Bit-o-feedback on my custom topical

[Only Natural]

I'm on my second bottle of my latest  custom topical, which consists of Nanosomal SOD, biotin, and royal jelly etc.  Things are still going good thanks to this and the other products(including most of the other Elsom topicals) I'm using.  This custom I use at least every other morning.

Major plus for this product is it's lack of odor and  zero visibility on the scalp.  Absorbs very quickly.

Just added NanoFibrin and Giga-C...so we shall C how things proceed.

This was brought to my attention in another forum(I wonder how this will affect what NanoFibrin is made to do... Dr Yechiel?)

Antifibrotic action of Cu/Zn SOD is mediated by TGF-beta1 repression and phenotypic reversion of myofibroblasts.

[My paper] M C Vozenin-Brotons, V Sivan, N Gault, C Renard, C Geffrotin, S Delanian, J L Lefaix, M Martin Laboratoire de Radiobiologie et Etude du Génome, DRR, DSV, CEA, Saclay, France.

Skin fibrosis is characterized by the proliferation and accumulation of activated fibroblasts called myofibroblasts. They exhibit specific cytoskeletal differentiation, overexpress the fibrogenic cytokine TGF-beta1, synthesize excess extracellular matrix compounds and exhibit a depleted antioxidant metabolism. Recently, SOD was successfully used as an antifibrotic agent in vivo, thus challenging the postulate of established fibrosis irreversibility. We postulated that myofibroblasts could be a direct target for this therapeutic effect. To test this hypothesis, we used three-dimensional co-culture models of skin, in which specific phenotypes of normal fibroblasts versus myofibroblasts are retained. These 3-D models were treated with liposomal and carrier-free Cu/Zn SOD, and examined for their effects on cell number, cell death, and phenotypic differentiation. The results show that SOD did not induce myofibroblast cell death, whereas it significantly reduced TGF-beta1 expression, thus demonstrating that SOD might be proposed as a potent antagonist of this major fibrogenic growth factor. We also found that SOD significantly lowered the levels of the myofibroblast marker alpha-sm actin, of beta-actin, and of the extracellular matrix components alpha1(I) collagen and tenascin-C. In conclusion, our results suggest that SOD antifibrotic action occurred in vitro through the reversion of myofibroblasts into normal fibroblasts.

[DrYechiel]

Hello Only Natural,

The article you refer to was written in the year 2000 and published in 2001. Before commenting on it, it is necessary to give credit to the authors and publisher.

The title of the article is “ANTIFIBROTIC ACTION OF Cu/Zn SOD IS MEDIATED BY TGF-b1 REPRESSION AND PHENOTYPIC REVERSION OF MYOFIBROBLASTS”

The authors, from diferent organizations in France, are: “MARIE-CATHERINE VOZENIN-BROTONS, VIRGINIE SIVAN, NATHALIE GAULT, CHRISTINE RENARD, CLAUDINE GEFFROTIN, SYLVIE DELANIAN, JEAN-LOUIS LEFAIX, and MICHELE MARTIN.

The article was published  in the journal Free Radical Biology & Medicine, Vol. 30, No. 1, pages 30–42, 2001. Free Radical Biology & Medicine is available through Science Direct, so any good public or university library should be able to provide the full text electronically.

As usual, when one reads the entire article the focus point of the article may somewhat shift from that hinted at by the abstract. I believe that the most important statement in the article is “the above observations suggest that the myo-fibroblastic differentiation is reversible” which means that myo-fibroblasts which are predominant in fibrotic tissue can be replaced with normal fibroblasts and that fibrosis is reversible. Though these are not the first researchers who believe in that possibility, the statement is well corroborated by their experiments. Moreover, they show that this is not only very likely but that it is also a practical target to achieve rather than one more utopian, hard-to-implement mechanism which is sometimes taken to be practical by readers. The reduction in TGF-b1 is significant for the modulated fibroblasts (myo-fibroblasts) which comprise fibrotic or scar tissue but may not be the modus operandi via which myo-fibroblasts are replaced by fibroblasts. Myo-fibroblasts express protein with contractile abilities such as a-sm actin b-actin (thus, the attribute “myo” which is typical of muscle cells). The authors show that Cu/Zn-SOD directly induced significant down regulation of a-sm actin and b-actin at both the protein and mRNA levels in myo-fibroblasts rather than via TGF-b1.

