Are Hairs in balding area different or is it solely from the environment?

The question I am asking are the hair follicles themselves on the top of the head programmed to die from dht or is it just from the bad blood flow environment they are in. Like if you took a follicle from the balding area alone and exposed it to dht would it continue to grow. People on the other hair loss forums seem to think the follicles themselves have different resistance to dht, which I do not think it is true and its just the bad environment built of toxins and bad flow.

There is no scientific evidence at all that suggest that hairfollicles from the side or back of the head is any different that those on top of the head. It is a big lie. Other people
have suggested that there are bacteria that only attack follicles on the top of the head
and for some reason leave the follicles on the side of the head alone, due to some intrinsic property not in the follicle - but in the bacteria. This is anotehr absurd lie. The only reason like you say, and I believe that makes any sense logically - is that the scalp environment
is different from top to side in some essential way, which causes the MPB pattern to appear, IMHO.

cpio wrote:
There is no scientific evidence at all that suggest that hairfollicles from the side or back of the head is any different that those on top of the head. It is a big lie.

you want to change that answer before I make you look stupid?

Mobydick you look stupid all the time.

Hi all

Most of the scientifc thought is that the follicles on back of the head are resistant to dht for what reason though, there are various theories,depends on who you talk to.

Regards
Mikeyc.

If you look at the two follicles, one from the top of the head and one from the side, and compare them under a microscope, or compare the dna sequences - if you dont find
any difference it follows logically that they are the same kind. Therefore it is a
paradox to say that one hair is vulnerable to dht and the other is not.

mikeyc wrote:Hi all

Most of the scientifc thought is that the follicles on back of the head are resistant to dht for what reason though, there are various theories,depends on who you talk to.

Regards
Mikeyc.

Cpio,

I'm not arguing on anyone's side here because I simply don't know the answer to this one.

Just pointing out that the DNA in every cell of the human body is the same. The DNA from one of my hair follicle cells will be identical to the DNA from a cell on my tongue. Its about expression, and its about epigenetics. We have to consider the proteins being produced by the genes that are expressed, and what proteins are not being produced.

For this reason, the nuclear receptors in cells from one area of the body could be completely different, in terms of number, type and distribution, from another cell, and could make those cells more sensitive to hormonal messengers in comparison. It all depends.

Anthonyspencer -thank you for the clarification. But if we assume that the problem
of MPB is an factor intrinsic to the hair follicle, then there must be a way to compare
follicles from non-balding areas balding ones, and identify a difference that is responsible
for the vulnerability to DHT. Otherwise from a scientific standpoint it is just mumbo-jumbo to say that some hair follicles are intrinsincly vulnerable to DHT but there is no way to prove this, IMHO. It is false and probably that is why it cannot be proven, IMHO.

anthonyspencer54 wrote:Cpio,

I'm not arguing on anyone's side here because I simply don't know the answer to this one.

Just pointing out that the DNA in every cell of the human body is the same. The DNA from one of my hair follicle cells will be identical to the DNA from a cell on my tongue. Its about expression, and its about epigenetics. We have to consider the proteins being produced by the genes that are expressed, and what proteins are not being produced.

For this reason, the nuclear receptors in cells from one area of the body could be completely different, in terms of number, type and distribution, from another cell, and could make those cells more sensitive to hormonal messengers in comparison. It all depends.

Agreed. There is some intrinsic difference. I know its been spoken of here that the cells of the dermal papilla and surrounding connective tissue have a higher distribution of not only 5AR, but also of androgen nuclear receptors. Whether this is that intrinsic difference, I don't know. This is a very interesting idea and would make for a great topic of research. We would not only need to examine the structure of the hair itself but also the local tissues, as its been noted there are differences in the subcutaneous fat in the MPB region. Whether the galea plays a role as the theories supporting manual methods suggests would also need to be investigated. Is there something related to the vasculature, adipose variations or other factors that makes the top of the scalp more prone to inflammation, what processes are occurring there that are causing the immunoreactivity and what are the predisposing factors? There seems to be a lot of evidence that points to a pathogenic component in MPB, but again, what factors are causing this to manifest in the MPB pattern and why aren't the remaining hairs effected? I just don't know.

This study is a pretty ubiquitous one. Its probably been posted here before. (http://www.nature.com/jid/journal/v116/n3/abs/5601004a.html) But it does demonstrate that the polymorphisms effecting the androgen receptor genes are much more prevalent in balding men, and more specifically, there seems to be a functional mutation of the restriction site and also shorter strings of CAG and GGC bases. But again, we would expect to see this mutation in every cell in the human body. So are the nonbalding regions still subject to the same androgen receptor overexpression? If they are, why isn't miniaturization occurring there?

This one (http://www.nature.com/jid/journal/v109/n3/abs/5610071a.html) shows that both men and women with hair loss had higher levels of 5-a reductase and androgen receptors in frontal scalp regions than in occipital scalp regions, but the occipital regions had higher aromatase. This is very interesting. As expected, women had almost 40% less androgen receptor and 5AR content in the frontal scalp, and six times more aromatase. These differences could suggest a reason for less prevalence of hair loss in women. It looks as though cross-talk between estrogens and androgens is an important factor, with aromatase levels seemingly appearing to be protective in terms of maintaining hair. But again, why is aromatase so much higher in the occipital regions with androgen receptor and 5AR content so much higher in the frontal region?

