Male pattern baldness

Cancer, Diabetes, Osteoporosis etc.
dime
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Re: Male pattern baldness

Post by dime »

It doesn't seem like such a topical (nor oral actually) inhibitor is available.
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RRM
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Re: Male pattern baldness

Post by RRM »

Hmm, too bad.
Kasper
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Re: Male pattern baldness

Post by Kasper »

My older and little brother both are loosing much hair on their temples.
I seem to have a little bit more luck, but I'm quite sure every year my hair line goes up a little bit.

A couple of years I go, I noticed that my little brother grow back hair in the summer on his temples.
My younger brother was something like 17 back than.
Last summer I noticed it again, and I asked him, and he said he always grew hair back in the summer, and loosing it again in the winter.
He is still young, and it's not that you would say he's balding, same for me, but you just say very much little hair growing in the summer.

So, there could be a lot of reasons he grows back hair in the summer, and I guess that has mainly to do that he's still young, because with older people, even on medication you don't see many people regrow hair in bald spots.

It could be vitamin D? Or it could be because he's living much healthier in the summer? Much more active, much more outdoors, much less gaming etc.

I know one person (who also posted succes photo's) who had great succes with this:
http://www.vitacost.com/jarrow-formulas-toco-sorb

He had a diffuse balding pattern.
I know other people who tried it and had no success at all. Which may has to do with that they didn't had a diffuse balding pattern.

http://newsroom.heart.org/pr/aha/tellta ... 39569.aspx
A receding hairline, baldness, earlobe crease and yellow fatty deposits on the eyelids were among signs of aging associated with an increased risk of heart disease.
Kasper
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Re: Male pattern baldness

Post by Kasper »

bbmine
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Re: Male pattern baldness

Post by bbmine »

mario91
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Re: Male pattern baldness

Post by mario91 »

I've just started using Nizoral. Although it is not officially recognized as a hair loss treatment, it seems to work:

"Preliminary research suggests ketoconazole shampoo may be beneficial in men suffering from androgenic alopecia. Support for this comes from a study in 1998 that compared ketoconazole 2% to the proven hair loss drug minoxidil 2% in men with androgenic alopecia.[13] In a sample of 27 men, "[h]air density and size and proportion of anagen follicles were improved almost similarly by both ketoconazole and minoxidil regimens."" (Wikipedia)

And it doesn't have any side effects, unlike minoxidil 2%.

Seems that alfatradiol doesn't have any serious side effects either, but it isn't available in my country.

Will post about how I'm doing in a few months :)
Kasper
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Re: Male pattern baldness

Post by Kasper »

http://www.hairlosshelp.com/forums/messageview.cfm?catid=7&threadid=100845&STARTPAGE=2&FTVAR_FORUMVIEWTMP=Linear&#lastunread wrote:Okay guys that's it. I have said this before on other topics, But I will say it again.
Its hard for me to watch people wasting their time on the wrong path..

PGD2 in hair folicles is not caused by HPGDS - hematopoietic prostaglandin D synthase BUT, by LPGDS lipocalin pgds.

Source? read the 22 march study of DR. cots. LPGds levels are highly elevated....

Image


Increased PGD2 pathway activity in balding scalp of men with AGA. (A) Expression of lipocalin-type PTGDS mRNA in bald versus haired scalp, as tested by qPCR. Data are means ± SEM (n = 4). (B and C) The amount of PTGDS protein in paired bald (B) and haired (H) scalps (n = 4), as shown by Western blotting with Ponceau stain used for verification of equal loading (B) and its quantitation as normalized to haired scalp (C). Data are means ± SEM. (D) PGD2 production in bald scalp, as tested by ELISA. Data are means ± SEM (n = 3). (E and F) Fold change in PGD2 (n = 17), 15-dPGJ2) (n = 7), and PGE2 (n = 17) expression in bald scalp compared to haired scalp (E). Total prostaglandin content is quantified in (F). Data are means ± SEM. *P < 0.05; **P < 0.01. In (F), P value compares haired versus bald samples for each prostaglandin.

