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ALA as a solution for discoloration


ALA as a solution for discoloration

Massappeal is right it is hemosiderin.

My understanding is that during jelqing blood is forced into the interstices where it is consumed by macrophages. Over time the macrophage hemosiderin accumulates because of overloading the removal mechanism.

The way that this is treated dermatologically is with lasers.

However when hemosiderin accumulates in the body it is treated with chelation. Desferal bind to hemosiderin and not hemoglobin.

So, for our purposes I believe a topical chelating agent would be the best bet.

My suggestion is Alpha Lipoic Acid. It is an anti-oxidant, water and fat soluble, small enough to absorb through the skin, has wide spread cosmetic use and is cheap and readily available.

I am currently experimenting with adding it to my minoxidil/contact lense growth accelerator lube solution. The only caution I have about ALA is that it could be unstable in liquid, so you might have to mix it every couple of days.

Or you could try any number of commercially available ALA creams.


gstlynx -

Do you have any product names of these commercial ALA creams?


Dr. Perricone is making a fortune of these things right now, so that is one brand. But just search google. Personally, I buy bulk ALA from beyond a century for health/bodybuilding and now just add it to my minox solution.

By what mechanism would alpha lipoic acid help?

Here are my thoughts about long-lasting discoloration.


I read your ideas before, and actually I got some good direction from it. Your mention of Vitamin C is interesting in this regard because Vitamin C is used in conjuction with chelation in hemosiderosis in order to speed clearance of iron.

I am pretty sure that chelation is the direction to take, now whether or not ALA is the perfect chelator in this regard, I don’t know. IP6 looks good too.

But here are some abstracts guiding my investigations now.


Int J Legal Med. 1994;107(2):60-8. Related Articles, Links

Histological and enzyme histochemical parameters for the age estimation of human skin wounds.

Betz P.

Department of Legal Medicine, University of Munich, Germany.

Routine histological staining techniques form the basis of a forensic age estimation of human skin wounds and the determination of vitality is aided by the detection of neutrophilic granulocytes which appear earliest about 20-30 min after wounding. A clear granulocyte infiltration and a significant increase in the number of macrophages indicates a post infliction interval of at least several hours. Macrophages containing incorporated particles such as lipophages, erythrophages or siderophages appear earliest at a wound age of 2-3 days similarly to extracellular deposits of hemosiderin, whereas the rarely detectable iron-free pigment hematoidin and spot-like lymphocytic infiltrates in the granulation tissue appear approximately one week or more after wounding. A complete reepithelialization of surgically treated and primarily healing human skin lesions can be expected earliest 5 days after wound infliction and the absence of a complete new epidermal layer indicates a survival time of less than 21 days. Enzyme histochemical methods allow a wound age differentiation especially in the range of a few hours. An increase in nonspecific esterases can be observed earliest approximately 1 hour after wounding followed by other enzymes such as acid phosphatase (approximately 2 h), ATPase (approximately 4 h), aminopeptidase (approximately 4 h) or alkaline phosphatase (approximately 4 h). Positive results, however, cannot be regularly found. Therefore, the detection of reactive changes is useful for a wound age estimation whereas negative findings, which in general must be interpreted with caution, can provide information only in a limited number of histological parameters.

Int J Legal Med. 1996;108(5):262-4. Related Articles, Links

Morphometrical analysis of hemosiderin deposits in relation to wound age.

Betz P, Eisenmenger W.

Department of Legal Medicine, University of Munich, Germany.

A morphometrical analysis of the extent of hemosiderin deposits in 71 human skin wounds with post-infliction intervals between 2 days and 7 months was performed. Earliest positive findings were detectable in a lesion aged 3 days, and with increasing wound age an increase in the amount of hemosiderin occurred. A value of more than 20% of the microscopic field with hemosiderin deposits was found earliest 8 days after wounding and therefore the detection of considerable amounts of hemosiderin (arbitrarily defined as 20% or more of the evaluated area) indicates a minimum wound age of approximately 1 week. Since the extent of hemosiderin formation depends upon the extent of the initial hemorrhage and a “physiological” reduction in the amount of this pigment with advanced wound age, slight or absent hemosiderin deposits cannot provide information on the post-infliction interval.

Exp Eye Res. 2003 Feb;76(2):241-8. Related Articles, Links

Alpha lipoic acid changes iron uptake and storage in lens epithelial cells.

Goralska M, Dackor R, Holley B, McGahan MC.

Department of Molecular Biomedical Sciences, North Carolina State University, 4700 Hillsborough Street, Raleigh, NC 27606, USA.

