- Joined
- Aug 8, 2025
- Messages
- 634
- Time Online
- 1d 21h
- Reputation
- 2,541
Ultimate Skincare Actives Showdown: Tretinoin vs. GHK-Cu vs. Accutane vs. Vitamin C vs. Niacinamide for Collagen, Elastin & Skin Quality
Introduction
The quest for youthful, resilient skin has led to the development of powerful skincare actives that target collagen synthesis, elastin production, and overall skin quality. This comprehensive comparison examines five heavy hitters: tretinoin, GHK-Cu (copper peptides), Accutane (isotretinoin), vitamin C, and niacinamide - analyzing their mechanisms, efficacy, and ideal applications for skin rejuvenation.
Mechanisms of Action
- Tretinoin:
- Primary mechanism: Retinoic acid receptor agonist
- Collagen effects: Strong stimulation of Types I & III
- Elastin effects: Improves elastin fiber organization
- Skin quality effects: Gold standard for anti-aging, texture improvement
- GHK-Cu:
- Primary mechanism: Copper peptide signaling
- Collagen effects: Moderate stimulation
- Elastin effects: Significant elastin production
- Skin quality effects: Wound healing, firmness, anti-inflammatory
- Accutane:
- Primary mechanism: Systemic retinoid (sebum suppression)
- Collagen effects: Indirect via scar prevention
- Elastin effects: Minimal direct effect
- Skin quality effects: Acne clearance, prevents deep scarring
- Vitamin C:
- Primary mechanism: Antioxidant, cofactor for collagen synthesis
- Collagen effects: Boosts production, prevents degradation
- Elastin effects: Mild stabilization
- Skin quality effects: Brightening, UV protection, glow
- Niacinamide:
- Primary mechanism: NAD+ precursor, barrier support
- Collagen effects: Prevents collagen breakdown
- Elastin effects: Minimal direct effect
- Skin quality effects: Barrier repair, redness reduction, even tone
Collagen Synthesis: Head-to-Head Comparison
- Tretinoin: The Gold Standard
- Proven to increase collagen by 80%+ in clinical studies
- Upregulates collagen gene expression directly
- Most effective for mature skin with existing photodamage
- Requires 3-6 months for visible results
- GHK-Cu: The Regenerative Peptide
- Stimulates collagen production through growth factor modulation
- Particularly effective for elastin production (superior to tretinoin in this aspect)
- Ideal for post-procedure healing and maintaining skin resilience
- Vitamin C: The Antioxidant Booster
- Works synergistically with tretinoin
- Protects existing collagen from UV damage
- Immediate brightening effects with long-term collagen benefits
- Niacinamide: The Protective Stabilizer
- Doesn't directly boost collagen but prevents glycation and breakdown
- Excellent for maintaining results from stronger actives
- Accutane: The Indirect Player
- Only collagen benefits come from preventing severe acne scarring
- Not a true anti-aging treatment despite being a retinoid
Elastin Production: Special Focus
- GHK-Cu stands out for elastin regeneration:
- Increases elastin production by up to 300% in studies
- Improves skin snap-back and elasticity
- More effective than tretinoin specifically for elastin
- Tretinoin improves elastin organization but doesn't stimulate new production as dramatically.
Skin Quality Improvements
Side Effect Profiles
Optimal Combinations
For Comprehensive Anti-Aging:
- AM: Vitamin C + Niacinamide + SPF
- PM: Tretinoin (3-4x weekly) + GHK-Cu (on off nights)
For Acne-Prone Skin:
- AM: Niacinamide + SPF
- PM: Tretinoin (if mild) or Accutane (if severe, under derm care)
For Sensitive Skin:
- AM: GHK-Cu + Niacinamide
- PM: Low-dose tretinoin (0.025% short contact therapy)
Final Recommendations
1. Best Overall for Anti-Aging: Tretinoin + GHK-Cu combination
2. Best for Prevention: Vitamin C + Niacinamide duo
3. Best for Acne: Accutane for severe cases, tretinoin for maintenance
4. Best for Sensitive Skin: GHK-Cu as primary active with niacinamide
How Carbohydrates Cause Facial Water Retention: The Insulin-Sodium Connection
Do you ever wake up with a puffy face after eating a carb-heavy meal? That bloated look isn't just in your head-it's often caused by water retention triggered by insulin, and the subsequent sodium reabsorption in the kidneys. Here's how carbohydrates lead to facial puffiness and what you can do about it.
The Science: Carbs, Insulin, and Sodium Retention
1. Carbs Spike Blood Glucose and Insulin
When you eat refined or high-glycemic carbohydrates (like white bread, pasta, pastries, or sugary snacks), your body quickly breaks them down into glucose, causing a rapid rise in blood sugar.
In response, the pancreas releases insulin, a hormone that helps cells absorb glucose for energy. However, high insulin levels also have another effect: they directly bind to insulin receptors in the kidneys to increase sodium reabsorption.
2. Insulin Increases Sodium Reabsorption in the Kidneys
Normally, your kidneys filter excess sodium into the urine to maintain fluid balance. But insulin enhances sodium reabsorption in the renal tubules, primarily through stimulating the epithelial sodium channel (ENaC), meaning:
- More sodium stays in your bloodstream.
- Sodium attracts water, leading to fluid retention (edema).
- Sodium is concentrated extracellularly, meaning it is pulling water outside of your cells, which is the location that leads to the perception of facial bloating.
The Treatment: ENAC inhibitors
These potassium-sparing diuretics block sodium reabsorption in the kidneys through a key mechanism:
1. They Directly Inhibit ENaC (Epithelial Sodium Channel)
- Insulin increases sodium retention by activating ENAC in the kidney's collecting ducts.
- Amiloride and triamterene block ENaC, preventing sodium reabsorption.
- Result: More sodium (and water) is excreted in urine → Less facial bloat.
2. They Don't Deplete Potassium (Unlike Thiazides/Loop Diuretics)
- Most diuretics (like furosemide or hydrochlorothiazide) cause potassium loss, leading to side effects like fatigue and cramps.
