RENIN-ANGIOTENSIN-ALDOSTERONE SYSYTEM And HAIR LOSS PROCESS

Estradiol

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Keep in mind that they also have less chance to get a heart disease. Hair and hearth are definitely connected.

Women and children look alike. They have less body hair, more scalp hair, less chance to get a heart disease.
 

GorillaHead

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When i start to work on the computer my feet get cold.


Knowing the stuff about the angiotensin system is this related?


what can cause this? I am either wasy too sensitive to adrenaline. Or over secrete it
 

lvysaur

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okay but why is dht locally elevated in the scalp why don’t we see this in other areas of the body.
Is DHT not found in other follicles?
My suspicion is that head hair is just a fundamentally different type of hair. Scalp hair grows "oxidatively" while body hair grows "fermentatively", is my suspicion.

Body hair always grows in much faster, but ends up shorter. Scalp hair grows slowly but reaches a much longer potential.
 

rei

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You can continue the wild goose chase forever looking into what are the results but it will not yield any result as the cause is still in the dark.

All hair loss, in all places, is mediated by postural damage causing fascial tension, which directly stresses the tissue, and at some point it is unable to maintain normal function. Almost all chronic disease is caused by this mechanism. If the continuous stress is removed the tissue will heal.
 

GorillaHead

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You can continue the wild goose chase forever looking into what are the results but it will not yield any result as the cause is still in the dark.

All hair loss, in all places, is mediated by postural damage causing fascial tension, which directly stresses the tissue, and at some point it is unable to maintain normal function. Almost all chronic disease is caused by this mechanism. If the continuous stress is removed the tissue will heal.


Nah dude just nah.

Tell me how postural tension causes leg hairloss
 

rei

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your body is a tensegrity system with lines of tension going from every extremity to every other. From top of head down to your toes. From fingers of one hand to the fingers of the other, and also from both all the way to toes, top of head etc. Postural damage causes tension along these lines according to where the issue is. As yoga teaches, the most important health issue is to have a completely straight spine which perhaps 1% of the population has today. Otherwise there is chronic tension in the body and effect on hair is only one very small aspect.
 

mrchibbs

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You can continue the wild goose chase forever looking into what are the results but it will not yield any result as the cause is still in the dark.

All hair loss, in all places, is mediated by postural damage causing fascial tension, which directly stresses the tissue, and at some point it is unable to maintain normal function. Almost all chronic disease is caused by this mechanism. If the continuous stress is removed the tissue will heal.

These types of comments are not helpful.
 

lampofred

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your body is a tensegrity system with lines of tension going from every extremity to every other. From top of head down to your toes. From fingers of one hand to the fingers of the other, and also from both all the way to toes, top of head etc. Postural damage causes tension along these lines according to where the issue is. As yoga teaches, the most important health issue is to have a completely straight spine which perhaps 1% of the population has today. Otherwise there is chronic tension in the body and effect on hair is only one very small aspect.

I notice I am able to keep a straight spine easily when my calcium to phosphate ratio is high. Too much fat, starch, phosphate and I begin slouching and I have to make a conscious effort to straighten my back
 

GorillaHead

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I notice when i am warm my body posture is great. But when i am cold it is not. My feet are always freezing to this day even after increasing my food consumption. Seriously beating this is becoming very difficult. I am gonna try upping my salt intake way more i guess
 

lvysaur

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I notice I am able to keep a straight spine easily when my calcium to phosphate ratio is high.
I notice when i am warm my body posture is great. But when i am cold it is not.
All hair loss, in all places, is mediated by postural damage causing fascial tension
I think this is another nofap red herring. In the same way that nofap confuses an effect of good health (lower and non-insatiable sex drive) as the cause of it, it's likely that better posture is also an effect rather than a direct cause.
 

GorillaHead

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I think this is another nofap red herring. In the same way that nofap confuses an effect of good health (lower and non-insatiable sex drive) as the cause of it, it's likely that better posture is also an effect rather than a direct cause.


All i know for the past 2 years ive been trying to solve this cold feet problem. Doctors can help. This forum has failed to help. Other forum also a fail.

