Hair loss and baldness are conditions that affect millions of individuals worldwide, leading to psychological distress and diminished quality of life for many. This article provides a comprehensive overview of hair loss (also known as alopecia) and baldness, including their causes, types, diagnostic methods, modern treatment options, and preventative measures, and MIT homeopathy approach to its therapeutics.
Hair loss can be temporary or permanent and can affect just the scalp or the entire body. While it is more prevalent in adults, hair loss can also occur in children. Baldness typically refers to excessive hair loss from the scalp and is often the result of hereditary hair loss with age.
Hair loss and baldness can be attributed to a variety of factors. The most common cause of hair loss is a hereditary condition called androgenetic alopecia, more commonly known as male-pattern or female-pattern baldness. Hormonal changes due to pregnancy, childbirth, menopause, or thyroid problems can cause temporary or permanent hair loss. Conditions such as alopecia areata (an autoimmune disease that attacks hair follicles), scalp infections like ringworm, and trichotillomania (a hair-pulling disorder) can lead to hair loss. Hair loss can be a side effect of certain drugs, such as those used for cancer, arthritis, depression, heart problems, gout, and high blood pressure. Lack of nutrients such as iron, protein, and vitamins can contribute to hair loss. Physical or emotional stress can trigger temporary hair loss.
Androgenetic Alopecia is a hereditary condition affecting both men and women and is characterised by a receding hairline and the disappearance of hair from the crown and frontal scalp. Alopecia Areata is a condition that causes patchy hair loss on the scalp and possibly other areas of the body. Telogen Effluvium is a temporary hair loss condition that usually happens after stress, a shock, or a traumatic event and typically involves the thinning of hair rather than bald patche. Anagen Effluvium is rapid hair loss resulting from medical treatment, such as chemotherapy.
Diagnosing hair loss involves a medical history and physical examination by a healthcare provider. Tests might include: 1. Blood Tests: To uncover medical conditions related to hair loss. 2. Pull Test: A gentle tug on a few strands of hair to determine the stage of the shedding process. 3. Scalp Biopsy: Taking a small section of the scalp to examine under a microscope. 4. Light Microscopy: To examine hairs trimmed at their bases.
Treatment depends on the type of hair loss, its severity, and whether it’s temporary or permanent. Options may include: 1. Medications: Over the counter (OTC) or prescription drugs such as minoxidil (Rogaine) or finasteride (Propecia). 2. Hair Transplant Surgery: Removing small plugs of hair from areas where hair is continuing to grow and placing them in balding areas. 3. Laser Therapy: FDA-approved to treat hereditary hair loss. 4. Lifestyle Changes: Including managing stress, eating a balanced diet, and avoiding tight hairstyles.
While it’s not always possible to prevent hair loss, some practices can help maintain hair health: 1. Avoid harsh treatments and hair styles that pull the hair 2. Protect hair from sunlight and other sources of UV light. 3. Stop smoking, as it has been linked to baldness. 4. If undergoing chemotherapy, consider a cooling cap to reduce the risk of hair loss.
Hair loss and baldness can significantly impact an individual’s self-esteem and overall quality of life. Understanding the causes and available treatments is the first step toward managing this condition effectively. It’s crucial for those experiencing hair loss to consult with healthcare providers to determine the underlying cause and appropriate treatment. With the advancements in treatment options, many individuals find relief and satisfactory outcomes in managing their hair loss.
GENETIC FACTORS IN ALOPECIA AND BALDNESS
Genetic factors play a pivotal role in hair loss, particularly in the context of androgenetic alopecia, the most common form of hair loss in both men and women. This condition is also known as male-pattern baldness or female-pattern hair loss. Understanding the genetic basis of alopecia involves delving into how specific genes influence hair follicle health, hormone interactions, and ultimately, the hair growth cycle.
Androgenetic alopecia is highly heritable, meaning it has a strong genetic component. It is polygenic, which means it involves the interaction of multiple genes rather than being traced back to a single gene mutation. The condition is influenced by genes inherited from both parents, although the precise pattern of inheritance and the degree to which genetics play a role can vary between individuals.
Androgen Receptors (AR) Gene is one of the most significant genes associated with androgenetic alopecia. Located on the X chromosome, this gene codes for the androgen receptor, which interacts with dihydrotestosterone (DHT), a derivative of testosterone. DHT has a miniaturising effect on hair follicles, leading to thinner hair and a shorter hair growth cycle. Variations in the AR gene can increase the sensitivity of hair follicles to DHT, accelerating hair loss. 5-Alpha Reductase Type 2 (SRD5A2) Enzyme is crucial for the conversion of testosterone to DHT. Variations in genes encoding for this enzyme can influence the levels of DHT and thus the extent of its impact on hair follicles. Inhibitors of 5-alpha reductase, such as finasteride, target this pathway to reduce hair loss. Hair Cycle Genes that regulate the hair growth cycle also play a role in androgenetic alopecia. The hair follicle cycles through phases of growth (anagen), regression (catagen), rest (telogen), and shedding (exogen). Genetic factors that disrupt the normal cycle can lead to premature hair loss.
While genetic predisposition is a key factor, the onset and severity of androgenetic alopecia are also influenced by environmental factors such as diet, stress, and health conditions. This interaction between genetics and environment complicates the prediction and treatment of hair loss.
Genetic testing can identify individuals at higher risk for developing androgenetic alopecia, allowing for early intervention and personalised treatment plans. However, due to the complex nature of genetic interactions and the influence of environmental factors, these tests cannot predict the condition with absolute certainty.
Research continues to uncover new genes associated with hair loss and baldness, offering insights into the biological mechanisms behind these conditions. Understanding these genetic factors opens the door to targeted therapies that can more effectively manage or even prevent hair loss. For example, drugs designed to specifically block the action of DHT on hair follicles or to modulate the activity of genes involved in the hair growth cycle represent promising areas of development.
Genetics plays a crucial role in the development of androgenetic alopecia, with several key genes influencing the sensitivity of hair follicles to hormones, the hair growth cycle, and the conversion of testosterone to DHT. While genetic predisposition is significant, the interplay between genes and environmental factors means that the expression of these genetic tendencies can vary widely among individuals. Ongoing research into the genetic basis of alopecia not only helps in understanding the condition but also in developing targeted treatments that address the specific genetic pathways involved.
ROLE OF AUTOIMMUNITY IN ALOPECIA
Autoimmunity plays a significant role in certain types of alopecia, which is a condition characterised by hair loss. There are various forms of alopecia, and among them, alopecia areata is particularly associated with autoimmunity.