- Amiloride/triamterene preserve potassium, making them safer for long-term use (when medically appropriate).
3. They Counteract Insulin's Sodium-Retaining Effect
- Since insulin's bloating effect works through ENaC activation, blocking ENaC directly out-competes this mechanism.
4. The Dose Is The Poison
In both theory and practice, there is obviously a dosage of amiloride/triamterene that sufficiently counteracts the excess sodium retention from insulin without going overboard and ruining overall electrolyte balance. It is important to be conservative with the dosage and start at a low dosage, and titrate up if necessary. Begin with 5mg of amiloride or 37.5mg triamterene and gauge water retention. Diuretics are only dangerous when they cause significant electrolyte imbalances. There is nothing unhealthy about correcting an electrolyte imbalance (which excess insulin causes) with diuretics in order to maintain better electrolyte balance, in fact this has health benefits, such as lower blood pressure.
Introduction
Facial bloating and water retention are common side effects of both anabolic steroid use and elevated estrogen levels. These effects are primarily driven by hormonal interactions with fluid-regulating pathways, including the renin-angiotensin-aldosterone system (RAAS), mineralocorticoid receptor (MR) agonism, and vasopressin (antidiuretic hormone, ADH). Below, we explore how these mechanisms contribute to facial puffiness and what other factors may exacerbate fluid retention.
1. Estrogen and Water Retention
Estrogen promotes sodium and water retention through several mechanisms:
- Increased Aldosterone Secretion: Estrogen enhances angiotensinogen production in the liver, leading to higher angiotensin II levels, which stimulate aldosterone release from the adrenal glands. Aldosterone acts on the kidneys to increase sodium reabsorption, leading to water retention.
- Vasopressin (ADH) Stimulation: Estrogen can upregulate vasopressin secretion, which reduces water excretion by the kidneys, further contributing to edema.
- Mineralocorticoid Receptor (MR) Agonism: Some estrogen metabolites (e.g., 2-hydroxyestradiol) have weak mineralocorticoid activity, directly promoting sodium retention and potassium excretion.
2. Androgens and Water Retention
Many anabolic steroids, particularly those with progestogenic or estrogenic activity, can cause water retention through similar pathways:
A. Progestogenic Androgens (e.g., Nandrolone, Trenbolone)
- Progesterone and MR Activation: Progestins (like those found in nandrolone and trenbolone) can bind to the mineralocorticoid receptor (MR), mimicking aldosterone and promoting sodium retention.
- RAAS Stimulation: Some androgens increase angiotensin II levels, indirectly raising aldosterone and causing fluid retention.
B. C17-Alpha Alkylated Oral Steroids (e.g., Dianabol, Anadrol, Winstrol)
- Liver Stress and Reduced Albumin: These steroids can impair liver function, lowering albumin production. Since albumin helps maintain oncotic pressure, a deficiency leads to fluid leakage into tissues (edema).
- Direct MR Agonism: Some oral steroids may weakly activate MR, worsening water retention.
- Glucocorticoid receptor (GR) antagonists: Some oral steroids (such as oxandrolone) antagonise GR, which prevents cortisol from binding to GR, meaning it can freely bind to MR. This can cause a marginal increase in water retention.
C. Testosterone and Estrogenic Side Effects
- Aromatization to Estrogen: High testosterone doses (especially without an aromatase inhibitor) lead to elevated estrogen, exacerbating fluid retention via the previously mentioned estrogen-mediated water retention pathways.
Treatment for Androgenic/Estrogenic Water Retention
1. Mineralocorticoid antagonist: Eplerenone. This will attenuate the issues stemming from mineralocorticoid receptor agonism, which includes angiotensin II, aldosterone and cortisol too (as they bind to the MR). Recommended starting dose: 50mg. Titrate up accordingly.
2. ENAC inhibitor: Amiloride/Triamterene. Just as with insulin, vasopressin causes sodium reabsorption through ENaC stimulation. ENaC inhibitors will attenuate vasopressin-related water retention (which stems from estradiol).
3. Aromatase inhibitor: Least effective option because not all water retention is caused by estrogen, and it is unhealthy if you decrease your estrogen too much, but it is a decent option to take a small amount of an aromatase inhibitor, provided that you are still well within the estradiol reference range (or even still above it). Exceptions necessary if heavy Al usage is happening to prevent epiphyseal plate closure.
Melanotan 2: Mechanism of Action, Skin Effects, and Phenotypic Changes Introduction
Melanotan 2 (MT2) is a synthetic analog of a-melanocyte-stimulating hormone (a-MSH) that induces skin tanning, affects appetite, and may influence libido. Originally developed as a potential sunless tanning agent and protective measure against UV radiation, it has gained popularity for cosmetic use despite lacking FDA approval. This article examines its mechanism of action, effects on skin pigmentation, and broader phenotypic changes. Mechanism of Action
1. Binding to Melanocortin Receptors
MT2 primarily acts on melanocortin receptors (MCRs), particularly:
- MC1R (melanocytes → tanning)
- MC3R/MC4R (appetite, libido, energy homeostasis)
By activating these receptors, MT2 mimics natural a-MSH but with longer-lasting effects due to its synthetic resistance to enzymatic degradation.
2. Melanogenesis Stimulation
- Eumelanin Production:
- MC1R activation in melanocytes triggers tyrosinase upregulation, converting tyrosine into melanin.
- Unlike UV-induced tanning, MT2 promotes eumelanin (dark pigment) over pheomelanin (red/yellow pigment), leading to a darker, more even tan.
- UV-Independent Effects:
- MT2 can induce pigmentation without sun exposure, though UV exposure greatly enhances
3. Secondary Effects on Appetite & Libido
- MC4R activation suppresses appetite (potential weight loss effect).
- Increased sexual arousal (anecdotal reports suggest enhanced erectile function). Effects on Skin & Phenotype
1. Tanning Response
- Rapid Onset: Darkening begins within days to weeks of administration.
- Dose-Dependent: Higher doses → deeper tan.
- Long-Lasting: Effects persist for weeks to months after discontinuation.
2. Skin Protection
- Increased eumelanin reduces UV damage risk by absorbing free radicals.
