For the last few years my fingertips have been very dry and cracked. I am in my mid-sixties, and on the STAT4 gene I have the rs7574865-GT SNP according to 23andme, with an OR of 1.24 for "Limited Cutaneous Schleroderma", so I pay a lot of attention to "keeping skin looking young". I also have minor symptoms associated with the T risk allele (occasional hard dry patches of skin on hands) most of my life, not that visible but annoying (Sometimes I will go several months without symptoms). Fortunately I am heterozygotic with GT rather than homozygotic with TT at rs7574865.
After trying just about everything in this thread and other threads over the years (including ointments, lotions...), I tried 500-1000 mg of oral hyaluronic acid daily. I compared brands and found results consistent with what piet3r is reporting with Jarrow HA. I actually notice results in the (4 caps * 50mg) daily range, and by 16-20 caps my skin is clear during active flareup.
Some of the other brands at much higher doses (2-3 times higher) still didn't have the impact that Jarrow did (they advertise a lower average molecular weight HA). I usually notice a small improvement by the next day and by 3-7 days my symptoms are almost gone. It is about the same schedule for the symptoms to reappear after halting oral HA. I understand that different molecular weight HA versions are "advertised" as targeting different problems. For me the issue is skin and not arthritis, so low weight HA seems to be best.
Since HA is expensive, and ingesting large amounts raises other concerns, I decided to look into hyaluronidase inhibitors to try to modify the hyaluronan creation/destruction cycle. I wanted to use known inhibitors with citable research, and that also might be useful for other things in my case (minor allergies like hay fever)
Here is a thread discussing port-site metastasis of cancer following surgery:http://www.longecity...plements/page-4
http://www.ncbi.nlm....pubmed/11353970
I asked my dermatologist if oral HA was a risk, and he didn't seem too concerned... which concerns me! The doc then prescribed prescription topical HA. Topical HA wasn't nearly effective as oral HA in my case.
Hyaluronidase Inhibitor Supplements:
1.) Quercetin, 800 mg, BID loading dose, cut back to 1/day.
Since I also have allergies this addition might have other benefits.
2.) Horse Chestnut, 250 mg (22% Aescin) BID
3.) NAC, 600 mg
4.) Fucoidan, 300 mg (77% fucoidan), 1-2/day, usually 1
Some people on this site are using Triphala for hyaluronidase inhibition. I decided to try fucoidan.
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After increasing the intake of the hyaluronidase inhibitors listed above, I was able to drastically reduce my intake of oral HA (75% reduction or more) to achieve similar effects, and save $$$ (20 caps of Jarrow HA per day works out to about $100/month at Swanson).
I also take other skin supplements, like collagen, Biosil, pomegranate, K2, etc., but HA is the only supplement with the "wow" factor for skin.
"ingesting large amounts raises other concerns"
What are these concerns?
There is a lot of conflicting information over the net.
http://www.denvernat...uronicacid.html
and a reply http://www.denvernat...ews/sardiHA.htm
actually, niner and ironfistx were talking about this in the thread I linked to above. Here is a link to niner's actual response:
http://www.longecity...ndpost&p=566342
The issue is that there continues to be discussion and concern... and published papers (as linked). I guess niner's comment does raise questions:
"It seems like a bad plan to take HA if you have a known cancer. The tricky part would be the case of the unknown cancer..."
So... given that HA is extremely effective in my case at higher doses (as described), similar to the reports from piet3r, I just wanted to experiment on getting similar effects by lowering the external oral HA and increasing hyaluronidase inhibitors, at lower cost. It worked. (Your Mileage May Vary)
I have been experimenting for about 1.5 years on an N=1 sample. So far, oral HA is extremely fast acting and effective at improving my skin (and friends not part of the N=1 study since I do not have their genetics after extreme prodding). The hyaluronidase inhibitors are not fast acting, in contrast to the fast acting direct HA supplementation.
The fast acting nature of HA is what first made me consider the hyaluronidase inhibitors. However... there remain concerns open to debate on HA, as illustrated in recent posts on this forum.
Obviously there are also concerns about all of the hyaluronidase inhibitors I take in my list. Perhaps one of the things that might be a next test would be to substitute luteolin for quercetin. Triphala for fucoidan might be a good switch too (some folks on this site take triphala, and it is cheaper!)
http://www.ncbi.nlm....les/PMC2615542/
I guess I was just trying to save $$$, since HA is expensive and I take other things too.
Once I got into the longer term hyaluronidase inhibitor phase (about 2 months), I found I could save money and have better results than HA only - and *possibly* lower the overall risk profile. There are a lot of hyaluronidase inhibitors out there, so I focused on those that might bring added benefit to my particular case, in addition to their hyaluronidase inhibiting properties.
Thanks for the question. I am just learning from you folks on this forum!
