The hair that we see is only but a part of its entire structure. Its health and overall quality depend on numerous influences that are constantly at play- that’s largely why a change in our general health status almost immediately affects the health of our hair.
Read on to explore the entire cycle of our hair and get a deep understanding of the series of events that lead to its growth.
Why Do We Have Hair?
The human body is covered in as many as 5 million hairs, of which between 80,000 and 150,000 are found on the scalp alone.
You may just see it for its aesthetics, but our hair actually has a number of functions. Physically, it helps regulates our body temperature (by rising when we’re cold, to trap air and insulate the skin, and laying flat when we’re warm) and shields the scalp from the sun’s UV rays. Some of its structures serve as a source of stem cells (cells that can turn into other types of cells, based on the immediate need) and help secrete sweat and pheromones (chemicals that trigger attraction between individuals).
Even the type of hair determines its function. For instance, eyebrow hairs can protect our eyes (to an extent) from dirt, sweat and rain, while eyelashes protect the eyes from (and can even sense) dirt.
Regardless of the hair type and its specific purpose, though, every hair strand is composed of the same structure.
A section of the hair runs under the skin and is called the hair follicle, while the part you can see above the skin is called the hair shaft.
Let’s take a closer look at each.
The Hair Follicle
The section of hair that’s found inside the skin is called the hair follicle. This is the part that regulates its growth, through a complex interaction between our hormones, signalling molecules and immune system cells.
The way each component of the hair follicle functions is determined by its ‘hair cycle’. Each hair follicle follows three stages: i) the anagen stage, during which our hair actively grows, ii) the catagen stage, where changes in the hair follicle put a stop to hair growth and finally, iii) the telogen stage- a ‘resting’ period before the hair naturally falls out.
Note: The duration of these stages depends on the part of the body a follicle is in; for instance, the anagen stage of hair follicles in our scalp lasts for 2 to 8 years, while eyebrow hair follicles only grow for about 2 to 3 months (which is why they only produce short hairs).
For now, let’s take a look at what happens during the anagen stage of the hair follicle.
During this stage, the hair follicle contains living, growing and dividing cells, all of which communicate and work with each other. There are 20 different types of cells in the hair follicles, but in this article, we’re only going to be looking at the ones that comprise the regions of the hair follicle that are most significant to hair growth.
Here are the various regions –
The Hair Bulb:
The bottom area of a hair follicle is called the hair bulb. This area, along with the rest of the follicle, is surrounded by something known as the dermal sheath (DS), which contains cells designed to generate new cells, depending on the requirement. For now, we’ll only be looking at their ability to create cells for the dermal papilla (DP).
The DP is incredibly important for hair growth. It’s a structure found at the base of the hair bulb and plays host to the blood capillaries that supply a hair follicle with its required nutrients. These capillaries also bring in signalling molecules that allow the DP to regulate the growth of cells in the hair follicles- especially the ones in the hair matrix, where our hair shaft’s cells are grown.
The Hair Matrix:
There are various types of cells in the hair matrix, that play their own roles in the formation of the hair shaft.
For instance, keratinocytes are cells that produce keratin, the protein that makes up the hair shaft. Melanocytes secrete melanin, the pigment that gives colour to hair. The amount and type of melanin that seeps into other cells of the hair shaft influence an individual’s hair colour. (Damage to melanocytes, whether because of genetics, stress or regular ageing, leads to the greying of hair.)
The cells in the hair matrix actively grow and divide, creating a stream of production that pushes all the cells upwards and further away from the blood capillaries. Being out of reach of their nutrient supply, these cells begin to die. This general area of the follicle is known as the ‘keratinisation zone’, because, in their death, these cells leave behind a hard, dry bag of keratin known as cornified cells.
That’s what goes on to form the bulk of the hair shaft, outside the hair follicle: dead, hardened cells, filled with keratin.
The Hair Shaft
The keratin structures created in the hair follicle are pushed upwards as they form the hair shaft, which finally surfaces out of the skin- that’s the part we actually see, cut and style. This is made up of three concentric regions: the medulla, the cuticle and the cortex.
This is the innermost part of the hair shaft, made up of a thin core of transparent cells and air spaces. You’ll find the medulla in coarser hair like grey hair, thick hair and beard hair; it isn’t generally seen in fine hair. That doesn’t seem to be a problem, though, because the medulla is believed to contribute negligibly to the mechanical properties of hair fibres; its function is largely unknown.
The bulk of our hair’s structure can be found in the cortex and is largely composed of cortical cells. These are packed with the protein keratin.