I started drinking half a teaspoon of salt with zero improvement.

theres only two times when my feet are warm. The first 5 minutes of being awake in bed and when ive been drinking. Super warm.
 

rei

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well i speak from personal experience, the only thing not directly related to this thread is that i did not suffer from baldness, but extremely coarse and spotty beard growth, after fixing postural problems it is much more normal feeling/softer, and most important almost completely even and less sparse than before. Also my pubes became more normal feeling/less coarse. Almost certainly result of decreased local DHT production. I could mention 10 other issues that also got fixed that you would never ever guess could be result from postural issues, but it would be OT. Ignore this at your own peril.

as GorillaHead found, warmth is important for energy in the fascia, i have used long warm showers while doing my yoga to great effect in my "protocol". Alcohol helps with circulation and energy in fascia, and postural problems easily result in reduced circulation in extremeties, especially legs.
 
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ilhanxx

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All i know for the past 2 years ive been trying to solve this cold feet problem. Doctors can help. This forum has failed to help. Other forum also a fail.

I started drinking half a teaspoon of salt with zero improvement.

theres only two times when my feet are warm. The first 5 minutes of being awake in bed and when ive been drinking. Super warm.
Did you try topical potassium iodide or povidone iodine on your feet, correct iodine deficiency helped my cold hands in past
 

lvysaur

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but extremely coarse and spotty beard growth, after fixing postural problems it is much more normal feeling/softer, and most important almost completely even and less sparse than before. Also my pubes became more normal feeling/less coarse.
And how did you fix these postural problems? Was it as simple as forcing it? If it was yoga, then it could be due to the biochemical effects of relaxation, rather than the posture itself.
My point is that the posture and hair could both be fixed by the same thing. If that's the case, chasing the posture would be a false lead.
 

rei

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And how did you fix these postural problems? Was it as simple as forcing it? If it was yoga, then it could be due to the biochemical effects of relaxation, rather than the posture itself.
My point is that the posture and hair could both be fixed by the same thing. If that's the case, chasing the posture would be a false lead.
I have called it chiropractic yoga before in my posts here, started by stretching my neck, then pushing my back against the wall, then against the corner of a wall once the worst curvature was gone and i needed to still get external force to the spine, and then later mainly "swinging/stretching" my arms and legs around and bend my body in such a fashion that the tension i could feel reduced. At the beginning i thought it would be over in couple weeks, yet i'm coming in at couple years soon doing it and it finally feels i'm seeing the finish line. I had absolutely no idea what i was getting myself into when i started the process.

Here are the videos i have found that are closest to what i "invented"
 
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L_C

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@md_a

I have been taking B vitamins for a long long time. Does nothing for my vitiligo.
 
OP
md_a

md_a

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@md_a

I have been taking B vitamins for a long long time. Does nothing for my vitiligo.
My mother has been suffering from vitiligo since she was young, recently at the age of 65, a good part of her body spots have disappeared since she started using red light as a treatment. For vitiligo I would focus on getting enough folic acid, B2, copper and zinc from food. Sun exposure / red light.
 

johnwester130

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I think excess cortisol-aldosterone- mineralocorticoid activation trough angiotensin system are main players in balding by cytokine activation and progressing to fibrosis. Focusing on TGF-β₁, which shuts off the anagen phase of the hair cycle, and 11β-HSD₁ expression should fix to the problem. Angiotensin 2 receptor (AT-1) is involved in the inflammation pathway.

Angiotensin - Aldosterone has been shown to upregulate TGF-β₁. DHT upregulates 11β-HSD₁ expression.

Cortisol synthesis depends on the enzyme 11β-HSD1 and it converts the inactive cortisone into the active cortisol.


RENIN-ANGIOTENSIN-ALDOSTERONE SYSYTEM AND HAIR LOSS PROCESS

Although hair follicles express almost a full set of RAAS-associated receptors, the role of this system in the regulation of hair growth has not yet been described.


The data describing serum ACE activity in patients with alopecia areata are not consistent; however, both of the studies performed to date have exploited relatively small groups (102, 103). Moreover, one study has shown that in patients with mild or moderate alopecia areata, ACE tissue activity is decreased in the epidermis, as well as in follicular epithelium and endothelium.


The role of RAAS in the hair loss process should be considered as highly possible due to reports linking to the intake of ACE-I to hair loss. Interestingly, discontinuation of ACE-I treatment or switching patients from ACE-I to ARB has resulted in hair regrowth. However, the mechanism of ACE-I-induced alopecia is unknown.