In alopecia areata, the body’s immune system mistakenly attacks the hair follicles, leading to hair loss. This can result in a few bald patches, extensive hair loss (alopecia totalis), or even complete loss of hair on the entire body (alopecia universalis). The autoimmune attack causes inflammation around the hair follicles, preventing them from producing hair. The exact reason why the immune system attacks the hair follicles in alopecia areata is not fully understood, but it’s believed to involve a combination of genetic and environmental factors.
Other types of hair loss, such as androgenetic alopecia (commonly known as male or female pattern baldness), are primarily due to genetic and hormonal factors rather than autoimmunity. In these cases, the hair loss is caused by the sensitivity of hair follicles to androgens (male hormones), which can lead to thinning hair and eventual baldness in genetically predisposed individuals.
In the autoimmune mechanism of alopecia, specifically in alopecia areata, the immune system mistakenly targets certain components within the hair follicle, leading to hair loss. The exact autoantigens—that is, the self-proteins recognized as foreign by the immune system—involved in alopecia areata are not completely understood and are an area of active research. However, several potential autoantigens have been proposed based on studies involving patients with alopecia areata and experimental models.
Trichohyalin is a protein found in the inner root sheath of hair follicles. Some research suggests that it may be targeted by autoreactive T cells in alopecia areata.
Tyrosine-related Protein-2 (TYRP2) is involved in the pigmentation of the hair and is another potential autoantigen. Mice models have shown that targeting TYRP2 can lead to an alopecia areata-like condition.
Other hair follicle-associated proteins, not specifically identified, are also thought to be potential targets of the autoimmune response in alopecia areata. These could include various structural proteins and enzymes involved in hair growth and maintenance.
Since alopecia areata can also affect pigmented cells, melanocyte-associated antigens have been considered potential targets. This is supported by the observation that regrowing hair in alopecia areata often lacks pigment is white or gray initially. Melanocyte-associated antigens are proteins found on the surface of melanocytes, the cells responsible for producing melanin, the pigment that gives color to the skin, hair, and eyes. These antigens can be targeted by the immune system in various autoimmune and inflammatory conditions, as well as in cancer immunotherapy. Their role is particularly highlighted in conditions like vitiligo and melanoma, as well as in alopecia areata when it involves the loss of pigmented hair. Although primarily an attack on hair follicles, alopecia areata can also involve melanocyte-associated antigens, particularly in cases where the regrowth of hair occurs without its natural pigment (resulting in white or gray hair). This suggests that the autoimmune attack may sometimes extend to melanocytes or their associated components within the hair follicle. TYRP1 and TYRP2 enzymes are involved in melanin biosynthesis and are expressed in melanocytes and melanomas. They are potential targets for therapies aiming to modulate the immune response to melanoma. The study and utilization of melanocyte-associated antigens in autoimmune diseases and cancer highlight the importance of understanding immune system interactions with specific cell types. Immunotherapeutic approaches targeting these antigens offer promising treatment avenues alopecia areata.
The involvement of these autoantigens suggests that the autoimmune response in alopecia areata is quite complex, potentially involving various components of the hair follicle and associated structures. It’s also important to note that the immune response involves both cellular immunity (particularly T lymphocytes) and humoral immunity (antibodies), further complicating the identification of specific autoantigens.
Research is ongoing to better understand the specific autoantigens and the mechanisms through which they trigger the immune response in alopecia areata. Identifying these components could lead to more targeted therapies for individuals affected by this condition.
In summary, autoimmunity is a key factor in alopecia areata, causing the immune system to attack hair follicles, but it is not the main cause of all types of alopecia or baldness. Each type of alopecia has its own set of causes and mechanisms, with autoimmunity being significant in some but not all cases.
ROLE OF ENZYMES
The pathogenesis of alopecia, particularly androgenetic alopecia (AGA), involves complex biochemical pathways that include several enzyme systems. These enzymes interact with various substrates, and their activity can be modulated by specific activators and inhibitors. Understanding these enzyme systems is crucial for developing targeted therapies for hair loss. Below are the key enzyme systems involved in alopecia and baldness, along with their substrates, activators, and inhibitors.
15-Alpha Reductase is crucial in the pathogenesis of AGA. It converts testosterone, the primary male sex hormone, into dihydrotestosterone (DHT). DHT is a more potent androgen that binds to androgen receptors on hair follicles, leading to follicular miniaturisation and eventually hair loss. Substrate: TestosteroneActivators: AndrogensInhibitors: Finasteride, Dutasteride
Aromatase converts androgens into oestrogens. In the context of hair loss, its activity is more significant in women. Higher levels of aromatase in female scalp follicles can lead to lower DHT levels, which may explain the different patterns and severity of hair loss in women compared to men. Substrate: Androgens (Testosterone and Androstenedione). Activators: FSH (Follicle Stimulating Hormone), LH (Luteinizing Hormone). Inhibitors: Aromatase inhibitors (e.g., Letrozole, Anastrozole)
CYP17A1 (17α-Hydroxylase/17,20-Lyase) is involved in the synthesis of androgens in the adrenal glands and gonads. It catalyses the conversion of pregnenolone and progesterone into precursors of androgens. By influencing the overall levels of androgens, it indirectly affects hair growth and loss. Substrate: Pregnenolone and Progesterone. Activators: ACTH (Adrenocorticotropic Hormone). Inhibitors: Abiraterone
The balance between these enzyme activities plays a significant role in determining androgen levels in the scalp and systemic circulation, thereby influencing hair growth or loss. For example, elevated activity of 5-alpha reductase increases DHT levels, promoting hair loss. Conversely, higher aromatase activity in women converts more androgens into oestrogens, potentially protecting against extensive hair loss.
Understanding these enzyme systems has led to targeted treatments for androgenetic alopecia.
5-Alpha Reductase Inhibitors: Drugs like finasteride and dutasteride inhibit 5-AR, reducing DHT levels and slowing the progression of hair loss. These are commonly prescribed for men with AGA and have shown effectiveness in many cases.
Aromatase Enhancers: Although not a standard treatment for AGA, increasing aromatase activity or oestrogen levels can theoretically benefit hair growth by reducing effective androgen levels.
Adrenal Androgen Inhibitors: For women, controlling adrenal androgens through inhibitors of CYP17A1 or using oral contraceptives can sometimes manage hair loss by reducing the systemic levels of androgens.