Here, hundreds of keratin fibres wind around each other to form bigger bunches that in in turn wind around each other. This tight winding of keratin is made possible by the presence of cysteine, an amino acid that’s rich in sulphur, in keratin’s molecular structure. When cysteine molecules are adjacent, the sulphur in them bind to each other, creating a ‘di-sulphide bond’- a chemical bond that’s incredibly strong and makes the keratin structures coil into each other.
Visualise a telephone’s curly cords as a keratin structure; now imagine a sulphur bond present at every point that the cord coils into itself- that’s basically how a di-sulphide bond strengthens our hair. When you pull on a strand of curly hair, what you’re doing is straightening out the coils formed by the di-sulphide bonds- this immediately recoils when you stop pulling.
This arrangement is what lends strength and elasticity to our hair- but it can be broken by alkaline solutions, which is what is used in perms and chemical hair straightening.
Part of the hair’s strength also comes from hydrogen bonds, which are weaker than the di-sulphide bonds but similarly help the hair’s keratin structure stay intact.
The outermost layer of our hair shaft is the cuticle. This layer is also made up of cells that contain keratin, but they arrange themselves in a slightly different way to cortex cells.
As the cuticle cells are produced, they lay over the cortex cells and flatten out into overlapping structures (like a roof’s tiles). Each cuticle cell is covered with a lipid layer of fat. This lipid layer restricts the entry of water into the inner layers of hair, but repeated hair treatments deplete this layer, leading to dull and damaged hair.
In addition to the hair follicle and shaft, a few associated structures play a vital role in the functionality and health of hair.
Sebaceous glands: these are present just outside the hair follicle and secrete sebum, a mixture of healthy fats, antioxidants and cholesterol. Sebum serves two purposes: it covers the hair shaft and nourishes it (in fact, it’s what forms the lipid layer on the cuticle), as well as provides a protective coating against moisture. It also delivers antioxidants in the form of vitamin E to the surface of the skin.
Arrector pili: These are small muscles attached to the hair follicle. When these muscles contract, they cause hair to straighten out and stand on end. This helps the body release heat and is the reason we get goosebumps in the cold.
The ‘bulge’ of the hair follicle: The bulge is a reservoir of stem cells, which differentiate into the various cell types involved in hair growth. During the telogen phase, DP and DS cells rest near the bulge. Once the stem cells are activated, they begin differentiating into the various cell types required to restart the anagen phase of the hair cycle.
The hair plexus: The hair plexus or root hair plexus is a special group of nerve fibre endings that allow us to sense touch. Each hair plexus forms a network around a hair follicle and is a receptor, which means it sends and receives nerve impulses to and from the brain when the hair moves.
The Other Phases of the Hair Cycle
Everything we’ve seen until now has been happening in the anagen stage of the hair cycle, which, as you’ll remember, is the stage of hair growth. Here’s a closer look at what happens in the other two.
The Catagen Phase:
Catagen is a degenerative process driven by apoptosis, or programmed cell death. It is a short, transitional phase of the hair cycle between anagen and telogen, which lasts between two and four weeks.
At the beginning of the catagen phase, the hair matrix cells significantly slow down their pace of growth and division, the melanocytes stop producing melanin and the production of our hair shaft is completed.
The hair follicle receives a signal that triggers apoptosis, and it reduces to about one-sixth of its normal size.
Towards the end of the catagen stage, the dermal papilla is pulled upward, to the side of the follicles, until it separates from the matrix. The blood flow to the hair matrix subsequently stops, which hinders the supply of nutrients to the matrix cells.
The catagen phase is a natural part of the hair cycle, but can also be triggered by physiological stress and environmental factors.
The Telogen Phase:
After catagen, the hair follicle enters the telogen, or resting, phase. During the transition from telogen to anagen, stem cells get activated by the now adjacent dermal papilla, which enables the stem cells to divide into matrix cells and start a new hair growth cycle, a process that continues throughout life.
Factors that influence hair growth and the hair shaft
While the growth, loss and regrowth of hair is a natural process that continues throughout life, there are a number of factors that can adversely affect this cycle, compromising both hair quality and hair growth – even to a point of permanent loss of hair. These factors include:
i) Nutritional Deficiencies:
The dividing cells of the hair follicle require a constant supply of nutrients to facilitate their growth. Vitamin D3 helps cells multiply and mature, vitamins B6, B12 and biotin help with cellular metabolism, and minerals such as iron, zinc as well as amino acids (that are the building blocks of keratin) are essential for healthy hair growth.
