Natural androgenetic alopecia treatment & Etiology of Male Pattern Baldness.
Studies show that men who experience advanced balding under the age of 35 tend to have high blood insulin levels. Additionally, there is a strong prevalence of insulin resistance with androgenetic alopecia.Lancet. 2000 Sep 30;356(9236):1165-6.
Chronic elevations of insulin result in increased circulating levels of Insulin Growth Factor-1 (IGF-1) and lower levels of Insulin like growth factor binding protein 3 (IGFBP-3).When we eat, our blood sugar is suppose to rise, yet when we eat foods that are high glycemic, more insulin is needed to convert sugar into fat (Triglycerides). Higher and higher blood sugar levels, due to chronic ingestion of high glycemic foods could lead to insulin resistance. A few very notable studies have shown correlations between insulin resistance and balding, as well as heart disease, which is also "positively" associated with insulin resistance.
The higher our triglyceride count is, the more of a fatty build-up occurs in the liver, hence the more of a prevalence of high triglycerides in the blood. High density lipoprotein (HDL), also known as the "good" cholesterol carrys triglycerides in the blood to the liver. If it exhibits this action frequently, your HDL levels will be low as a result. One of the functions of the liver is to remove insulin from the bloodstream. However the more triglycerides carried to the liver via HDL (leading up to a fatty liver) the less efficient the liver is at removing the insulin from the blood stream.
As a result, the pancreas has to release more insulin to lower the blood sugar, hence triglyceride levels go up, the livers fatty deposits build up, more insulin is needed, which acts on the fat cells (called adipocyte differentiation) and the brain as a feedback loop to make you crave more insulin producing foods.
Chronically elevated glucose levels lead to increased cortisol release and a cascade of inflammatory cytokines, a rise in Reactive Oxygen Species (ROS) which has been shown to be elevated in balding dermal papilla cells.
Hair follicle regeneration are dependent upon a complex series of cross-talks involving cytokines from dermal papilla cells via paracrine and autocrine mechanisms. These are mitogenic substances influenced by way of hormonal signaling.
British Journal of Dermatology Volume 154 Page 609 - April 2006
Lowering your insulin isn't everything, yet it is fundamental for everything else you do. Insulin, as a matter of speaking is the "hormone of death." A study on mice revealed an interesting finding. Genetically altered mice rendered in a manner that allowed their fat cells to be unresponsive to insulin, ate as much food as they desired. Despite that, they remained thin. While they actually consumed 55 percent more food than the control mice, they had 70 percent less body fat than the control group. Additionally, the genetically altered mice lived 18 percent longer than the control mice. This study shows control of insulin is probably why calorie restriction helps with life extension. However, it is the insulin control that is important, not necessarily the the amount of food consumed. Insulin release is stimulated in response to grain, starch and sugar consumption.
Extended Longevity in Mice Lacking the Insulin Receptor in Adipose Tissue
According the results, published in the journal Nature, higher levels of reactive oxygen species (ROS) set off resistance, while low levels of reactive oxygen species decrease insulin resistance significantly.
Nature. 2006 Apr 13;440(7086):944-8.
While oxidative stress leaves our hair subject to accelerated loss, it is also involved in the process of graying follicles. Melanocytes, which are responsible for the pigmentation of hair, go through a rapid cell death (apoptosis), particularly in the aging human hair follicle. As oxidative stress increases, melanocytes eventually die off, leaving no pigmentation left.
The FASEB Journal 2006;20:1567-1569.
A multitude of insulin resistance related conditions are greatly helped by anti-oxidant therapy. One of the most important antioxidants is Lipoic acid.
The value of Lipoic Acid.
Lipoic acid, also known as Alpha Lipoic acid is a lipid (fat) and water soluble anti-oxidant. Lipoic acid boosts the body's endogenous anti-oxidants like Superoxide Dismutase (SOD) & Glutathione, it also increases the bioavailability of exogenous (outside the body) anti-oxidants like vitamins C & E. Lipoic acid recycles and acts as a carrier or transport for anti-oxidant protection into the mitochondria (cell factory engine).
Lipoic acid offers strong protection against oxidative stress, and not only reactivates vitamins C & E, but regenerates Co-enzyme Q10. Besides these benefits of anti-oxidant protection on multiplicity of actions, the main benefit of Lipoic acid is its effect on glucose metabolism.
