Aspirin With Castor Oil For Hair Loss

[eddiem991]

i don't know, there are tons of theory sites that show the muscles in the skull getting tight, something with the galea. there was some study where they put botox into some guys head to relax the muscles and the guy managed to regrow his hair. someone else did it, but it didn't work, but not really sure how it went or if they even did it right.

all those guys that look into it though they think if they do scalp massage or something, it will fix the problem. i don't think it is accurate, i don't think that fixes the problem. its the cortisol is high, or lack of magnesium, or a backed up digestive system, or lack of pregnenlone, i'm not sure what it is exactly, but it causes the muscles in the head to get strained, like on the side of the head. you notice people who are bald, their skull is shiny, like it was stretched out somehow. i don't know the process though.

but it seems like the right course of events, like fungus buildup, lack of vitamin A, digestion problems, it leads to this chain of events where the muscles get strained. it doesn't make sense why it doesn't happen to women though, i don't know why, maybe it's the DHT that causes the muscles to strain, i really don't know as i keep saying lol, but i have felt the muscle strain and felt it relax as well.

I think that the hardening of the scalp is caused by fibrosis. Stiff muscles doesn't explain the pattern, but the location of blood vessels in the head can explain it.

 

[Travis]

About artery constriction/dilation, do you think co2 could help with hair loss if you were to have, say, an airtight bag over your scalp and fill it with co2? I've wondered this and I've got a co2 tank but haven't tried it.

Garza had shown about four times the prostaglandin D₂ levels in hairless areas—when measuring two areas of one person. This was done by radioimmunoassay, and the HPLC determinations indicated a slightly less—but still appreciable (~3×)—elevated levels.

I think prostaglandin D₂ is so involved that it should be the primary concern. Even doing everything right to reverse ischemia—like magnesium chloride, infrared light, saunas, and scalp massage—wouldn't do anything about these elevated prostaglandin D₂ levels, although one might expect them to help to a degree with hair loss.

 

[Koveras]

I haven't seen any evidence showing that serotonin, parathyroid, or prolactin were etioligical factors.

Perhaps the Ca²⁺/Mg²⁺ ratio is nearly as important as linoleic acid? These are two things that separate humans from the other primates: Besides eating much less linoleic acid, other primates would consume far more magnesium for their body weight. I don't think any other animals get alopecia besides the spotty type seen during parasitic infection (i.e. canine leishmaniasis, a.k.a. interferon-γ creating PGD₂ in spots by upregulating phospholipase A₂).

Are you eating any immunogenic proteins, such as those found in wheat and oats? These can release interferon-γ and interferon-6 shown to induce phospholipase A₂ and cyclooxygenase‐2, respectively. These two enzymes, when working in tandem, powerfully increase all prostaglandins.

Immune activation has been shown to cause diffuse thinning. I think the phospholipase A₂ upregulated mice had diffuse thinning . .

Danny's references

"Subsequent actions of prolactin may involve the following: a) an increased intracellular concentration of potassium and a reduced level of sodium, b) an increased level of cGMP and a reduced level of cAMP, c) an enhanced rate of prostaglandin biosynthesis mediated by a stimulation of phospholipase A2 activity, and d) a stimulation of polyamine synthesis."

Rillema, J. A. Mechanism of prolactin action. Federation Proceedings [1980, 39(8):2593-2598]​

"Our findings showed a significant elevation of F [cortisol] in both male and female AH patients compared to controls, pointing to the suprarenes as a contributing factor in AH. This is confirmed by the observation of exacerbated AH in periods of increased stress.” "The mainly peripheral activity of this hormone and elevated E2 levels in males stress the importance of androgen metabolism especially at the peripheral level.” "Another significant finding was elevated PRL after TRH stimulation. Thus, the androgen-stimulating effect of PRL may also play a role in female AH. Our findings show multilayered hormonal influences in AH."

Schmidt JB. Hormonal basis of male and female androgenic alopecia: clinical relevance. Skin Pharmacol. 1994;7(1-2):61-6.​

"PRL has also been implicated in the pathogenesis of androgenetic alopecia by modulation of androgens, and hyperprolactinemia is associated with an androgenetic alopecia-type hair loss pattern, along with hirsutism (in females)."