- Not a substitute for sunscreen-MT2 does not fully prevent DNA damage from UV rays.
3. Side Effects & Unwanted Phenotypic Changes
- Nausea (common initially, subsides with use)
- Facial flushing (due to vasodilation)
- Darkening of existing moles/freckles (requires monitoring)
4. Long-Term Considerations
- Mole Changes: Existing nevi may darken, requiring dermatological monitoring.
- Tolerance Development: Some users report diminished effects over time.
Practical Application: Dosing and UV exposure
- Typical Protocol:
- Loading Phase: 0.25-0.5 mg/day (subcutaneous injection) for 10-14 days.
- Maintenance: 1-2 doses per week.
- UV Exposure:
- It is important to get enough UV exposure to "use up" the melanin released by MT2. The higher the dose, the more time should be spent in sun (to avoid uneven/dirty pigmentation and darkening of moles/freckles).
- Try to get 30-45 minutes of 7-10 UV exposure.
The Science of Tanning & Sunscreen: UV Protection, Tanning Effects, and Best Choices Introduction
Tanning is the skin's response to ultraviolet (UV) radiation, leading to increased melanin production for protection. However, excessive UV exposure accelerates aging and raises skin cancer risk. Sunscreen helps mitigate damage while allowing controlled tanning. However, you cannot maximize tanning efficiency and skin health; they are on opposite ends of the spectrum.
1. The Biology of Tanning
UV Radiation & Melanin Production
- UVB (290-320 nm):
- Penetrates the epidermis (outer skin layer).
- Causes direct DNA damage, sunburn, and stimulates melanocytes to produce melanin.
- Responsible for immediate tanning (delayed by 48-72 hours).
- UVA (320-400 nm):
- Deeper penetration into the dermis.
- Triggers oxidative stress, leading to premature aging (wrinkles, loss of elasticity).
- Causes immediate pigment darkening (IPD)—a temporary tan that fades within hours.
- Contributes to long-term tanning by oxidizing existing melanin.
2. Sunscreen: How It Blocks UV & Affects Tanning
Sunscreens use chemical (organic) or physical (inorganic) filters to absorb or reflect UV rays.
A. Chemical (Organic) Sunscreens
- Absorb UV radiation and convert it into heat.
- Common Filters & Their Coverage:
- UVB Blockers:
- Octinoxate, Octisalate, Homosalate
- UVA Blockers:
- Avobenzone (unstable alone, needs stabilizers like Octocrylene)
- Mexoryl SX (ecamsule), Meroxyl XL (UVA/UVB)
- Broad-Spectrum (UVA+UVB):
- Tinosorb S/M, Uvinul A Plus
Effect on Tanning:
- Low SPF (15-30): Allows some UVB for melanin stimulation (mild tan).
- High SPF (50+): Blocks most UVB, reducing tanning but still permits UVA exposure (higher aging risk).
B. Physical (Mineral) Sunscreens
- Reflect/scatter UV rays using zinc oxide or titanium dioxide.
- Coverage:
- Zinc Oxide: Full UVA+UVB protection.
- Titanium Dioxide: Strong UVB, partial UVA.
Effect on Tanning:
- Less tanning due to broad-spectrum blocking.
- Better for sensitive skin (less irritation).
3. Can You Tan While Wearing Sunscreen?
Yes, but differently:
- Low SPF (15-30): Permits UVB-induced tanning (slow, longer-lasting).
- High SPF (50+): Mostly blocks UVB but allows UVA tanning (faster fade, higher aging risk).
Best for Safe Tanning:
- SPF 30+ UVA protection (avoids burning while allowing some melanin production).
- Reapply every 2 hours (especially after swimming/sweating).
4. Sunscreen Choices for Different Tanning Goals
5. Myths vs. Facts About Tanning & Sunscreen
- Myth: "SPF 100 blocks all tanning."
- Fact: No sunscreen blocks 100% UV-SPF 100 still allows ~1% UVB through.
- Myth: "Base tans protect against burns."
- Fact: A "base tan" only provides ~SPF 3, insufficient for real protection.
- Myth: "Chemical sunscreens are unsafe."
- Fact: FDA-approved filters are rigorously tested; mineral options exist for sensitive skin.
6. Best Practices for Tanning Safely
1. Use SPF 30+ broad-spectrum sunscreen (reapplied often).
2. Avoid peak UV (10 AM-4 PM) OR avoid long tanning sessions.
3. Moisturize post-sun (aloe vera, hyaluronic acid).
4. Monitor moles for changes (see a dermatologist if new dark spots appear).
Conclusion
Tanning is a biological response to UV damage, not a sign of "healthy" skin. You cannot tan efficiently without keeping your skin subject to DNA damage from the sun. While sunscreen can modulate tanning, no tan is completely safe from aging or cancer risks.
Key Takeaways
- UVB = Sunburn & Delayed Tanning | UVA = Immediate Tan & Aging
- Chemical SPF 30+ UVA protection = Best balance for safe tanning
Introduction
Bone is a dynamic tissue that constantly undergoes remodeling-a balance between bone resorption by osteoclasts and bone formation by osteoblasts. While major fractures are easily detectable, micro traumas and micro fractures are small-scale injuries that accumulate over time due to repetitive stress, mechanical loading, or minor impacts. These microscopic damages play a crucial role in bone adaptation and repair, influencing osteoblast activity and overall bone remodeling.
What Are Micro Traumas and Micro Fractures?
Micro traumas refer to tiny, often undetectable injuries in bone tissue caused by repetitive stress, such as in athletes or individuals with physically demanding jobs. Micro fractures are slightly more defined, representing small cracks in the bone matrix that do not disrupt overall bone integrity but can weaken the structure if left unrepaired.
These micro-damages are common in weight-bearing bones (e.g., tibia, femur) and trabecular bone (spongy bone), where cyclic loading creates stress concentrations. Unlike major fractures, micro fractures do not always cause immediate pain but can lead to chronic conditions like stress fractures or osteoporosis if repair mechanisms fail.