Ukr Biokhim Zh. 2005 May-Jun;77(3):20-6.
The role elevated glucose levels play in the body is highly detrimental to health and hair loss. Lipoic acid boosts mitochondrial production of Superoxide Dismutase (SOD) and serves as a protectant against decreased microvascular profusion, which would otherwise deprive oxygen transport along tiny endothelial passages.
Invest Ophthalmol Vis Sci. 2006 Apr;47(4):1594-9.
Lipoic acid acts as an insulin mimic, increases glucose transport through muscle cells and reduces glycation. The combination of Lipoic acid and Acetyl L-Carnitine has been shown to reverse neurogenerative deficits in aged rats back to near normalcy. The list of attributes is seemingly endless.
While insulin resistance is a driving force of male pattern baldness, the underlying cause maybe thyroid problems, and or hypothyroidism.
Thyroid problems, both hypothyroid and hyperthyroid are epidemically undiagnosed. This is because the standard thyroid test, known as thyroid stimulating hormone (TSH) is not a reliable indication of thyroid status, except in advanced cases. The reason is due to thyroid hormone resistance, in which tissues are insensitive to thyroid hormone.
Under performing thyroid is strongly correlated with elevated Lipoprotein(a) which is not only linked with androgenetic alopecia, but appears to be linked with Dickkopf-related protein 1 (DKK-1), a gene that is significantly upregulated in balding scalps.
Both insufficient and excess levels of thyroid hormones T3 and/or T4 can result in hair loss. For example, T4 prolongs the duration of the hair growth phase (anagen) possibly due to the down-regulation of TGF-beta2.
J Clin Endocrinol Metab. 2008 Nov;93(11):4381-8.
Neurotrophins, including nerve growth factor (NGF) and brain-derived-neurotrophic factor (BDNF) are involved in human hair growth control. Therefore, neurotrophins effectors may be of good use with some unexplained types of hair loss, such as telegen effluvium. The role of neurotrophin agonists and antagonists have paradoxical actions dependent on their application, some increase anagen, while others induce catagen stages. Topical capsiacin increases facial skin elasticity and promotes hair growth by increasing dermal insulin-like growth factor-I (IGF-I) production through activation of sensory neurons.
Prog Brain Res. 2004;146:493-513.
Growth Horm IGF Res. 2008 Aug;18(4):335-44.
However, Capsiacin has been found to induce early catagen (sleep phase) and promote the miniaturization of the hair follicle in a dose-dependent manner by activation of the transient receptor potential vanilloid-1 receptor, (TRPV1).
(American Journal of Pathology. 2005;166:985-998.)
Fortunately, the inflammation caused from neurotrophins can be thwarted by a combination of Curcumin and Resveratrol. This is achieved by selectively blocking the CB1 receptor (Cannanbinoid), which is a significant regulator of hair growth.
J Pharmacol Exp Ther. 2009 Jul;330(1):31-9.
Bioorg Med Chem Lett. 2009 May 1;19(9):2546-50.
Elevated reactive oxygen species are involved in the pathogenesis of sebaceous gland hyperplasia in male pattern baldness. Antioxidant therapy is essential to blunt these free radicals in scalp follicles.
J Invest Dermatol. 1996 Aug;107(2):154-8.
A cytokine known as Transforming growth factor (TGF) has been found to suppress the growth of dermal papilla cells, while Basic fibroflast growth factor (bFGF) and platelet-derived growth factor (PDGF) act as proliferators of hair follicle cells.
J. Cell Physiol 1992 Apr;151(1):41-9.
More recent evidence shows that Transforming growth factor-beta1 (TFG-beta1) has been implicated as one of the paracrine mediators induced by androgens causing male pattern baldness.
J Investig Dermatol Symp Proc. 2005 Dec;10(3):209-11.
Transforming growth factor-beta1 (TFG-beta1) stimulates production of Gelatinase B, also known as Metalloproteinase 9 (MMP-9)
Biochem Biophys Res Commun. 2002 Aug 16;296(2):267-73.
In addition to protecting mitochrondrial DNA, Lipoic acid inhibits Matrix Metalloproteinase-9 (MMP-9) a collagen enzyme that induces apoptosis in the hair bulb.
Can J Physiol Pharmacol. 2005 Mar;83(3):301-8.
The value of Ecklonia Cava (Seanol).
