Lets put together a compilation of evidence against the donor dominance theory; CS your input requested

I've been debating with some chaps over on other forums over whether or not the donor dominance theory is accurate.
Obviously I am against it, I believe it is a condition of low oxygen. So far I have the following evidence to support my argument:

1. The Botox study proved that hair loss can be reversed by loosening the scalp, which essentially loosens the scalp and improves bloodflow; their comeback is to say that it has nothing to do with bloodflow, that it must work by affecting other parameters.
2. The scalp tension relaxer (str) invention loosens the scalp and has been clinically proven to reverse hair loss; the comeback being it can't work since that aren't popula, even though they were clinically proven to work.
3. The Goldman study outlined balding scalps having low blood flow, the comeback being the condition is CAUSED by the hair loss, which may hold SOME merit.
4. The Goldman study outlined hair loss to the legs was found when oxygen levels fell below mmhg, balding scalps have 32 and normal scalps have 53
5. The Goldman study outlined how keratin production is severely hampered below 40mmhg
6. The Goldman study outlined how estradiol production is hampered in low oxygen environments, which causes local shy levels to elevate.

As you can see, most of my research involves low oxygen levels caused by tight scalp/ poor circulation, microvascular or general.

I was hoping to get some scientific evidence compiled based on other avenues, such as thyroid, pathogenic or other causes of hair loss.

Thanks!

Hi SlowMoe, I agree with you...it really comes down to oxygen (low oxygen/hypoxia).

In case there is an argument about hypoxia (there is some evidence that short term hypoxia is good for hair, but the key is, only short term hypoxia, since it stimulates VEGF, PDGF, HIF, etc.

How this low oxygen is created or caused by is essentially almost entirely my focus when it comes to this sort of research.

In part, it's a mitochondrial problem, which could either involve the thyroid, or a co-factor for thyroid hormone synthesis or involve one of the glands or organs that affect it.

When it's not the thyroid, it is inflammation. Inflammation in of itself creates a low oxygen environment.

Stress can increase cortisol and reduce testosterone simultaneously. This sea saw effect not engenders inflammation and hair loss (the hair organ system produces its own cortisol, independent of HTPA). Having low testosterone can increase agitation (lack of calmness).

Getting back to the thyroid (once again), a low thyroid and/or impaired function (which is typically missed by 'gold standard' approach) precipitates a state of infection.

An infection precipitates inflammation.

Back in the "good old bad days"...or before the advent of antibiotics, people literally died if they had low thyroid function, because they would become more susceptible to infection.

Of course, people do not generally die right away...and conditions such as heart disease and diabetes are in large part...infections or caused by infections.

Here is an example. If one takes Berberine, which is an alkaloid that neutralizes various infections, blood sugar will often normalize, because the prior infection precipitated an elevation in blood sugar.

When diabetic rats were given thyroid hormone (active form), their blood sugar levels normalized (no longer diabetic).

When iodine is sufficiently concentrated in the thyroid (it belongs in all other cells as well), it will filter the blood every 17 minutes. Being that iodine is a natural antiseptic, antibiotic, antifungal, antibacterial, etc. infectious microbes will have more difficulty setting up "shop" to create an chronic infection.

There are many things today that prevent uptake of iodine or thyroid hormones, such as halides (or halogens) or toxins that take the place of iodine...since thyroid hormones cannot be produced without this and other co-factors, the tests do not distinguish this...nor do they qualify thyroid hormone resistance either.

There are many things that go beyond iodine and the co-factors as well. Some infections can occur (particularly bacterial endotoxins), which deplete electrons...this invites an infection with open arms and stimulates a chronic inflammation, that begets continued inflammation.

Further, as we age we can no longer produce sufficient enzymes to chemically tag cytokines to be destroyed and so the
inflammatory cascade continues.

I could go on, however I think it might be worth your time to argue with those other posters, because there's a lot of people who would rather think they are right than be interested in the truth. Telling a cancer patient they do not have to take chemo is a good example. Most of them are too scared to do it.