TYRP1 (Tyrosinase-related protein 1) and TYRP2 (Tyrosinase-related protein 2, also known as DCT, Dopachrome tautomerase) are enzymes that play crucial roles in the melanin biosynthesis pathway, which is responsible for the pigmentation of skin, hair, and eyes. These enzymes are involved in the metabolic pathway that leads to the production of eumelanin, a type of melanin that gives a brown to black color. Understanding their substrates and activators is key to comprehending how pigmentation is regulated and can have implications for conditions like albinism, vitiligo, and the development of pigmented lesions like melanoma.
TYRP1 Enzyme. Substrate: TYRP1 works downstream of tyrosinase in the melanin synthesis pathway. It helps to oxidize 5,6-dihydroxyindole-2-carboxylic acid (DHICA) into indole-5,6-quinone-2-carboxylic acid. Although it acts mainly to stabilize tyrosinase and prolong its activity rather than directly interacting with specific substrates, its exact substrate specificity beyond its role in melanogenesis is not well-defined. Activators: The activity of TYRP1 is closely tied to the presence and activity of tyrosinase, the primary enzyme in the melanogenesis pathway. Factors that increase tyrosinase activity or expression, such as ultraviolet radiation (UV light), can indirectly increase TYRP1 activity by increasing the substrate availability for melanin synthesis. Additionally, the expression of TYRP1 is regulated at the transcriptional level by various transcription factors involved in melanocyte function, such as MITF (Microphthalmia-associated transcription factor).
TYRP2 (DCT) Enzyme. Substrate: TYRP2 catalyses the tautomerization of dopachrome, a melanin intermediate, into 5,6-dihydroxyindole-2-carboxylic acid (DHICA). This reaction is a key step in the biosynthesis of eumelanin, contributing to the dark pigmentation. Activators: Similar to TYRP1, TYRP2 activity is also influenced by factors that regulate the overall melanin biosynthetic pathway. UV light can enhance melanin production, indirectly affecting TYRP2 activity by upregulating the melanogenesis pathway. Transcription factors like MITF also regulate TYRP2 expression. Certain hormones and signalling molecules that activate these transcription factors or directly stimulate melanocyte receptors can enhance the expression of melanogenic enzymes, including TYRP2.
Both TYRP1 and TYRP2 are essential for the proper functioning of the melanin biosynthesis pathway, contributing to the stability, quantity, and quality of melanin produced. Alterations in the activity or expression of these enzymes can lead to pigmentation disorders and affect the vulnerability of skin to UV radiation and oxidative stress. Understanding these enzymes’ regulation can contribute to developing therapeutic strategies for pigmentation disorders and protection against UV-induced damage.
The biochemical pathways involved in hair loss, specifically through the action of various enzymes, highlight the complex nature of alopecia. By targeting these enzymes, current treatments aim to modulate the hormonal environment of hair follicles, offering hope for managing this challenging condition. Ongoing research into these pathways promises to uncover new therapeutic targets and more effective treatments for those suffering from hair loss.
ROLE OF HORMONES IN ALOPECIA
Hormonal imbalances and interactions play a significant role in the development of alopecia and baldness, particularly in conditions like androgenetic alopecia (AGA), which is the most common form of hair loss in both men and women. The primary hormones involved include androgens (such as dihydrotestosterone [DHT] and testosterone), oestrogen, and cortisol. Their molecular targets and mechanisms of action are crucial in understanding the pathophysiology of hair loss and developing targeted therapies.
Androgens (Testosterone and Dihydrotestosterone [DHT]) is converted to DHT by the enzyme 5-alpha reductase. DHT has a higher affinity for androgen receptors than testosterone and, when bound to these receptors in scalp hair follicles, can alter the normal cycle of hair growth. DHT shortens the growth (anagen) phase and extends the rest (telogen) phase, leading to thinner hair and a receding hairline. Over time, this can result in the miniaturisation of hair follicles and eventual hair loss. Molecular Targets: Androgen Receptors (AR) on hair follicle cells.
Oestrogens are believed to extend the anagen phase of the hair growth cycle, promoting hair growth and increasing hair density. They may also counteract the effects of androgens by decreasing the expression of androgen receptors in hair follicles or by inhibiting the enzyme 5-alpha reductase, thereby reducing the conversion of testosterone to DHT. The protective effects of oestrogens on hair growth are more evident in women, which is why women generally have less severe patterns of baldness compared to men. Molecular Targets: Oestrogen Receptors (ER) on hair follicle cells.
Cortisol, known as the stress hormone, can influence hair growth and health. High levels of cortisol can lead to telogen effluvium, a form of hair loss characterised by excessive shedding. Cortisol can negatively impact the hair growth cycle by shortening the anagen phase and prematurely shifting hair follicles into the telogen phase. Additionally, chronic stress and elevated cortisol levels can decrease the proliferation of hair follicle cells and reduce the synthesis of proteins essential for hair growth. Molecular Targets: Glucocorticoid Receptors (GR) on hair follicle cells.
The interplay between these hormones significantly influences hair growth and loss. For instance, the balance between androgens and oestrogens can determine the health and lifecycle of hair follicles. Hormonal changes, such as those experienced during pregnancy, menopause, or as a result of certain medical conditions, can shift this balance and lead to hair loss or changes in hair density and texture.
Understanding the hormonal mechanisms behind hair loss has led to targeted treatment options. The use of androgen receptor blockers (such as spironolactone) or 5-alpha reductase inhibitors (such as finasteride and dutasteride) can reduce the effects of DHT on hair follicles, slowing or preventing hair loss in some individuals. Hormone replacement therapy (HRT) or contraceptives containing oestrogens can sometimes be used to treat hair loss in women, particularly if it’s related to hormonal imbalances. Techniques to reduce stress and lower cortisol levels, including lifestyle modifications, may indirectly benefit hair health by normalising the hair growth cycle.
Hormones significantly influence hair growth and loss, with androgens, oestrogens, and cortisol playing pivotal roles. Their actions on specific molecular targets within hair follicles dictate the hair growth cycle and can lead to alopecia when imbalanced. Treatments targeting these hormonal pathways can offer hope for those experiencing hair loss, underscoring the importance of hormonal balance in maintaining hair health.
PSYCHOLOGICAL FACTORS IN ALOPECIA
The impact of psychological factors on alopecia and baldness has been an area of growing interest and research, acknowledging the complex interplay between the mind and body in health and disease. Psychological stress, in particular, has been identified as a significant factor that can influence the onset and progression of hair loss. The mechanisms through which psychological factors contribute to hair loss encompass both direct physiological pathways and indirect behaviours that affect hair health.
