ABOUT HAIR TRANSPLANTHAIR LOSS SOLUTION

Genetic Hair Loss (AGA) Guidelines

Why Does Hair Fall Out?
Quick Summary

Hair loss is actually a chronic condition, just like diabetes, prostate problems, cancer, or heart disease. There’s no clear cure for these illnesses, but they all have something in common: chronic inflammation in the body. Over time, this inflammation can lead to diseases like these — and yes, including hair loss.

The first step to stop hair loss is to reduce or prevent this inflammation. In Turkey (and actually many other places), most people are intolerant to gluten and dairy. And if you’re dealing with Androgenetic Alopecia (AGA), chances are high that you’re sensitive to one or both. Cutting these out of your life can make a big difference.

Now, here’s the interesting part: many drugs used to treat hair loss are also used in diseases like prostate issues, heart conditions, and even cancer (in low doses for AGA). This is not a coincidence.

Another big myth: DHT is not the cause or the result of hair loss. It’s just a middleman. DHT actually has anti-inflammatory effects, meaning it helps reduce inflammation in the scalp. So in a way, DHT is helping us, not harming. Also, DHT is responsible for hair growth in general — without it, body hair wouldn’t even develop.


Detailed Explanation

There are two terms you need to know here. First is calcification, which basically means mineral buildup or hardening in tissues — like a kind of internal “scaling.” The second is fibrosis on the scalp — where connective tissue starts forming randomly under the skin. These changes happen before visible hair loss starts.

A lot of people notice their head shape changing, or that their scalp looks shinier. That’s not your imagination. In fact, the reason bald heads shine is because the skin there has changed. Do we have any other shiny skin areas on our body? Yes — knuckles. And guess what, there’s no hair on knuckles either.

So what’s happening is that healthy scalp tissue slowly starts transforming into a type of skin that looks like the one over our knuckles — smooth, shiny, tight. This process is part of why hair stops growing.

There’s even a disease related to this called Scleroderma, which involves extreme fibrosis of the skin.

In this disease (scleroderma), fibrosis usually appears randomly, often in the hands. But when scleroderma happens on the scalp, it also leads to hair loss. You can even see pictures of this in some studies [1].

Too much collagen and fibrosis blocks proper blood circulation. It’s already been observed that bald scalps have reduced blood flow [2]. There are also studies showing that blood flow decreases in scleroderma [3]. And when blood flow drops, oxygen levels also decrease. There’s evidence showing that the oxygen level in the scalp goes down in hair loss [4]. In fact, in one study, the balding areas had only 60% of the oxygen compared to areas with full hair [5].

But fibrosis isn’t the only thing that restricts blood to hair follicles — there’s also calcification, or mineral build-up in the tissues [6]. Many people think calcification just comes with aging, but that’s not really true [7]. Fibrosis and calcification are not directly related — one doesn’t cause the other (no solid link has been found yet). They’re both separate issues.

Here’s something interesting: Men are twice as likely to have calcified blood vessels compared to women [8]. The main suspect here? DHT (Dihydrotestosterone). In one study on mice, injecting DHT increased vascular calcification up to 4 times [9]. But in humans, DHT alone isn’t the problem. Another key factor is the increase in androgen receptors [10].

Think of it like a puzzle — the androgen hormone and its receptor have to fit together. More androgen receptors were also linked to heart fibrosis [11]. That’s why it’s not surprising that bald men have 3 times the risk of heart attacks. So the big question is: if DHT helps grow body hair, and doesn’t cause fibrosis or calcification in other areas, why does it do this only on the scalp?

Honestly, we don’t know for sure. But here’s one thing we do know: if you inject DHT into mice that don’t have androgen receptors, no calcification occurs [12]. This means there are other things in the body — mostly proteins — that regulate all of this, depending on the location

All of the known inducers (triggers) are also linked with hair loss. Right now, there are three main things we know about hair loss:

  • Increased DHT

  • Increased Androgen Receptors

  • Imbalanced Calcification Regulators

While short-term inflammation (like from microneedling or scalp massage) is helpful and promotes healing, chronic inflammation is harmful and should be constantly kept under control. Actually, DHT is doing us a favor in some ways [13].

Both calcification and fibrosis happen as a result of long-term chronic inflammation. That’s also the reason why most hair loss medications don’t fully work. These two conditions — fibrosis and calcification — are the biggest blocks in the way of scalp recovery.

Drugs like Finasteride can reduce the amount of DHT on the scalp, but they do very little to reverse existing fibrosis or calcification. Because of this, most hair loss drugs only slow down or temporarily stop hair shedding, but they rarely regrow what’s already lost.