Bone Remodelling and the Role of Osteoblasts
Bone remodelling is a tightly regulated process involving:
1. Osteoclasts - Break down damaged bone.
2. Osteoblasts - Synthesize new bone matrix (osteoid) and promote mineralization.
When micro traumas occur, the bone initiates a repair response:
- Microdamage Detection: Osteocytes (bone's mechanosensors) detect strain and release signalling molecules (e.g., RANKL, sclerostin).
- Osteoclast Activation: Osteoclasts resorb damaged bone, creating resorption pits.
- Osteoblast Recruitment: Mesenchymal stem cells differentiate into osteoblasts, which deposit new bone.
How Micro Fractures Affect Osteoblasts
1. Increased Osteoblast Activity - Small, controlled microdamage stimulates osteoblast proliferation, enhancing bone formation as an adaptive response (Wolff's Law).
2. Chronic Overload and Suppressed Repair - Excessive microdamage without adequate recovery can overwhelm osteoblasts, leading to:
- Accelerated bone loss if resorption outpaces formation.
- Fatigue-induced apoptosis (cell death) of osteoblasts, impairing repair.
3. Altered Signalling Pathways - Prolonged stress may dysregulate Wnt/ß-catenin (critical for osteoblast differentiation) and increase sclerostin (an osteoblast inhibitor), reducing bone formation.
Clinical Implications
- Stress Fractures - Common in athletes and military recruits due to repetitive microdamage.
- Osteoporosis - Aging or hormonal changes can impair microdamage repair, weakening bone.
- Bone Healing Therapies - Understanding osteoblast responses may improve treatments (e.g., anabolic drugs like teriparatide).
Conclusion
Micro traumas and micro fractures are essential for bone adaptation but can become detrimental if repair mechanisms falter. This means it is important to combine bonesmashing with usage of compounds that increase osteoblasts (PTH analogs, androgens, growth factors). Osteoblasts play a pivotal role in maintaining bone integrity, and their response to microdamage determines whether bone strengthens or deteriorates.
Intensity and technique:
- Use your fist or another hard/heavy object to hit your facial bones.
- Do at an intensity that basically is the maximum that you can tolerate - your tolerance will increase over-time due to increased bone density and reduced nerve sensitivity (the same adaptations that happen to muay thai / kickboxing trainers who condition their shins).
Duration and frequency:
- Hit a certain area for 1-2 minutes at a high intensity.
- Start off doing this 1-2 times a week and gauge recovery of your skin and how long the area remains sensitive to touch.
- Increase the frequency towards every other day as you see fit.
Bracing:
- It is extremely important to brace in order to minimize brain movement during bonesmashing.
- The only reason fighters end up with CTE (chronic traumatic encephalopathy) is because of the movement of their head when punched which causes their brain to rattle around in their skull.
- When you are going to begin a bonesmashing session, brace at the very least against your other arm/hand.
- Optimal bracing is against a seat that supports your head, or bracing by lying down in bed.
- Bracing against your hand and a hard wall is also effective.
Introduction to localized fat dissolvers
Whilst it is likely you will have a lean enough face if you cut down to 5% body fat... many people have unfortunate fat distribution, where they need to get extremely lean to get the last bit of fat off their face. While liposuction remains a popular surgical option, non-invasive fat-dissolving treatments such as injectable solutions are also effective.
1. What Are Fat Dissolvers?
Fat dissolvers are non-surgical treatments that break down fat cells, allowing the body to metabolize and eliminate them naturally. They come in two main forms:
- Injectable fat dissolvers (e.g., Aqualyx, Kybella) - Injected directly into fat.
- Topical fat dissolvers (e.g., creams with phosphatidylcholine) - Applied to the skin (less effective than injections).
These treatments target localized fat pockets (double chin, love handles, belly fat) rather than overall weight loss.
2. Key Ingredients in Fat-Dissolving Solutions
A. Deoxycholic Acid (Kybella, Aqualyx)
- Primary mechanism: Breaks down fat cell membranes, causing permanent adipocyte death (kills the fat cell).
How it works:
- Disrupts fat cell structure → releases triglycerides
- Triglycerides are metabolized by the liver and excreted
- FDA-approved for submental fat (double chin) but used off-label elsewhere.
B. Phosphatidylcholine (Lipostabil, Cellutrix)
- Often combined with deoxycholate for better fat emulsification.
- Originally used for cholesterol management but repurposed for cosmetic fat reduction.
- Works by breaking down fat into fatty acids, which are then processed by the body.
- Does not cause adipocyte death, therefore the fat can come back.
C. Sodium Deoxycholate (Aqualyx's Main Ingredient)
- Aqualyx is a European injectable that uses sodium deoxycholate to dissolve fat.
- Similar to Kybella but with a different formulation (includes vitamins and amino acids).
D. Other Common Ingredients in Topical Fat Creams
- Caffeine - Temporarily reduces water retention, making skin appear tighter.
- L-carnitine - May help transport fatty acids for metabolism (weak evidence).
- Retinol - Improves skin texture but does not dissolve fat.
Note: Topical creams are far less effective than injectables because they cannot penetrate deeply enough to destroy fat cells.
3. How Do Fat-Dissolving Injections Work?
1. Injection - The solution is injected into the fat layer (subcutaneous tissue).
2. Fat Cell Destruction - Deoxycholic acid or phosphatidylcholine disrupts fat cell membranes.
3. Inflammatory Response - The body sends macrophages to clear out damaged fat cells.
4. Metabolism & Elimination - Fat is processed by the liver and excreted over weeks. Results appear gradually over 4-12 weeks as the body removes the fat naturally.
4. Risks & Side Effects
- Swelling, bruising, and tenderness (common, lasts days to weeks).
- Nodules or lumps (usually temporary).
- Skin irregularities (if injected improperly).
- Rare (likely temporary) nerve damage (if injected too deeply).
Disclaimer: Always consult a licensed practitioner for these treatments.