knowing this, explain why cetrizine and other mastcell stabelizers, will NOT help against the elevated PGD2 in hairflocles.. so your basically missing the boat with hpgds stabilizers.

this leaves us 2 options at this point, antagonizing the CRTH2 receptor, or using Anti androgens to reduce LPGds and pgd2. there is currently No on humans tested LPGDS antagonist.

all info I have collected on my pc, including all AGA studies in the past, Does fit in the puzzle/ chain reaction, dkk1. lpgds, androgen receptors sensitivity , progenitor cells, caspease3/pks activation, ... it fits perfectly . in my other posts I have explained some parts of it regarding p53, dkk1 , decreased igf1 etc....
it explains me perfectly how the hairgrowth is inhibited.
Kasper
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Re: Male pattern baldness

Post by Kasper »

"PGD2 can be produced by two distinct types of PGD2 synthase (PGDS), lipocalin-type PGDS (LPGDS) and hematopoietic PGDS (HPGDS), but only LPGDS is related to sleep. Three potential sites for PGD2 synthesis by LPGDS have been identified in the brain, i.e. oligodendrocytes (OD), epithelial cells of the choroid plexus (CP) and arachnoid trabecular cells of the leptomeninges (LM).
...
We recorded electroencephalogram, electromyogram and locomotor activity to measure sleep of 10 weeks old animals with a specific knockdown of LPGDS in one of the 3 target tissues. By using selenium tetrachloride, a specific PGDS inhibitor, we demonstrated that sleep was inhibited in OD-LPGDS and CP-LPGDS KO mice, but not in the mice lacking LPGDS in the LM. "

http://www.abstractstosubmit.com/ibro20 ... g77c6g1i70

PDG2 seems to induces sleep by activating DP1 receptor. DP2 seems to be more relevant regarding hair loss.
I was thinking caffeine may help, but caffeine works by inhibiting the DP1 pathway.
"PGD2 stimulates DP1 receptors on leptomeningeal cells of the basal forebrain to release adenosine as a paracrine signaling molecule to promote sleep."
"Consumption of caffeine antagonizes adenosine."
Kasper
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Re: Male pattern baldness

Post by Kasper »

This is information I found about L-PGDS. Read it if you're intrested:

"L-PGDS has at least two known functions. It is capable of synthesizing D-series prostaglandins, and it also can act as a carrier of lipophilic molecules (15). It has been reported to have a protective role in the development of atherosclerosis (16)."

"In summary, L-PGDS appears to regulate the balance between carbohydrate and lipid metabolism in BAT (Brown Adipose Tissue). The association between metabolic health and an ability to switch between carbohydrate and lipid metabolism is
already established; however, the ability of L-PGDS to control the balance between lipid and carbohydrate utilization, with only minor effects on metabolic rate, highlights a new type of control mechanism for whole organism substrate handling that could potentially be used to bypass states of nutritionally induced or genetic insulin resistance."

"We previously reported that mice lacking PPARγ2 had an unexpectedly normal metabolic phenotype [1]. In this study we have demonstrated that L-PGDS was up-regulated selectively in BAT and subcutaneous white adipose tissue and that L-PGDS in part compensated for a loss of PPARγ2 function. Simultaneous loss of PPARγ2 and L-PGDS synergistically caused glucose intolerance. Additionally mice lacking PPARγ2 and L-PGDS had elevated serum triglyceride compared to any other genotype."

"Lipocalin-type prostaglandin D synthase (L-PGDS) reportedly well predicts cardiovascular injuries in humans. ... In conclusion, patients with hypertension exhibited a higher level of L-PGDS in serum and urine, and this became increasingly obvious along with advance in renal dysfunction. These data suggest that L-PGDS metabolism is related to blood pressure and kidney injuries associated with hypertension. "

"Urinary L-PGDS excretion increased in the early stage of kidney injury in patients with type-2 diabetes mellitus. The urinary excretion was correlated independently with urinary protein excretion even when there was no difference in urinary protein or albumin excretions, thereby suggesting that urinary L-PGDS excretion is possibly a more sensitive indicator of renal injuries than proteinuria. Urinary L-PGDS may thus predict the progression of renal injuries in diabetic patients."