HAIR LOSS AND GENETICS

Let’s talk a little bit about genetics. So far, no single gene has been 100% linked to androgenetic alopecia (AGA). It’s probably a polygenic disorder, which means there are multiple gene variations that increase your risk [14].

Newer studies are showing that in AGA, prostate issues, cancer and similar diseases, genetics only play a 10% role [15]. That means 90% is due to environmental factors – this is where epigenetics comes in.

You can actually test your genetic risk for baldness using websites like 23andme.com.

And here’s an interesting example:
The founder of Perfect Hair Health, who was diagnosed with AGA, carries 10 baldness-related genes and comes from a mostly bald family – and yet he still has hair.

There are also photos showing the difference in hair between identical twins – despite having identical DNA, one goes bald, the other doesn’t.

CAN HAIR LOSS BE REVERSED DESPITE GENETICS?

Contrary to popular belief, hair loss can be stopped – and even reversed. Just because hair loss “runs in your genes” doesn’t mean it’s your destiny. What we’re talking about here is gene expression – and it can be changed.

Let’s look at a fascinating example.

There’s a type of mouse called the Agouti mouse that was once believed to be doomed by its genetics. These mice have a mutation in the agouti gene, which normally controls fur color. Most mice are brown or black. But agouti mice are yellow due to this mutation.

But here’s the real kicker: these yellow agouti mice are obese, tend to overeat, and are way more likely to suffer from diabetes, cancer, and heart disease. In extreme cases, this mutation is even called a “lethal allele.”

Now here’s where it gets interesting.

Scientists wondered – what if we gave pregnant agouti mice mega doses of specific nutrients early on in development, while their babies were still in the womb? Could we change the outcome?

So they split the agouti mothers into two groups and fed them different diets:

  • One group got a standard lab mouse diet.

  • The other got a diet rich in vitamin B12, folic acid, betaine, and choline – all nutrients known to influence gene expression.

Then they let both groups get pregnant.

Twenty days later, the babies were born – and the results were shocking:

  • The standard diet group had babies that were yellow and obese – just like their genes predicted.

  • But the nutrient-rich group gave birth to brown, lean babies – normal-looking mice, despite carrying the same agouti mutation.

How is that possible?

These mice were genetically identical. They should have looked and behaved the same.

But those nutrients had actually turned off the agouti gene – a process known as DNA methylation.

The gene didn’t change. But how it was expressed did.

That’s the core idea behind epigenetics – that genes can be turned on or off, depending on environmental factors like diet, stress, toxins, sleep, or even inflammation.

So when someone says, “You can’t fight your genetics” – they’re not entirely right.

Your genes are not your destiny.

And if a mouse programmed to be obese and die young can change its fate with better nutrition, what does that say about us?

HOW METHYLATION AFFECTS GENE EXPRESSION (AND WHAT IT MEANS FOR HAIR LOSS)

Let’s break this down simply.

Every cell in your body contains DNA, and within that DNA are genes. When we eat, our cells break down food for energy. If that food contains methyl donors (nutrients like B12, folate, choline, betaine), these donors enter the cell and leave tiny chemical tags on the DNA.

These tags tell your cell which genes to turn on or off.

  • A non-methylated gene is active or “turned on” (upregulated).

  • A methylated gene is inactive or “turned off” (downregulated).

What’s wild is that in the Agouti mice study, a diet rich in methyl donors not only methylated the agouti gene – it shut it down completely. And even crazier: when these brown, healthy agouti offspring reproduced, they passed on that same fur color.

Their babies were also brown.

This changed everything we thought we knew about genetics. It showed that we can influence gene expression. Your genes may be the blueprint, but they don’t decide your fate.

Even more interesting, new research suggests epigenetic differences might explain why one identical twin goes bald and the other doesn’t [16].


Contents [hide]

What Hurts Gene Expression?

  • Alcohol

  • Cigarette smoke

  • Chronic sleep deprivation

What Helps?

  • Regular exercise

  • Meditation

  • A healthy gut microbiome

You could carry a gene for a rare cancer. But if you live in a way that never activates that gene, you might never develop it.

The same goes for hair loss.