5. Recommended Fat Dissolver
- The best fat dissolvers will be ones containing deoxycholic acid or sodium deoxycholate, as this is the compound that will actually permanently kill fat cells. Phosphatidylcholine being included in the product is a bonus because this synergizes with deoxycholate to emulsify the fat once the adipocytes have been killed. The best options for this are Aqualyx and Dr. Lipo+
Introduction
The quest for youthful, resilient skin has led to the development of powerful skincare actives that target collagen synthesis, elastin production, and overall skin quality. This comprehensive comparison examines five heavy hitters: tretinoin, GHK-Cu (copper peptides), Accutane (isotretinoin), vitamin C, and niacinamide - analyzing their mechanisms, efficacy, and ideal applications for skin rejuvenation.
Mechanisms of Action
- Tretinoin:
- Primary mechanism: Retinoic acid receptor agonist
- Collagen effects: Strong stimulation of Types I & III
- Elastin effects: Improves elastin fiber organization
- Skin quality effects: Gold standard for anti-aging, texture improvement
- GHK-Cu:
- Primary mechanism: Copper peptide signaling
- Collagen effects: Moderate stimulation
- Elastin effects: Significant elastin production
- Skin quality effects: Wound healing, firmness, anti-inflammatory
- Accutane:
- Primary mechanism: Systemic retinoid (sebum suppression)
- Collagen effects: Indirect via scar prevention
- Elastin effects: Minimal direct effect
- Skin quality effects: Acne clearance, prevents deep scarring
- Vitamin C:
- Primary mechanism: Antioxidant, cofactor for collagen synthesis
- Collagen effects: Boosts production, prevents degradation
- Elastin effects: Mild stabilization
- Skin quality effects: Brightening, UV protection, glow
- Niacinamide:
- Primary mechanism: NAD+ precursor, barrier support
- Collagen effects: Prevents collagen breakdown
- Elastin effects: Minimal direct effect
- Skin quality effects: Barrier repair, redness reduction, even tone
Collagen Synthesis: Head-to-Head Comparison
- Tretinoin: The Gold Standard
- Proven to increase collagen by 80%+ in clinical studies
- Upregulates collagen gene expression directly
- Most effective for mature skin with existing photodamage
- Requires 3-6 months for visible results
- GHK-Cu: The Regenerative Peptide
- Stimulates collagen production through growth factor modulation
- Particularly effective for elastin production (superior to tretinoin in this aspect)
- Ideal for post-procedure healing and maintaining skin resilience
- Vitamin C: The Antioxidant Booster
- Works synergistically with tretinoin
- Protects existing collagen from UV damage
- Immediate brightening effects with long-term collagen benefits
- Niacinamide: The Protective Stabilizer
- Doesn't directly boost collagen but prevents glycation and breakdown
- Excellent for maintaining results from stronger actives
- Accutane: The Indirect Player
- Only collagen benefits come from preventing severe acne scarring
- Not a true anti-aging treatment despite being a retinoid
Elastin Production: Special Focus
- GHK-Cu stands out for elastin regeneration:
- Increases elastin production by up to 300% in studies
- Improves skin snap-back and elasticity
- More effective than tretinoin specifically for elastin
- Tretinoin improves elastin organization but doesn't stimulate new production as dramatically.
Skin Quality Improvements
Side Effect Profiles
Optimal Combinations
For Comprehensive Anti-Aging:
- AM: Vitamin C + Niacinamide + SPF
- PM: Tretinoin (3-4x weekly) + GHK-Cu (on off nights)
For Acne-Prone Skin:
- AM: Niacinamide + SPF
- PM: Tretinoin (if mild) or Accutane (if severe, under derm care)
For Sensitive Skin:
- AM: GHK-Cu + Niacinamide
- PM: Low-dose tretinoin (0.025% short contact therapy)
Final Recommendations
1. Best Overall for Anti-Aging: Tretinoin + GHK-Cu combination
2. Best for Prevention: Vitamin C + Niacinamide duo
3. Best for Acne: Accutane for severe cases, tretinoin for maintenance
4. Best for Sensitive Skin: GHK-Cu as primary active with niacinamide
How Carbohydrates Cause Facial Water Retention: The Insulin-Sodium Connection
Do you ever wake up with a puffy face after eating a carb-heavy meal? That bloated look isn't just in your head-it's often caused by water retention triggered by insulin, and the subsequent sodium reabsorption in the kidneys. Here's how carbohydrates lead to facial puffiness and what you can do about it.
The Science: Carbs, Insulin, and Sodium Retention
1. Carbs Spike Blood Glucose and Insulin
When you eat refined or high-glycemic carbohydrates (like white bread, pasta, pastries, or sugary snacks), your body quickly breaks them down into glucose, causing a rapid rise in blood sugar.
In response, the pancreas releases insulin, a hormone that helps cells absorb glucose for energy. However, high insulin levels also have another effect: they directly bind to insulin receptors in the kidneys to increase sodium reabsorption.
2. Insulin Increases Sodium Reabsorption in the Kidneys
Normally, your kidneys filter excess sodium into the urine to maintain fluid balance. But insulin enhances sodium reabsorption in the renal tubules, primarily through stimulating the epithelial sodium channel (ENaC), meaning:
- More sodium stays in your bloodstream.
- Sodium attracts water, leading to fluid retention (edema).
- Sodium is concentrated extracellularly, meaning it is pulling water outside of your cells, which is the location that leads to the perception of facial bloating.
The Treatment: ENAC inhibitors
These potassium-sparing diuretics block sodium reabsorption in the kidneys through a key mechanism:
1. They Directly Inhibit ENaC (Epithelial Sodium Channel)
- Insulin increases sodium retention by activating ENAC in the kidney's collecting ducts.
- Amiloride and triamterene block ENaC, preventing sodium reabsorption.
- Result: More sodium (and water) is excreted in urine → Less facial bloat.
2. They Don't Deplete Potassium (Unlike Thiazides/Loop Diuretics)
- Most diuretics (like furosemide or hydrochlorothiazide) cause potassium loss, leading to side effects like fatigue and cramps.
- Amiloride/triamterene preserve potassium, making them safer for long-term use (when medically appropriate).
3. They Counteract Insulin's Sodium-Retaining Effect
- Since insulin's bloating effect works through ENaC activation, blocking ENaC directly out-competes this mechanism.
