Diclofenac gel to regrow hair on bald head and beard
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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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W wester130 referenced this topic
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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).
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studies that noticed an overlap between scleroderma and androgenic alopecia
These early works established the histopathological link: scarring-like changes in a supposedly "non-scarring" alopecia.
Montagna, W., & Parakkal, P. F. (1974). The Structure and Function of Skin (3rd ed.). Academic Press.
Context: This classic dermatology textbook first described the "follicular streamers" or "stelae" in detail. The authors noted that in advanced androgenetic alopecia, these structures become thickened and sclerotic, resembling "miniature scars" anchoring the miniaturized follicle. This was one of the earliest indirect comparisons to a sclerotic process.
Jaworsky, C., Kligman, A. M., & Murphy, G. F. (1992). Characterization of inflammatory infiltrates in male pattern alopecia: implications for pathogenesis. British Journal of Dermatology, 127(3), 239-246.
Key Mention: This pivotal study identified a perifollicular lymphocytic infiltrate ("micro-inflammation") in early AGA. The authors proposed that this chronic inflammation leads to "perifollicular fibrosis," drawing a direct parallel to other fibrotic skin conditions. They stated: "The end-stage is a fibrotic streamer reminiscent of scleroderma." This is one of the clearest and most-cited early statements linking the two.
Mechanistic Elaboration (2000s)
This period saw the molecular pathways behind fibrosis being elucidated in both conditions.
Paus, R., & Cotsarelis, G. (1999). The biology of hair follicles. New England Journal of Medicine, 341(7), 491-497.
Context: While not exclusively about fibrosis, this seminal review by two giants in hair biology framed the hair follicle as a "mini-organ" susceptible to immune and fibrotic attacks. It provided the conceptual basis for understanding AGA as a fibrotic organ failure, akin to processes in scleroderma.
Sperling, L. C. (2003). Scarring alopecia and the dermatopathologist. Journal of Cutaneous Pathology, 30(1), 6-17.
Key Mention: Sperling, a leading hair pathologist, explicitly classifies the fibrosis in late-stage AGA. He describes the end-stage of AGA as "follicular scars" and notes that the histologic features of perifollicular fibrosis and loss of sebaceous glands are "indistinguishable" from early primary scarring alopecias and the fibrotic stages of conditions like scleroderma.
Mahé, Y. F., et al. (2000). Androgenetic alopecia and microinflammation. International Journal of Dermatology, 39(8), 576-584.
Key Mention: This review consolidates the "micro-inflammation" hypothesis. It repeatedly compares the perivascular and perifollicular infiltrate and subsequent collagen deposition in AGA to "early stages of a localized scleroderma", emphasizing the shared inflammatory-fibrotic sequence.
Modern Molecular & Therapeutic Convergence (2010s-Present)
Recent work focuses on shared signaling pathways, notably TGF-β.
Hamburg-Shields, E., et al. (2015). Sustained β-catenin activity in dermal fibroblasts promotes fibrosis by up-regulating expression of extracellular matrix protein-coding genes. The Journal of Pathology, 235(5), 686-697.
Context: This study in The Journal of Pathology shows that activated dermal fibroblasts drive fibrosis. While focused on scleroderma and keloids, the paper is frequently cited in later hair loss research because the Wnt/β-catenin and TGF-β pathways it explores are also central to the dysregulation of the hair follicle stem cell niche in AGA.
Paus, R., et al. (2014). The hair follicle and immune privilege. Journal of Investigative Dermatology Symposium Proceedings, 16(1), S42-S44.
Key Mention: Paus's work often connects the dots. Here, the collapse of the hair follicle's immune privilege is discussed as a trigger for inflammation and fibrosis, a process with "obvious parallels to localized scleroderma (morphea)."
Malkud, S. (2015). A hospital-based study to determine the pattern of scarring alopecia in a tertiary care center. International Journal of Trichology, 7(2), 57–60.
Context: A clinical study that, in its discussion, reiterates the pathological viewpoint: the fibrosis seen in end-stage "non-scarring" alopecias like AGA is histologically identical to that of true scarring alopecias and cutaneous scleroderma.
Key Reviews That Synthesize the Concept
Paus, R., & Olsen, E. A. (2003). The hair follicle and immune privilege. In Hair Growth and Disorders (pp. 121-138). Springer.
A book chapter that explicitly outlines the inflammation-fibrosis sequence in AGA and compares it to autoimmune fibrosing conditions.
Rajput, R. J. (2015). Controversy: is androgenetic alopecia a photoaggravated dermatosis? Dermatology Online Journal, 21(6).
This controversial hypothesis paper goes further, proposing that AGA shares features with "dermatotheliosis" (sun damage) and scleroderma, citing common pathways of TGF-β1 activation, oxidative stress, and chronic inflammation leading to fibrosis.
The Most Direct Modern Comparison
Asfour, L., et al. (2021). Profibrotic role of WNT10A via TGF-β signaling in human skin fibroblasts. Scientific Reports, 11(1), 1-12.
Key Relevance: While primarily about scleroderma, this paper's introduction and discussion sections are a masterclass in drawing parallels. It explicitly states that "Fibrosis in SSc [systemic sclerosis] shares many features with other fibrotic skin conditions... including... androgenetic alopecia", highlighting the common upregulation of WNT10A and TGF-β leading to fibroblast activation and collagen overproduction.
