Here's a guide for improving:
-Acne
-Psoriasis
-Eczema
-Rosacea
-Vitiligo
-Seborrheic dermatitis
that will finally make you understand the driving factors each one and the biggest levers you can pull to improve them.
Thread🧵
-Acne
-Psoriasis
-Eczema
-Rosacea
-Vitiligo
-Seborrheic dermatitis
that will finally make you understand the driving factors each one and the biggest levers you can pull to improve them.
Thread🧵
*Standard disclaimer that nothing in this thread should be used as a substitute for medical advice*
Now it’s quite common to think that the skin is this very simple and almost purely aesthetic part of the body when in reality it is quite fascinating and complex.
So let’s begin this thread with a basic anatomical model of the skin's layers, since i believe it will help you understand the issue you are facing better and more easily.
Now it’s quite common to think that the skin is this very simple and almost purely aesthetic part of the body when in reality it is quite fascinating and complex.
So let’s begin this thread with a basic anatomical model of the skin's layers, since i believe it will help you understand the issue you are facing better and more easily.
We have:
1. The epidermis (the outermost layer of the skin).
The epidermis is an avascular (lacking blood vessels) epithelium that serves as a protective barrier and varies in thickness depending on the part of the body (it’s thicker in your palms for example, compared to the eyelids).
The main epidermal cell types are:
-Keratinocytes (the majority), whose main roles are to produce keratin and undergo keratinization to replenish the upper layers (keratinization is a process where keratinocytes “mature”, then fill with keratin, lose organelles and die in order to form the stratum corneum).
Keratinocytes in the epidermis also convert 7-dehydrocholesterol to vitamin D3 upon UV exposure
-Melanocytes (5–10%) whose main role is to synthesize melanin in melanosomes to protect against UV damage.
-Langerhans cells (2–4%) that are antigen-presenting cells for immune defense.
-Merkel cells (<1%) that are sensory cells for touch detection.
It is also composed of the following sublayers:
-Stratum corneum.
This is made out of 15–30 layers of flattened, dead, anucleate keratinocytes (corneocytes) filled with keratin, embedded in a lipid matrix (ceramides, cholesterol) that acts as a waterproof barrier against mechanical abrasion, pathogens and so on.
-Stratum lucidum.
This is only found in parts such as your palm and soles, it’s made out of 2–3 layers of tightly packed keratinocytes with no nuclei or organelles, containing keratin precursor such as elidin that enhances barrier function in thick skin.
-Stratum granulosum.
This is made out of 3–5 layers of flattened keratinocytes with keratohyalin granules and lamellar bodies that are lipid-secreting organelles whose function is to initiate keratinization and release lipids to form the waterproof barrier.
-Stratum spinosum.
This is made out of 8–10 layers of polyhedral keratinocytes connected by desmosomes, giving a "spiny" appearance under a microscope that contains pre-keratin filaments and provides structural strength and flexibility.
-Stratum basale.
This one is a single layer of cuboidal/columnar cells anchored to the basement membrane via hemidesmosomes, whose function is a stem cell layer for keratinocyte regeneration.
1. The epidermis (the outermost layer of the skin).
The epidermis is an avascular (lacking blood vessels) epithelium that serves as a protective barrier and varies in thickness depending on the part of the body (it’s thicker in your palms for example, compared to the eyelids).
The main epidermal cell types are:
-Keratinocytes (the majority), whose main roles are to produce keratin and undergo keratinization to replenish the upper layers (keratinization is a process where keratinocytes “mature”, then fill with keratin, lose organelles and die in order to form the stratum corneum).
Keratinocytes in the epidermis also convert 7-dehydrocholesterol to vitamin D3 upon UV exposure
-Melanocytes (5–10%) whose main role is to synthesize melanin in melanosomes to protect against UV damage.
-Langerhans cells (2–4%) that are antigen-presenting cells for immune defense.
-Merkel cells (<1%) that are sensory cells for touch detection.
It is also composed of the following sublayers:
-Stratum corneum.
This is made out of 15–30 layers of flattened, dead, anucleate keratinocytes (corneocytes) filled with keratin, embedded in a lipid matrix (ceramides, cholesterol) that acts as a waterproof barrier against mechanical abrasion, pathogens and so on.
-Stratum lucidum.