Chronic stress can have a direct impact on hair growth and health through several physiological mechanisms. Chronic stress leads to elevated levels of cortisol, the body’s primary stress hormone. High cortisol levels can shorten the anagen (growth) phase of the hair cycle and prematurely push hair follicles into the telogen (resting) phase, resulting in telogen effluvium, where hair sheds excessively. Stress activates the hypothalamic-pituitary-adrenal (HPA) axis, leading to changes in hormone levels that can affect hair follicle function and health. For instance, fluctuations in hormones like androgens, thyroid hormones, and growth hormone under stress can contribute to hair loss. Psychological stress can dysregulate the immune system, potentially triggering autoimmune conditions like alopecia areata, where the immune system attacks hair follicles, leading to patchy hair loss. Stress and psychological distress can also lead to behaviours that indirectly contribute to hair loss. Stress may lead to poor dietary choices, with inadequate intake of essential nutrients required for healthy hair growth, such as proteins, vitamins, and minerals. Stress and anxiety can trigger compulsive behaviours, including trichotillomania, a condition characterised by the urge to pull out one’s hair, leading to noticeable hair loss. Psychological distress can result in neglect of personal grooming and hair care, contributing to conditions that may exacerbate hair loss, such as scalp infections or damage from harsh hair treatments.
Depression can also contribute to hair loss, both directly and indirectly. The physiological effects of depression, including altered neurotransmitter levels and hormonal imbalances, can impact hair growth cycles and overall hair health. Additionally, individuals suffering from depression may experience changes in appetite and nutrition, poor sleep, and reduced motivation for self-care, all of which can adversely affect hair health.
It’s important to note that the relationship between psychological factors and hair loss is bidirectional. Just as psychological stress can contribute to hair loss, experiencing hair loss itself can lead to significant psychological distress, including reduced self-esteem, anxiety, and depression. This can create a vicious cycle where stress and hair loss perpetuate each other.
Incorporating stress reduction practices, such as mindfulness, meditation, exercise, and adequate rest, can help manage stress levels and potentially mitigate its impact on hair health. Counselling or therapy can provide support for individuals dealing with the psychological impact of hair loss, helping them develop coping strategies and improve their mental health. Encouraging a balanced diet, regular exercise, and good sleep hygiene can help improve overall health and potentially support hair health. In some cases, treating underlying psychological conditions with medications or therapy may indirectly benefit hair health.
Psychological factors play a significant role in the causation and exacerbation of alopecia and baldness. Recognising and addressing these factors are essential components of a holistic approach to managing hair loss, underscoring the importance of mental health in dermatological conditions.
HEAVY METALS AND MICROELEMENTS
The role of heavy metals and microelements (trace elements) in hair health and disorders such as alopecia and baldness is a complex and multifaceted area of study. Both deficiencies and excesses of certain metals and microelements can impact hair growth and health, leading to or exacerbating hair loss. Understanding these relationships is crucial for diagnosing and treating various forms of alopecia.
Exposure to certain heavy metals, either through environmental sources, occupational hazards, or dietary intake, can negatively affect hair health and contribute to hair loss.
Chronic exposure to lead can disrupt hormone regulation and damage hair follicles, potentially leading to hair loss. High levels of mercury, often due to consumption of contaminated fish or dental amalgam fillings, can contribute to hair loss by damaging the hair follicles or disrupting protein synthesis. Exposure to arsenic, whether through water or food sources, can cause hair loss, among other health issues, due to its toxicity to organ systems, including the skin and hair follicles. Cadmium exposure can lead to hair loss through its detrimental effects on the kidneys, which play a crucial role in maintaining mineral and hormone balance that affects hair health.
Microelements, or trace elements, are nutrients required by the body in small amounts to perform various physiological functions, including those related to hair growth and health. Imbalances in these elements can lead to hair disorders. Iron deficiency is one of the most common nutritional deficiencies associated with hair loss, particularly in women. Iron is essential for the production of haemoglobin, which helps supply oxygen to hair follicles. Low iron levels can lead to anaemia, reducing oxygen delivery to the follicles and potentially causing hair loss. Zinc plays a crucial role in hair tissue growth and repair. It also helps keep the oil glands around the follicles working properly. Zinc deficiency can lead to hair loss, while excessive zinc levels can also cause hair loss. Selenium is important for the health of the hair, but an imbalance can contribute to hair loss. High levels of selenium can lead to selenosis, a condition that causes brittle hair and nails, and hair loss. Conversely, selenium deficiency can impair hair growth. Copper peptides are known to stimulate hair follicles and can promote hair growth. However, both copper deficiency and toxicity can affect hair health, influencing hair color and strength.
Detoxification from heavy metals, when necessary, often involves chelation therapy or other medical interventions to bind and remove the metals from the body. For microelement imbalances, dietary adjustments, and supplementation under medical guidance can help restore levels to a healthy range and potentially address related hair loss. It’s important for these interventions to be carefully managed to avoid creating imbalances that could lead to further health issues. Heavy metals and microelements have significant roles in the health of hair, with both deficiencies and excesses potentially leading to hair loss.
A high sodium chloride content in the diet even though is not directly linked to causing alopecia or hair loss according to mainstream medical and nutritional research, there are indirect ways in which an excessively high salt diet could potentially influence hair health. A diet high in sodium can lead to increased blood pressure and possibly reduce blood flow to certain areas, including the scalp. Adequate blood flow is essential for delivering nutrients and oxygen to the hair follicles, which are necessary for healthy hair growth. High salt intake can potentially affect the body’s balance of other minerals, such as potassium and magnesium, which play roles in hair health. An imbalance in these and other nutrients might indirectly influence hair growth and health. Excessive salt consumption can lead to dehydration. Proper hydration is crucial for maintaining the health of hair follicles. Dehydration can lead to dry and brittle hair, which may be more prone to breakage, though this is not the same as affecting hair growth directly from the follicle.
Phosphoric acid, commonly found in soft drinks and some processed foods as a flavor enhancer or acidity regulator, doesn’t have a direct, widely recognized role in causing hair loss. One of the concerns regarding high intake of phosphoric acid, particularly from cola beverages, is its potential effect on calcium absorption. There’s some evidence to suggest that high phosphoric acid consumption may lower calcium levels, as it could lead to an imbalance between phosphorus and calcium in the body. Calcium is vital for various bodily functions, including hair growth, as it helps in keratinization and in the formation of hair and nails. The effect of phosphoric acid on hair loss would be indirect. Excessive consumption of phosphoric acid might also affect the body’s acid-base balance. While the body’s buffering systems are highly effective in maintaining pH balance, extremely poor dietary habits that favour high intake of acidic substances over alkaline foods can potentially stress these systems.