4. The Dose Is The Poison
In both theory and practice, there is obviously a dosage of amiloride/triamterene that sufficiently counteracts the excess sodium retention from insulin without going overboard and ruining overall electrolyte balance. It is important to be conservative with the dosage and start at a low dosage, and titrate up if necessary. Begin with 5mg of amiloride or 37.5mg triamterene and gauge water retention. Diuretics are only dangerous when they cause significant electrolyte imbalances. There is nothing unhealthy about correcting an electrolyte imbalance (which excess insulin causes) with diuretics in order to maintain better electrolyte balance, in fact this has health benefits, such as lower blood pressure.
Introduction
Facial bloating and water retention are common side effects of both anabolic steroid use and elevated estrogen levels. These effects are primarily driven by hormonal interactions with fluid-regulating pathways, including the renin-angiotensin-aldosterone system (RAAS), mineralocorticoid receptor (MR) agonism, and vasopressin (antidiuretic hormone, ADH). Below, we explore how these mechanisms contribute to facial puffiness and what other factors may exacerbate fluid retention.
1. Estrogen and Water Retention
Estrogen promotes sodium and water retention through several mechanisms:
- Increased Aldosterone Secretion: Estrogen enhances angiotensinogen production in the liver, leading to higher angiotensin II levels, which stimulate aldosterone release from the adrenal glands. Aldosterone acts on the kidneys to increase sodium reabsorption, leading to water retention.
- Vasopressin (ADH) Stimulation: Estrogen can upregulate vasopressin secretion, which reduces water excretion by the kidneys, further contributing to edema.
- Mineralocorticoid Receptor (MR) Agonism: Some estrogen metabolites (e.g., 2-hydroxyestradiol) have weak mineralocorticoid activity, directly promoting sodium retention and potassium excretion.
2. Androgens and Water Retention
Many anabolic steroids, particularly those with progestogenic or estrogenic activity, can cause water retention through similar pathways:
A. Progestogenic Androgens (e.g., Nandrolone, Trenbolone)
- Progesterone and MR Activation: Progestins (like those found in nandrolone and trenbolone) can bind to the mineralocorticoid receptor (MR), mimicking aldosterone and promoting sodium retention.
- RAAS Stimulation: Some androgens increase angiotensin II levels, indirectly raising aldosterone and causing fluid retention.
B. C17-Alpha Alkylated Oral Steroids (e.g., Dianabol, Anadrol, Winstrol)
- Liver Stress and Reduced Albumin: These steroids can impair liver function, lowering albumin production. Since albumin helps maintain oncotic pressure, a deficiency leads to fluid leakage into tissues (edema).
- Direct MR Agonism: Some oral steroids may weakly activate MR, worsening water retention.
- Glucocorticoid receptor (GR) antagonists: Some oral steroids (such as oxandrolone) antagonise GR, which prevents cortisol from binding to GR, meaning it can freely bind to MR. This can cause a marginal increase in water retention.
C. Testosterone and Estrogenic Side Effects
- Aromatization to Estrogen: High testosterone doses (especially without an aromatase inhibitor) lead to elevated estrogen, exacerbating fluid retention via the previously mentioned estrogen-mediated water retention pathways.
Treatment for Androgenic/Estrogenic Water Retention
1. Mineralocorticoid antagonist: Eplerenone. This will attenuate the issues stemming from mineralocorticoid receptor agonism, which includes angiotensin II, aldosterone and cortisol too (as they bind to the MR). Recommended starting dose: 50mg. Titrate up accordingly.
2. ENAC inhibitor: Amiloride/Triamterene. Just as with insulin, vasopressin causes sodium reabsorption through ENaC stimulation. ENaC inhibitors will attenuate vasopressin-related water retention (which stems from estradiol).
3. Aromatase inhibitor: Least effective option because not all water retention is caused by estrogen, and it is unhealthy if you decrease your estrogen too much, but it is a decent option to take a small amount of an aromatase inhibitor, provided that you are still well within the estradiol reference range (or even still above it). Exceptions necessary if heavy Al usage is happening to prevent epiphyseal plate closure.
Melanotan 2: Mechanism of Action, Skin Effects, and Phenotypic Changes Introduction
Melanotan 2 (MT2) is a synthetic analog of a-melanocyte-stimulating hormone (a-MSH) that induces skin tanning, affects appetite, and may influence libido. Originally developed as a potential sunless tanning agent and protective measure against UV radiation, it has gained popularity for cosmetic use despite lacking FDA approval. This article examines its mechanism of action, effects on skin pigmentation, and broader phenotypic changes. Mechanism of Action
1. Binding to Melanocortin Receptors
MT2 primarily acts on melanocortin receptors (MCRs), particularly:
- MC1R (melanocytes → tanning)
- MC3R/MC4R (appetite, libido, energy homeostasis)
By activating these receptors, MT2 mimics natural a-MSH but with longer-lasting effects due to its synthetic resistance to enzymatic degradation.
2. Melanogenesis Stimulation
- Eumelanin Production:
- MC1R activation in melanocytes triggers tyrosinase upregulation, converting tyrosine into melanin.
- Unlike UV-induced tanning, MT2 promotes eumelanin (dark pigment) over pheomelanin (red/yellow pigment), leading to a darker, more even tan.
- UV-Independent Effects:
- MT2 can induce pigmentation without sun exposure, though UV exposure greatly enhances
3. Secondary Effects on Appetite & Libido
- MC4R activation suppresses appetite (potential weight loss effect).
- Increased sexual arousal (anecdotal reports suggest enhanced erectile function). Effects on Skin & Phenotype
1. Tanning Response
- Rapid Onset: Darkening begins within days to weeks of administration.
- Dose-Dependent: Higher doses → deeper tan.
- Long-Lasting: Effects persist for weeks to months after discontinuation.
2. Skin Protection
- Increased eumelanin reduces UV damage risk by absorbing free radicals.
- Not a substitute for sunscreen-MT2 does not fully prevent DNA damage from UV rays.
