Scalp Calcification & Hair Loss: Is There a Connection?

Calcification of blood vessels can happen anywhere in the body, including the scalp.

But, is there any connection to scalp calcification and hair loss?

In this article, I’ll explain what scalp calcification is, why it might be the culprit behind your hair loss, why it happens, and ways you may be able to reverse it.

Just keep reading!

Also, make sure you take the free hair quiz further down this article.

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What Is Scalp Calcification?

Scalp calcification is a factor in hair loss. It happens when the blood vessels underneath the scalp accumulate calcium in their walls (1).

As a result, the blood vessels become stiff and inflexible, impairing blood flow.

Decreased blood flow is serious anywhere in the body. Blood provides our tissues with the nutrients they need to continue doing their jobs.

This is true in the scalp as well. Reduced blood flow, as a result of vascular calcification, reduces the number of nutrients available to the hair follicle.

Hair growth is dependent on the ability of the hair follicle to initiate follicle cell proliferation (cell division). Cell proliferation is a complex process that requires the precursors to make cells and the co-factors needed for cell function and signaling.

Proteins, fatty acids, glucose (from carbohydrates), vitamins, minerals, and other micronutrients all work in synergy to support proper hair follicle cell function and proliferation.

Vascular calcification decreases nutrient delivery which means less of the building blocks and co-factors required to initiate hair growth.

So, maintaining healthy blood vessels by reducing calcification is important for supporting hair growth.

In the sections below, I’ll explain the root cause of vascular calcification to help you better understand how you may be able to reverse it.

Key Takeaways:

  • Calcification of blood vessels in the scalp reduces blood flow.
  • Reduced blood flow diminishes nutrient delivery to the follicle required for hair growth.
  • Maintaining healthy blood vessels by reducing calcification is important for supporting hair growth.
  • Understanding the root cause of vascular calcification can help you better understand how to reverse it.

Scalp Calcification and Hair Loss: Androgenetic Alopecia

There is one clear connection between scalp calcification and hair loss: Androgenetic Alopecia (AGA), which is pattern hair loss that can affect both men and women) (2).

Scalp calcification is a component of hair follicle miniaturization, a hallmark of AGA. Combined with scarring around the hair follicle and decreased nutrient supply, the number, size, and growing capacity of hair strands is reduced.

The process of hair follicle miniaturization
The process of hair follicle miniaturization.

AGA is a complex and not fully understood condition that is characterized by hair loss that involves male hormone (androgen) activity, specifically dihydrotestosterone (DHT).

DHT is a powerful male hormone that stimulates the activity of androgen receptors in the cell much more efficiently compared to regular testosterone. It is created by the interaction of testosterone with the enzyme 5α-reductase (5α-R) that converts it into DHT.

DHT production is dependent on the levels of circulating testosterone, the expression of 5α-R (which is controlled by genetics and the environment), and the number of androgen receptors available for DHT to bind to.

Excess DHT mediates a lot of the symptoms of AGA, including scalp calcification. However, simply chalking it up to DHT activity isn’t accurate.

How Does It Happen?

As many like to say, “genetics load the gun, but the environment pulls the trigger.” This is a perfect metaphor to explain how scalp calcification occurs.

We know this because identical twins who have a genetic predisposition to AGA don’t always progress in the same way (2). This tells us that external, non-genetic factors can also impact the way AGA develops.

The genetic predisposition to AGA involves the genes that control the production of the 5α-R enzyme, androgen receptors (ARs), which are the catalyst for the effects of androgens, and the androgen co-activator Hic-5/ARA55.

A higher expression of 5α-R enzymes, controlled by genetics, increases the production of DHT.

Androgen receptors are distributed throughout the hair follicle. The density of these receptors is determined by genetics.

The activity of DHT is also influenced by the co-activator Hic-5/ARA55. This co-activator is like a bridge and determines the sensitivity of cell functions to androgens (3).

