Natural androgenetic alopecia treatment & Etiology of Male Pattern Baldness.
What causes hair loss? In short, an imbalance in the thyroid and/or the hypothalamic-pituitary-adrenal-gonadotropic axis.
How does it become imbalanced? Stress, environmental pollutants, heavy metals, lack of bio-available minerals, excess storage of toxins.
Are there other factors involved? Yes, however they are too numerous to mention, everyone is different.
The following are abstracts and well as excerpts from some of my writings over the years on hair loss.
Sci Transl Med. 2012 Mar 21;4(126):126ra34.
Prostaglandin D2 Inhibits Hair Growth and Is Elevated in Bald Scalp of Men with Androgenetic Alopecia.
Testosterone is necessary for the development of male pattern baldness, known as androgenetic alopecia (AGA); yet, the mechanisms for decreased hair growth in this disorder are unclear. We show that prostaglandin D(2) synthase (PTGDS) is elevated at the mRNA and protein levels in bald scalp compared to haired scalp of men with AGA. The product of PTGDS enzyme activity, prostaglandin D(2) (PGD(2)), is similarly elevated in bald scalp. During normal follicle cycling in mice, Ptgds and PGD(2) levels increase immediately preceding the regression phase, suggesting an inhibitory effect on hair growth. We show that PGD(2) inhibits hair growth in explanted human hair follicles and when applied topically to mice. Hair growth inhibition requires the PGD(2) receptor G protein (heterotrimeric guanine nucleotide)-coupled receptor 44 (GPR44), but not the PGD(2) receptor 1 (PTGDR). Furthermore, we find that a transgenic mouse, K14-Ptgs2, which targets prostaglandin-endoperoxide synthase 2 expression to the skin, demonstrates elevated levels of PGD(2) in the skin and develops alopecia, follicular miniaturization, and sebaceous gland hyperplasia, which are all hallmarks of human AGA. These results define PGD(2) as an inhibitor of hair growth in AGA and suggest the PGD(2)-GPR44 pathway as a potential target for treatment.
Dermatol Surg. 2012 Mar 8. doi: 10.1111/j.1524-4725.2012.02378.x.
Caspase-1 Level Is Higher in the Scalp in Androgenetic Alopecia.
Inflammasomes that activate caspase-1 govern the innate immune inflammatory response. In vitro studies of human keratinocytes were conducted to establish effects of finasteride, dihydrotestosterone (DHT), and testosterone on caspase-1 levels using immunoblot Caspase-1 is expressed in normal human adult epidermal keratinocytes. Caspase-1 expression is greater in men with AGA.
Ecklonia Cava can help manage inflammatory response along with normalizing thyroid function.
Exp Dermatol. 2012 Mar;21(3):223-6. doi: 10.1111/j.1600-0625.2011.01432.x.
Calcitonin gene-related peptide (CGRP) may award relative protection from interferon-„-induced collapse of human hair follicle immune privilege.
Interferon-„ (IFN„)-induced collapse of hair follicle (HF) immune privilege (IP) is a key element in the pathogenesis of alopecia areata. In this pilot study, we investigated whether the immunosuppressive neuropeptide, calcitonin gene-related peptide (CGRP), can protect from and/or restore IFN„-induced HF-IP collapse. After showing that human scalp HFs express CGRP receptor-like receptor (CRLR) immunoreactivity, anagen HFs were cultured in the presence of IFN„, with CGRP added before or after. Adding CGRP after IFN„ administration ('restoration assay') failed to downregulate IFN„-induced ectopic MHC class I expression, while MHC class II expression was reduced. However, administering CGRP before IFN„ application ('protection assay') significantly reduced the IFN„-induced overexpression and ectopic expression of MHC class I and II and reduced the increased degranulation of perifollicular mast cells induced by IFN„. This suggests that CGRP may not restore HF-IP once it has collapsed, but may protect it from collapsing. Therefore, CRLR stimulation might help to retard AA progression.
Revisiting Important Findings - Implications for De novo Hair Growth
The following is the mechanism required to stimulate a variety of factors to stimulate new hair growth. Most notably Platelet-derived growth factor (PDGF) and VEGF.