Foitzik, K., et al. Human scalp hair follicles are both a target and a source of prolactin, which serves as an autocrine and/or paracrine promoter of apoptosis-driven hair follicle regression. Am J Pathol. 2006 Mar;168(3):748-56.​

“In addition we show that PRL exerts functional effects on anagen hair follicles in murine skin organ culture by down-regulation of proliferation in follicular keratinocytes.””The regressing (catagen) follicle showed a strong expression of PRL in the proximal ORS.” “Addition of PRL (400 ng/ml) to anagen hair follicles in murine skin organ culture for 72 hours induced premature catagen development in vitro along with a decline in the number of proliferating hair bulb keratinocytes. These data support the intriguing concept that PRL is generated locally in the hair follicle epithelium and acts directly in an autocrine or paracrine manner to modulate the hair cycle.”

Foitzik, K., et al. Prolactin and its receptor are expressed in murine hair follicle epithelium, show hair cycle-dependent expression, and induce catagen. Am J Pathol. 2003 May;162(5):1611-21.​

“PRL has also been implicated in the pathogenesis of androgenetic alopecia by modulation of androgens, and hyperprolactemia is associated with an androgenetic alopecia-type hair loss pattern, along with hirsutism (in females).

Foitzik, K., et al. Human scalp hair follicles are both a target and a source of prolactin, which serves as an autocrine and/or paracrine promoter of apoptosis-driven hair follicle regression. Am J Pathol. 2006 Mar;168(3):748-56. ”​

"The mean prolactin level decreased from 11.3 to 8.6 ng/mL after spironolactone treatment. The 5 participants who had hyperprolactinemia at baseline also experienced a significant decrease in serum prolactin levels. Levels of testosterone, androstenedione, and DHEA were significantly decreased after spironolactone therapy.""

Spritzer, P.M., et al. Spironolactone as a single agent for long-term therapy of hirsute patients. Clin Endocrinol (Oxf). 2000 May;52(5):587-94. "​

 

[Travis]

I'm getting the feeling that they are emphasizing androgens not because the are particularly influenced by prolactin, but because nearly all 'acceptable' pre‐2012 explanations would seem to require that. The increased calcium and prostaglandins are more direct, as well as the influence of the Na⁺/K⁺ changes on aldosterone.

What is interesting about vitamin D receptor‐knockout mice is that they are totally hairless. Almost equally interesting is that equalizing Ca²⁺, parathyroid, and prolactin had reversed all symptoms but alopecia:

Xie, Zhongjion, et al. "Lack of the vitamin D receptor is associated with reduced epidermal differentiation and hair follicle growth." Journal of investigative dermatology (2002)
Li, Yan Chun. "Normalization of Mineral Ion Homeostasis by Dietary Means Prevents Hyperparathyroidism, Rickets, and Osteomalacia, But Not Alopecia in Vitamin D Receptor-Ablated Mice." Endocrinology (1998) ​

Since Valerie Randall had shown DHT to actually stimulate the growth of scalp hair, any negative effect of androgens cannot be from the androgen–receptor interaction at the follicle or the ancillary papilla cells. I am of the opinion that androgens influence hair growth by raising interferon-γ and cortisol; both the thymus and the adrenals have androgen receptors. Finasteride has been shown to significantly lower interferon-γ levels, as has acyline. This has been clinically demonstrated:

click to embiggen (Page, 2006)​

Page, Stephanie T. "Effect of medical castration on CD4 CD25 T cells, CD8 T cell IFN-expression, and NK cells: a physiological role for testosterone and/or its metabolites." Am J Physiol Endocrinol Metab (2006)​

The ability of interferon-γ to cause hair loss is undeniable. Interferon-gamma, like interleukin-six, is a phoshpolipase A₂‐inducing cytokine. After invading the cell, interferon-γ causes increased phospholipase A₂ expression for days.

Not all cytokines do this. Some of them induce cyclooxygenase, and some of them are beneficial. Interleukin-four, for instance, induces the interleukin-1 binding protein—deftly inactivating it.

The interesting thing about vitamin D is that it's required for hair loss; the hair protein keratin 31 is under transcriptional control of vitamin D. But most people do seem to have enough. Although vitamin D likely plays a role, I think it's secondary to prostaglandin D₂.

But vitamin D has also shown capable of reducing the induction of interleukin-6 after UV-irradiation, on the skin, by 75–90%:

De Haes, Petra. "1, 25‐dihydroxyvitamin D₃ inhibits ultraviolet B‐induced apoptosis, Jun kinase activation, and interleukin‐6 production in primary human keratinocytes." Journal of cellular biochemistry (2003)​

And the outer root sheath itself has interleukin-6 receptors, as verified by flourophore‐congugated antibody immunohistochemical staining.