It works like this:

  1. 5α-R converts testosterone into DHT in various tissues throughout the body, including the hair follicle.
  2. DHT enters into cells and binds to ARs.
  3. The DHT-AR complex moves to the nucleus.
  4. Hic-5/ARA55 is influenced by the cellular environment to translocate from the cytoplasm of the cell to the nucleus.
  5. Once in the nucleus, Hic-5/ARA55 acts as a bridge between the DHT-AR complex and the genetic material of the cell. Without Hic-5/ARA55, DHT can’t effectively influence gene transcription.
  6. This allows the DHT-AR complex to influence gene transcription in a DHT-specific way.
  7. Gene transcription takes place and influences the expression of enzymes, inflammatory mediators, and more molecules inside the cell. This will ultimately determine the fate of the cell and collective tissue that the cells make up.

One of the genes that DHT influences is TGF-β. DHT activity increases TGF-β expression which is the mediating growth factor in scalp calcification.

TGF-β increases the activity and expression of an enzyme called alkaline phosphatase (4). This enzyme digests inorganic pyrophosphates which are responsible for blocking calcium deposits in blood vessels (5). However, when alkaline phosphatase is increased by TGF-β, this enzyme reduces the number of pyrophosphates. As a result, calcium can be deposited in blood vessels.

But, what determines the translocation of Hic-5/ARA55 to the nucleus?

Evidence suggests free radicals and inflammation may mediate this process. According to studies looking at cellular mechanisms, oxidative stress from free radicals stimulate the shuttling of Hic-5/ARA55 to the nucleus, which increases androgen activity.

Cells before and after free radicals
Free radicals, which lead to cellular damage, may play a role in AGA progression.

Inflammatory mediators produce free radicals as a byproduct. Free radicals also accumulate as a result of antioxidant depletion (which can be caused by a myriad of factors), metabolic processes, and exposure to environmental toxins.

This isn’t surprising considering oxidative stress and inflammation are closely linked to AGA.

TGF-β itself also enhances the expression of Hic-5/ARA55, exacerbating this vicious cycle that is AGA.

However, it’s hard to determine which, TGF-β or free radicals and inflammation, is the initiating factor.

Nonetheless, breaking this DHT-inflammation/free radical-Hic-5/ARA55-TGF-β cycle in some way is prudent to reduce scalp calcification.

Key Takeaways:

  • Genetics set the predisposition for AGA, but the environment influences the progression of AGA.
  • The environment may impact AGA development through the activity of the androgen co-activator Hic-5/ARA55.
  • Hic-5/ARA55 is responsible for allowing DHT to influence gene expression of TGF-β which mediates scalp calcification through its enzymatic effects.
  • Free radicals and inflammation (which increases the production of free radicals) are closely intertwined with AGA. This may be because free radicals stimulate the shuttling of Hic-5/ARA55 to the nucleus, where it allows androgens to effectively influence gene expression.
  • TGF-β itself also enhances the expression of Hic-5/ARA55, exacerbating the cycle.
  • It’s hard to determine whether TGF-β or free radicals and inflammation are the initiating factor in AGA. Nonetheless, breaking the cycle in some way is prudent to reduce scalp calcification.

How to Decalcify the Scalp

No studies have currently examined the ability of nutrients to reduce scalp calcification specifically. However, there are some plausible ways you can naturally decalcify the scalp.

Address Inflammation and Oxidative Stress

Inflammation and oxidative stress are closely linked (6). Inflammation produces free radicals and free radicals stimulate inflammation.

Inflammation is initiated by a synergy between pro-inflammatory signaling molecules like cytokines and mediators like prostaglandins, thromboxanes, and leukotrienes.

Pro-inflammatory prostaglandins, thromboxanes, and leukotrienes are created by the interaction between arachidonic acid, an omega-6 fatty acid, and cyclooxygenase (COX) and lipooxygenase (LOX) enzymes.

The production of pro-inflammatory cytokines and pro-inflammatory mediators is influenced by gene expression. The gene expression of these inflammatory molecules is mediated by a transcription factor called NF-κB.