"In this context, Melegos et al. [5] and Hoffman et al. [6] have recently reported that the plasma level of L-PGDS increases in various forms of renal diseases and that the levels are correlated with plasma creatinine concentrations."

"As often happens in the history of proteins, lipocalin type prostaglandin D-synthase (L-PGDS) has been known and studied for many years under another name: β-trace. The protein was initially identified in the cerebrospinal fluid (CSF) in the early 1960s [1] but later found in many other tissues and biologic fluids. It is now well known that L-PGDS is very abundant in compartments beyond blood-tissue barriers, that is, in the CSF [2], [3], [4] and [5], in the aqueous humor [6], in the amniotic fluid [7], and in the seminal fluid (SF) [8](Fig. 1). The reason for such peculiar distribution is not known but must be related to its biologic role, which is still not understood completely."

Image

http://www.sciencedirect.com/science/ar ... 2402002809

"In the last few years, it has been shown that L-PGDS binds with high affinity bile pigments such as biliverdin and bilirubin [15], retinoids such as retinaldehyde and retinoic acid [16], thyroid hormones [15], and essential fatty acids such as docosahexanoic acid [17](Fig. 2). Thus, it was speculated that L-PGDS would act as a scavenger of toxic metabolites like bile pigments and/or a carrier of essential molecules for brain [18] and [19], retina [20], fetus [21], and sperm development [22]. Interestingly, the protein would not be capable of exerting both activities simultaneously because its ligands inhibit, in a reversible noncompetitive fashion, its enzymatic activity [15](Fig. 2)."

DHA may have a therapeutic role here? If you make sure L-PGDS is to bush with DHA etc, it won't be able to convert PGH2 to PGD2, and there may be more PGH2 left to convert to PGE2 (which seems beneficial for hair).
overkees
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Re: Male pattern baldness

Post by overkees »

I had terrible hairloss when I ate +4 avocados a day. I have alot of hair and was terrified of my severe hairloss after shampooing in the shower... One of the reasons I quit the avocados and began researching PUFAs again.

Now, with alot of coconut oil I now still have some hairloss (probably still from the avocados), but it's rapidly reducing. Avocados have 3500-5000 PUFAs in them, mainly n-6s. You can imagine eating 5-6 of them day after day. (30g of omega 6)
Kasper
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Re: Male pattern baldness

Post by Kasper »

Intersting overkees. However, PGE2 is associated with hair growth, which is also an AA product. Therefore I don't think that limiting omega-6 will solve all hair loss problems.

"In the CNS, L-PGDS gene expression is regulated by glucocorticoid, thyroid, and estrogen hormones [58], [59] and [60], whereas expression in the heart is regulated by estrogen alone [57]."

Fact: L-PGDS is upregulated in the scalp of MPB
Question 1: Where does this L-PGDS come from?

"L-PGDS is a member of the lipocalin superfamily [47] and is localized in the choroids plexus, leptomeninges, oligodendrocytes, and associated organs of the CNS [48], male genital organs of various mammals [49] and [50], and in the human and monkey heart [51] (Table 1) and is secreted into the cerebrospinal fluid, bloodstream, amniotic fluid, interphotoreceptor matrix, urine, and seminal plasma [52]. "

I'm not able to answer this question, but I would guess the L-PGDS in the scalp must comes from the CNS ??

Question 2: Which factors regulate L-PGDS gene experssion?