Alpha lipoic acid (LA) is a cofactor in mitochondrial dehydrogenase complexes. Previous studies have shown that when administered exogenously LA has antioxidant properties, which include free radical scavenging, metal chelation and regeneration of other antioxidants. The cells convert LA into dihydroplipoic acid (DHLA), which in the presence of iron can act as a prooxidant. In vitro DHLA reduces Fe(+3) to Fe(+2) and removes iron from ferritin, increasing the risk of Fe catalyzed free radical formation. In the present study we examined the in vivo effects of lipoic acid treatment on Fe metabolism in cultured lens epithelial cells, and found that LA decreases Fe uptake from transferrin, increases Fe deposition into ferritin and increases the concentration of this protein. When administered together with ascorbic acid, lipoic acid changes the characteristic heavy to light chain ratio of ferritin makeup. The decreased Fe uptake and increased storage diminishes the size of the cytosolic highly reactive Fe pool (LIP). These changes are associated with increased cell resistance to H(2)O(2) challenge. Therefore, LA may reduce the risk of Fe induced oxidative damage and also might be useful as a treatment of Fe overload. Copyright 2003 Elsevier Science Ltd.

Ok, so if ALA isn’t the right way to go, then there is always IP-6, phytic acid,
probably a combination of the two for chelation and then something else to cause a skin flush to facilitate removal of remaining chelates.

Biochem J. 1993 Sep 15;294 ( Pt 3):929-34. Related Articles, Links

Inhibition of iron-catalysed hydroxyl radical formation by inositol polyphosphates: a possible physiological function for myo-inositol hexakisphosphate.

Hawkins PT, Poyner DR, Jackson TR, Letcher AJ, Lander DA, Irvine RF.

Department of Biochemistry, AFRC Institute of Animal Physiology and Genetics Research, Babraham, Cambridge, U.K.

1. The ability of myo-inositol polyphosphates to inhibit iron-catalysed hydroxyl radical formation was studied in a hypoxanthine/xanthine oxidase system [Graf, Empson and Eaton (1987) J. Biol. Chem. 262, 11647-11650]. Fe3+ present in the assay reagents supported some radical formation, and a standard assay, with 5 microM Fe3+ added, was used to investigate the specificity of compounds which could inhibit radical generation. 2. InsP6 (phytic acid) was able to inhibit radical formation in this assay completely. In this respect it was similar to the effects of the high affinity Fe3+ chelator Desferral, and dissimilar to the effects of EDTA which, even at high concentrations, still allowed detectable radical formation to take place. 3. The six isomers of InsP5 were purified from an alkaline hydrolysate of InsP6 (four of them as two enantiomeric mixtures), and they were compared with InsP6 in this assay. Ins(1,2,3,4,6)P5 and D/L-Ins(1,2,3,4,5)P5 were similar to InsP6 in that they caused a complete inhibition of iron-catalysed radical formation at > 30 microM. Ins(1,3,4,5,6)P5 and D/L-Ins(1,2,4,5,6)P5, however, were markedly less potent than InsP6, and did not inhibit radical formation completely; even when Ins(1,3,4,5,6)P5 was added up to 600 microM, significant radical formation was still detected. Thus InsP5s lacking 2 or 1/3 phosphates are in this respect qualitatively different from InsP6 and the other InsP5s. 4. scyllo-Inositol hexakisphosphate was also tested, and although it caused a greater inhibition than Ins(1,3,4,5,6)P5, it too still allowed detectable free radical formation even at 600 microM. 5. We conclude that the 1,2,3 (equatorial-axial-equatorial) phosphate grouping in InsP6 has a conformation that uniquely provides a specific interaction with iron to inhibit totally its ability to catalyse hydroxyl radical formation; we suggest that a physiological function of InsP6 might be to act as a ‘safe’ binding site for iron during its transport through the cytosol or cellular organelles.

PMID: 8379947 [PubMed]

In Vitro Cell Dev Biol. 1986 Apr;22(4):177-9. Related Articles, Links

Phosphate compounds as iron chelators in animal cell cultures.

Rasmussen L, Toftlund H.

We have studied the capacity of a number of phosphate compounds to act in the double role as a phosphate source and a detoxifier of ferric chloride hydroxo compounds, i.e. as Fe(III) chelators. The tested compounds were: orthophosphate, trimetaphosphate, alpha-glycerophosphate, beta-glycerophosphate, phytic acid, and phosphorylcholine; the test organism the ciliate protozoon Tetrahymena thermophila, an animal cell; and the nutrient medium was synthetic, consisting solely of low-molecular-weight compounds. We assessed growth rates of cells in two experimental series. First, phosphate-starved cells were exposed to the tested phosphate compound as the only phosphate source and the ferric chloride concentrations were varied stepwise from 0 to 1000 microM. Second, we offered the cells orthophosphate as a phosphate source and selected phosphate compounds as chelators. The cell growth results allow the following conclusions: orthophosphate, trimetaphosphate, alpha-glycerophosphate, and beta-glycerophosphate are excellent phosphate sources; trimetaphosphate, alpha-glycerophosphate, beta-glycerophosphate, and phytic acid are excellent Fe(III) chelators; of the tested compounds trimetaphosphate, alpha-glycerophosphate, and beta-glycerophosphate are excellent in the double role as a phosphate source and a ferric chloride hydroxo detoxifier, i.e. as a Fe(III) chelator.