There are some studies indicating the potential role of aldosterone and MR in hair loss. Postnatal MR overexpression in keratinocytes in mice has resulted in delayed alopecia, hair follicle dystrophy, and abnormalities of the hair cycle, without alternation of the interfollicular epidermis. Moreover, clinical studies have shown that both male and female patients with androgenic alopecia have higher aldosterone serum levels. The mechanism underlying this process may be associated with the skin microinflammation found in those patients. Despite the potential role of aldosterone, there is only one study evaluating the influence of MR blockade on hair. This showed that spironolactone treatment reduced hair shaft size and weight resulting in softer, finer hair and a slower growth rate in patients with hirsutism. In this study, the action of spironolactone was mainly associated with its antiandrogenic activity. Nevertheless, the potential role of MR blockade cannot be excluded.

JPP No 3/2019 article 01
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Both aldosterone and cortisol have a similar affinity for the mineralocorticoid receptor. To prevent over-stimulation of the mineralocorticoid receptor by cortisol, 11β-HSD converts the biologically active cortisol to the inactive cortisone, which can no longer bind the mineralocorticoid receptor. 11β-HSD co-localizes with intracellular adrenal steroid receptors. Licorice, which contains glycyrrhizinic acid and enoxolone, can inhibit 11β-HSD and lead to a mineralocorticoid excess syndrome. Cortisol levels consequently rise, and cortisol binding to the mineralocorticoid receptor produces clinical signs and symptoms of hypokalemia, alkalosis and hypertension (i.e. mineralocorticoid excess).

11β-hydroxysteroid dehydrogenase is expressed in the central nervous system of aged individuals. It is essential in Hypothalamo-Pituitary-Adrenal Axis function. 11β-hydroxysteroid dehydrogenase also partakes involvement in the decline of conscious intellectual activity due to ageing.

11β-HSD1 is responsible for activating glucocorticoids while 11β-HSD2 is responsible for deactivating them.

https://en.wikipedia.org/wiki/11β-Hydroxysteroid_dehydrogenase


Mineralocorticoid overexpression is expressed in hyper-keratinization. Mineralocorticoid excess is due to cortisol. Elevated mineralocorticoid is the consequence of defective cortisol metabolism, thus implicating impaired 11β-HSD2 activity.

A syndrome of apparent mineralocorticoid excess associated with defects in the peripheral metabolism of cortisol. - PubMed - NCBI


The local renin-angiotensin-aldosterone system (RAAS) is fully expressed in the human skin at the mRNA and protein level. Local RAAS is known to play a regulatory function in epidermal proliferation, wound healing, scarring, cutaneous heating adaptation, and aging. There are also some indications of its role in the regulation of hair growth and sebum secretion. Impaired wound healing, skin diseases associated with diabetes, cancer development, psoriasis, and scleroderma may be related to changes in skin RAAS activity. Extensive research has shown that RAAS-modulating drugs can affect the skin when applied orally or topically, creating new therapeutic approaches against dermatological diseases.

https://www.researchgate.net/public...ayer_in_skin_biology_beyond_the_renal_horizon


Linoleic acid - Arachidonic acid – Iron (heavy metals) are involved in inflammation – lipid peroxidation – hair loss.

Our data suggest that iron overload increases both lipid peroxidation and TGF-beta1 expression, which together could promote hepatic injury and fibrogenesis.

Excess iron induces hepatic oxidative stress and transforming growth factor beta1 in genetic hemochromatosis. - PubMed - NCBI

Arachidonic acid is synthesized from α-linolenic acid derived from linoleic acid, an essential fatty acid, by the enzyme Δ6-desaturase. ... Cyclooxygenase is an enzyme that transforms arachidonic acid into endoperoxides which are used to synthesize prostaglandins, prostacyclin, or thromboxanes.

Arachidonic Acid - an overview | ScienceDirect Topics



Oxidative Stress in Ageing of Hair

Ageing of hair manifests as decrease of melanocyte function or graying, and decrease in hair production or alopecia. There is circumstantial evidence that oxidative stress may be a pivotal mechanism contributing to hair graying and hair loss.