"In the CNS, L-PGDS gene expression is regulated by glucocorticoid, thyroid, and estrogen hormones [58], [59] and [60], whereas expression in the heart is regulated by estrogen alone [57]."
"Our results provide a molecular basis for the reported down-regulation of the PGDS gene in the hypothyroid rat brain. Interestingly, the lipocalin-type PGDS is together with the major urinary protein in mouse liver the second member of the lipocalin family found to be regulated by T3 [8]."
"Dexamethasone induces lipocalin-type prostaglandin D synthase gene expression in mouse neuronal cells"
"Estradiol differentially regulates lipocalin-type prostaglandin D synthase transcript levels in the rodent brain: evidence from highdensity oligonucleotide arrays and in situ hybridization"
"We have previously demonstrated that estradiol differentially regulates L-PGDS transcript levels in the rodent brain. In hypothalamic nuclei, estradiol increases L-PGDS transcript expression, whereas in the ventrolateral preoptic area L-PGDS gene expression is reduced after estradiol treatment"

This information suggest that hypothyroidism and estradiol may be helpfull against balding.
But in reality things are probably a million times more complicated...

"Consequently, the regrowth of normally pigmented hair shafts after chemotherapy-induced alopecia was significantly accelerated in the 17-beta-estradiol treated group. Our data encourage one to explore topical estrogens as a potential stimulant for hair re-growth after chemotherapy-induced alopecia."

"Due to unwanted side effects like gynecomastia, E2 should not be used in men because very high topical doses seem to be required to obtain measurable hair growth effects (84), whereas the inactive stereoisomer 17α-estradiol may also be prescribed for men. "

"Treatment of chondrocytes with IL-1beta upregulated L-PGDS mRNA and protein expressions as well as PGD2 production in a dose- and time-dependent manner. "
Kasper
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Re: Male pattern baldness

Post by Kasper »

http://www.hairlosshelp.com/forums/mess ... did=103373

This one explains a bit more about L-PGDS/PGD2/DHT connection.
dime
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Re: Male pattern baldness

Post by dime »

17α-estradiol is Alfatradiol/Pantostin, this is what I put on my scalp. It has like 10% efficacy in 6 months if I'm not mistaken.
Kasper wrote: "In the last few years, it has been shown that L-PGDS binds with high affinity bile pigments such as biliverdin and bilirubin [15], retinoids such as retinaldehyde and retinoic acid [16], thyroid hormones [15], and essential fatty acids such as docosahexanoic acid [17](Fig. 2). Thus, it was speculated that L-PGDS would act as a scavenger of toxic metabolites like bile pigments and/or a carrier of essential molecules for brain [18] and [19], retina [20], fetus [21], and sperm development [22]. Interestingly, the protein would not be capable of exerting both activities simultaneously because its ligands inhibit, in a reversible noncompetitive fashion, its enzymatic activity [15](Fig. 2)."

DHA may have a therapeutic role here? If you make sure L-PGDS is to bush with DHA etc, it won't be able to convert PGH2 to PGD2, and there may be more PGH2 left to convert to PGE2 (which seems beneficial for hair).
At some point I got measured really high bilirubin, 2.5x the normal; last time I measured it was 1.4x. Maybe there's some connection to L-PGDS..
overkees
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Re: Male pattern baldness

Post by overkees »

PGD2 is derived from Arachidonic acid (an omega 6).
Some more light on the PGD2 and baldness connection:

Prostaglandin D2 Inhibits Hair Growth and Is Elevated in Bald Scalp of Men with Androgenetic Alopecia
Kasper
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Re: Male pattern baldness

Post by Kasper »

Yes, PGD2 inhibits hair growth.
It is shown that PGD2 is high in balding scalp and L-PGDS is upregulated.
L-PGDS converts PGH2 to PGD2.
PGE2 is downregulated in balding scalps.
RRM wrote:How about trying a topical H-PGDS inhibitor?
I've heard that some people try this, but without any effect. This may be because that not H-PGDS, but L-PGDS causes PGD2 to be upregulated.
Some people speculate that COX inhibitors may be effective, to lower PGD2 in the balding scalp. However, you will not only downregulate PGD2 but also PGE2, and it is thought that PGE2 is important for hair growth.
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