Hair loss & Thin hair

Most common types


Getting to the ROOT Cause of your hair loss is key. You can try all the creams, oils, shampoos, etc - which are basically band aids to the issue. And often, they do NOTHING and you waste your money.

You need to find out WHY and WHAT is causing your hair loss. Extensive laboratory testing will give you a good picture of what your health issue is. Once we determine the reason for your hair loss, we work to get on you on a customized nutrition protocol coupled with a supplement regime that helps to get the infection/parasite/pathogen OUT of your body. Once we get that out, we can work to add the RIGHT nutrition back INTO your body so your can actually absorb the nutrition, vitamins and minerals in your CELLS so that your body can begin to work as it is supposed to. The goal is NOT to keep you on supplements - but rather feed your body while it detoxes, repairs and rebuilds itself. Once you are working at an optimal level, you decide if you want to continue adding supplements or get your nutrition from the right foods. I work with you to educate you on all this and why and how you do this.

Telogen Effluvium      What is telogen effluvium?     Increased shedding or thinning of a person's hair is characteristic of telogen effluvium.   A person is described as having chronic telogen effluvium if they frequently experience periods of hair shedding for more than  6 months . Telogen effluvium is generally reversible.  A person with this condition does not lose all their hair, although it may become noticeably thin.  Telogen effluvium is a form of hair loss characterized by hair thinning or an increase in hair shedding. It occurs  more often  in women and is usually triggered by a disturbance to the hair cycle.  The hair cycle typically has three phases:   Anagen = growth phase    Catagen = transitional phase    Telogen = resting phase   Telogen effluvium is associated with the telogen phase. Normally,  5 to 10 percent  of a person's hair is in the telogen phase at any one time.  With telogen effluvium, the anagen phase slows down, meaning that fewer hairs enter the next two stages. With this condition, around  30 percent of hair follicles  move into the telogen phase, which means that hair shedding occurs.     *Source: Medical News Today       Abstract    Telogen effluvium was first described by Kligman in 1961. It is a most common cause of diffuse hair loss. Women with telogen effluvium more frequently present to dermatologist. A wide variety of potential triggers have been implicated in the pathogenesis of telogen effluvium. Diffuse shedding of telogen hair are seen after 3-4 months of triggering event. The observation of increased telogen hair shedding does not infer a cause. Establishing aetiology of telogen effluvium requires elicitation of relevant history and appropriate laboratory investigations to exclude endocrine, nutritional and autoimmune disorders.     *Source: NCBI, PubMed.gov

Telogen Effluvium

What is telogen effluvium?

Increased shedding or thinning of a person's hair is characteristic of telogen effluvium.

A person is described as having chronic telogen effluvium if they frequently experience periods of hair shedding for more than 6 months. Telogen effluvium is generally reversible.

A person with this condition does not lose all their hair, although it may become noticeably thin.

Telogen effluvium is a form of hair loss characterized by hair thinning or an increase in hair shedding. It occurs more often in women and is usually triggered by a disturbance to the hair cycle.

The hair cycle typically has three phases:

Anagen = growth phase

Catagen = transitional phase

Telogen = resting phase

Telogen effluvium is associated with the telogen phase. Normally, 5 to 10 percent of a person's hair is in the telogen phase at any one time.

With telogen effluvium, the anagen phase slows down, meaning that fewer hairs enter the next two stages. With this condition, around 30 percent of hair follicles move into the telogen phase, which means that hair shedding occurs.

*Source: Medical News Today

Abstract

Telogen effluvium was first described by Kligman in 1961. It is a most common cause of diffuse hair loss. Women with telogen effluvium more frequently present to dermatologist. A wide variety of potential triggers have been implicated in the pathogenesis of telogen effluvium. Diffuse shedding of telogen hair are seen after 3-4 months of triggering event. The observation of increased telogen hair shedding does not infer a cause. Establishing aetiology of telogen effluvium requires elicitation of relevant history and appropriate laboratory investigations to exclude endocrine, nutritional and autoimmune disorders.

*Source: NCBI, PubMed.gov

Alopecia Areata    Alopecia areata is an autoimmune disorder characterized by transient, non-scarring hair loss and preservation of the hair follicle. Hair loss can take many forms ranging from loss in well-defined patches to diffuse or total hair loss, which can affect all hair-bearing sites. Patchy alopecia areata affecting the scalp is the most common type. Alopecia areata affects nearly 2% of the general population at some point during their lifetime. Skin biopsies of affected skin show a lymphocytic infiltrate in and around the bulb or the lower part of the hair follicle in the anagen (hair growth) phase. A breakdown of immune privilege of the hair follicle is thought to be an important driver of alopecia areata. Genetic studies in patients and mouse models have shown that alopecia areata is a complex, polygenic disease. Several genetic susceptibility loci were identified to be associated with signalling pathways that are important to hair follicle cycling and development. Alopecia areata is usually diagnosed based on clinical manifestations, but dermoscopy and histopathology can be helpful. Alopecia areata is difficult to manage medically, but recent advances in understanding the molecular mechanisms have revealed new treatments and the possibility of remission in the near future.     *Source: NCBI, Pubmed.gov