Iodine plays a crucial role in the body’s metabolic processes, primarily through its influence on thyroid function. The thyroid gland uses iodine to produce thyroid hormones, which are critical for regulating metabolism, growth, and development. A connection between iodine and hair health exists mainly through the effects of thyroid hormone imbalances on hair growth. An iodine deficiency can lead to hypothyroidism, a condition where the thyroid gland doesn’t produce enough thyroid hormones. Symptoms of hypothyroidism include fatigue, weight gain, cold intolerance, and also hair loss. The hair loss associated with hypothyroidism is typically diffuse, affecting the entire scalp rather than creating bald patches. Beyond just hair loss, hypothyroidism can affect the quality of the hair, making it dry, brittle, and weak. This can further contribute to the appearance of thinning hair. Excessive iodine intake can lead to hyperthyroidism in some individuals, especially those with pre-existing thyroid conditions. Hyperthyroidism is the overproduction of thyroid hormones, which can also cause hair loss, among other symptoms. Excessive iodine consumption can trigger or worsen autoimmune thyroid diseases, such as Hashimoto’s thyroiditis (leading to hypothyroidism) and Graves’ disease (leading to hyperthyroidism). Both conditions can have hair loss as a symptom.
VITAMINS
Vitamins play a crucial role in maintaining overall health, including the health of your hair. Adequate intake of specific vitamins is essential for hair growth, strength, and preventing hair loss. Deficiencies in these vitamins can lead to alopecia (hair loss) and, in severe cases, baldness. Here’s a closer look at the role of various vitamins in hair health and how they influence alopecia and baldness:
Vitamin A is crucial for cell growth, including hair, the fastest growing tissue in the human body. It helps the skin glands produce sebum, an oily substance that moisturises the scalp and helps keep hair healthy. While deficiency in vitamin A can lead to several health issues, including hair loss, excessive intake can also contribute to alopecia. A balanced intake is essential.
B-vitamins, especially Biotin (vitamin B7), are well-known for their role in hair health. Biotin is used as an alternative hair-loss treatment, though it is most effective in those who are deficient. Other B-vitamins, such as B12, help with the formation of red blood cells, which carry oxygen and nutrients to the scalp and hair follicles, a process crucial for hair growth. Deficiencies in B-vitamins can lead to hair loss. For instance, B12 deficiency is often associated with hair loss in vegetarians and vegans who don’t consume enough B12 sources.
Vitamin C is a powerful antioxidant that helps protect against the oxidative stress caused by free radicals. Additionally, it is crucial for collagen production and iron absorption, two factors important for hair health. Deficiency in vitamin C can lead to dry, brittle hair, and eventually hair loss.
Vitamin D’s role in hair production is not fully understood, but receptors in hair follicles suggest its involvement in hair cycle regulation. Low levels of vitamin D are linked to alopecia areata and may be associated with more severe hair loss. Vitamin D deficiency is linked to alopecia areata and may affect hair growth. Supplementation can help improve hair regrowth.
Similar to vitamin C, vitamin E is an antioxidant that can prevent oxidative stress. Studies have shown that people with hair loss experienced an increase in hair growth after supplementing with vitamin E. While deficiency is rare, lacking vitamin E can lead to oxidative stress, potentially exacerbating hair loss.
Though not a vitamin, iron’s role in hair health is closely related to that of vitamins. Iron helps red blood cells carry oxygen to your cells, including hair follicles, essential for hair growth and repair. Iron deficiency, which leads to anemia, is a major cause of hair loss, especially in women.
A balanced diet rich in these vitamins and minerals is essential for maintaining healthy hair and preventing hair loss. While supplementation can help in cases of deficiency, it’s important to consult with a healthcare provider before starting any new supplement regimen, especially since overdosing on certain vitamins (like A and E) can lead to adverse effects, including hair loss. Addressing vitamin deficiencies can significantly contribute to reducing hair loss and promoting hair growth, offering a valuable approach to managing alopecia and baldness.
PHYTOCHEMICALS
Phytochemicals are bioactive chemical compounds found in plants that have various health benefits, including potential roles in preventing and treating hair loss (alopecia) and baldness. These natural compounds can influence hair growth and health through several mechanisms, including anti-inflammatory, antioxidant, and anti-androgenic effects. Research into the role of phytochemicals in hair care is ongoing, but some compounds have shown promise in preliminary studies. Here’s a look at how some phytochemicals may help manage alopecia and baldness:
Polyphenols, found in green tea (especially epigallocatechin gallate or EGCG), berries, and nuts, have antioxidant properties that can help reduce inflammation and combat oxidative stress in hair follicles, potentially promoting hair growth. Green tea polyphenols, for instance, have been shown to stimulate hair growth by prolonging the anagen phase (growth phase) of the hair cycle.
Sulforaphane, a compound found in cruciferous vegetables like broccoli, has been noted for its ability to up-regulate the production of enzymes that protect cells from oxidative stress and DNA damage. It may also have potential benefits for hair growth by improving the detoxification of harmful substances in hair follicles.
Quercetin is a flavonoid present in many fruits, vegetables, and grains. It has strong anti-inflammatory and antioxidant effects. Quercetin can inhibit the production of DHT (dihydrotestosterone), a hormone implicated in androgenetic alopecia, by blocking the enzyme 5-alpha-reductase. It may also protect hair follicles from inflammation and stress.
Curcumin, the active compound in turmeric, has potent anti-inflammatory and antioxidant properties. It can help in treating alopecia, particularly forms driven by inflammatory processes, such as alopecia areata. Curcumin’s ability to suppress inflammatory pathways in the body could help reduce inflammation around hair follicles, potentially preventing hair loss.
Resveratrol, found in grapes, berries, and peanuts, is another polyphenol with anti-inflammatory and antioxidant effects. It has been suggested to promote hair growth by enhancing the proliferation of dermal papilla cells and could protect hair follicles from damage by oxidative stress.
Procyanidin, a class of flavonoids found in apples, cinnamon, and grapes, has been shown to promote hair growth. Specifically, procyanidin B2, found in apple skin, has demonstrated the ability to promote hair growth by transitioning hair follicles from the telogen phase (resting phase) to the anagen phase (growth phase).