So, CS, do you think that MPB is completely reversible if we take every action necessary?

although i have been heavily lambasted for suggesting that the dht molecule gradually clogs up the cytoplasm and hinders oxygen processing within the mitochondria, I still consider it a very plausible factor.

it's argued that the dht molecule is too small to have a clogging effect within cells, but the cytoplasmic membrane is also incredibly small.

if not enough oxygen is reaching the cell, then atp will be low, and i think it's likely that the cell will not have the energy to metabolize large quantities of dht; the hormone would probably fill up the cell and interfere with oxygen / energy production, not to mention waste matter / c02 expulsion. A build up of toxins = heightened inflammation.

so, slowmoe, i think you're right in what you say in regards to scalp tension being a major culprit, but i think a tight scalp ultimately leads to cells with androgen receptors becoming clogged, toxic, inflamed, then destroyed.

p.s. despite many dismissing what i've previously stated regarding the galea being strongly compressed against a pillow when we sleep, it has to play a role in lowering circulation to the scalp. this could be comparable to wearing a tight swimming cap for hours every day. this + a tight scalp would vastly accelerate mpb.

What about the two experiments where hairs were transplanted to/ from balding regions and the balding hairs continued to die.

I know that somehow those experiments were flawed; any ideas?

SlowMoe wrote:What about the two experiments where hairs were transplanted to/ from balding regions and the balding hairs continued to die.

I know that somehow those experiments were flawed; any ideas?

Well, I have two remaining terminal hairs in symmetrical locations on my temples + a couple of remaining hairs where my widows peak formerly existed. I have often wondered why these hairs remained, yet the surrounding temple hair withered away.

some men bald differently also -- front to back, back to front, vertex thinning, etc. This may suggest that there is an upregulation of receptors in certain follicles, and the cell takes in more testosterone than it is able to metabolize. Why this happens is a mystery -- perhaps caused by a mutation within the genome nucleotide sequence.

it seems that follicles with extra receptors require extra oxygen to help them metabolize superfluous amounts of dht, and this may be how minoxidil helps.

Growdamnit wrote:So, CS, do you think that MPB is completely reversible if we take every action necessary?

The possibility of an existing hair follicle to reverse it's miniaturization process--yes, definitely. The progenitor cell still exists.

However, with the absence of a hair follicle, the possibility becomes less certain. It depends entirely if a progenitor cell has some regenerative capacity at some later point in time.

One way to look at it is similar to telomeres. There is a finite number of basis pairs, and when they run out, there is no more regenerative capacity. In the case of hair follicles, the progenitor cell which governs their regenerative capacity (number of times they can become new hairs) is diminished as we age. And not surprisingly, the telomeres are much shorter relative to other tissues for balding scalps.

Xenon - Your ideas about the galea, sweat and other info is very interesting. It would be amazing if a group eventually figures out by some study about the effect of the pillow on the vertex area. Makes a lot of sense. Another thing is that people who sweat a lot (there seems to be an unusual number who have MPB) or hyperhydrosis with MPB. I do know that at least in part, iodine can help correct this to some extent.

I should point out that serum levels of DHT are inversely correlated with MPB. In other words, a high blood level of DHT actually means more hair, not less.

However, an elevated serum 5-alpha reductase level is correlated with MPB.

SlowMoe wrote:What about the two experiments where hairs were transplanted to/ from balding regions and the balding hairs continued to die.

I know that somehow those experiments were flawed; any ideas?

Based on what is in the medical literature, dermal papilla contains various growth factors and/or growth inhibitors.
So when balding dermal papillas are transplanted, they further miniaturize in the new host.

I suppose one question might be, is this permanent? If somehow the dermal papilla could be salvaged or maintained for longer, could the environment of the host epigenetically modify the expressions? I'm guessing the answer is yes.

I don't use a pillow and im a NW 2.5. I have never used a pillow my whole life.