One of the most common causes of hair loss in premenopausal women is nutritional deficiency of iron. In this case, screening for serum ferritin (a protein that stores iron) and haemoglobin can help identify the cause of hair loss. Severe protein deficiency, caloric restriction, vitamin D deficiency, zinc deficiency and chronic starvation can also induce hair loss.
The good news is that hair loss due to nutritional deficiencies is, for the most part, reversible by bringing back the levels of these nutrients.
ii) Mechanical Influences:
Excess physical forces on the hair shaft can damage hair cuticles, causing them to flake and tear. These forces can be caused by combing, back-combing, and the use of a hair curler. Wet hair is particularly susceptible as the cuticles are swollen, potentially exposing the inner cortex.
Additionally, wet hair can be stretched more, and combing wet hair is more likely to stretch hair to its breaking point. Extensive brushing and tying tight ponytails or braids can lead to breakage in dry and brittle hair, and in some cases ‘traction alopecia’. That’s a form of hair loss, caused primarily by force being applied to the hair.
iii) Environmental factors:
The sun’s UV rays, salt and chlorinated water can all contribute to the breakdown of chemical bonds within the hair’s structure.
Overexposure to sunlight degrades melanin and can alter the structure of hair proteins, making the hair very brittle and susceptible to damage. A humid environment, on the other hand, opens up pores and cuticles, leaving them exposed to damaging influences. When the cuticle is open, the hair’s porous cortex is exposed to environmental moisture, which causes it to swell with water and push against the cuticle, giving a ‘frizzy’ appearance.
iv) Heat treatments:
Using a curling iron, straighteners, blow dryer or dryer hood repeatedly can lead to breakage of hair. Heat breaks down the temporary bonds i.e. the hydrogen bonds, which hold together keratin protein chains within the hair, making it easier to style. However, over-exposure to heat can irreparably damage the structure of hair and may also damage the scalp, leading to hair loss.
v) Chemical factors:
Colouring, lightening and perming are designed to penetrate the outer protective cuticle, so as to affect the inner cortex directly. Perming chemicals break down disulphide bonds, which hold together the chains of keratin. If hair and scalp are over exposed to these chemicals, severe damage can occur. Shampooing daily cleanses off the protective layer of sebum that covers the hair, causing the shaft to dry out so it easily gets statically charged and consequentially more prone to friction. Using sulfate-free shampoos can be considered to reduce damage and maintain moisture.
The transition between phases of the hair cycle are controlled by finely tuned changes in the local signalling. This signalling is based on several growth factors, cytokines, hormones, neurotransmitters and their receptors as well as transcription factors and enzymes.
A number of hormones have been shown to directly affect hair. Testosterone, the primary male sex hormone, when in excess, is converted by a specific enzyme to Dihydrotestosterone (DHT). DHT binds to receptors on the hair follicle leading to a shortening of the anagen phase and a prolongation of the telogen phase, combined with miniaturization of the hair follicle. Symptoms of hair thinning and male pattern baldness (androgentetic alopecia) are a common result of excess DHT. Excess circulating testosterone in conditions such as PCOS and even anabolic steroid use can promote this type of hair loss.
Oestrogen, on the other hand, prolongs your hair’s growing stage (anagen) of the hair growth cycle, overriding the effects of testosterone. As oestrogen levels decline, the greater influence of testosterone shortens the growth phase, and the subsequent hair loss is usually gradual but can become noticeable over time. Low oestrogen levels are most common during menopause and just after pregnancy but can happen to women at any age.
Thyroid hormones T3 and T4, affects the development of hair at the follicle. Hair falls out and may not be replaced by new growth, resulting in thinning across your scalp and other areas such as your eyebrows.
One study published in the European Journal of Cardiovascular Risk found that women with some markers of insulin resistance have a greater risk for androgenic alopecia (AGA), or female pattern baldness.
In autoimmune disorders, inflammatory molecules attack healthy cells in the body (those of the hair follicle included). Alopecia areata, a common autoimmune disorder that interferes with hair follicle regeneration and causes patients to lose hair in patches from their scalp, eyebrows, and faces.
Inflammation (caused by nutritional imbalances and other reasons) can also damage the hair follicle and lead to hair loss.
Telogen effluvium is a major hair growth disorder, and is closely related to stress. Occurring mainly in women, telogen effluvium can be induced as a result of stress or extreme hormonal imbalance. This creates a disruption to the normal hair growth cycle in which anagen (growing) hairs prematurely enter the telogen (resting) phase. Consequently, symptoms begin to appear in the form of short, sudden bouts of hair shedding with little to no hair growth. Stress also induces significant changes in actively growing hair follicles and promotes their transition into the involution phase i.e. progressive degeneration of cells.
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