S
SemenDemon
Iron
- Joined
- Jul 9, 2023
- Posts
- 22
- Reputation
- 17
The Incentives To Use Topical Estriol:
As society progresses, the demand for novel topical products that can either reverse
or slow the progression of both intrinsic and extrinsic age-related factors becomes
increasingly desirable.
Retinoids are commonly utilized, although they carry detrimental side effects, limiting
their use among many individuals.
Topical Hormonal Therapy (THT) has garnered interest. The use of THT originates
from treatments for postmenopausal women and men with hypogonadism. Other
forms of hormonal therapy include supplementation with DHEA, pregnenolone, and
phytoestrogens. Among all the THTs trialed, topical estriol and estradiol are the most
commonly used and researched for both reversing and slowing the inevitable
progression of aging.
How Estriol Works and Why It Works:
Estrogen receptors (ERs), specifically ER beta (ERβ), decline with age. Peripheral
synthesis of estradiol decreases due to the declining production of DHEA and its
sulfated form.
Estrogen exerts its effects through a wide array of interactions, including:
- Receptor coactivation
- Enhancement of mitochondrial dynamics
- Non-genomic signaling
- Genomic signaling
- Antioxidative and anti-inflammatory activity
Estrogen can bind to ERα and ERβ, initiating canonical genomic effects. To activate
these receptors, a large coactivator complex is recruited, composed of p160
coactivators including GRIP1, SRC-1, histone acetyltransferases (p300/CREB-binding
protein), and pCAF. After activation, estrogen response elements (EREs) interact
with DNA to promote transcription.
Through ERβ and ERα, estrogen also elicits effects via protein-protein interactions,
including enhanced transcription at AP-1 sites such as those for the Jun/Fos complex.
Additionally, activation of second messengers such as cAMP, adenylate cyclase,
phospholipase C, and mitogen-activated protein kinase (MAPK) can also occur.
Its non-genomic interactions are equally extensive.
- Increases intracellular Ca²⁺ by activating voltage-gated ion channels
- Activates Nrf2 via CK2 and EGFR-Ras-PI3K-Akt axis, inhibiting GSK3β
- Restores mitochondrial function via Nrf2/ARE activation
- Promotes glutathione transport, preventing UV-induced toxicity
- Activates Erk1/2, increasing keratinocyte proliferation
- Inhibits NF-κB and promotes M2 macrophage phenotype
Estriol vs Estradiol in GPR30 Modulation:
- 17β-estradiol activates GPR30
- Estriol inhibits GPR30 (beneficial in rosacea phenotypes)
Human Data:
S-Equol Study (Men):
- 12 weeks oral → 55–73% improvement in hydration, tone, discoloration, smoothness, wrinkles
- Topical → reversed mid-depth wrinkles, improved multiple skin parameters
(Topical S-equol Results)
Estriol (0.3%) & Estradiol (0.1%) Study (Women):
Estriol results (Week 12 vs placebo):
- Radiance: +48%
- Tactile roughness: -57%
- Visual roughness: -57%
- Hydration: +70%
- Elasticity: +88%
- Overall skin health: +68%
Estradiol results (Week 12 vs placebo):
- Radiance: +50%
- Tactile roughness: -62%
- Visual roughness: -58%
- Firmness: +67%
- Hydration: +76%
- Overall skin health: +67%
Surprising Note: Estriol increased TEWL by 13% at week 12, while estradiol & placebo did not change barrier integrity.
Conclusion: Topical estriol 0.3% generally outperformed estradiol 0.1% in most parameters.
Determination of S- and/or R-equol in plant-based food products and efficacy of topical or oral 4′,7-isoflavandiol (R/S equol) to improve skin health in adult men, a Placebo-controlled pilot study
https://assets.ctfassets.net/md0kv0ejg0xf/4gaULAkbHbgNZtNMOgg1PI/91329de08abacf438fb83d99e756ee99/Alloy_M4_Report_063024.pdf
Estrogens and aging skin
Mechanism of Rapid Nuclear Factor-E2-Related Factor 2 (Nrf2) Activation via Membrane-Associated Estrogen Receptors: Roles of NADPH Oxidase 1, Neutral Sphingomyelinase 2 and Epidermal Growth Factor Receptor (EGFR)
7587 The Estrogen Receptors and ARE/Nrf2 are Involved in Protecting Human Dermal Fibroblasts from Damage Caused by Mitochondrial Disfunction
Novel Locally Active Estrogens Accelerate Cutaneous Wound Healing-Part 2
Estriol acts as a GPR30 antagonist in estrogen receptor-negative breast cancer cells
17β-Estradiol promotes LL37-induced rosacea-like skin inflammation via G protein-coupled estrogen receptor 30
As society progresses, the demand for novel topical products that can either reverse
or slow the progression of both intrinsic and extrinsic age-related factors becomes
increasingly desirable.
