As a counterpoint: I have a small amount of Daxxify (a longer-lasting variant of Botox) injected around the outside of my eyes (i.e. crow’s feet) every six months. It’s partly aesthetic, but the decrease in my facial tension was life-changing.
I hold stress in my face, and tension around my eyes had been a near-constant since my mid 20s. I tried various relaxation techniques, facial exercises, and topicals. I saw an optometrist and later an ophthalmologist to rule out a vision issue (like squinting ). I even tried a muscle relaxant once. Nothing worked. And the constant tension would eventually give me base-of-skull headaches.
The morning after my first Daxxify injection, I woke up to a fully relaxed face. It became a permanent part of my budget after that. I can’t speak to more extensive treatments (e.g. brow and forehead), but the amount I receive doesn’t impair my facial expressions. It does soften the smile lines around my eyes, which I suspect slows the appearance of wrinkles—and makes me look younger.
For HA serum I don’t use transcutol, only na-pca. I posted a link on Amazon some time ago. It’s only $10. Search on this forum. There are several posts about it.
That’s an excellent use of Botox!!! That makes sense because a lot of people also have success using it for migraines. If you have documented headaches that your doc has been helping you with, there is a chance you could get it covered by insurance. Might be worth checking out?
For clarity, I was responding someone who didn’t want it but was being pressured with a fear tactic. In her case, she discovered it was not true. I am in no way anti Botox, my face is basically Chernobyl
I was referring to people in 20s, most of whom can’t even afford their rent, using it for prevention because they are being told the wrong thing. For most people, 20s is long before they would have a wrinkle forming.
If the elastin problem can’t be solved all the topical creams and lotions in the world won’t save your skin.
There is no known way to restore elastin, with any significance.
Our system stops producing elastin around puberty and does not make any new elastin after that.
Elastin has a 70 year half life. Think about what that means. Making too much elastin would be harmful due to it’s incredibly long half life. If a way to restart elastin production was developed it would also need a way to shut it off due to the extremely long half life.
Where else is elastin important? any part of your body that can stretch and rebound has an elastin component. Your heart, your lungs, your tendons and ligaments, etc.
Without elastin we die.
This is one of the most rate limiting process for humans and one of the main reasons we can’t live past 120.
Until the elastin problem is solved there is no “rejuvenation” and there is no real “longevity”
Everything is a balancing act. As Doxy is an antibiotic it has the potential for harming the gut microbiome. It may be possible to counteract that negative effect with diet and pre and pro biotics, exercise, etc.
Interesting find, thanks for bringing this information to the table!
Some publications suggest doxy- or minocycline taken at low doses do not exert significant antimicrobial activity, which may prevent the disruption of normal flora and reduce the risk of developing antibiotic resistance. Low dose doxy- or minocycline is mostly used for its potential anti-inflammatory effects.
But on the other hand: a recent study concluded that a year after one time antibiotic use, there were still observable changes in the intestinal microbiome. Whereas earlier studies suggested after one-time use the microbiome commonly recovers within months. Imho this confirms again there are likely so many things about the microbiome that we don’t known yet.
Personally I wouldn’t dare to use doxy- or monocycline on a regular basis; let alone taking a low dose daily.
I’m always a bit surprised when it is brought up that some pre- and probiotics can resolve dysbiosis caused by antibiotics. Most commonly the ability of probiotics to establish permanent residence is limited. (That’s besides the fact that we’re just randomly using some strains with no idea whether they may start to dominate/outcompete other strains while using the probiotic, etc. And that’s besides the fact that many probiotics may not even be active anymore - albeit some research suggests ‘dead’ probiotics may still have some effects on the microbiome, potentially apparently because of ‘bioactive compounds that are released when bacterial cells dissolve in the digestive system’).
I concur (always wanted to use that one) that taking low dose antibiotics is not for me either due to the high potential for unintended consequences. At least with our fav experimental drug Rapa it appears to have some benefit to the gut microbiome.
Agreed on the gut “helpers” thing as it remains a significant mystery and there are significant “works”, “doesn’t work” studies on how to restore/maintain it.
I just did a quick headline review on the Doxy effects and one thing it appears to do is change gene expression of various gut microbes that could lead to microbial resistance.
This particular study is one of the more extreme use cases as it involves HIV positive and exposed folks who are on higher doses.
Results and discussion
Significant tetracycline resistance genes (ARGs) were detected among the analyzed samples, revealing that tetracycline ARGs were the most prevalent in the resistome, accounting for a substantial portion of the mass.
