated platelets are sources of this cytokine. IL-1 has both

paracrine effects on cells in the vicinity, e.g.,
causing them to produce tissue factor and thus triggering the blood clotting cascade. [Link]
stimulating the synthesis and secretion of a variety of other interleukins
helping to activate T cells and thus initiate an adaptive immune response
endocrine (hormonal) effects as it is carried in the blood throughout the body.
decreasing blood pressure
inducing fever.

IL-1 causes fever by stimulating the release of prostaglandins, which act on the temperature control center of the hypothalamus.
Inflammasomes

IL-1 is synthesized from a larger precursor that is cleaved by a caspase (caspase-1). Caspase-1 is part of two (or more) multi-protein complexes in the cytosol of macrophages and neutrophils that are called inflammasomes. Inflammasomes are activated by several different products produced by invading bacteria. Some of these are first "seen" by toll-like receptors (TLRs) thus providing a link between the innate immune system and inflammation.
Bradykinin

Bradykinin is a nonapeptide (9 amino acids).

It is synthesized by proteolytic cleavage of an inactive precursor (a kininogen) that is produced by the liver and circulates at all times in the blood (one of the alpha-globulins).
Bradykinin

relaxes the smooth muscle walls of the arterioles lowering blood pressure and increasing blood flow to the tissue and
makes the capillaries leakier, allowing blood components to enter the tissue space.
These effects (like those of histamine) produce the redness, warmth, and swelling of inflammation.

The process:

Hageman factor (also known as clotting factor XII [12]) normally circulates in the blood as inactive precursor.
When tissue damage allows blood to escape into the tissue space, Hageman factor comes in contact with the collagens in the tissue space and becomes activated.
Activated Hageman factor is a serine protease that cleaves an inactive precursor called prekallikrein into another serine protease — kallikrein.
Kallikrein then cleaves kininogen forming bradykinin.

Bradykinin also

stimulates the release of nitric oxide;
stimulates phospholipase to increase the production of prostaglandins and
(mediates the closing of the ductus arteriosus when a baby is born).

Prostaglandins and Leukotrienes

These potent mediators of inflammation are derivatives of arachidonic acid (AA) a 20-carbon unsaturated fatty acid produced from membrane phospholipids.
The principal pathways of arachidonic acid metabolism are

the cyclooxygenase (COX) pathway, which produces prostaglandin H2 (PGH2). PGH2 serves as the substrate for two enzymatic pathways: one leading to the production of several
prostaglandins (PG); the other leading to the production of
thromboxanes (Tx).
the 5-lipoxygenase pathway, which produces a collection of leukotrienes (LT)


Acute Inflammation: The Good Side of Inflammation
The acute inflammatory response to tissue damage is of great value. By

isolating the damaged area,
mobilizing effector cells and molecules to the site, and — in the late stages —
promoting healing,

inflammation protects the body.

Its importance is demonstrated by the problems people with inherited defects in components of the process have with infections.

Some examples:

a failure to produce reactive oxygen species (ROS) leads to chronic granulomatous disease (CGD) [Link to discussion]
inherited defects in the ability to produce the later complement components (C5, C6, C7, C8, C9) increase the risk of certain infections.

Chronic Inflammation: The Bad Side of Inflammation

In chronic inflammation, the inflammatory response is out of proportion to the threat it is faced with or is directed against inappropriate targets. In the first case, the result can be more damage to the body than the agent itself would have produced.
Allergies and Autoimmune Diseases

All the many types of allergies and
many of the autoimmune diseases

are examples of inflammation in response to what should have been a harmless agent.

Some examples:

Asthma
Rheumatoid Arthritis (RA)
Multiple Sclerosis (MS)
Systemic Lupus Erythematosus (SLE)

In many of these cases, the problem is made worse by the formation of antibodies against

self antigens or
persistent antigens from smoldering infections.

The antibodies complex with the antigens triggering the complement system with all its mediators of inflammation.

The result: immune complex disorders.

anthonyspencer54 wrote:Xenon,

Heat can be a byproduct of inflammation because the histamine release causes dilation of the blood vessels in the local tissue. As far as I know, a modest increase in heat does not by itself produce inflammation. It simply dilates blood vessels. Very high temperatures can be a problem but telling someone that the heat generated from exercise is causing their hairloss is a joke. And your understanding of DHT is off as well. Clogging capillaries and sweat glands?