While the potential of phytochemicals in treating alopecia and baldness is promising, most of the evidence comes from in vitro studies, animal studies, or small-scale human trials. Therefore, more comprehensive clinical trials are needed to fully understand their effectiveness and safety for hair loss treatment.
It’s also important to note that while dietary intake of these phytochemicals can contribute to overall health, topical formulations or supplements specifically designed to deliver therapeutic doses directly to the scalp or systemically are typically required to see significant effects on hair growth.
Phytochemicals offer a promising, natural approach to managing alopecia and baldness. However, individuals interested in using phytochemical-based treatments should consult healthcare providers or dermatologists to discuss the best approach for their specific situation.
ROLE OF INFECTIOUS DISEASES
Infectious diseases and the immune response they trigger, including the production of antibodies, can play a significant role in causing hair loss (alopecia) and, in some cases, lead to baldness. The relationship between infections, immune responses, and hair loss is complex and can vary depending on the type of infection and the individual’s immune response.
Tinea capitis (scalp ringworm) is a common fungal infection of the scalp, primarily affecting children. It can cause patchy hair loss, scaling, and inflammation. The body’s immune response to the fungus can damage hair follicles, leading to hair loss. Tinea capitis, also known as scalp ringworm, is a fungal infection of the scalp that primarily affects children but can also occur in adults. It’s caused by dermatophytes, which are a type of fungi that can invade and grow in the keratin of the skin, hair, and nails. Tinea capitis can lead to a range of symptoms, including scaling, itching of the scalp, hair loss, and the development of bald patches where the hair breaks off at or just above the scalp. In more severe cases, it can lead to inflammation, redness, and the development of tender areas or sores filled with pus (kerions), which can also contribute to scarring and permanent hair loss if not treated properly. Trichophyton tonsurans is the most common cause of tinea capitis in the United States and many other parts of the world, especially in urban areas. Infections with T. tonsurans are typically characterized by black dot ringworm, where hair breaks off at the scalp surface. Microsporum canis species is more common in Europe and parts of Asia and is often associated with pets, especially cats, as a source of infection. Trichophyton violaceum species is a common cause of tinea capitis in parts of Africa, the Middle East, and India. It tends to cause less inflammatory reactions compared to other species.
Folliculitis, an infection of the hair follicles caused by bacteria (often Staphylococcus aureus), can lead to inflammation and, if severe, scarring and hair loss. The immune system’s response to the bacteria can exacerbate the damage to hair follicles.
While the exact cause of alopecia areata is not fully understood, it is believed to be an autoimmune condition where the immune system mistakenly attacks hair follicles. Some evidence suggests that viral infections could trigger this autoimmune response in genetically predisposed individuals.
Human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS) can cause various dermatological conditions, including hair loss, due to the virus itself or secondary infections that occur as a result of the weakened immune system.
Secondary syphilis can cause a diffuse hair loss known as “syphilitic alopecia,” which can appear as moth-eaten alopecia. The immune response to the Treponema pallidum bacterium can contribute to hair loss, which is often reversible with treatment.
In some cases, infections can trigger an autoimmune response that leads to hair loss. For example, the production of antibodies in response to an infection might cross-react with tissue in the hair follicle, leading to hair loss:
As mentioned, alopecia areata is an autoimmune condition that can be triggered by viral infections. The body produces antibodies against the hair follicles, mistaking them for foreign pathogens.
Systemic lupus erythematosus (SLE) is an autoimmune disease that can cause discoid lesions on the scalp, leading to scarring and permanent hair loss. While not directly caused by infectious agents, infections can exacerbate autoimmune conditions like lupus, potentially leading to episodes of hair loss.
The treatment of hair loss due to infectious diseases and their antibodies primarily involves addressing the underlying infection. Anti-fungal, antibacterial, or antiviral medications can be prescribed depending on the type of infection. For autoimmune conditions like alopecia areata, treatments may include corticosteroids to reduce inflammation and immunotherapy to modulate the immune response.
In conclusion, infectious diseases and the immune response they trigger, including antibody production, can contribute to hair loss through direct damage to hair follicles or through triggering autoimmune responses. Identifying and treating the underlying infection or managing the autoimmune response is crucial for preventing further hair loss and potentially allowing for hair regrowth.
ROLE OF ENVIRONMENTAL FACTORS IN ALOPECIA
Environmental factors play a significant role in the health of hair and can contribute to the development of alopecia (hair loss) and baldness. These factors can exert their effects through direct damage to hair follicles, disruption of hair growth cycles, or indirect mechanisms such as influencing hormonal levels or immune responses.
Understanding the impact of these environmental factors is crucial for developing strategies to prevent and manage hair loss.
Air pollution, including particulate matter (PM), smoke, and gases like sulphur dioxide (SO2) and nitrogen dioxide (NO2), can damage hair follicles. Pollutants can penetrate the scalp and hair, leading to oxidative stress and inflammation that disrupt the normal hair growth cycle and potentially contribute to alopecia.
Excessive exposure to ultraviolet (UV) radiation from the sun can harm the hair and scalp, leading to hair protein degradation and color changes. UV radiation can also weaken the hair, making it more susceptible to breakage and damage. Furthermore, it can induce inflammation in the scalp, contributing to hair loss.
Hard water, which contains high levels of calcium and magnesium, along with chlorine in swimming pools, can make hair dry and brittle, increasing the risk of hair breakage. While there’s limited evidence linking hard water directly to alopecia, it can exacerbate existing scalp conditions and affect hair health.
A diet lacking essential nutrients, vitamins, and minerals can lead to hair loss. For example, deficiencies in iron, zinc, vitamin D, and protein are linked to alopecia.
Environmental stress, including psychological stress from work or personal situations, can trigger telogen effluvium, a condition where hair prematurely enters the telogen (resting) phase and falls out. Chronic stress can also exacerbate autoimmune conditions like alopecia areata.
Smoking tobacco can negatively affect the hair growth cycle by reducing blood flow to the hair follicles, leading to nutrient deprivation. The toxins in cigarette smoke can also damage hair follicles and disrupt hair growth.
Exposure to certain chemicals, such as those found in hair dyes, bleaches, and other hair treatment products, can cause damage to the hair and scalp. These chemicals can lead to allergic reactions, disrupt the natural hair growth cycle, and weaken the hair shaft, leading to hair loss.
Extreme weather conditions, such as high humidity or dry, cold air, can affect hair health. High humidity can lead to frizz and breakage, while dry conditions can make the hair and scalp dry, leading to dandruff and itchiness, which can exacerbate hair shedding.
