Diclofenac gel to regrow hair on bald head and beard
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@heyman i'm going off topic but re-read what I wrote
i think you should change strategy to combat hair loss
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@wester130 how is it heart disease root cause? I think it is metabolic dysfunction thats why I use a redlight infrared hat, make my own shampoo etc
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Nah you're on topic. This thread is kind of the "hairloss/hair regrowth" general now lol.
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@wester130 according to Peat, cardio diseases are down stream of metabolism. Reverse soft tissue calcification with increased temperature, and stop soft tissue calcification by lowering PTH via dietary calcium.
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@LetTheRedeemed soft tissue calcification is due to low temperatur?
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@heyman no, it's due to elevated pth (parathyroid hormone) pulling calcium from the bones, leeching them into the soft tissues -- this is an emergency response due to lack of dietary calcium, since it's vitally involved in metabolism.
this is super layman description: basically, high local metabolic rate will "disolve" the calcium deposits back into the bloodstream to be used properly by the body. calcium deposits are not permanent like bones built by genes (even bones are not permanently one size).
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@wester130 50ml mentioned in point 2: is that a topical? 50ml of what? water?
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@tubert it means like an energy drink shot
50ml orange juice, mix in lysine/taurine and shake
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microvascular circulation might be better than things like cayenne
Grok says
burdock root
diosmin/hesperdidin
Cleavers
Echinacea
gotu kola // Ginkgo bilobamove the lymph, and some people confuse lymph circulation with arterial circulation
maybe bald people have reduced lymph circulation but their arteries are still okay
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@Mauritio just curious if you continued along on the oleic experiment, (looks like it’s been nearly a month now). Always interested to hear about what you’re tinkering with. Thanks in advance!
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@evan.hinkle i did. not every day but most days I apply it. I feel like the hair where I apply it grows faster (I have a lot of new hair coming in from scalp exercises) but I'm not sure yet. Im also applying it to one side of my hand to see if it is effective.
Did you ask your wife about the 100% oleic acid ?
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@Mauritio she only could find 75% from soap suppliers, but I found this:
https://www.amazon.com/Oleic-Natural-General-Purpose-Liquid/dp/B088F5QF1G
Is there any reason to worry that such a high concentration could be irritating?
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@evan.hinkle if it were, I think mixing it with a dab of mct or better yet, mitolipin from Georgi would solve that problem
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@evan.hinkle ok.
I would always inquire if it's really 100% . But I also don't think that a little less should destroy the whole process.Yes it is irritating at first but I got used to it. Although it seems to make my skin quite dry.
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Scleroderma Skin: The collagen is overproduced and laid down in thick, parallel, densely packed bundles (like stacks of lumber). This squeezes out and destroys the normal structures—sweat glands atrophy, hair follicles disappear, fat is replaced, and blood vessels are constricted. This dense matrix extends deep into the tissue.
The Fibrotic Cycle in Scleroderma: A Vicious Loop
In scleroderma, fibrosis isn't just a scar that sits there. It's a dynamic, ongoing faulty repair process. Here's a simplified view:
Initial Insult: Immune dysfunction & vascular damage cause chronic inflammation and injury to tissues (e.g., in skin, lungs).
The "On" Signal: Cells called fibroblasts, which normally produce collagen to heal wounds, receive constant chemical signals (like TGF-β) telling them to activate.
Activated State: These activated fibroblasts, called myofibroblasts, become the primary problem cells. They:
Over-produce the wrong types of collagen (type I and III) and other extracellular matrix (ECM) components.
Contract, pulling tissue tight.
Resist normal cell death (apoptosis) and become long-lived.
Fibrotic Tissue Accumulates: The excess, disorganized collagen and ECM build up, hardening tissue and disrupting its normal architecture and function.
The Loop Continues: The stiff, fibrotic tissue itself creates a microenvironment that sends more "on" signals, recruiting and activating more fibroblasts. The process becomes self-sustaining.