Alopecia Areata

Alopecia areata is an autoimmune disorder characterized by transient, non-scarring hair loss and preservation of the hair follicle. Hair loss can take many forms ranging from loss in well-defined patches to diffuse or total hair loss, which can affect all hair-bearing sites. Patchy alopecia areata affecting the scalp is the most common type. Alopecia areata affects nearly 2% of the general population at some point during their lifetime. Skin biopsies of affected skin show a lymphocytic infiltrate in and around the bulb or the lower part of the hair follicle in the anagen (hair growth) phase. A breakdown of immune privilege of the hair follicle is thought to be an important driver of alopecia areata. Genetic studies in patients and mouse models have shown that alopecia areata is a complex, polygenic disease. Several genetic susceptibility loci were identified to be associated with signalling pathways that are important to hair follicle cycling and development. Alopecia areata is usually diagnosed based on clinical manifestations, but dermoscopy and histopathology can be helpful. Alopecia areata is difficult to manage medically, but recent advances in understanding the molecular mechanisms have revealed new treatments and the possibility of remission in the near future.

*Source: NCBI, Pubmed.gov

Anagen Effluvium    Anagen effluvium is the abrupt loss of hairs that are in their growing phase (anagen) due to an event that impairs the mitotic or metabolic activity of hair follicle. Chemotherapy, radiation and toxic chemicals, and sometimes inflammatory diseases like alopecia areata and pemphigus are also capable of diminishing the metabolic activity of hair follicles resulting in anagen hair loss. Although it is reversible, and hair regrowth occurs after a delay of 1-3 months; sometimes it can lead to permanent alopecia and can be psychologically devastating with negative impact on individual perceptions of appearance, body image, sexuality, and self-esteem.     *Source: NCBI, Pubmed.gov

Anagen Effluvium

Anagen effluvium is the abrupt loss of hairs that are in their growing phase (anagen) due to an event that impairs the mitotic or metabolic activity of hair follicle. Chemotherapy, radiation and toxic chemicals, and sometimes inflammatory diseases like alopecia areata and pemphigus are also capable of diminishing the metabolic activity of hair follicles resulting in anagen hair loss. Although it is reversible, and hair regrowth occurs after a delay of 1-3 months; sometimes it can lead to permanent alopecia and can be psychologically devastating with negative impact on individual perceptions of appearance, body image, sexuality, and self-esteem.

*Source: NCBI, Pubmed.gov


Breakdown of immune privilege in alopecia areata     a ) Immune privilege of the hair follicle can be achieved through several strategies including: down regulation of MHC class I and β2 microglobulin, which normally stimulate natural killer (NK) cells; local production of immunosuppressants; expression of immunoinhibitory signals (for example, CD200; also known as OX2 membrane glycoprotein); and repression of intrafollicular antigen-presenting cell (APC), perifollicular NK cell and mast cell functions owing to increased levels of macrophage migration inhibitory factor (MIF). Vasoactive intestinal peptide (VIP), released by perifollicular sensory nerve fibers, is also believed to be an immunoinhibitory neuropeptide that might have a role in immune privilege.  b ) Late anagen hair follicles in patients with alopecia areata have perifollicular infiltrations of APCs, CD4+ and CD8+ T cells, and abnormal expression of MHC class I and II molecules. CD8+ T cells also infiltrate into the hair follicle root sheaths. Molecules involved in the lymphocyte co-stimulatory cascade are involved in the pathogenesis of alopecia area and provide targets for therapeutic intervention. No inflammatory cells are found in the surrounding of nomal follicles in late anagen phase. INFγ, interferon gamma; IFNγR, interferon gamma receptor; IL2RB, IL2 receptor subunit beta; IL15RA, IL15 receptor subunit alpha; JAK, Janus kinase; NKG2D, NK cell receptor D; NKG2DL, NKG2D ligand; P, phosphorylated; POMC, pro-opiomelanocortin; STAT1, signal transducer and activator of transcription 1; TCR, T cell receptor; TGFB, transforming growth factor beta, VIPR, VIP receptor.

Breakdown of immune privilege in alopecia areata

a) Immune privilege of the hair follicle can be achieved through several strategies including: down regulation of MHC class I and β2 microglobulin, which normally stimulate natural killer (NK) cells; local production of immunosuppressants; expression of immunoinhibitory signals (for example, CD200; also known as OX2 membrane glycoprotein); and repression of intrafollicular antigen-presenting cell (APC), perifollicular NK cell and mast cell functions owing to increased levels of macrophage migration inhibitory factor (MIF). Vasoactive intestinal peptide (VIP), released by perifollicular sensory nerve fibers, is also believed to be an immunoinhibitory neuropeptide that might have a role in immune privilege. b) Late anagen hair follicles in patients with alopecia areata have perifollicular infiltrations of APCs, CD4+ and CD8+ T cells, and abnormal expression of MHC class I and II molecules. CD8+ T cells also infiltrate into the hair follicle root sheaths. Molecules involved in the lymphocyte co-stimulatory cascade are involved in the pathogenesis of alopecia area and provide targets for therapeutic intervention. No inflammatory cells are found in the surrounding of nomal follicles in late anagen phase. INFγ, interferon gamma; IFNγR, interferon gamma receptor; IL2RB, IL2 receptor subunit beta; IL15RA, IL15 receptor subunit alpha; JAK, Janus kinase; NKG2D, NK cell receptor D; NKG2DL, NKG2D ligand; P, phosphorylated; POMC, pro-opiomelanocortin; STAT1, signal transducer and activator of transcription 1; TCR, T cell receptor; TGFB, transforming growth factor beta, VIPR, VIP receptor.