When activated, NF-κB translocates to the nucleus and communicates for the production of the genes that create these inflammatory signaling molecules.

But, what activates NF-κB?

Free radicals are a well-established activator of NF-κB (7).

Considering inflammation produces free radicals, lowering inflammation is a key factor in reducing NF-κB activation. Utilizing nutrients to reduce oxidative stress may also inhibit NF-κB.

One of the most effective ways to reduce inflammation is to incorporate more omega-3s into the diet (8). Their anti-inflammatory effects are potent due to their multifaceted effects on the inflammatory signaling pathways of the body.

When the tissues of the body are effectively saturated with DHA & EPA, two powerful omega-3 fatty acids, they compete with arachidonic acid for binding with COX and LOX enzymes.

When DHA and EPA bind to COX and LOX enzymes preferentially over arachidonic acid, they not only reduce the amount of pro-inflammatory mediators produced, but they also produce weakly inflammatory mediators in their place.

Additionally, two byproducts of DHA and EPA, resolvins and protectins, also help to regulate inflammation and resolve it, reducing the propensity for inflammation’s negative effects.

Moreover, DHA, EPA, and even their oxidized byproducts inhibit NF-κB and activate Nrf2, the transcription factor that increases antioxidant enzyme expression in the cell (9, 10).

Thus, DHA and EPA are essential for reducing excessive inflammatory responses in the body.

DHA and EPA can be obtained through the consumption of cold-water fatty fish, shellfish, and fish oil.

Antioxidants in the diet also help reduce the oxidative load on the body.

They work by neutralizing free radicals. Some antioxidants also activate Nrf2, which enhances the expression of antioxidant enzymes in the cell like glutathione peroxidase and superoxide dismutase.

This combined enhanced antioxidant activity reduces the oxidative stress load on the body and prevents cellular structures from being damaged. It may also reduce androgen sensitivity and scalp calcification by preventing Hic-5/ARA55 translocation.

Antioxidant-rich foods and Nrf2 activators include:

  • Broccoli sprouts
  • Organic berries
  • Red grapes
  • Leafy greens
  • Dark chocolate
  • White, green, black, and red teas
  • Carotenoid-rich foods like sweet potato, mango, avocados, and peppers
  • Extra virgin organic olive oil
  • Shellfish and wild-caught salmon
  • Raw, organic, sprouted nuts and seeds
  • Blue-green algae like spirulina and chlorella
  • Herbs like rosemary and oregano
  • Vitamin-C rich foods like bell peppers, guava, and kiwis

Striving to eat the rainbow every day is a great way to guarantee adequate antioxidant consumption.

Combined, anti-inflammatory foods and antioxidant-rich foods can help reduce the oxidative stress load on the body that may contribute to scalp calcification.

Key Takeaways:

  • Both inflammation and free radicals contribute to the oxidative stress load on the body.
  • Omega-3 DHA and EPA lower inflammation and oxidative stress in a multifaceted way. DHA and EPA can be obtained through wild-caught fish and shellfish consumption along with supplementation of fish oils.
  • Antioxidant rich foods not only neutralize free radicals but help support the antioxidant systems of the body responsible for reducing the oxidative stress load.
  • Striving to eat the rainbow is a great way to encourage antioxidant consumption.
  • Together anti-inflammatory and antioxidant foods reduce the oxidative stress load that contributes to scalp calcification.

Magnesium for Scalp Calcification

Magnesium is a mineral in the body with various roles. It’s a co-factor in over 300 enzymes.

One of its jobs is to regulate calcium balance. Through this, it helps reduce vascular calcification like in the scalp.

The anti-mineralization properties of magnesium have been well-studied (11).

Magnesium is also often lacking in the diet, attributed to a lack of spring water consumption and depleted soil quality. So, it’s important to actively consume magnesium.