Oxidative Stress in Ageing of Hair \


A hypothetical pathogenesis model for androgenic alopecia: clarifying the dihydrotestosterone paradox and rate-limiting recovery factors

AGA is the result of chronic GA-transmitted scalp tension mediated by pubertal and post-pubertal skull bone growth and/or the overdevelopment and chronic contraction of muscles connected to the GA. This tension induces a pro-inflammatory cascade (increased ROS, COX-2 signaling, IL-1, TNF-α, etc.) which induces TGF-β1 alongside increased androgen activity (5-αR2, DHT, and AR), which furthers TGF-β1 expression in already-inflamed AGA-prone tissues. The concomitant presence of DHT and TGF-β1 mediates perifollicular fibrosis, dermal sheath thickening, and calcification of the capillary networks supporting AGA-prone hair follicles. These chronic, progressive conditions are the rate-limiting factors in AGA recovery. They restrict follicle growth space and decrease oxygen and nutrient supply to AGA-prone tissues – leading to tissue degradation, hair follicle miniaturization, and eventually pattern baldness.

A hypothetical pathogenesis model for androgenic alopecia: clarifying the dihydrotestosterone paradox and rate-limiting recovery factors - ScienceDirect


Induction of transforming growth factor-beta 1 by androgen is mediated by reactive oxygen species in hair follicle dermal papilla cells

The progression of androgenetic alopecia is closely related to androgen-inducible transforming growth factor (TGF)-β1 secretion by hair follicle dermal papilla cells (DPCs) in bald scalp. Physiological levels of androgen exposure were reported to increase reactive oxygen species (ROS) generation. In this study, rat vibrissae dermal papilla cells (DP-6) transfected with androgen receptor showed increased ROS production following androgen treatment. We confirmed that TGF-β1 secretion is increased by androgen treatment in DP-6, whereas androgen inducible TGF-β1 was significantly suppressed by the ROS scavenger, N-acetyl cysteine. Therefore, we suggest that induction of TGF-β1 by androgen is mediated by ROS in hair follicle DPCs.

Induction of transforming growth factor-beta 1 by androgen is mediated by reactive oxygen species in hair follicle dermal papilla cells


Clove oil (eugenol) inhibited 97.3% lipid peroxidation and decreases TGF‐β1 expression

Expression of TGF‐β1 was increased significantly in the diabetic control group. However, eugenol treatment decreases this increased expression.

Results suggest that treatment with eugenol involved amelioration of diabetic nephropathy by decreasing TGF‐β1 expression.

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Clove oil inhibited 97.3% lipid peroxidation of linoleic acid emulsion at 15 μg/mL concentration. However, under the same conditions, the standard antioxidant compounds such as butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), α-tocopherol and trolox demonstrated inhibition of 95.4, 99.7, 84.6 and 95.6% on peroxidation of linoleic acid emulsion at 45 μg/mL concentration, respectively. In addition, clove oil had an effective DPPH scavenging, ABTS+ scavenging, superoxide anion radical scavenging, hydrogen peroxide scavenging, ferric ions (Fe3+) reducing power and ferrous ions (Fe2+) chelating activities.

Antioxidant activity of clove oil – A powerful antioxidant source - ScienceDirect



Multiple nutritional, environmental and lifestyle factors can directly affect hair follicles, to weaken and make them sensitive to the action of androgens. Hair loss can be corrected and hair growth can be improved by addressing these non-androgenic factors. Patients having hair fall, thinning, loss of volume and poor growth can be precursors to androgenetic alopecia. Recent research has shown that androgens inhibit hair growth through release of Transforming Growth Factor (TGF) ß1. Further study of this mechanism reveals that generation of Reactive Oxygen Species (ROS) induced by androgens leads to release of TGF ß1 and use of ROS scavengers can block the release of TGF ß1, explaining beneficial role of antioxidants in hair growth. The binding of ROS to intracellular proteins also causes hair loss by altering the protein structure, changing their immune recognition and converting them to new antigens targeted by inflammatory and immune systems. Calorie restriction and individual micronutrient deficiencies lead to a new process of intracellular destruction or autophagy before cell apoptosis, which could explain cessation of hair growth. Telogen is not a resting phase but now defined as active conservation of follicles under unfavorable conditions. Thus any stress, trauma, metabolic change or insult causes telogen. Micronutrients zinc, copper, selenium maintains immunity, control inflammation and preserve antioxidant activity of the cells. Vitamins A, C, D have a role in phagocytosis and antibodies maintaining resistance. Vitamin D3 modulates the hair-inductive capacity of dermal papilla cells. Vitamin and micronutrient deficiencies are prevalent among all the population of the world. Nutritive value of the foods has reduced over the years by 30%. Endocrine Disrupting chemicals are creating further damage to the hormonal balance of the body. All these can be countered by use of antioxidants and a well-planned nutritional program which will ensure strengthening and regrowth of hair follicles, without the use of Finasteride. https://www.researchgate.net/public...n_Hair_loss_and_Hair_Regrowth_Review_Articlen