The most powerful inhibitor of Matrix Metalloproteinase-9 (MMP-9) is a brown algae-based polyphenol, called Ecklonia Cava. It is a brown algae which grows at a depth of about 100 feet. Seanol is effectively extracted from Ecklonia Cava and has an interconnected phenolic ring structure capable of trapping ten to 100 times the free radicals of either Green tea and Resveratrol extracts.
Life Sci. 2006 Sep 5;79(15):1436-43.
Ecklonia Cava is also known as a phlorotannin and is 40% fat soluble, this means it acts as both a water and fat soluble anti-oxidant. Ecklonia cava is by far the most versatile supplement I've ever discovered to treat hair loss. Besides it potent inhibition of MMP-9, it effects a whole array of systems.
While it is widely thought that Dihydrotestosterone (DHT) via 5-alpha-reductase enzyme is soley responsible for androgenetic alopecia (AGA) or male-pattern baldness. The theory of 5-alpha-reductase inhibition is far from replete. 5-alpha-reductase is relentlessly targeted for enlarged prostate (BPH) and androgenetic hair loss, yet there are many other mitogenic substances with strong influence.
Przegl Lek. 2005;62(9):908-15.
Isoenzymes such as 17beta-hydroxysteriod dehydrogenase (17beta-HSD) and 5-alpha-reductase are key mediators in the pathogenesis of AGA. Thus (17beta-HSD) has been largely ignored.
The 17beta-HSD type 1 enzyme (17beta-HSD1) converts estrone to estradiol, which is adversely expressed in estrogenic based cancers (i.e., prostate and breast). Moreover, 17beta-hydroxysteriod dehydrogenase is responsible for increases in androstenedione from testosterone.
Simply put, androstenedione equals hair loss. Pro-hormones in general equate to increased hair loss. Reducing endogenous androstenedione conversion from testosterone by way of inhibiting 17beta-hydroxysteriod dehydrogenase is a significant piece to the hair loss puzzle.
Androstenedione presents a problem. Several studies have elucidated the effects of androstenedione supplementation in younger males. Increases in testosterone were negligible, yet supplementation of androstenedione produced significant increases in estrone (E1) and estradiol (E2). Conversely, women experienced significant increases in testosterone.
Estrogen is the enemy, testosterone is your ally. Estrogen increases in men accompany a series of adverse side-effects; namely, gynecomastia (breast enlargement), testicular shrinkage, loss of libido, glucose intolerance (impaired blood sugar metabolism) and acne.
A number of factors increase endogenous estrogen increases in the male. The largest influence is of a dietary nature, excess starches and sugars, which lead to insulin resistance. The problem with insulin resistance is a simple one, a strong prevalence in the narrowing of micro vascular tissue creating a significant lack of circulation. This basically a thickening of smooth muscle of the endothelium, the same mechanism seen in cardiovascular disease.
Men with sub-normal levels of Sex Hormone Binding Globulin (SHBG) have increased exposure to circulating androgens, augmenting hormonal exposure to receptor sites.
Lower levels SHBG has been found to be inversely correlated with insulin resistance. In other words, high insulin levels due to poor blood sugar metabolism are usually associated with sub-normal levels of SHBG. Predominate dietary consumption of sugars and starches not only encourage insulin resistance and impaired blood glucose levels, but elevate DHT levels.
Endocr Regul. 2005 Dec;39(4):127-31.
Men at earlier ages who suffer from Androgenetic Alopecia (AGA) have lower circulating SHBG (Sex Hormone Binding Globulin), and in some a higher free androgen index (FAI). Elevated testosterone for example, causes SHBG synthesis to decrease, whereas high estrogen stimulates SHBG production. Older men have ever increasing levels of SHBG and as a consequence their estrogen levels rise instructing prostate tissue to follow suit.
Cancer Epidemiology Biomarkers & Prevention Vol. 10, 25-33, January 2001
A diet higher in protein and Omega-3 fatty acids, very low in starches and sugars will help lower DHT levels and improve blood sugar metabolism. Improving glucose metabolism is essential if hair loss is advanced or premature. Avoidance in sugars and starches is critical to that end.
Nutrition & Metabolism 2005, 2:34
Improving glucose metabolism through diet and supplementation of vitamins, vitamin catalysts, minerals, amino acids, essential fatty acids, and antioxidants will help normalize regulation of SHBG synthesis. This is such the case whether SHBG levels are too high or too low.