AGA – STILL FULL OF MYSTERIES

There’s still a lot we don’t know about Androgenetic Alopecia (AGA):

  1. Which genes are exactly responsible?

  2. Why does DHT increase specifically in balding areas?

  3. How does DHT actually shrink the follicles?

Nobody knows for sure. But here’s what current research suggests:

There seems to be a strong link between DHT and a signaling protein called Transforming Growth Factor Beta 1 (TGF-ß1). In vitro studies show that TGF-ß1:

  • Helps with wound healing

  • Encourages the buildup of fibrotic scar tissue

So when TGF-ß1 levels increase in the scalp, they may drive follicle miniaturization – a core feature of AGA. Even worse, androgen activity increases TGF-ß1, and TGF-ß1 further boosts androgen effects. This feedback loop may create a vicious cycle that accelerates hair loss.

Think of it like this:

  • If you get a small cut, your body heals it cleanly.

  • But if the wound is deep, your body panics and fills it with random fibrotic tissue.

  • That’s why scars form – and that same process may be happening in your scalp.


BUT WHY IS DHT GROWING BEARD HAIR WHILE DESTROYING SCALP HAIR?

Ironically, DHT promotes facial and body hair growth – despite its role in scalp hair loss. One theory? Beard follicles have 3–5x more 5-alpha reductase activity, which converts testosterone into DHT differently than in the scalp.


WHY THE “PATTERN” IN PATTERN BALDNESS?

Why does hair loss often start at the temples, then the crown, and finally result in full baldness?

No one knows for sure – but we’ll try to explain it as best we can in the next section.

SCALP TENSION THEORY & HAIR LOSS: A DIFFERENT PERSPECTIVE ON AGA

When hair transplants first became popular, the scalp tension theory was dismissed. Why? Because it was believed that the hair on the back and sides of the head was resistant to DHT.

But here’s the issue: if there’s no hair on the crown, yet hair grows just 1mm below, how can DHT sensitivity alone explain that? It turns out, all follicles may be equally sensitive to DHT. The real difference might be environmental — or mechanical.

And now we know: even transplanted hair can fall out over time.


The Tension Map

Some studies have mapped areas of the scalp with the most mechanical tension — and guess what? It almost perfectly mirrors the typical pattern of male pattern baldness.

Research shows that balding men and women tend to have chronically tighter scalps compared to those who retain their hair. Across the body, chronic tension can trigger inflammation and fibrosis — the buildup of scar tissue. We’ve seen this in:

  • The eyelids of people with Graves’ disease

  • The prostate in men with BPH

  • The hands of patients with scleroderma

In each case, more tension = more inflammation = more fibrosis. And fibrosis limits blood flow, oxygen, and nutrients to the tissue — just like what we see in balding scalps.


So Here’s the Chain Reaction:

  1. Chronic scalp tension

  2. Inflammatory response

  3. Fibrotic scarring (collagen buildup)

  4. Restricted blood flow and oxygen

  5. Hair follicle miniaturization

  6. Pattern hair loss

In fact, bald scalp regions contain up to 4x more collagen (scar tissue) than hairy regions [17]. And as we’ve learned from scleroderma research, hair does not grow in scar tissue.


Can Reducing Scalp Tension Help Hair Regrow?

Yes. A study by Dr. Brian Freund used botox injections to relax chronically contracted scalp muscles in AGA patients. The result? A +18% increase in hair count [18]. A follow-up study confirmed his findings [19].

Another approach? Tension-relief devices, which have shown significant regrowth in 3–12 month periods in AGA patients.


Why Does the Crown Respond Worse to Hair Transplants?

In my opinion, the crown responds poorly because it’s the first area to calcify, even before it shows visible signs of thinning. Over time, it becomes less vascularized and more fibrotic, putting stress on nearby regions like the temples. So while the crown doesn’t bald first, it’s likely in the worst condition from the beginning.


Myth Busted: Bald Men Don’t Necessarily Have High Testosterone

One common myth is that men with male pattern baldness (MPB) must have high testosterone. In reality, even men with low testosterone can go bald.

Studies show that serum testosterone and DHT levels are not correlated with baldness [20]. Instead, it’s the local DHT levels in scalp tissue that matter.

And here’s the twist: if your testosterone is low and you’re still balding, it might be worse for you. Why? Because your body may compensate by converting more testosterone into DHT — which is 5x more potent.

In the past 50 years, average male testosterone levels have dropped by 20%, yet baldness has increased.

PGD2 and Hair Loss: What You Should Know

So what is PGD2 actually?

PGD2 stands for prostaglandin D2. Prostaglandins are a group of lipids that are produced in our body during injury or infection. They are basically part of our body’s inflammation response – that means PGD2 levels go high in inflamed areas.