And perhaps even more alarming, vitamin D downreguates cyclooxygenase and upregulates hydroxyprostaglandin dehyrogenase— an enzyme that degrades prostaglandins:

​

Krishnan, Aruna V.. "Analysis of vitamin D‐regulated gene expression in LNCaP human prostate cancer cells using cDNA microarrays." The Prostate (2004)​

It also upregulates interleukin‐1 receptor‐like protein, a dummy receptor which binds interleukin‐1 yet does nothing. This is another anti‐cytokine/prostaglandin effect of vitamin D (on prostate cells, admittedly).

Also notable are:

Vitamin D 24-hydroxylase +79.15×
Insulin-like growth factor binding protein three +33.2×
Interleukin 1 receptor-like +9.41×
Hydroxyprostaglandin dehydrogenase +7.30×
Bone morphogenetic protein +3.92×
Nicotinamide N-methyltransferase −3.63×
Insulin-like growth factor 1 −2.22×
​

The first one on the list is induced the greatest, and happens to be the enzyme which inactivates calcitriol by introducing a fourth hyroxyl group; vitamin D induces an enzyme which inactivates it, perhaps why blood levels seem to top‐out at around 90·ng/ml. The second protein inactivates IFG‐1 by binding to it, and vitamin D also downregulates IFG‐1 itself. Nicotonamide N-methyltransferase of course N‐methylates niacin, tautologically, into a form which is excreted. Perhaps this is another way that vitamin D inhibits proliferation? by lowering the NADH concentration?

Peehl, Donna M. "Molecular activity of 1, 25-dihydroxyvitamin D 3 in primary cultures of human prostatic epithelial cells revealed by cDNA microarray analysis." The Journal of steroid biochemistry and molecular biology (2004)​

 

[General Orange]

Tachykinins and Their Receptors: Contributions to Physiological Control and the Mechanisms of Disease

Stress-induced hair loss
The hair follicle apparatus expresses tachykinins, NKRs, and endopeptidases, and tachykinins have been implicated in stress- and autoimmune-evoked hair loss. Stress-induced premature induction of catagen and hair follicle apoptosis in mice requires expression of the NK1R and the presence of mast cells (15). ...

Mast cells
Mast cells are closely associated with SP-positive sensory nerves in many tissues, and there is a bidirectional communication between mast cells and primary sensory neurons, whereby sensory neuropeptides stimulate mast cells, and mast cell products control neuropeptide release. SP induces the release of TNF-α (78) and vascular endothelial growth factor (301) from mast cells, thereby contributing to inflammation, immunity, and angiogenesis.

Mast cell deficient and neurokinin-1 receptor knockout mice are protected from stress-induced hair growth inhibition. - PubMed - NCBI
Despite the lack of insight on distinct mediators in the skin orchestrating the pathophysiological response to stress, hair loss has often been reported to be caused by stress. Recently we revealed the existence of a "brain-hair follicle axis" by characterizing the neurokinin (NK) substance P (SP) as a central element in the stress-induced threat to the hair follicle, resulting in premature onset of catagen accompanied by mast cell activation in the skin.
...These results indicate that the cross-talk between SP and mast cell activation via NK-1R appears to be the most important pathway in the regulation of hair follicle cycling upon stress response.

...Observations of human skin biopsies and hair follicles in culture indicate that Substance P downregulates production of prolactin, which is important for hair growth (178):

Human scalp skin and hair follicles (HFs) are extra-pituitary sources of prolactin (PRL). However, the intracutaneous regulation of PRL remains poorly understood. Therefore we investigated whether well-recognized regulators of pituitary PRL expression, which also impact on human skin physiology and pathology, regulate expression of PRL and its receptor (PRLR) in situ.
...This study identifies substance P, TNFα and IFNγ as novel modulators of PRL and PRLR expression in human skin, and suggests that intracutaneous PRL expression is not under dopaminergic control. Given the importance of PRL in human hair growth regulation and its possible role in the pathogenesis of several common skin diseases, targeting intracutaneous PRL production via these newly identified regulatory pathways may point towards novel therapeutic options for inflammatory dermatoses.
Tumour necrosis factor alpha, interferon gamma and substance P are novel modulators of extrapituitary prolactin expression in human skin. - PubMed - NCBI

Substance P, NK1R, and neprilysin regulate the inflammatory response in a murine model of alopecia areata, an autoimmune disorder of the hair follicle associated with inflammatory cell influx around growing hair follicles (306).