WellI know that the grafts used in those experiments were very large; 4 to 12mm in diameter...Could it be that the degraded microvascular environment that was transferred is the reason why the follicles failed to survive? What if just one follicle was transferred; would the follicle have flourished?

CausticSymmetry wrote:I should point out that serum levels of DHT are inversely correlated with MPB. In other words, a high blood level of DHT actually means more hair, not less.

However, an elevated serum 5-alpha reductase level is correlated with MPB.

Can you elaborate more on this?

I thought the more DHT that was exposed to a dermal papilla cell the more "overworked" it became.. And more 5AR eventually means more DHT, because there is more competition for the aromatase...

And doesn't finasteride lower serum DHT levels, and slow MPB?

Only serum levels....so the DHT = bad for hair still applies...

Xenon - Your ideas about the galea, sweat and other info is very interesting. It would be amazing if a group eventually figures out by some study about the effect of the pillow on the vertex area. Makes a lot of sense. Another thing is that people who sweat a lot (there seems to be an unusual number who have MPB) or hyperhydrosis with MPB. I do know that at least in part, iodine can help correct this to some extent.

It's all a huge confusing labyrinth lol. But I just want to say, I read a pubmed study that said that androgen receptors exist within the papilla and matrix region of the follicle, yet an in vivo experiment was carried out in the removal of the matrix and papilla, yet because the hair bulge housed so many progenitor cells, both the papilla and matrix had completely regenerated and produced terminal hair once again.

So if surplus DHT is binding to receptors within the papilla / matrix, I presume that the hormone is creating a toxic environment (for the reasons stated earlier); this triggers inflammation and then cellular healing, but this constant cycle of destruction and rebirth might cause progenitor cells to become prematurely exhausted, and cell division no longer takes place.

The boar brushers report severe shedding during the first few months of their regime, but then some also report terminal hair growth many more months on. I read that progenitor cells start to migrate en masse to injured tissue, yet in tissue not subject to injury there is a surprisingly low number of progenitors to be found there. So I think that this is what is happening with the regular boar brushers -- progenitors are migrating to the bulge, and the matrices and papillas are regenerating.

As for the hyperhydrosis, i also read this. In burns victims, it stated that inflammation occurs due to acute fluid loss, Due to the high concentration of sweat glands within the temples, this severe perspiration may also trigger an inflammatory response.

But ultimately it seems that DHT is the catalyst for MPB. I mean, you take a F2M transsexual on testosterone therapy and some of them start to suffer from MPB in the same way a regular guy would. So testosterone / DHT has to be the trigger here. It must progressively weaken the follicle to the point where it becomes susceptible to inflammation from several other factors.

For instance, if my follicles are exposed to extremes of cold air: inflammation. If I'm sitting in a stuffy room with high C02: inflammation. If I work out too heavily: inflammation. All localized to the galea, yet when i was younger I never suffered from these issues anywhere near as bad as i do now that I'm older.

If there are no more telomeres, how do we grow back hair? We can't just manifest telomeres from thin air.

Growdamnit wrote:If there are no more telomeres, how do we grow back hair? We can't just manifest telomeres from thin air.

Apparently, the enzyme telomerase slows down telomere shortening and prevents it from prematurely reaching the 'hayflick limit':

I remember reading about how telomerase is boosted by regular exercise, healthy diet and low stress levels. ...not exactly the magic bullet, but I'm going to devote more study into this issue and hopefully achieve immortality as well as a full head of hair

Could someone explain to me again why the most morbidly obese men will have full heads of hair while a health freak like myself has to battle hairloss. I haven't touched a hydrogenated oil in two years and haven't drank in 5 and yet I still have to spend $150 a month on supplements just to maintain what I have left. I work in the construction field and I see guys on lunch break eating the worst possible foods you could eat yet a lot of the really fat guys I see have awesome hair. Could all the extra estrogen these guys have in their system be protecting their hair bc obviously these guys have to have health issues.