3. Side Effects & Unwanted Phenotypic Changes
- Nausea (common initially, subsides with use)
- Facial flushing (due to vasodilation)
- Darkening of existing moles/freckles (requires monitoring)
4. Long-Term Considerations
- Mole Changes: Existing nevi may darken, requiring dermatological monitoring.
- Tolerance Development: Some users report diminished effects over time.
Practical Application: Dosing and UV exposure
- Typical Protocol:
- Loading Phase: 0.25-0.5 mg/day (subcutaneous injection) for 10-14 days.
- Maintenance: 1-2 doses per week.
- UV Exposure:
- It is important to get enough UV exposure to "use up" the melanin released by MT2. The higher the dose, the more time should be spent in sun (to avoid uneven/dirty pigmentation and darkening of moles/freckles).
- Try to get 30-45 minutes of 7-10 UV exposure.
The Science of Tanning & Sunscreen: UV Protection, Tanning Effects, and Best Choices Introduction
Tanning is the skin's response to ultraviolet (UV) radiation, leading to increased melanin production for protection. However, excessive UV exposure accelerates aging and raises skin cancer risk. Sunscreen helps mitigate damage while allowing controlled tanning. However, you cannot maximize tanning efficiency and skin health; they are on opposite ends of the spectrum.
1. The Biology of Tanning
UV Radiation & Melanin Production
- UVB (290-320 nm):
- Penetrates the epidermis (outer skin layer).
- Causes direct DNA damage, sunburn, and stimulates melanocytes to produce melanin.
- Responsible for immediate tanning (delayed by 48-72 hours).
- UVA (320-400 nm):
- Deeper penetration into the dermis.
- Triggers oxidative stress, leading to premature aging (wrinkles, loss of elasticity).
- Causes immediate pigment darkening (IPD)—a temporary tan that fades within hours.
- Contributes to long-term tanning by oxidizing existing melanin.
2. Sunscreen: How It Blocks UV & Affects Tanning
Sunscreens use chemical (organic) or physical (inorganic) filters to absorb or reflect UV rays.
A. Chemical (Organic) Sunscreens
- Absorb UV radiation and convert it into heat.
- Common Filters & Their Coverage:
- UVB Blockers:
- Octinoxate, Octisalate, Homosalate
- UVA Blockers:
- Avobenzone (unstable alone, needs stabilizers like Octocrylene)
- Mexoryl SX (ecamsule), Meroxyl XL (UVA/UVB)
- Broad-Spectrum (UVA+UVB):
- Tinosorb S/M, Uvinul A Plus
Effect on Tanning:
- Low SPF (15-30): Allows some UVB for melanin stimulation (mild tan).
- High SPF (50+): Blocks most UVB, reducing tanning but still permits UVA exposure (higher aging risk).
B. Physical (Mineral) Sunscreens
- Reflect/scatter UV rays using zinc oxide or titanium dioxide.
- Coverage:
- Zinc Oxide: Full UVA+UVB protection.
- Titanium Dioxide: Strong UVB, partial UVA.
Effect on Tanning:
- Less tanning due to broad-spectrum blocking.
- Better for sensitive skin (less irritation).
3. Can You Tan While Wearing Sunscreen?
Yes, but differently:
- Low SPF (15-30): Permits UVB-induced tanning (slow, longer-lasting).
- High SPF (50+): Mostly blocks UVB but allows UVA tanning (faster fade, higher aging risk).
Best for Safe Tanning:
- SPF 30+ UVA protection (avoids burning while allowing some melanin production).
- Reapply every 2 hours (especially after swimming/sweating).
4. Sunscreen Choices for Different Tanning Goals
5. Myths vs. Facts About Tanning & Sunscreen
- Myth: "SPF 100 blocks all tanning."
- Fact: No sunscreen blocks 100% UV-SPF 100 still allows ~1% UVB through.
- Myth: "Base tans protect against burns."
- Fact: A "base tan" only provides ~SPF 3, insufficient for real protection.
- Myth: "Chemical sunscreens are unsafe."
- Fact: FDA-approved filters are rigorously tested; mineral options exist for sensitive skin.
6. Best Practices for Tanning Safely
1. Use SPF 30+ broad-spectrum sunscreen (reapplied often).
2. Avoid peak UV (10 AM-4 PM) OR avoid long tanning sessions.
3. Moisturize post-sun (aloe vera, hyaluronic acid).
4. Monitor moles for changes (see a dermatologist if new dark spots appear).
Conclusion
Tanning is a biological response to UV damage, not a sign of "healthy" skin. You cannot tan efficiently without keeping your skin subject to DNA damage from the sun. While sunscreen can modulate tanning, no tan is completely safe from aging or cancer risks.
Key Takeaways
- UVB = Sunburn & Delayed Tanning | UVA = Immediate Tan & Aging
- Chemical SPF 30+ UVA protection = Best balance for safe tanning
Introduction
Bone is a dynamic tissue that constantly undergoes remodeling-a balance between bone resorption by osteoclasts and bone formation by osteoblasts. While major fractures are easily detectable, micro traumas and micro fractures are small-scale injuries that accumulate over time due to repetitive stress, mechanical loading, or minor impacts. These microscopic damages play a crucial role in bone adaptation and repair, influencing osteoblast activity and overall bone remodeling.
What Are Micro Traumas and Micro Fractures?
Micro traumas refer to tiny, often undetectable injuries in bone tissue caused by repetitive stress, such as in athletes or individuals with physically demanding jobs. Micro fractures are slightly more defined, representing small cracks in the bone matrix that do not disrupt overall bone integrity but can weaken the structure if left unrepaired.
These micro-damages are common in weight-bearing bones (e.g., tibia, femur) and trabecular bone (spongy bone), where cyclic loading creates stress concentrations. Unlike major fractures, micro fractures do not always cause immediate pain but can lead to chronic conditions like stress fractures or osteoporosis if repair mechanisms fail.
Bone Remodelling and the Role of Osteoblasts
Bone remodelling is a tightly regulated process involving:
1. Osteoclasts - Break down damaged bone.
2. Osteoblasts - Synthesize new bone matrix (osteoid) and promote mineralization.
When micro traumas occur, the bone initiates a repair response:
- Microdamage Detection: Osteocytes (bone's mechanosensors) detect strain and release signalling molecules (e.g., RANKL, sclerostin).