Xenon wrote:
As for my understanding of DHT being well off, I don't mind you saying this, so long as you can present a reasonable argument as to why this is, and then I will take your remark serious.

https://immortalhair.forumotion.com/t7534-conventional-hair-loss-meets-alternative-views-the-role-of-inflammation-in-the-gene-expression-and-activation-of-sex-hormone-receptor-sites

if you can't present a reasonable argument, then it goes to show you haven't got one because you have no knowledge of this subject.

My point exactly.

Xenon wrote:Admin, thanks for your reply. I appreciate it, as it has made me think.

No sweat, it's what we're all here for.

"DHT doesn't clog anything, it's too small to do so, if this were the case people would be dropping dead on the street like flies."

I have read many sources (which were also in national newspaper articles documenting scientific discoveries) about how DHT plaques capillaries of balding men, thus making them higher candidates for coronary heart disease and heart attacks. I'm not a scientist, so i can only go with their findings on this issue.

This issue has been talked about a lot on this site, and it's very multifactoral. It's become very accepted based on newer research and a lot of personal experience from users past and present that the old DHT clogging theory has a lot of holes in it, and much of what we read in big articles regarding it are a very dumbed down media freindly half version of the truth. DHT is very much a part of hairloss, but 1 + 1 = 2 isn't the type of equation it would look like, there's many more variables. An example would be a condition very associated with mpb, that is prostatitis and prostate cancer, inflammation often happens prior to the androgen mediated effects as opposed to before it, as I posted in the link above inflammation upregulates different hormone receptors, the androgen receptor being one of them. After such a point the prostate tissue becomes completely seperate from androgens once again after androgen lowering therapies are induced or andropause, provided certain inflammitory factors are still present.

If what the scientists findings suggest are true, then it's plausible to suggest that DHT will clog the capillaries of cells with DHT receptors. You say the DHT molecule is too small to cause clogging, yet the capillaries connecting to the follicles are also minute. I don't find it an absurd notion to suggest that an overload of the DHT molecule could gradually cause clogging of capillaries around target sites.


DHT under certain circumstances can cause the capillaries to narrow, essentially making everything clog, blood, nutrients, etc. If you look deeper through large amounts of studies you'll see a trend, androgens slow wound healing and can cause narrowing of bloodvessels, whereas estrogens are protective of blood vessels / capillaries and can cause angiogenesis. SHBG is the real make or break factor here, which is very much tied into insulin, which is very much tied into thyroid, which is very much tied into liver, which is very much tied into the gut, which is yadda yadda yadda on and on forever in a nasty tangle of factors that are self perpetuating after one of many possible single dominoes falls.


"I do this everyday and I can definitely tell you that you're wrong about it causing hairloss for me"

Fair enough. This is not the case for me, as well as other cases i've come across. The inflammation does not occur immediately in my case, rather, if i work out intensively for a week or two, then I will begin noticing inflammation and thinning hair soon follows.

Working out can cause insulin resistance depending on how you do it, what you eat, etc. It wasn't until drastically altering my diet and spending almost a grand in chelation of multiple forms was I able to work out again to no ill effect. Iodine helped tremendously too, as well as dealing with dental issues (which can be like a 24/7 IV drip of poison for some).

"Heat just ends up not being the type of factor your theory says it is, if it were the case metabolic syndrome would increase the closer you get to the equator, but its exactly the opposite."

Well, for one, no one who lives in hot regions of the world are going to wear thick clothing, nor would they consume many hot drinks. So, the main heat source would come from the sun, yet they constantly sweat to cool down. Like i say, the less clothing you wear in hot weather (or during exercise), then the more the sweat glands of your body can release heat and keep you cool. Yet, wearing thick clothing in hot climates / during exercise, would absorb the sweat from your body and cause you to develop hyperthermia. (not to be confused with hypothermia), and I'm sure inflammation would result, especially if the follicles are clogged by DHT.

I'd be interested to see more research on this if you have it.

"To get a better idea of prostoglandins, inflammation, here's some good simplified articles that will hopefully broaden your view and help you fill in some of the gaps your current theory has."

Thanks for this. This is an interesting read. Appreciated.

And I know for sure that if I eat wheat or cooked oil or any kind of junk, it triggers inflammation = hair loss.

LawOfThelema wrote:

And I know for sure that if I eat wheat or cooked oil or any kind of junk, it triggers inflammation = hair loss.

evidence that wheat causes inflammation in those who don't have gluten intolerance?

scottyc33 wrote:

LawOfThelema wrote:

And I know for sure that if I eat wheat or cooked oil or any kind of junk, it triggers inflammation = hair loss.

evidence that wheat causes inflammation in those who don't have gluten intolerance?