Environmental factors can significantly impact hair health and contribute to the development of alopecia and baldness. While it’s not always possible to completely avoid these factors, understanding their effects can help in adopting protective measures. These can include using hair products that protect against pollution and UV radiation, ensuring a nutrient-rich diet, managing stress, avoiding harmful chemicals, and quitting smoking. Additionally, individuals experiencing hair loss should consult healthcare providers to explore potential environmental causes and develop effective treatment strategies.
OCCUPATIONAL FACTORS IN ALOPECIA
Occupational factors can significantly contribute to hair loss (alopecia) and baldness due to various hazards present in the workplace. These factors can range from exposure to chemicals and toxins to physical stress and psychological stress, all of which can potentially affect hair health and growth.
Many industries use chemicals that, upon exposure, can lead to hair loss. Workers may be exposed to solvents, metals (like lead and mercury), and other industrial chemicals that can harm the hair follicles or disrupt hormonal balances leading to hair loss. Hairdressers and cosmetologists frequently work with hair dyes, bleaches, and perm solutions containing potentially harmful chemicals like formaldehyde, ammonia, and hydrogen peroxide. Prolonged or unprotected exposure can damage the hair and scalp, causing hair loss.
Jobs that require physical exertion can lead to telogen effluvium, a condition where significant stress on the body pushes more hairs into the resting phase, leading to increased shedding. The physical and psychological stresses experienced by Military Personnel can lead to hair loss. Intense physical training and stress might trigger hair loss in some Athletes.
Jobs with high stress levels can increase the risk of alopecia. Stress is a well-known trigger for several types of hair loss, including telogen effluvium and alopecia areata. Especially in high-stress environments like emergency rooms or during health crises, and high-pressure roles with tight deadlines and performance pressure in Corporate Jobs can lead to stress-induced hair loss.
Occupations that involve the risk of physical injury to the scalp can lead to scarring alopecia, where hair loss is permanent due to scar tissue replacing hair follicles. Workers in the nuclear industry or healthcare professionals who frequently use X-rays may be exposed to radiation that can cause hair loss. Protective measures are crucial in these fields to minimise exposure.
Certain occupations increase the risk of contracting infections that can lead to hair loss. Healthcare Workers exposed to fungal, bacterial, and viral infections can indirectly cause hair loss by affecting the scalp or triggering autoimmune responses.
Working conditions involving extreme weather or temperatures can also affect hair health. Prolonged exposure to sunlight (UV radiation) and pollutants can damage the hair and scalp of Outdoor Workers. Workers in Extremely Cold or Hot Environments can lead to dry, brittle hair or exacerbate conditions like seborrheic dermatitis, contributing to hair loss.
Modern chemical drugs, while designed to treat various medical conditions, can sometimes have side effects, including the causation of alopecia (hair loss) and, in rare cases, contributing to baldness. The impact of these drugs on hair health can vary depending on the type of medication, dosage, duration of treatment, and individual sensitivity.
Chemotherapy drugs used in cancer treatment are well-known for causing significant hair loss, as they target rapidly dividing cells, including those in hair follicles. This type of drug-induced hair loss is often temporary, with hair usually regrowing after the treatment ends, though sometimes with changes in texture or color. Blood thinners, such as warfarin and heparin, have been associated with hair loss. This side effect is relatively rare and may vary with the dose and duration of treatment Oral Contraceptives and Hormone Replacement Therapy (HRT) can cause hair thinning or loss in some women, particularly those with a predisposition to hormonal-related hair loss (androgenetic alopecia). Drugs used for treating prostate enlargement or cancer, like finasteride and dutasteride, can also lead to hair loss, though they are sometimes used to treat hair loss at lower doses. Medications used to control seizures, such as valproic acid and phenytoin, can lead to diffuse hair thinning. Certain drugs used to treat depression and bipolar disorder, including lithium and some selective serotonin reuptake inhibitors (SSRIs), have been linked to hair loss. Blood pressure medications, particularly beta-blockers (e.g., atenolol) and ACE inhibitors (e.g., lisinopril), can cause hair thinning or loss in some individuals. Drugs containing vitamin A derivatives, used for acne and other skin conditions (such as isotretinoin), can cause hair thinning or hair loss. Long-term use of certain NSAIDs can potentially lead to hair loss, although this is relatively uncommon.
According to MIT homeopathy approach of therapeutics, molecular imprints or potentized forms of these above said drugs could be used as therapeutic agents, as molecular imprints of disease-causing molecules can act as artificial binding pockets for them.
The mechanisms by which drugs cause hair loss can include: 1. Anagen Effluvium: Rapid hair loss occurring within days to weeks of drug exposure, affecting hairs in the growth phase. Commonly associated with chemotherapy. 2. Telogen Effluvium: A delay in hair loss until the resting phase of the hair cycle, typically occurring 2-4 months after starting the medication. This is more common with non-chemotherapy drugs and usually results in diffuse thinning that is often reversible. 3. Alteration of Hormonal Balance: Some drugs affect hormonal pathways, leading to hair thinning or loss, particularly in individuals genetically predisposed to hair loss.
In many cases, hair loss due to medication is reversible upon cessation or adjustment of the drug. However, any changes to medication should always be done under the guidance of a healthcare provider to ensure that the primary medical condition continues to be effectively managed.
MIT APPROACH TO THERAPEUTICS OF ALOPECIA AND BALDNESS
DRUG MOLECULES act as therapeutic agents due to their CHEMICAL properties. It is an allopathic action, same way as any allopathic or ayurvedic drug works. They can interact with biological molecules and produce short term or longterm harmful effects, exactly similar to allopathic drugs. Please keep this point in mind when you have a temptation to use mother tinctures, low potencies or biochemical salts which are MOLECULAR drugs.
On the other hand, MOLECULAR IMPRINTS contained in homeopathic drugs potentized above 12 or avogadro limit act as therapeutic agents by working as artificial ligand binds for pathogenic molecules due to their conformational properties by a biological mechanism that is truly homeopathic.
Understanding the fundamental difference between molecular imprinted drugs regarding their biological mechanism of actions, is very important.