That mechanism is short-term hypoxia (without oxygen), which stimulates a production of factors which will help further the factors (cytokines) necessary to facilitate better oxygen transport to the dermal papilla.
Biomed Res. 2010 Feb;31(1):27-34.
Hair growth stimulated by conditioned medium of adipose-derived stem cells is enhanced by hypoxia: evidence of increased growth factor secretion.
Adipose-derived stem cells (ADSCs) and their secretomes mediate diverse skin-regeneration effects, such as wound-healing and antioxidant protection, that are enhanced by hypoxia. We investigated the hair-growth-promoting effect of conditioned medium (CM) of ADSCs to determine if ADSCs and their secretomes regenerate hair and if hypoxia enhances hair regeneration. If so, we wanted to identify the factors responsible for hypoxia-enhanced hair-regeneration. We found that ADSC-CM administrated subcutaneously induced the anagen phase and increased hair regeneration in C(3)H/NeH mice. In addition, ADSC-CM increased the proliferation of human follicle dermal papilla cells (HFDPCs) and human epithelial keratinocytes (HEKs), which are derived from two major cell types present in hair follicles. We investigated the effect of hypoxia on ADSC function using the same animal model in which hypoxia increased hair regrowth. Forty-one growth factors in ADSC-CM from cells cultured under hypoxic or normoxic conditions were analyzed. The secretion of insulin-like growth factor binding protein (IGFBP)-1, IGFBP-2, macrophage colony-stimulating factor (M-CSF), M-CSF receptor, platelet-derived growth factor receptor-beta, and vascular endothelial growth factor was significantly increased by hypoxia, while the secretion of epithelial growth factor production was decreased. It is reasonable to conclude that ADSCs promote hair growth via a paracrine mechanism that is enhanced by hypoxia.
Full Study: http://www.jstage.jst.go.jp/article/biomedres/31/1/27/_pdf
J Dermatol Sci. 2006 Aug;43(2):105-15. Epub 2006 May 24.
PDGF isoforms induce and maintain anagen phase of murine hair follicles.
It is known that platelet-derived growth factor (PDGF) receptors are expressed in hair follicle (HF) epithelium.
The aim of the present study was to clarify the effects of PDGF-AA and -BB on the cyclic growth of HFs.
PDGF-AA or -BB was injected into the dorsal skin of C3H mice during the second telogen phase once daily for five consecutive days, or PDGF-AA or -BB dissolved in hyaluronic acid was injected only once. In order to confirm the effects of different PDGF isoforms, anti-PDGF-AA antibody or anti-PDGF-BB antibody was injected just after each injection of PDGF-AA or -BB. In addition, anti-PDGF antibodies were injected into the skin of C3H mice during the second anagen phase once daily for 5 days. We studied expression of signaling molecules in the skin where anagen phase had been induced by PDGF injection by real-time RT-PCR.
Both PDGF-AA and -BB injection experiments immediately induced the anagen phase of the hair growth cycle at the injection sites. The induction of anagen was interfered by anti-PDGF antibody treatment. Real-time RT-PCR using extracted RNA from the PDGF injected sites of skin samples showed upregulated expression of HF differentiation-related key signaling molecules, Sonic hedgehog (Shh), Lef-1 and Wnt5a.
These results indicate that both PDGF-AA and -BB are involved in the induction and maintenance of the anagen phase in the mouse hair cycle. Local application of PDGF-AA and -BB might therefore prove to be an effective treatment option for alopecia associated with early catagen induction and elongated telogen phase.
J Drugs Dermatol. 2011 Dec 1;10(12):1404-11.
The role of inflammation and immunity in the pathogenesis of androgenetic alopecia.