PMID: 3700321 [PubMed]…ytic%20acid.htm

Phytic Acid: Derived from Rice Bran, Phytic Acid (IP6) offers high level, varied benefits to cosmetics

Phytic Acid (inositol hexaphosphate / IP6) has been researched widely in recent years for its anti-cancer action. Phytic Acid is found in Rice Bran at high levels (approx. 10-15%). More recently, the cosmetic effects of Phytic Acid have been researched and the results are impressive.

Overview of researched effects:
Phytic acid has been proven to have the following cosmetic effects:
- Increases the elasticity of skin
- Anti-wrinkle agent
- Sebum regulation
- Moisturising
- Antioxidant

As well as the above reported effects, Phytic acid is possibly the most potent natural chelating agent. It also has more ‘in-depth’ activity, for example Inhibition of UVB-induced signal transduction (see below ‘further information’ for details).

Effects in figures:
Through the research and tests that have been performed, just 0.5% of our Phytic Acid in cosmetic formulae (versus placebo) has been proven to have the following effects:

- Increases skin moisturisation by 42%
- Improved elasticity by 7% (people in 20s-30s) and 14% (people in 40s-50s)
- Sebum values were normalised in both dry and oily skins
- Skin lightening improvement of 6%
- Wrinkle reduction of 16.9%

Those are my thoughts for now.

I hope you’re on to something. Are you using straight R-ALA or the more common stuff that is a mix of R-ALA and S-ALA?


I use R-ALA because I have read that it is more bioactive. It is not that expensive if bought in bulk, like from beyond-a-century.

Originally Posted by gstlynx
I am currently experimenting with adding it to my minoxidil/contact lense growth accelerator lube solution. The only caution I have about ALA is that it could be unstable in liquid, so you might have to mix it every couple of days.


Can you explain why you are doing this - is it simply to create your own personal solution instead of using an otc cream, or is there more to the idea?

Thanks - - very interesting stuff.


I take it that you have just started using your “special mix”. Please keep us updated as to its effectiveness. Are you going to document with before and after photos? Do you have bad discoloration? And just one more, what method of PE do you think has contributed most to your discoloration?


Here is an update on my ALA as a way to chelate the hemosiderin causing the bronze look to my penis skin from Jelqing.

I tried 2% ALA in a solution of 50% minoxidil(5%)/50% Boston RGP Contact lense solution. This was too strong. ALA is a weak acid, but acid nontheless, so it caused the skin to peel.

Next, I diluted it down to .5%, same solution. And this is working. My skin is returning to a more tanned look, rather than bronze, the skin folds are not really changing as fast as the rest.

Unfortunately, I don’t have pictures, but I will keep everyone posted on the ongoing experiment.

As an aside, I have reduced my use of minoxidil in jelqing , to just the first application. Which means 1 ml of above solution(50% minox/50%Boston,.5% ALA).

I was noticing rapid eyebrow growth. I am pretty sure that this is because the jelqing causes much more absorption of the solution than does simply applying it to my head, where I use it to prevent further receding of my hairline.

I wonder how much effect is from exfoliation vs. chelation. For a while I used a mild alpha hydroxy acid cream on my shaft. I didn’t stick with it long enough to tell if it helped or not. I’ll try it again since I’m on a break. Thanks for reminding me. :)


Is this the thing to use?

>And this is working. My skin is returning to a more tanned look, rather than bronze, the skin folds are not really changing as fast as the rest. <

OK, this is very cool. I wonder why the skin folds are changing more slowly. How long have you been using the cream, and also how much would you say the discolouration has faded, like maybe as a %?

>Unfortunately, I don’t have pictures, but I will keep everyone posted on the ongoing experiment. <

Awesome stuff dude, please do.


That link doesn’t work, but if it was some sort of cream then that could work, but it is not my style. I always make it myself.

In this case I buy bulk, powdered R-ALA from beyond-a-century, I mix it as I stated above, now @ .5%, originally 2%.

Minoxidil releases Nitric Oxide (miNOxidil). As we all know NO is key to initiating and maintaining erections by relaxing smooth muscle. Additionally, Minoxidil increases VEGF, IGF-1, etc.


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