Prostaglandins have different roles in inflammation and healing – like controlling blood flow, forming blood clots, expressing cytokines, and even regulating hormones. They kind of act like hormones themselves, changing how cells behave.

Normally, prostaglandins are good (and necessary). But when they are elevated for a long time, they become a problem. Chronic high PGD2 levels are linked to allergies, autoimmune diseases, atherosclerosis… and yes, even hair loss.

There are many types of prostaglandins, but PGD2 is the one that got the spotlight when it comes to baldness.

To affect the body, PGD2 must bind to a receptor on a cell. There are few types of these receptors, but in hair loss, the main one is called GPR44.

And when PGD2 binds to GPR44, hair loss usually follows.

Just like we have DHT blockers, there are also PGD2 inhibitors. Here’s some of them:

  • Setipiprant (blocks GPR44 receptor)

  • Ramatroban (also a GPR44 antagonist)

  • Ricinoleic Acid (blocks the enzyme that makes PGD2). Yes it sounds scary (from castor oil actually), but it’s not poison like “ricin” even if it sounds similar.

Do PGD2 Inhibitors Regrow Hair?

Well… the truth is we haven’t heard much from the clinical trials. Which probably means they didn’t have impressive results.

But that didn’t stop people from trying. Some biohackers and hair loss researchers started mixing their own PGD2 blockers and testing on themselves. Most popular one? Setipiprant.

The results? Sadly, no major regrowth even after 1 year of using.

However, some researchers started combining PGD2 blockers with something that increases PGE2 (think of it like the opposite of PGD2 – it supports hair growth). That combo actually showed better results.

PGD2 Doesn’t Just Cause Hair Loss… It Also Causes Calcification

Calcification is when calcium builds up in soft tissues – like skin or arteries – where it shouldn’t be. And PGD2 has been shown to trigger this process.

That means, when PGD2 is overexpressed, calcification might follow soon after.
So if PGD2 causes calcification, and calcification reduces blood flow to the hair follicles, then of course… hair starts to miniaturize and eventually disappear.

This is probably why PGD2 inhibitors don’t reverse baldness, they only slow it down. Because they can stop new PGD2… but can’t remove the damage (calcification) that’s already there.

So How Can We Reduce PGD2 Naturally?

  • Eat less Omega-6, more Omega-3

  • Go out into the sun more often. UVB light increases PGE2 (the good one). You’ll also get Vitamin D which helps in hair loss too.

MOST IMPORTANT: AVOID SUGAR
Sugar is linked to all chronic diseases. It increases androgen receptors (bad news for hair).
Also, many people have food intolerances without knowing – gluten and dairy are common ones.
You might feel fine after bread or milk, but still be reacting. Celiac people react strongly, but most of us don’t even notice.

Only fermented dairy like homemade kefir or yogurt are ok. Especially yogurt is the most allergenic dairy product among all.

Sources

1-https://www.nature.com/articles/sj.bdj.2010.252
2-https://journals.lww.com/plasreconsurg/Abstract/1996/05000/Transcutaneous_Po2_of_the_Scalp_in_Male_Pattern.3.aspx
3-https://medicine.umich.edu/dept/intmed/divisions/rheumatology/research/scleroderma-program/patients/raynauds.htm
4-https://journals.lww.com/plasreconsurg/Abstract/1996/05000/Transcutaneous_Po2_of_the_Scalp_in_Male_Pattern.3.aspx
5-https://pubmed.ncbi.nlm.nih.gov/8628793/
6-https://care.diabetesjournals.org/content/27/10/2409
7-https://www.ncbi.nlm.nih.gov/books/NBK2015/
8-https://pubmed.ncbi.nlm.nih.gov/19176322/
9-https://pubmed.ncbi.nlm.nih.gov/19176322/
10-https://www.nature.com/articles/srep24807
11-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3560513/
12-https://www.nature.com/articles/srep24807
13-https://pubmed.ncbi.nlm.nih.gov/22562653/
14-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441445/
15-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841276/
16 -https://www.researchgate.net/publication/234104444_Eleven_pairs_of_Japanese_male_twins_suggest_the_role_of_epigenetic_differences_in_androgenetic_alopecia
17-https://link.springer.com/article/10.1007/s00403-007-0826-x
18-https://pubmed.ncbi.nlm.nih.gov/21042071/
19-https://onlinelibrary.wiley.com/doi/abs/10.1111/dth.12785
20-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4171668/
21-https://pubmed.ncbi.nlm.nih.gov/2930558/
22-http://carcin.oxfordjournals.org/content/19/5/723.full.pdf

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