Background: Female pattern hair loss affects many women; its pathogenetic basis has been held to be similar to men with common baldness. Objective: The objective of this study was to determine the role of immunity and inflammation in androgenetic alopecia in women and modulate therapy according to inflammatory and immunoreactant profiles. Materials and Methods: 52 women with androgenetic alopecia (AA) underwent scalp biopsies for routine light microscopic assessment and direct immunofluroescent studies. In 18 patients, serologic assessment for antibodies to androgen receptor, estrogen receptor and cytokeratin 15 was conducted. Results: A lymphocytic folliculitis targeting the bulge epithelium was observed in many cases. Thirty-three of 52 female patients had significant deposits of IgM within the epidermal basement membrane zone typically accompanied by components of complement activation. The severity of changes light microscopically were more apparent in the positive immunoreactant group. Biopsies from men with androgenetic alopecia showed a similar pattern of inflammation and immunoreactant deposition. Serologic assessment for antibodies to androgen receptor, estrogen receptor or cytokeratin 15 were negative. Combined modality therapy with minocycline and topical steroids along with red light produced consistent good results in the positive immunoreactant group compared to the negative immunoreactant group. Conclusion: A lymphocytic microfolliculitis targeting the bulge epithelium along with deposits of epithelial basement membrane zone immunoreactants are frequent findings in androgenetic alopecia and could point toward an immunologically driven trigger. Cases showing a positive immunoreactant profile respond well to combined modality therapy compared to those with a negative result.
This is the first study I have seen that confirms that androgenic hair loss in large part, a result of an infection.
An infection always produces inflammation. The existance of chronic inflammation reduces blood flow and oxygen to the affected area.
The suggested 'treatment' in the study above is not so safe. However, steps can be taken to resolve this infection natuarally.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.
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.
Live longer and grow your hair by reducing your insulin levels.
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.
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.
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).
J Med Chem. 2006 May 4;49(9):2812-2820.
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.
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.
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).
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.
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.
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
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.
Ecklonia cava, on the Promotion of Hair Growth
Ecklonia cava possesses anti-bacterial, anti-inflammatory properties. It contains polyphenols with various antioxidant actions, among them is reducing 5-alpha-reductase activity in a natural manner (without side-effects). Ecklonia cava extract, eckol and dieckol significantly inhibited 5-alpha-reductase activities in a dose-dependent manner.
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.The polyphenols of Ecklonia cava can last up to 12 hours in human metabolism, while compared to most plant-based tannins have a half-life of just 30 minutes. Ecklonia cava's oxygen radical absorbance capacity (ORAC) value, the score for anti-oxidation potential is 8,300, is much higher than most land-based polyphenols.
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.
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.
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.
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.
Constituents of flax seed hulls, known as lignans contain Secoisolariciresinol Diglycoside (SDG). Ingested plant lignans are converted by intestinal bacteria to biological (mammalian) forms of lignans, enterodiol and enterolactone.
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.
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.
Another ally in the fight against MPB is Green tea polyphenols or Catechins and their Galates, which offer reduced expression of the Matrix Metalloproteinaseís (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.
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.J. Cardiovasc Pharmacol 2005 Dec;46(6):856-62.
Stress is unavoidable, all we can do is buffer what stresses we are dealt. Stress can cause a decrease in thyroid output and acute stress can lead to or create a temporary hypothyroid (under active thyroid level) condition.
Iodine levels could be off and supplementing with an optimal amount of iodine (12.5 to 14 milligrams) along with Vitamin E (to increase uptake) is recommended. Take note that 12.5 to 14 milligrams of iodine is well above the RDA, which is a paltry 0.125 milligrams
Guy Abraham MD, whom through serious research has cultivated significant findings on the importance of using higher intakes of iodine.
Alzheimer Dis Assoc Disord. 1995 Fall;9(3):128-31.
Acetyl L-Carnitine (ALC) can help normalize thyroid function and modulate stress hormones like cortisol. Under stress ALC can act as a buffer to stress, act as a catalyst to neurotransmitters, improve mood and has been shown to out perform testosterone in males suffering from loss of libido.
Muscle Nerve. 2005 Sep;32(3):357-9.
Mol Cell Biochem. 2005 Dec;280(1-2):83-9.
Acetyl L-Carnitine becomes especially potent when used along with Lipoic acid. This combination has been shown to reduce oxidative stress, improve fatty-acid combustion, increase ATP, which helps anagen growth, and supplies energy.
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.
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.