Changes in Gut Microbiota Induced by Doxycycline Influence in Vascular Function and Development of Hypertension in DOCA-Salt Rats
Abnormal Weight Gain and Gut Microbiota Modifications Are Side Effects of Long-Term Doxycycline and Hydroxychloroquine Treatment
I’ve read this before, one of the plastic surgery publications, I think. No salvation until genetic therapy is perfected. Likely that would be in 1,000 years.
I take it daily at the low dose range because of my unique risk - reward. I want to reduce the risk from impact on microbes but I want the benefits - in my case impact on inflammation (I’ve got MS so reductions in inflammation is good for me)
Inflammation is often site and condition specific, are you targeting a specific site or is this for systemic inflammation ? I see you have noted a specific condition.
There are quite a few things that can reduce inflammation, some systemic, some site specific. I’m going to be trying (GLY14)-HUMANIN soon and may add Dulaglutide to one of my stacks as GLP1-R’s are being studied for systemic and brain inflammation.
The gene therapy thing may be an answer as long as it can be controlled. We’re talking about stimulating the production of something with a 70 year half life which if not controlled could turn us into a ball of rubber LoL! and that is why we stop making it around puberty.
I’ve mentioned this before, evolution does not care how long we live, only that we procreate and continue the species. After that, evolution is done with us.
Aren’t there stool-based tests for microbiotic health that you can do? Would be interesting to see how things are after being on the low-dose doxy protocol. I prescribe low dose doxy on occasion for patients with rosacea who are recalcitrant to topical therapies. I prefer the 20mg tablets twice daily with food (to keep the total dose and the peaks low). There’s a 40mg sustained release version, but I’ve given up on it for now due to prior authorization headaches even though it’s gone generic. There’s also a new 40mg branded sustained release minocycline that just got approved.
Will you use CRP as your measure for inflammation? Keep us posted. I’m watching/waiting to try low dose GLP1 for systemic inflammation - osteoarthritis in my hands is inhibiting my life at age 64.
I have old skin and it has seen a lot of sun. I watch this topic with interest and have tried oneskin and a few others just to see what they do. Not that I care very much, but I like to try things.
I recently bought a bottle of Tremella mushroom capsules. Tremella was of interest when I was starting to grow mushrooms, but it’s a little harder than most because it’s a fungus that grows on another fungus and I’m not that good at just one fungus so never gave it a try. It has been used for thousands of years as a skin moisturizer and is supposed to be able to hold 500 times it weight in water.
I think the capsules work better than anything I’ve tried. My skin is very smooth. I bought this from @Joseph_Lavelle and forgot the web site but it’s not that expensive.
I’m very limited in the testing I can get done here for a reasonable price. So I’m more interested in the visible/physical effects and some basic measurements I can do at home.
For osteo, clearing out senescent cells appears to be one way to reduce inflammation that may be closely tied to that condition.
What is interesting about senescent cells is how many conditions they play a part in. I tell people to pick their favorite disease/condition and do a google search like this > heart disease senescent cells <> osteoarthritis senescent cells < just tack on > senescent cells < to any condition and you may be surprised.
I’ve been “killing” my senescent cells for about 4 years but the method I’ve been using is tissue specific and does not appear to fully address the tissues involved in OA. One of the reasons I’m about to try an interesting peptide called FOXO4-DRI in January. I have arthritis in my left hand, and my little finger is where it’s most prevalent, so I’m interested to see if FOXO4-DRI helps.
Asking Google AI > osteoarthritis senescent cells < I get this answer.
" AI Overview
Yes, senescent cells are a key factor in the development of osteoarthritis (OA). Senescent cells are cells that have undergone a process of cellular senescence, which can occur in many tissues, including cartilage, synovium, and subchondral bone. In OA, senescent cells contribute to the disease in a number of ways, including:
Creating an inflammatory environment: Senescent cells secrete cytokines that impact the immune system and can contribute to inflammation.
Altering the synovial microenvironment: Senescent cells can alter the synovial microenvironment, which can lead to OA-like arthropathy.
Degrading cartilage: Senescent cells can contribute to cartilage degradation.
Some markers of cellular senescence include: Beta-galactosidase expression, Telomere length, Mitotic activity, and Senescence-associated secretory phenotype (SASP).
). I even tried a muscle relaxant once. Nothing worked. And the constant tension would eventually give me base-of-skull headaches.