Retinoids are commonly utilized, although they carry detrimental side effects, limiting
their use among many individuals.
Topical Hormonal Therapy (THT) has garnered interest. The use of THT originates
from treatments for postmenopausal women and men with hypogonadism. Other
forms of hormonal therapy include supplementation with DHEA, pregnenolone, and
phytoestrogens. Among all the THTs trialed, topical estriol and estradiol are the most
commonly used and researched for both reversing and slowing the inevitable
progression of aging.
How Estriol Works and Why It Works:
Estrogen receptors (ERs), specifically ER beta (ERβ), decline with age. Peripheral
synthesis of estradiol decreases due to the declining production of DHEA and its
sulfated form.
Estrogen exerts its effects through a wide array of interactions, including:
- Receptor coactivation
- Enhancement of mitochondrial dynamics
- Non-genomic signaling
- Genomic signaling
- Antioxidative and anti-inflammatory activity
Estrogen can bind to ERα and ERβ, initiating canonical genomic effects. To activate
these receptors, a large coactivator complex is recruited, composed of p160
coactivators including GRIP1, SRC-1, histone acetyltransferases (p300/CREB-binding
protein), and pCAF. After activation, estrogen response elements (EREs) interact
with DNA to promote transcription.
Through ERβ and ERα, estrogen also elicits effects via protein-protein interactions,
including enhanced transcription at AP-1 sites such as those for the Jun/Fos complex.
Additionally, activation of second messengers such as cAMP, adenylate cyclase,
phospholipase C, and mitogen-activated protein kinase (MAPK) can also occur.
Its non-genomic interactions are equally extensive.
- Increases intracellular Ca²⁺ by activating voltage-gated ion channels
- Activates Nrf2 via CK2 and EGFR-Ras-PI3K-Akt axis, inhibiting GSK3β
- Restores mitochondrial function via Nrf2/ARE activation
- Promotes glutathione transport, preventing UV-induced toxicity
- Activates Erk1/2, increasing keratinocyte proliferation
- Inhibits NF-κB and promotes M2 macrophage phenotype
Estriol vs Estradiol in GPR30 Modulation:
- 17β-estradiol activates GPR30
- Estriol inhibits GPR30 (beneficial in rosacea phenotypes)
Human Data:
S-Equol Study (Men):
- 12 weeks oral → 55–73% improvement in hydration, tone, discoloration, smoothness, wrinkles
- Topical → reversed mid-depth wrinkles, improved multiple skin parameters
(Topical S-equol Results)
Estriol (0.3%) & Estradiol (0.1%) Study (Women):
Estriol results (Week 12 vs placebo):
- Radiance: +48%
- Tactile roughness: -57%
- Visual roughness: -57%
- Hydration: +70%
- Elasticity: +88%
- Overall skin health: +68%
Estradiol results (Week 12 vs placebo):
- Radiance: +50%
- Tactile roughness: -62%
- Visual roughness: -58%
- Firmness: +67%
- Hydration: +76%
- Overall skin health: +67%
Surprising Note: Estriol increased TEWL by 13% at week 12, while estradiol & placebo did not change barrier integrity.
Conclusion: Topical estriol 0.3% generally outperformed estradiol 0.1% in most parameters.
Determination of S- and/or R-equol in plant-based food products and efficacy of topical or oral 4′,7-isoflavandiol (R/S equol) to improve skin health in adult men, a Placebo-controlled pilot study
https://assets.ctfassets.net/md0kv0ejg0xf/4gaULAkbHbgNZtNMOgg1PI/91329de08abacf438fb83d99e756ee99/Alloy_M4_Report_063024.pdf
Estrogens and aging skin
Mechanism of Rapid Nuclear Factor-E2-Related Factor 2 (Nrf2) Activation via Membrane-Associated Estrogen Receptors: Roles of NADPH Oxidase 1, Neutral Sphingomyelinase 2 and Epidermal Growth Factor Receptor (EGFR)
7587 The Estrogen Receptors and ARE/Nrf2 are Involved in Protecting Human Dermal Fibroblasts from Damage Caused by Mitochondrial Disfunction
Novel Locally Active Estrogens Accelerate Cutaneous Wound Healing-Part 2
Estriol acts as a GPR30 antagonist in estrogen receptor-negative breast cancer cells
17β-Estradiol promotes LL37-induced rosacea-like skin inflammation via G protein-coupled estrogen receptor 30
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