Magnesium-rich foods include:

  • Leafy greens
  • Blue-green algae like spirulina and chlorella
  • Dark chocolate
  • Avocados
  • Nuts and seeds

You can also supplement with magnesium. The most bioavailable form is chelated, amino acid-bound magnesium in the form of magnesium glycinate or magnesium citrate.

Key Takeaways:

  • Magnesium is a mineral that helps regulate calcium balance to help reduce calcification.
  • Magnesium is often lacking in the diet due to lack of spring water consumption and depleted soil quality.
  • You can ensure you’re getting enough magnesium by consuming magnesium-rich foods and supplementing with a chelated, amino-acid bound magnesium supplement.

Blocking DHT with 5α-Reductase Inhibitors

Since DHT is so intimately involved with scalp calcification, DHT blockers could be used to prevent it from occurring.

DHT blockers, or 5α-R inhibitors, are approved by the FDA to treat AGA, which is mediated in part by scalp calcification.

Currently, the FDA has approved finasteride as a 5α-R inhibitor for treating AGA.

However, pumpkin seed oil may be a natural alternative to prescription 5α-R inhibitors. In a randomized, placebo-controlled trial, supplementation of a capsule containing 400mg of pumpkin seed oil resulted in an average 40 percent increase in hair count after 24 weeks (12). It should be noted that pumpkin seed oil hasn’t been tested for efficacy in women.

Pumpkin seed oil

Many other natural 5α-R inhibitors have been proposed and are even frequently used (13). Unfortunately, many of these herbs don’t currently have a reliable body of research to back up their use.

While 5α-R inhibitors may solve part of the problem, DHT, they don’t resolve the underlying issue of excess DHT in the first place. We don’t know the exact culprit, but evidence points to inflammation and oxidative stress.

This means that the changes that result from using drugs like finasteride are usually restricted to the time of use. This means that when you stop taking it, scalp calcification and hair loss sets in all over again.

Messing with hormones is also tricky business. Each hormone doesn’t exist on its own, in fact, all hormones in the body exist in a delicate, synergistic concert with one another. Resolving issues that involve hormones, like AGA, is less about targeting one hormone and more about bringing the hormones into balance.

For this reason, opting for anti-androgens without resolving underlying issues may not give long-lasting results.

Key Takeaways:

  • DHT blockers like finasteride may benefit scalp calcification which plays a role in AGA.
  • Pumpkin seed oil may be a natural alternative. One randomized controlled trial of pumpkin seed oil supplementation resulted in an average 40% increase in hair count in men with AGA.
  • Many other natural 5α-R inhibitors have been proposed and are even frequently used but many don’t have much of a body of research to support their use.
  • Whether natural or synthetic, 5α-R inhibitors don’t resolve the underlying root cause of excess DHT. This means that once you stop taking them, you could lose your hair again.
  • Messing with hormones is tricky business because hormones function in a delicate balance. It’s less about targeting one specific hormone and more about bringing hormones into balance.

Vitamin K2 for Scalp Calcification

Vitamin K2 (as opposed to K1, which isn’t the active form) helps regulate calcium deposition in the body (14). Because of this, it helps prevent blood vessel calcification, as seen in AGA scalp calcification.

The way vitamin K2 accomplishes this is through matrix GLA protein (MGP), a calcification inhibitor.

The way MGP works to prevent vascular calcification is not fully understood yet, but it is believed to act on bone morphogenetic proteins which may be involved in this process.

For MGP to work, it has to be activated through a process called carboxylation (15). Without this, MGP can’t effectively prevent vascular calcification.

The enzyme responsible for the carboxylation of MGP is γ-glutamylcarboxylase. It transforms MGP into cMGP. For the γ-glutamylcarboxylase enzyme to function, it needs vitamin K2.

Without it, MGP goes uncarboxylated and is biologically inactive.

Vitamin K2 can be obtained through the diet and supplementation.