- Osteoclast Activation: Osteoclasts resorb damaged bone, creating resorption pits.
- Osteoblast Recruitment: Mesenchymal stem cells differentiate into osteoblasts, which deposit new bone.
How Micro Fractures Affect Osteoblasts
1. Increased Osteoblast Activity - Small, controlled microdamage stimulates osteoblast proliferation, enhancing bone formation as an adaptive response (Wolff's Law).
2. Chronic Overload and Suppressed Repair - Excessive microdamage without adequate recovery can overwhelm osteoblasts, leading to:
- Accelerated bone loss if resorption outpaces formation.
- Fatigue-induced apoptosis (cell death) of osteoblasts, impairing repair.
3. Altered Signalling Pathways - Prolonged stress may dysregulate Wnt/ß-catenin (critical for osteoblast differentiation) and increase sclerostin (an osteoblast inhibitor), reducing bone formation.
Clinical Implications
- Stress Fractures - Common in athletes and military recruits due to repetitive microdamage.
- Osteoporosis - Aging or hormonal changes can impair microdamage repair, weakening bone.
- Bone Healing Therapies - Understanding osteoblast responses may improve treatments (e.g., anabolic drugs like teriparatide).
Conclusion
Micro traumas and micro fractures are essential for bone adaptation but can become detrimental if repair mechanisms falter. This means it is important to combine bonesmashing with usage of compounds that increase osteoblasts (PTH analogs, androgens, growth factors). Osteoblasts play a pivotal role in maintaining bone integrity, and their response to microdamage determines whether bone strengthens or deteriorates.
Intensity and technique:
- Use your fist or another hard/heavy object to hit your facial bones.
- Do at an intensity that basically is the maximum that you can tolerate - your tolerance will increase over-time due to increased bone density and reduced nerve sensitivity (the same adaptations that happen to muay thai / kickboxing trainers who condition their shins).
Duration and frequency:
- Hit a certain area for 1-2 minutes at a high intensity.
- Start off doing this 1-2 times a week and gauge recovery of your skin and how long the area remains sensitive to touch.
- Increase the frequency towards every other day as you see fit.
Bracing:
- It is extremely important to brace in order to minimize brain movement during bonesmashing.
- The only reason fighters end up with CTE (chronic traumatic encephalopathy) is because of the movement of their head when punched which causes their brain to rattle around in their skull.
- When you are going to begin a bonesmashing session, brace at the very least against your other arm/hand.
- Optimal bracing is against a seat that supports your head, or bracing by lying down in bed.
- Bracing against your hand and a hard wall is also effective.
Introduction to localized fat dissolvers
Whilst it is likely you will have a lean enough face if you cut down to 5% body fat... many people have unfortunate fat distribution, where they need to get extremely lean to get the last bit of fat off their face. While liposuction remains a popular surgical option, non-invasive fat-dissolving treatments such as injectable solutions are also effective.
1. What Are Fat Dissolvers?
Fat dissolvers are non-surgical treatments that break down fat cells, allowing the body to metabolize and eliminate them naturally. They come in two main forms:
- Injectable fat dissolvers (e.g., Aqualyx, Kybella) - Injected directly into fat.
- Topical fat dissolvers (e.g., creams with phosphatidylcholine) - Applied to the skin (less effective than injections).
These treatments target localized fat pockets (double chin, love handles, belly fat) rather than overall weight loss.
2. Key Ingredients in Fat-Dissolving Solutions
A. Deoxycholic Acid (Kybella, Aqualyx)
- Primary mechanism: Breaks down fat cell membranes, causing permanent adipocyte death (kills the fat cell).
How it works:
- Disrupts fat cell structure → releases triglycerides
- Triglycerides are metabolized by the liver and excreted
- FDA-approved for submental fat (double chin) but used off-label elsewhere.
B. Phosphatidylcholine (Lipostabil, Cellutrix)
- Often combined with deoxycholate for better fat emulsification.
- Originally used for cholesterol management but repurposed for cosmetic fat reduction.
- Works by breaking down fat into fatty acids, which are then processed by the body.
- Does not cause adipocyte death, therefore the fat can come back.
C. Sodium Deoxycholate (Aqualyx's Main Ingredient)
- Aqualyx is a European injectable that uses sodium deoxycholate to dissolve fat.
- Similar to Kybella but with a different formulation (includes vitamins and amino acids).
D. Other Common Ingredients in Topical Fat Creams
- Caffeine - Temporarily reduces water retention, making skin appear tighter.
- L-carnitine - May help transport fatty acids for metabolism (weak evidence).
- Retinol - Improves skin texture but does not dissolve fat.
Note: Topical creams are far less effective than injectables because they cannot penetrate deeply enough to destroy fat cells.
3. How Do Fat-Dissolving Injections Work?
1. Injection - The solution is injected into the fat layer (subcutaneous tissue).
2. Fat Cell Destruction - Deoxycholic acid or phosphatidylcholine disrupts fat cell membranes.
3. Inflammatory Response - The body sends macrophages to clear out damaged fat cells.
4. Metabolism & Elimination - Fat is processed by the liver and excreted over weeks. Results appear gradually over 4-12 weeks as the body removes the fat naturally.
4. Risks & Side Effects
- Swelling, bruising, and tenderness (common, lasts days to weeks).
- Nodules or lumps (usually temporary).
- Skin irregularities (if injected improperly).
- Rare (likely temporary) nerve damage (if injected too deeply).
Disclaimer: Always consult a licensed practitioner for these treatments.
5. Recommended Fat Dissolver
- The best fat dissolvers will be ones containing deoxycholic acid or sodium deoxycholate, as this is the compound that will actually permanently kill fat cells. Phosphatidylcholine being included in the product is a bonus because this synergizes with deoxycholate to emulsify the fat once the adipocytes have been killed. The best options for this are Aqualyx and Dr. Lipo+
People pay money for this information.