Lisinopril-Induced Alopecia: A Case Report

The American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guidelines consider angiotensin-converting enzyme (ACE) inhibitors as one of the mainstay therapies in the management of heart failure. The widespread use of ACE inhibitors has been associated with several notable adverse effects such as hyperkalemia and an increased serum creatinine. There are no previous reports of alopecia associated with lisinopril use; however, a few previous cases of alopecia associated with other ACE inhibitors exist. This report discusses a case of lisinopril-induced alopecia of a 53-year-old male presenting to our outpatient heart failure clinic with a chief complaint of a new onset of alopecia. Upon evaluation, it was suspected that the patient’s alopecia was likely medication induced by lisinopril; therefore, lisinopril was discontinued and switched to an angiotensin receptor blocker (ARB), losartan potassium. Alopecia resolved in 4 weeks after the therapeutic intervention.

SAGE Journals: Your gateway to world-class research journals


The beneficial effect of Ang-(1-7) in alopecia can be attributed to their vasodilation action on blood vessels (Santos et al., 2000). The vasodilation of arterioles present in the dermis improves irrigation of the hair follicles, increasing the supply of nutrients and oxygen. Thus, the cells of the hair follicle increase their proliferation, accelerating hair growth

US20150313829A1 - Topical formulations for the prevention and treatment of alopecia and inhibition of hair growth - Google Patents


TGF-β plays important roles in the induction of catagen during the hair cycle. We examined whether TGF-β2 could activate a caspase in human hair follicles. Using active caspase-9 and -3 specific antibodies, we found that TGF-β2 activated these caspases in two regions, the lower part of the hair bulb and the outer layer of the outer root sheath. In addition, we searched for a plant extract that can effectively suppress TGF-β action. We found that an extract of Hydrangea macrophylla reduced synthesis of a TGDβ-inducible protein. We confirmed that the extract has a potential to promote hair elongation in the organ culture system. Furthermore, it delayed in vivo progression of catagen in a mouse model. Our results suggest that the induction of catagen by TGF-β is mediated via activation of caspases and that a suppressor of TGF-β could be effective in preventing male pattern baldness.

A Potential Suppressor of TGF-β Delays Catagen Progression in Hair Follicles - ScienceDirect



Angiotensin II is also well known in inducing reactive oxygen species and promoting inflammatory phenotype switch via its type 1 receptor. In clinic, Angiotensin II type 1 (AT1) receptor blocker like candesartan has been widely applied as an antihypertensive medication.

It was found that pre-treat with candesartan significantly suppressed transforming growth factor-β (TGF-β) and interleukin-6 (IL-6) expression after incubation with TNF-α.

Candesartan inhibits inflammation through an angiotensin II type 1 receptor independent way in human embryonic kidney epithelial cells


Related to stress


Angiotensin II type 1 (AT(1)) receptors are expressed within organs of the hypothalamo-pituitary-adrenal (HPA) axis and seem to be important for its stress responsiveness. Secretion of CRH, ACTH, and corticosterone (CORT) is increased by stimulation of AT(1) receptors. In the present study, we tested whether a blockade of the angiotensin II system attenuates the HPA axis reactivity in spontaneously hypertensive rats.


Gene expression of AT(1A), AT(1B), and AT(2) receptors within the HPA axis was not altered by any drug. We show for the first time that antihypertensive treatment by inhibition of AT(1) receptors or angiotensin-converting enzyme attenuates HPA axis reactivity independently of blood pressure reduction. This action is solely evident after CRH stimulation but not under baseline conditions. Both a reduced pituitary sensitivity to CRH and a down-regulation of hypothalamic CRH expression have the potential to reduce HPA axis activity during chronic AT(1) blockade or angiotensin-converting enzyme inhibition.

Angiotensin II inhibition reduces stress sensitivity of hypothalamo-pituitary-adrenal axis in spontaneously hypertensive rats - PubMed

so topical licorice/liquorice is an option?
 

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