The other argument in the article is that myo-fibroblasts are not simply dying and being replaced by normal fibroblasts but rather change or normalize or de-differentiate into normal fibroblasts. So, the reduction in TGF may not be the channel through which the de-differentiation of myo-fibroblasts into fibroblasts takes place but rather a coinciding effect. This argument still needs more work before it can be considered as a very likely possibility but it is quite interesting. In a paper that I published in the early eighties, there is an argument about liposomes that trigger de-differentiation of muscle cells, so I believe that the phenomenon may be valid but the article does not have enough data to make it a sound argument.

As for topical SOD, it will be useless on its own or with conventional vehicles but with a good delivery system with good penetration it could have some in vivo effect when applied on skin. The authors used liposomes to penetrate a multi-layer of cells and it is not clear whether this was more successful than their control, which did not use liposomes. However, I know that it is possible now to formulate liposomes for excellent topical penetration.

One more thing which relates to our NanoFibrin™. By removing many skin layers, topicals become more effective and more penetrating because they have fewer layers of dead skin to cross and penetrate before they come closer to the live cells. In addition, NanoFibrin™ stimulates rapid turnover of skin layers which means that new live fresh skin replaces the old fibrotic skin in a simple and natural way. And while we are at this, DO NOT use NanoFibrin™ in conjunction with any other physical or chemical treatment which penetrates to the live skin layers (such as puncturing the skin with multi needles attached to some roller).

[Only Natural]

Thanks for the response.  I'd be interested in your views on follicles dying or never dying or who-in-the-world knows for sure. Dealing with fibrosis should help if they're still "alive"..obviously. 

[DrYechiel]

Hello Only Natural,

Your question is a very difficult one and there is no solid answer to it. However, there is a good way to evaluate the large magnitude of data in a way that can strongly indicate that the likelihood of retrieving hair is high indeed and that the current knowledge about such a feat is not quite sufficient but not lightyears away from coming through.

I will start with an analysis of a related issue to explain the parameters on which I base my observations:

Every species of animal has a median life expectancy which can vary greatly from other animal species. There are also sub-groups within each species which can be categorized as different groups on the basis of median life expectancy. Rats can live an average of 2.5 years but there are certain rat sub-groups which have about 3 year median life expectancy (Group 1) and sub-groups with a 2 year median life expectancy (Group 2). Within each sub-group, there may be individual rats which live much longer than the median life expectancy of their group. If an individual rat from Group 1 and an individual rat from Group 2 both succeed in surviving 3.5 years, we may not even realize that they are from different groups. However, these extreme and rare individuals can hint at the potential life span of their groups. Life span is different from life expectancy in that it relates to the internal potential of a group. One exceptionally long-lived rat cannot alter the statistics of what is probable for other members of a very large group, but it is enough to change our thinking about the potential life expectancy of the entire group. This means that it may be possible to increase life expectancy of a group by changing external conditions, food, temperature and other such parameters by which the rats in that group will live longer. No rat in any of the sub-groups was ever reported to live 6 years, so 6 years is more than their potential life span but 3.5 years (which does occur, although very rarely) can be  considered the potential life span of the entire group and it may be possible to try to increase life expectancy to match life span by some intervention. So, one or a few individuals with long life spans have great value in telling us the “outer limits of that group’s life expectancy”, which is actually the groups’ life span. The same goes for humans as whole organisms, and for human biological processes such as balding.