I think I read somewhere that gluten causes inflammation of the intestines in 80% of people.

Xenon wrote:@Admin

The only thing I have to provide you with - in response to your request - is personal observations. i know that may not be of much use to you, but that's all I can provide you with right now, and I have done so in my previous postings.

Also, if i may just add: when i wear a bathrobe for too long, then I especially begin to experience inflammation. I wondered why Terry cloth or toweling, from which most bathrobes are made, would cause me to experience inflammation so much. I can only surmise that this is because Terry cloth is designed to absorb lots of water, while keeping the skin dry and insulated. So, I can only assume - as a possible explanation - that Terry cloth was causing sweat to be rapidly absorbed, and causing my body to generate too much heat. I know you don't necessarily agree that I'm correct, but I am just pointing out something which I noticed causes inflammation.

Also, I'd be interested in your views on the following...

I debated the inflammation / exercise issue with a friend online sometime ago. An alternative explanation for the inflammation, which I put forward, was acidosis caused by either lactic acid or carbonic acid. I read that when we work out too much, lactic acid forms in muscles because they are in oxygen debt, so to speak, and i wondered if it was this lactic acid which was a cause of the inflammation.

Also, I have noticed that if i sleep in a poorly ventilated room, I wake up the next morning with an inflamed scalp, not to mention feeling nervous and irritable. I discovered that a poorly ventilated room contains significant levels of carbon dioxide, which, when breathed in causes carbonic acids to form in the bloodstream. So i wondered if the CO2 was causing an inflammatory effect upon my follicles. So, I began leaving my bedroom window slightly open when I was asleep, and this seemed to do the trick, as i was breathing in fresh oxygen while i was asleep. When I woke up the next morning I experienced no inflammation at all, nor any feelings of irritability.

I read that breathing in more oxygen makes the blood less acidic and more alkaline.

What are your views on the things I've mentioned here?

http://paleodietlifestyle.com/11-ways-gluten-and-wheat-can-damage-your-health/

"Gluten causes gut inflammation in at least 80% of the population and another 30% of the population develops antibodies against gluten proteins in the gut. Furthermore, 99% of the population has the genetic potential to develop antibodies against gluten. Antibodies acting in the gut can actually be good news, because when the body doesn’t react against gluten right away, gluten proteins can enter the blood stream more easily, especially if the gut is already leaky, and trigger immune reaction elsewhere in the body."

mistyisland wrote:sanderson, that appears to be a link for health care practitioners exclusively. I couldn't find an area where an individual could order their own testing. No mention of any fees, except for cancellation fees.

Xenon wrote:

anthonyspencer54 wrote:Xenon,

Heat can be a byproduct of inflammation because the histamine release causes dilation of the blood vessels in the local tissue. As far as I know, a modest increase in heat does not by itself produce inflammation. It simply dilates blood vessels. Very high temperatures can be a problem but telling someone that the heat generated from exercise is causing their hairloss is a joke. And your understanding of DHT is off as well. Clogging capillaries and sweat glands?

I'm not talking about a modest increase in heat, I'm talking about a significant increase in heat

As for heavy exercise causing enough body heat to cause inflammation / hairloss, I'm not the only one who has observed this -- scientists did and it was reported in a national newspaper some years ago. Again, for the hard of hearing: 30% of body heat is lost through the scalp, when we exercise. Now, we wear clothing to keep us insulated, yes? So... if we wear thick clothing during exercise, we are going to generate even more body heat, yes? And when our bodies sweat, we begin to cool down. But when we are wearing clothes, the sweat is absorbed by the clothes, thus preventing our bodies from cooling down. As a result, massive amounts of body heat are produced and rushes to the scalp to escape, as it is a major release center for body heat. All of this heat overwhelms the sweat glands of the galea and not all of it can be released, which then leads to inflammation.

As for my understanding of DHT being well off, I don't mind you saying this, so long as you can present a reasonable argument as to why this is, and then I will take your remark serious. if you can't present a reasonable argument, then it goes to show you haven't got one because you have no knowledge of this subject.

sanderson wrote:

mistyisland wrote:sanderson, that appears to be a link for health care practitioners exclusively. I couldn't find an area where an individual could order their own testing. No mention of any fees, except for cancellation fees.

i got it through my naturepath doctor last year, not sure where you order it, but that is the one i got. it was around $300.