The value of Magnesium
The most critically underutilized mineral is Magnesium. Approximately 70% of United States and the West have diets containing less than the recommended 400 mg of magnesium per day and up to 20% have diets with less than one-half the recommended intake. Increased stress only builds up further worsening magnesium deficiency, with health issues such as depression and cardiovascular disease resulting. Magnesium deficiency symptoms are non-specific due to its necessity in over 325 enzymes.
Depletion of Magnesium has been found to accelerate the aging process. I believe the use of Magnesium is as important as Omega 3 fatty acid intake. Most in the medical field advocate the use of calcium, yet calcium is mishandled by the body when there a shortage of Magnesium. Many packaged foods fortified with some vitamins and minerals, but no amounts of Magnesium whatsoever. Insulin resistance is accelerated with a deficiency of Magnesium and the condition itself actually increases its excretion.
A Magnesium deficiency promotes inflammation of the skin.
Br J Dermatol. 2000 Apr;142(4):669-79.
Food stuffs that produce Enterolactone are a natural defense against the enzyme 17beta-hydroxysteriod dehydrogenase, the catalyst for androstenedione. Enterolactone also inhibits aromatase, which is necessary for estrogen synthesis.
J Steroid Biochem Mol Biol. 2005 Apr;94(5):461-7. Epub 2005 Mar 16.
Sesamin, a lignan of the sesame seed like flax seed is also an enterolactone precursor. The data supporting flax seed hull extract is considerably heavier.
J Nutr. 2006 Apr;136(4):906-12.
From the knots of the spruce tree is a lignan known as 7-Hydroxymatairesinol (7-HMR) is yet another enterolactone precursor. The most efficient way to increase blood levels of enterolactone. Unlike flax seed hull sources (SDG), spruce lignans or 7-HMR is metabolized quickly and remains in the serum for up to 24-hours.
Eur J Cancer Prev. 2002 Aug;11 Suppl 2:S48-57.
Drugs like finasteride were first touted for their effects on enlarged prostate, yet raising enterolactone levels has been found to be just as effective when compared to alpha adrenoceptor blockers and 5-alpha-reductase inhibitorsAnother ally in the fight against MPB is Green tea polyphenols or Catechins and their Galates, which offer reduced expression of the Matrix Metalloproteinase’s (MMP)-2 and MMP-9. Various pro-inflammatory cytokines induce the expression of theses maxtrix metalloproteinase's within the epithelial compartment of the hair bulb. However, Seanol from Ecklonia cava is significantly more potent. Nevertheless, Green tea polyphenols are excellent for immune health.
Int J Dermatol. 2001 Jun;40(6):385-92.
Certain green tea gallates can regulate androgen action in target tissues, reducing the oxidative and androgen induced apoptosis (programmed cell death) of the hair follicle. Induced up regulation of MMP-9 in the lower epithelial compartment of the human hair bulb is a major mechanism through which hair follicle involution (miniaturization) alopecia occurs.
Cytokine and epidermal growth factor receptor (EGFR) exhibits negative growth effects on certain carcinomas as well as hair follicle cells. Epigallocatechin-3-gallate (EGCG), the principal polyphenol in green tea, has been shown to inhibit the growth of many cancer cell lines and to suppress the phosphorylation of epidermal growth factor receptor (EGFR). Flax seed lignans also offer this protection.
Nutr Cancer 2002;43(2):187-92.
Vertex balding has strong associations with cardiovascular disease, addressing all factors in its pathogenesis will also help hair loss. Ecklonia Cava, Magnesium, Omega-3 fatty acids, and Enterolactone precursors will make significant, positive shifts in physiological health.
Hyperprolactinemia generally occurs in celiac disease, type 1 diabetes mellitus (type II), autoimmune diseases, as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) and organ-specific autoimmune diseases, Addison's disease, autoimmune thyroid diseases, etc.
Adrenal androgen production is increased by prolactin. The use of dopamine agonists can modulate elevated prolactin levels in hyperandrogenic patients.
J Reprod Med. 2001 Jul;46(7):678-84.
Chasteberry is an effective dopamine agonist.
Chasteberry (Vitex agnus-castus) in a dose dependent manner, decreases prolactin levels by way of dopaminergic effects. This is due to the inhibition of basal and thyotropin releasing hormone (TRH) stimulated prolactin release.