Alopecia areata (AA) is an autoimmune disorder of the hair follicle characterized by inflammatory cell infiltrates around actively growing (anagen) hair follicles. Substance P (SP) plays a critical role in the cutaneous neuroimmune network and influences immune cell functions through the neurokinin-1 receptor (NK-1R). To better understand the role of SP as an immunomodulatory neuropeptide in AA, we studied its expression and effects on immune cells in a C3H/HeJ mouse model for AA.
..Additional SP supply to the skin of AA-affected mice leads to a significant increase of mast cell degranulation and to accelerated hair follicle regression (catagen), accompanied by an increase of CD8+ cells-expressing granzyme B. These data suggest that SP, NEP, and NK-1R serve as important regulators in the molecular signaling network modulating inflammatory response in autoimmune hair loss.
Substance P as an immunomodulatory neuropeptide in a mouse model for autoimmune hair loss (alopecia areata). - PubMed - NCBI

 

[lvysaur]

Prostaglandin D₂ formation is impossible without linoleic acid.

This isn't true, PGD2 comes from arachidonic acid.

To neutralize PGD2, one would have to both avoid PUFA and eat a vegetarian diet. Only a fraction of linoleic acid gets converted to arachidonic, and in some people even this doesn't happen.

 

[StayPositive]

This combo works for me, completely stopped my shedding with aspirin and castor oil

 

[davvid_1]

This combo works for me, completely stopped my shedding with aspirin and castor oil

topical castor oil? how did you do it exactly?

 

[md_a]

Ricinoleic Acid: An Inhibitor of PGD2​

While clinical trials are underway to test the effectiveness of various pharmaceutical drugs on their abilities to reduce the effect of PGD2 by blocking the GPR44 receptor, a recent study by researchers in China shows that castor oil may provide a natural and readily-available alternative.

Fong et al selected 12 herbs commonly used in Traditional Chinese Medicine and tested various aspects of each.

The aim of the study was to determine whether any of the 12 herbs or their constitutents were inhibitors of prostaglandin D2 synthase (PTDGS) and, therefore, could be developed for use in the treatment of androgenetic alopecia (male-pattern baldness).

One of the herbs which was tested was, you guessed it, castor. Or, ‘ricinus communis’ as it was identified in the study.

As discovered by researchers, ricinoleic acid, a major component of castor, has a few properties which made it stand out as a potentially effective inhibitor of PDG2.

First and foremost, ricinoleic acid received a high docking score as tested by researchers.

Docking is an indicator of inhibitory prowess, as it shows an ability to interact and bind. In fact, the similarity in chemical structures between ricinoleic acid and prostaglandin is a good indicator of its ability to interact and bind with the molecule.

The striking similarities can be seen by comparing the below prostaglandin structures with the above image of ricinoleic acid.
https://www.umuziorganics.com/castor-oil-for-hair-loss-3-new-studies-reveal-the-truth/

In silico prediction of prostaglandin D2 synthase inhibitors from herbal constituents for the treatment of hair loss - PubMed

Overall, ricinoleic acid, acteoside, amentoflavone, quercetin-3-O-rutinoside and hinokiflavone were predicted to be PTGDS inhibitors with good pharmacokinetic properties and minimal adverse skin reactions. These compounds have the highest potential for further in vitro and in vivo investigation...

pubmed.ncbi.nlm.nih.gov

 

[Brandin]

Lol, so should I be talking to my hair like a plant, give it love ?

Castor oil and many other things have caused hair growth in studies tho

 

[Brandin]

But why do normal people get away with normal levels of cortisol and PUFA with a full head of hair?

They dont have the balding gene. This turns certain hormones into having opposite effects on hair follicles right? But assume it only happens when in bad health

 

[johnwester130]

Reckless? But how could it possibly be reckless when blood levels are undetectable after topical application?

Exhibit 1: Rey, F. O. "Lack of endocrine systemic side effects after topical application of spironolactone in man." Journal of endocrinological investigation (1988)​

​

'No changes in any levels of these hormones have been detected and plasma canrenone levels were undetectable during the 72 hours of topical treatment. Topically administered, spironolactone appears to have only a local skin impregnation.' ―Rey​

Canrenone is the metabolite, the result of dethioacetylation. There is no systemic absorption of spironolactone, or its metabolite, after topical application.