Human life expectancy used to be about 40 years and has almost doubled now, but human life span is still the same. Even when people routinely died at the ripe old age of 40, there were exceptional people living to 110 or even 120 years. Few achieved such long lives, but the fact that it could occur made a solid statement about the potential of the entire human species. We see, now that the human median life expectancy has almost doubled, there are still the same exceptional individuals who make it to 110-120 years. If we exclude the Biblical documentation of people living about a millennium for this discussion, as far as the records indicate no one is known to have survived 140 years in the last three millennia and 120-125 years seems to be about the high limit for humans or the human life span (maybe 127 year if we can trust every report). The doubling of life expectancy (for the group) with a constant (and un-changed) life span (for exceptionally long-lived individuals) over millennia proves the significance of one or a few exceptional cases as markers for the ability of the entire group. Even now there are societies with a median life expectancy of more than 90 years but none of that group has made it above 120-125 years. That group is living in a way which allows their routine life expectancy to reach close to their maximum life span and there can be many lessons learned from closely observing such a group.

There are actually many cases (though fewer could be enough for this purpose) where people grew healthy, thick, and quite long new hair including a case I observed personally of an old man who grew a nice head of black hair after receiving chemotherapy for cancer. Before that, he was almost completely bald and the sparse hair he had was white. He is now starting to bald again and getting gray again but still retains most of his new hair. Apparently, his follicles were rebooted (or re-generated?), woke up and went back to doing what they did when he was young; now they are returning to doing what they did when he was old. We know that shock can cause people to gray. People call it to “gray over night”. Well, it may not be overnight but the phenomenon is well known and documented. It was probably the shock of the cancer treatment which caused him to grow new black hairs. In fact, many of the suggested therapies for balding are based on injury/trauma to the scalp (needles…) for the purpose of inducing new growth. Injury/trauma causes different and also antagonizing chemicals to secrete and the system responds to trauma by awakening sleeping mechanisms for renewal. The big problem is that trauma is random as far as generating a positive response but the trauma is in itself very damaging to the tissues it affects. The chances are so much bigger that trauma will result in more injury, more baldness, more scar tissue, and less viable hair roots that it is risky (closer to the level of insanity) to tear down for the purpose of rebuilding because what you tear down is done but you may never build again. Also, deep peeling is not recommended as a method of rejuvenation because it injures live skin or scalp cell layers. Only mild peeling which accelerates removal of dead skin or scalp layers and facilitates resurfacing of new skin is safe and worthwhile to use. Mild peeling will stimulate the need for cell division by removing dead cell layers on the surface.

Even without understanding the complexities and intricacies of my theory of “Dynamic Synergy” (as discussed in the July 2008 Journal of Topical Formulations at http://www.topical-formulations.com/topical/200807/dynamic-synergy.htm), it should be clear that generating a multitude of different chemical environments over short time periods will trigger skin responses to these different chemical environments. As a result, renewal mechanisms are awakened (just as in “successful” trauma, but without the trauma), which may respond dramatically. The added benefit of Dynamic Synergy is that the different chemical environments are not arbitrary but well calculated to generate a large stimulating effect and with readjusted feedback interactions (which will better and longer maintain the outcomes from the renewal mechanisms).

If anything may currently close the gap between the outer limits of maintaining or regrowing hair and the median (average) time that people maintain hair or are able to regrow hair, it’s the implementation of the Dynamic Synergy theory. We have worked for this purpose for years and built a comprehensive scalp regimen on the premise of Dynamic Synergy (the regimen is described at http://www.elsomresearch.com/learning/how2/scalpcare-regimen.htm). Note: Our regimen is not medicinal and we make no claims that our regimen is intended to or can maintain or regrow hair because those would be medicinal claims.

[Only Natural]

Thanks again for the response.

I've never been that interested in wounding/needling for the reasons you laid out there.  Your Dynamic Synergy theory is something I'll have to read a few more times  I have, ever since using treatments, taken breaks from topicals and/or rotated a number of them, etc. I also like to ease on to new topicals so as not to shock my follicles out of my scalp.  Except for the NanoFibrin, which I used as recommended- once a day for a week.

I've gotten quite a few complements lately on my "new hair cut".  Nothing has changed in the way it was cut or anything, so after having it grown out a bit it's nice to hear such complements with the shorter style again.

I also swear I see smaller hairs peeping out,  nearly 2 weeks since the start of using NanoFibrin. Not the peach fuzz you normally see in certain lighting on slick areas, but longer ones. Whether they'll amount to anything in the long run remains to be seen.  I'm not one to study my scalp on a daily basis..so all of this could just be an ongoing development.