How Can Fibrosis Be Reversed or Halted? (The Therapeutic Targets)
The goal is to break this vicious cycle at different points.
Target Mechanism Example Agents- Reduce the "On" Signals Block the pro-fibrotic cytokines (e.g., TGF-β) that activate fibroblasts. Some investigational drugs (e.g., fresolimumab). Supplements like Quercetin may modestly modulate signaling.
- Deactivate/Kill Myofibroblasts Induce apoptosis in the hyperactive myofibroblasts OR revert them back to quiet fibroblasts. This is where EGCG (green tea) is thought to work. It promotes apoptosis specifically in these activated cells. Prescription drugs like nintedanib (Ofev) also target pathways in these cells.
- Degrade Existing Excess Matrix Boost the body's natural enzymes that break down collagen (matrix metalloproteinases - MMPs) while inhibiting the enzymes that protect it (TIMP). This is very difficult. Some drugs in trials aim at this. Physical therapy and movement help remodel tissue.
- Block Collagen Production Interfere with the cellular machinery that synthesizes and secretes collagen. Pirfenidone (Esbriet), an approved anti-fibrotic for lungs, works partly here.
- Improve the Microenvironment Fix underlying vascular damage and inflammation so the "wound-heal" signal stops. Vasodilators (for Raynaud's), immune suppressants, antioxidants (like NAC) aim here.
Your Specific Question Answered: "If EGCG kills fibrotic cells, is the new collagen also fibrotic?"
This is the key insight. The hope is that by removing the activated myofibroblasts, you are not just clearing a building site—you are removing the faulty construction crew.
In the diseased state: The myofibroblast crew is deaf to "stop building" signals. They lay down collagen in a chaotic, dense, scar-like pattern.
If EGCG promotes their apoptosis: Those specific, dysregulated cells die.
What happens next? The tissue microenvironment is now different (less inflammatory, with less constant TGF-β signaling). If the underlying disease activity is also controlled (e.g., with immunosuppressants), then any new fibroblasts that might be recruited to the area would be the normal, quiescent type. These normal fibroblasts produce collagen in a controlled, organized manner as part of healthy tissue remodeling.
So, no, the new collagen would not automatically be fibrotic. The cycle can be broken if the driving signals are also reduced.
The Crucial Caveat & Why It's So HardThe ECM Itself is "Sticky": The dense fibrotic matrix acts as a scaffold that helps keep myofibroblasts in their activated state. Just killing some cells might not be enough if the physical environment still screams "KEEP BUILDING!"
The Immune Driver Persists: If the autoimmune process isn't controlled, new myofibroblasts will just keep getting recruited. This is why immunosuppressants are foundational. EGCG or any anti-fibrotic agent would likely fail as a monotherapy.
Established Scars are Tough: Long-standing, dense fibrosis (like in chronic scleroderma skin) has a lot of cross-linked collagen that is extremely resistant to degradation. Early intervention is always more effective.
The Bottom Line Analogy:
Think of skin fibrosis like a city being rebuilt poorly after a constant, slow earthquake.
The earthquakes = the autoimmune/vascular damage (treated with immune/vascular drugs).
The bad construction crews = myofibroblasts (targeted by EGCG, nintedanib).
The shoddy buildings = the fibrotic collagen matrix (hardest to remove).
Green tea (EGCG) is a promising approach that targets the "bad construction crew" (myofibroblasts). For it to lead to meaningful improvement, it likely needs to be part of a strategy that also 1) reduces the "earthquakes" (immunosuppression), 2) improves the "city's infrastructure" (vascular care), and 3) maybe uses other methods to gently clear some "rubble" (physical therapy, possibly other matrix-modulating agents).
Important: The human studies on EGCG for scleroderma are still preliminary. It represents a promising adjunct strategy based on strong molecular science, not a proven cure. Any use should be monitored by a doctor, as high doses can have side effects (e.g., liver strain).