And spironolactone is, first and foremost, an antimineralcorticoid:

Exhibit 2: Sica, Domenic A. "Pharmacokinetics and pharmacodynamics of mineralocorticoid blocking agents and their effects on potassium homeostasis." Heart failure reviews (2005)​

​

'Spironolacotone and eplerenone are mineralocorticoid-blocking agents used for their ability to block both the epithelial and non-epithelial actions of aldosterone. Spironolactone is a non-selective mineralocorticoid receptor antagonist with moderate affinity for both progesterone and androgen receptors.' ―Sica​

Spironolactone has about 6.5 higher affinity for the mineralocorticoid receptor than it has for the androgen receptor:

View attachment 7744 click to embiggen​

But eplerenone has a better ratio, making this drug more antihypertensive and less antiandrogenic. However, this drug is more expensive and harder to find. Topical spironolactone is not antiandrogenic anywhere besides the skin, but Valerie Randall has shown there to be essentially no androgen receptors on the follicle and few on the surrounding dermal papilla.⁽¹⁾ Topically, spironolactone should be better because it's more antiandrogenic; Valerie Randall also has shown DHT to promote hair growth on the scalp⁽²⁾—just like it promotes hair growth on the beard.

[1] Randall, Valerie. "Cultured dermal papilla cells from androgen-dependent human hair follicles (e.g. beard) contain more androgen receptors than those from non-balding areas of scalp." Journal of Endocrinology (1992)​

[2] Randall, Valerie. "Mechanism of androgen action in cultured dermal papilla cells derived from human hair follicles with varying responses to androgens in vivo." Journal of investigative dermatology (1992).​

In your post above (#36), we have this:

'Spironolactone, an inhibitor of androgen synthesis, has been administered to castrated men with metastatic carcinoma of the prostate.'―unattributed​

Which I think is worded in a confusing manner. I think the logical explanation for the lowered androgens seen upon spironolactone ingestion is that the body is compensating for additional pseudoandrogen (canrenone), and lowering androgen biosynthesis in a negative feedback manner in the spirit of maintaining homeostasis. The same thing has been seen with withaferin—also with a concomitant increase in facial hair growth (despite the very low testosterone, in a female).⁽³⁾ If you define an antiandrogen by its ability to lower androgens, withaferin is both an androgen and an antiandrogen. This is of course absurd, and even full‐blown androgens like DHT when taken orally would almost certainly lower de novo androgen biosynthesis.

What spironolactone does to dihydrotestosterone—the most active androgen—is nothing in comparison to what finasteride does. This drug inhibits DHT production directly by postitioning itself, rather rudely, inside of the enzyme 5α-reductase. The levels of DHT can drop from roughly thirty nanograms per deciliter down to four:⁽⁴⁾

View attachment 7745​

Now this is dangerous. Androgens this low often cause impotence, as the nucleus of bulbocavernosus—a nervous offshoot from the spine found only in males which leads to the . . . — has androgen receptors and atrophies it their absence. Gynecomastia is also common.

Eplerenone is a better choice if taken orally since its less antiandrogenic, but topically I don't see much difference. Orally eplenerone would lower blood pressure just the same, but be nearly free of androgenic effects. But inhibiting androgens could be beneficial for those with prostatic hyperplasia, as the prostate has a relatively high density of androgen receptors which upon activation expresses the polyamine‐producing ornithine decarboxylase. Prostaglandin E₂ also upregulates this enzyme, an event that always leads to cell proliferation. Spironolactone and eplerenone both lower blood pressure, and lowering blood pressure can be considered beneficial in some people (but there are many other ways to accomplish this of course, and there are natural antimineralocorticoid agents found in certain plants).

Obviously, if anyone decides to ingest spironolactone it could be prudent to reduce the dose in the event of manboobs (unless of course, you're nursing an orphan squirrel or a lost kitten).

There is zero chance of manboobs—over that which would otherwise be expected to occur—upon the topical application of spironolactone, since doing so leads to undetectable circulating metabolite levels.

[3] Nguyen, Diep Dinh. "Effect of ashwagandha on adrenal hormones." Adrenal Insufficiency. Endocrine Society, 2013. ​

[4] Rittmaster, Roger. "Effect of finasteride on adrenal steroidogenesis in men." Journal of andrology (1994)​

Amazing post

Shame you have passed

 

[S.Holmes]

Amazing post

Shame you have passed

Travis passed? What happened?