At the risk of sounding like a broken record, I believe it all ties into thyroid dysfunction. Whatever the missing element is, whether it is a mineral, vitamin, presence of a toxin which disrupts the enzyme or receptor and ultimately disrupts thyroid hormone will negatively effect the androgen receptor. This I believe is intrinsically why a non-balding man is relatively unaffected by DHT vs a balding man.

In my own experience, at my worst level of health & hair, I had the following problems: bad breathe, poor diet, stress...my scalp was oily, gum health was poor.

Fast forward into the future - zero problems zero hair loss (+ more hair).

CS,

I have to agree about your last point. I am dealing with all of those problems at the moment and my hair loss has been pretty rapid, well not loss, but thinning. I don't seem to have lost hair but it has miniaturized extensively. It would seem that gut issues and thyroid issues are a common thread.

But here is my question: does T3 or T4 have any effect in down-regulating the androgen receptor or steroid conversion enzymes? I haven't researched this, but if there was a connection that would be huge. Thyroid hormone might at least effect fat metabolism, which plays a huge role in local inflammation, and possible immune response.

anthonyspencer54 wrote:CS,

I have to agree about your last point. I am dealing with all of those problems at the moment and my hair loss has been pretty rapid, well not loss, but thinning. I don't seem to have lost hair but it has miniaturized extensively. It would seem that gut issues and thyroid issues are a common thread.

But here is my question: does T3 or T4 have any effect in down-regulating the androgen receptor or steroid conversion enzymes? I haven't researched this, but if there was a connection that would be huge. Thyroid hormone might at least effect fat metabolism, which plays a huge role in local inflammation, and possible immune response.

Totally agree about gut issues and thyroid being related. In fact, they both affect each other.

Also there is evidence that AR expression is affected by T3, although it depends on cell type and probably other factors.
(J Endocrinol. 1998 Jan;156(1):43-50.), (Endocrinology. 2007 Jul;148(7):3485-95.).

T3 affects fat metabolism and as well as some co-factors, such as vitamin A (animal source only).

I totally agree about thyroid but how do we actually inherit such problems? Iodine deficiency changes some genes? Vitamin D is responsible for thousands of genes so I can only assume that iodine must be responsible for 10x as much

moby wrote:I totally agree about thyroid but how do we actually inherit such problems? Iodine deficiency changes some genes? Vitamin D is responsible for thousands of genes so I can only assume that iodine must be responsible for 10x as much

Before the advent of antibiotics, people simply died from hypothyroidism (they are more susceptible to infections), and therefore never had a proper opportunity to transfer that tendency into future generations. However, today is different because now the fetus will absorb up to two-thirds the heavy metals (thanks to the dentist and industrial production), the 100,000 toxic chemicals in the environment.

Many of those estrogen mimics (psuedoestrogens, xenoestrogens, bisphenol-a, lotions, creams, methylparabens, sun tan lotions)--they invite thyroid suppression. And of course there is the fear of iodine over the last three plus decades due to extrapolation of data extracted from erroneous rat studies and presumed in humans. So iodine intake has dropped and the rats drugs and assumptions amount (RDA) is 100 times less than the human body needs of iodine.

Since those who use imaging, radioactive contrast agents do not get a "positive" reading from those who intake sufficient iodine, there is no incentive in that area also.

Plenty of toxic substances that compete for iodine uptake into the thyroid and other cells that need it. Dentists not only cut, burn (drill) and leave rotten materials in the mouth, they also poison their patients with bisphenol-a (dental sealants), and fluoride "cleanings." Both of these inhibit thyroid function.

I would go on about health 'authorities' pressuring the public to reduce salt intake (a bad idea), which contains some iodine, but not nearly enough. Anyway, suffice to say there is a lot going against proper thyroid function. In fact, I'm leaving a lot of things out just for the sake of time.

Inspired by the recent conspiracy thread, I find it extremely interesting that in the past 60-70 years, iodine has been basically removed from the food supply when you consider than iodized salt has about a 10% rate of absorption. Then, while the food supply was robbed of iodine (also due to soil depletion), it was also being replaced with chemicals that are competitors with iodine for receptor sites: bromide and fluoride. The amount of both that we are receiving from food and water is ridiculous, especially if the diet contains a good deal of processed grains. A modern, sufficient diet according to authorities basically leaves your thyroid running on fumes. Hell of a eugenics plan if you ask me. I don't really believe its a conscious plot, but let's use the analogy of being a livestock owner. If the lot was getting too big for my farm to sustain, I'd have no choice but to depopulate. But let's also assume these cows are hyper-conscious and I need to do it in a way that won't cause a stir, i.e. I can't just blatantly slaughter them. What better way to do it then through the food supply, as 99% of these cows know next to nothing about what they're putting in their mouths. Epigenetic engineering. How many generations of cumulative epigenetic derangement does it take for people to become sterile?