Those people do not originate from Europe or other such regions where there is less Vitamin D thus less glutathione. Less glutathione equals more heavy metals who then in turn suppress thyroid and that essentially causes MPB? Just a theory. Is thyroid health 100% responsible for MPB?

Vince, we know and share your anguish! But in the long haul the benefits might be more visible.

Diet and local factors are two sides of the mpb coin. Deficiencies of this and that, diet, hormones must surely play a part. But then, local factors are definitely there- inflammation, calcification, impaired blood supply, 5AR/DHT, and more. If local factors weren't playing a part, for instance, I wouldn't be having a worse frontal/temporal hairline than many, and on other areas of the head a better hairline than many.

There has to be a better explanation than DHT in classic (and not to forget, gradual) frontal recession of MPB. Some local factor must be making that area of the head susceptible to DHT to begin with.

And that's just a rant on stemming the hair loss. Regrowth and reversal of the condition, phew, still black magic.

9rugrats5 wrote:
Some local factor must be making that area of the head susceptible to DHT to begin with.

Did you read my posts in other topics where low oxygen levels allow more DHT to be produced locally?

What it looks like to me is that the low oxygen level causes the DHT/ estradiol ratio to increase (2 times the DHT/ 3 times less estradiol). This hormonal slurry is what causes the cells to go haywire and ultimately overloads the follicle.

Did you read my posts in other topics where low oxygen levels allow more DHT to be produced locally?

I was going to comment on this point you previously made.

When follicles are constantly exposed to cold air, they contract byway of the erector pilli muscle. When in a state of contraction too long: reduced oxygen levels = increased dht. the temples are constantly being exposed to cold wind.

remember the sudden diffuse thinning i experienced when i kept spraying my hairline with cold water?

Lack of BAT makes these follicles susceptible to tension caused by cold air.

But there are obviously other factors such as scalp tightness - caused by overgrown skull bones, pillow compression, etc.

Xenon wrote:

Did you read my posts in other topics where low oxygen levels allow more DHT to be produced locally?

I was going to comment on this point you previously made.

When follicles are constantly exposed to cold air, they contract byway of the erector pilli muscle. When in a state of contraction too long: reduced oxygen levels = increased dht. the temples are constantly being exposed to cold wind.

remember the sudden diffuse thinning i experienced when i kept spraying my hairline with cold water?

Lack of BAT makes these follicles susceptible to tension caused by cold air.

But there are obviously other factors such as scalp tightness - caused by overgrown skull bones, pillow compression, etc.

Maybe I don't understand the pillow compression coincept properly...Wouldn't the sides of our heads bald since this is what mostly contacts the pillow?

I would also like to re-iterate what I said previously.

In those transplant experiments the donor dominance theory was based on, very large (1/4" to 1/2" diameter) grafts were taken, so basically the entire scalp environment was moved to another part of the body, like moving a flower pot from one side of the porch to another, without changing the soil.

So it's no wonder the inplants maintained their inherent characteristics.



I read somewhere that individual balding hairs implanted into mice will become full sized terminal hairs....What I would like here is more hard evidence from scientiffic experiments that contradict the silly donor dominance theory..

Maybe I don't understand the pillow compression coincept properly...Wouldn't the sides of our heads bald since this is what mostly contacts the pillow?

the lower back and sides of the head have muscles and BAT, which act as a protective cushion to the follicles. The temples / galea don't have these muscles, so when the temples are pressed against a pillow they are simultaneously pressing against the hard skull.



I am not suggesting that the pillow compression issue is the #1 cause of mpb, rather I'm suggesting it is a factor in reducing oxygen to the temples and consequently causes elevated levels of dht.

I suppose you could compare this to firmly pressing your palm against your scalp for 8 hours every day. surely oxygen levels would be compromised.

p.s. and apologies for hijacking your thread; someone i know was in a coma for a week or so. when he woke up he had a large bald patch in the back of his head from continual pillow compression. But i will also add that he was receding anyway, so this may have accelerated his mpb.

However idk if this happens in all comatose patients or just those genetically susceptible to mpb.