Foods rich in vitamin K2 include:

  • Grass-fed butter
  • Dark chicken meat
  • Egg yolks
  • Cheese
  • Liver
  • Natto (Japanese fermented soy)

Natto is the most bioavailable form of vitamin K2 because it produces a form of vitamin K2 called menaquinone 7 (MK-7).

When supplementing, this is the form you will want to look for as well.

Key Takeaways:

  • GLA is a protein that prevents vascular calcification.
  • For GLA to be biologically activate, it has to be carboxylated by γ-glutamylcarboxylase. For γ-glutamylcarboxylase to function, it needs vitamin K2.
  • You can obtain vitamin K2 by eating vitamin K2-rich foods.
  • Vitamin K2 MK-7 is the most bioavailable form of vitamin K2 which can be found in supplements and natto.

Support Proteoglycan Production

In the skin, there are molecules called proteoglycans. They have various functions.

One proteoglycan, decorin, has been shown to block the effects of TGF-β, the growth factor that contributes to scalp calcification (16).

The synthesis of decorin requires amino acids from proteins in the diet and a galactosaminoglycan called dermatan sulfate.

The synthesis of dermatan sulfate requires sulfation by an enzyme called sulfotransferases (17). Sulfation is a process by which sulfur is added to a molecule.

This process requires a sulfur donor. This can be achieved by dietary sulfur, however, many factors can limit sulfur absorption including extremely common imbalances in gut bacteria (18).

A majority of the sulfur supply is derived from homocysteine metabolism (19). This is a series of enzymatic conversions that detoxifies homocysteine to produce cysteine and methionine, two important sulfur donors.

Four B-vitamins are absolutely essential to this process:

  • Riboflavin (B2)
  • Pyridoxine (B6)
  • Folate — not folic acid (B9)
  • Cobalamin (B12)

B6 is essential for the transsulfuration of homocysteine to cysteine.

B6 and B2 are involved in the enzymatic conversion of folate to 5-methyltetrahydrofolate (5-MTHF) that allows 5-MTHF and B12 to convert homocysteine to methionine.

Because they exist in a cycle, all reactions are dependent on each other. So, while each nutrient is important for individual reactions, they all work synergistically for the functionality of the whole cycle.

Another way to boost sulfur levels is through the skin. Magnesium sulfate, in the form of Epsom salts or magnesium oil, is another possible route of absorption.

Bolstering sulfur levels in these ways may be beneficial for sulfotransferase reactions which play a role in decorin synthesis. However, this hasn’t been directly studied.

Key Takeaways:

  • Decorin is a proteoglycan that requires dermatan sulfate. Dermatan sulfate is produced through sulfotransferase reactions.
  • Sulfotransferase reactions require sulfur donors from the diet or sulfur produced by reactions in the body. However, sulfur absorption from the diet can be limited by a myriad of factors including the common gut dysbiosis.
  • B2, B6, B9, and B12 play key roles in the production of cysteine and methionine, two sulfur donors that are used for sulfotransferase reactions.
  • Magnesium sulfate from epsom salts and magnesium oil may also provide sulfur to the body through the skin, which bypasses the problematic digestive absorption.
  • Because sulfur is essential for sulfotransferase activity, dermatan sulfate is produced through sulfation, and decorin synthesis is dependent on dermatan sulfate, bolstering sulfur levels in this way may boost decorin synthesis. However this hasn’t been directly studied.

Can You Reverse Scalp Calcification Hair Loss?

Scalp calcification plays a role in hair loss but isn’t a direct cause. Reversing scalp calcification may improve hair growth, however, finding the root cause of scalp calcification in the first place is difficult.

Unfortunately, no studies have currently attempted to explicitly observe scalp calcification and interventions that may reverse or prevent it.

But, by understanding the physiology of the body, we can make some assumptions as to how certain methods might help. Most of these address the potential underlying causes of scalp calcification.

Although, it should be noted that most of these haven’t been directly studied for their effects on hair growth.

Have you tried any of these methods for reducing scalp calcification? Leave a comment below.

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