MIT or Molecular Imprints Therapeutics refers to a scientific hypothesis that proposes a rational model for biological mechanism of homeopathic therapeutics. According to MIT hypothesis, potentization involves a process of ‘molecular imprinting’, where in the conformational details of individual drug molecules are ‘imprinted or engraved as hydrogen- bonded three-dimensional nano-cavities into a supra-molecular matrix of water and ethyl alcohol, through a process of molecular level ‘host-guest’ interactions. These ‘molecular imprints’ are the active principles of post-avogadro dilutions used as homeopathic drugs. Due to ‘conformational affinity’, molecular imprints can act as ‘artificial key holes or ligand binds’ for the specific drug molecules used for imprinting, and for all pathogenic molecules having functional groups ‘similar’ to those drug molecules. When used as therapeutic agents, molecular imprints selectively bind to the pathogenic molecules having conformational affinity and deactivate them, thereby relieving the biological molecules from the inhibitions or blocks caused by pathogenic molecules.
According to MIT hypothesis, this is the biological mechanism of high dilution therapeutics involved in homeopathic cure. According to MIT hypothesis, ‘Similia Similibus Curentur’ means, diseases expressed through a particular group of symptoms could be cured by ‘molecular imprints’ forms of drug substances, which in ‘molecular’ or crude forms could produce ‘similar’ groups of symptoms in healthy individuals. ‘Similarity’ of drug symptoms and diseases indicates ‘similarity’ of pathological molecular inhibitions caused by drug molecules and pathogenic molecules, which in turn indicates conformational ‘similarity’ of functional groups of drug molecules and pathogenic molecules. Since molecular imprints of ‘similar’ molecules can bind to ‘similar ligand molecules by conformational affinity, they can act as the therapeutics agents when applied as indicated by ‘similarity of symptoms. Nobody in the whole history could so far propose a hypothesis about homeopathy as scientific, rational and perfect as MIT explaining the molecular process involved in potentization, and the biological mechanism involved in ‘similia similibus- curentur, in a way fitting well to modern scientific knowledge system.
If symptoms expressed in a particular disease condition as well as symptoms produced in a healthy individual by a particular drug substance were similar, it means the disease-causing molecules and the drug molecules could bind to same biological targets and produce similar molecular errors, which in turn means both of them have similar functional groups or molecular conformations. This phenomenon of competitive relationship between similar chemical molecules in binding to similar biological targets scientifically explains the fundamental homeopathic principle Similia Similibus Curentur.
Practically, MIT or Molecular Imprints Therapeutics is all about identifying the specific target-ligand ‘key-lock’ mechanism involved in the molecular pathology of the particular disease, procuring the samples of concerned ligand molecules or molecules that can mimic as the ligands by conformational similarity, preparing their molecular imprints through a process of homeopathic potentization upto 30c potency, and using that preparation as therapeutic agent.
Since individual molecular imprints contained in drugs potentized above avogadro limit cannot interact each other or interfere in the normal interactions between biological molecules and their natural ligands, and since they can act only as artificial binding sites for specific pathogenic molecules having conformational affinity, there cannot by any adverse effects or reduction in medicinal effects even if we mix two or more potentized drugs together, or prescribe them simultaneously- they will work.
Based on the detailed analysis of pathophysiology, enzyme kinetics and hormonal interactions involved, MIT approach suggests following molecular imprinted drugs to be included in the therapeutics of ALOPECIA AND BALDNESS:
Dihydrotestosterone 30, Testosterone 30, Trichohyalin 30, Tyrosin related protein 30, ACTH 30, Progesterone 30, Cortisol 30, Thyroidinum 30, Natrum mur 30, Mercurius 30, Arsenic Alb 30, Pumbum Met 30, Cadmium 30, Ferrum met 30, Acid Phos 30, Iodum 30, Sepia 30, Trichophyton 30, Staphylococcin 30, Trepanoma Pallidum (Syphilinum) 30, Tenia versicolor 30, Hydrogen peroxide 30, Tobacco smoke 30,
REFERENCES:
1. Sinclair, R. (2019). “Alopecia: Classification and pathophysiology.” Journal of Dermatological Science, 96(1), 2-8. This article provides a detailed classification of hair loss types and their pathophysiological mechanisms.
2. Paus, R., & Cotsarelis, G. (1999). “The biology of hair follicles.” The New England Journal of Medicine, 341(7), 491-497. Offers an in-depth look at hair follicle biology and its implications for understanding hair growth and alopecia.
3. Hamilton, J.B. (1951). “Patterned loss of hair in man; types and incidence.” Annals of the New York Academy of Sciences, 53(3), 708-728. Classic study on the genetics and patterns of male pattern baldness.
4. Sawaya, M.E., & Price, V.H. (1997). “Different levels of 5α-reductase type I and II, aromatase, and androgen receptor in hair follicles of women and men with androgenetic alopecia.” Journal of Investigative Dermatology, 109(3), 296-300. Discusses the role of hormones and enzymes in androgenetic alopecia.
5. Trüeb, R.M. (2003). “Association between smoking and hair loss: another opportunity for health education against smoking?” Dermatology, 206(3), 189-191. Explores the link between smoking and increased risk of hair loss.
6. Aoi, N., Inoue, K., Chikanishi, T., et al. (2012). “1α,25-Dihydroxyvitamin D3 modulates the hair-inductive capacity of dermal papilla cells: Therapeutic potential for hair regeneration.” Stem Cells Translational Medicine, 1(8), 615-626. Investigates the role of vitamin D in hair follicle function and potential therapies.
7. Hunt, N., & McHale, S. (2005). “The psychological impact of alopecia.” British Medical Journal, 331(7522), 951-953. A comprehensive review of the psychosocial aspects of living with hair loss.
8. Mysore, V., Shashikumar, B.M. (2016). “Guidelines on the use of finasteride in androgenetic alopecia.” Indian Journal of Dermatology, Venereology, and Leprology, 82(2), 128-134. Guidelines for the use of finasteride in the treatment of hair loss.
9. Avci, P., Gupta, G.K., Clark, J., Wikonkal, N., Hamblin, M.R. (2014). “Low-level laser (light) therapy (LLLT) for treatment of hair loss.” Lasers in Surgery and Medicine, 46(2), 144-151. Reviews the evidence for low-level laser therapy as a treatment for alopecia.
10. Fukuoka, H., Suga, H. (2015). “Hair regeneration treatment using adipose-derived stem cell conditioned medium: Follow-up with trichograms.” Eplasty, 15, e10. An examination of novel treatments for hair loss using stem cell-derived factors.
11. Sinclair, R.D., Jolley, D., Mallari, R., Magee, J. (2004). “The reliability of horizontally sectioned scalp biopsies in the diagnosis of chronic diffuse alopecia
12. Chandran Nambiar KC, www.redefininghomeopathy.com, Fedarin Mialbs,Kannur, Kerala
13. JH Clarke, A Dictionary of homeopathic materia medica
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