This is only found in parts such as your palm and soles, it’s made out of 2–3 layers of tightly packed keratinocytes with no nuclei or organelles, containing keratin precursor such as elidin that enhances barrier function in thick skin.
-Stratum granulosum.
This is made out of 3–5 layers of flattened keratinocytes with keratohyalin granules and lamellar bodies that are lipid-secreting organelles whose function is to initiate keratinization and release lipids to form the waterproof barrier.
-Stratum spinosum.
This is made out of 8–10 layers of polyhedral keratinocytes connected by desmosomes, giving a "spiny" appearance under a microscope that contains pre-keratin filaments and provides structural strength and flexibility.
-Stratum basale.
This one is a single layer of cuboidal/columnar cells anchored to the basement membrane via hemidesmosomes, whose function is a stem cell layer for keratinocyte regeneration.
2. The dermis (the middle layer of the skin/the primary structural layer).
The dermis is a thick, vascular connective tissue layer that sits beneath the epidermis and is the layer that provides structural support, elasticity and nourishment to the epidermis.
It contains blood vessels, nerves and skin appendages such as hair follicles, glands and is critical for thermoregulation, sensation and immune defense while it also serves as a scaffold for skin regeneration during wound healing.
The main dermal cell types are:
-Fibroblasts (majority), whose primary role is to synthesize extracellular matrix (ECM) components, including collagen, elastin and ground substance, providing structural integrity and supporting tissue repair.
-Macrophages (variable), which phagocytose pathogens, debris and apoptotic cells, contributing to immune defense and wound healing.
-Mast cells (sparse), which release histamine and cytokines to initiate inflammation and allergic responses.
-Adipocytes (in deeper dermis), which store fat and provide cushioning, especially near the hypodermis transition.
Now the dermis is composed of the following regions:
-Papillary dermis.
This is a thin, superficial layer of loose areolar connective tissue with type III collagen and elastic fibers that also contains dermal papillae (finger-like projections that interlock with the epidermis’s rete ridges).
Its main functions are to supply nutrients to the epidermis via capillary loops, houses sensory nerve endings for touch and pain and supports immune surveillance.
Its components include capillary loops that deliver oxygen and nutrients to the epidermis and regulate temperature, meissner’s corpuscles that are mechanoreceptors for light touch sensation and free nerve endings that detect pain, temperature, and itch.
This region also provides a vascular supply for granulation tissue formation during the proliferation phase of wound healing.
-Reticular dermis.
This is a thicker, deeper layer of dense irregular connective tissue with type I collagen and elastic fibers arranged in a network, giving it a fibrous texture.
Its main functions are to provide tensile strength and elasticity to resist mechanical stress.
Its components include blood vessels that are larger arteries and veins for systemic circulation and thermoregulation, lymphatic vessels that drain excess fluid and support immune responses, pacinian corpuscles that ar emechanoreceptors for deep pressure and vibration, ruffini endings that detect skin stretch and tension, plus skin appendages such asair follicles, sebaceous glands (secrete sebum), eccrine sweat glands (thermoregulation), and apocrine sweat glands (scented sweat).
Thus region also serves as a reservoir for fibroblasts and ECM components during wound healing, contributing to collagen deposition and scar formation in the remodeling phase.
The dermis is separated from the epidermis by a basement membrane, a thin layer of collagen IV, laminin, and proteoglycans that anchors the epidermis via hemidesmosomes and anchoring fibrils, facilitating nutrient diffusion and structural stability.
The dermis is a thick, vascular connective tissue layer that sits beneath the epidermis and is the layer that provides structural support, elasticity and nourishment to the epidermis.
It contains blood vessels, nerves and skin appendages such as hair follicles, glands and is critical for thermoregulation, sensation and immune defense while it also serves as a scaffold for skin regeneration during wound healing.
The main dermal cell types are:
-Fibroblasts (majority), whose primary role is to synthesize extracellular matrix (ECM) components, including collagen, elastin and ground substance, providing structural integrity and supporting tissue repair.
-Macrophages (variable), which phagocytose pathogens, debris and apoptotic cells, contributing to immune defense and wound healing.
-Mast cells (sparse), which release histamine and cytokines to initiate inflammation and allergic responses.
-Adipocytes (in deeper dermis), which store fat and provide cushioning, especially near the hypodermis transition.
Now the dermis is composed of the following regions:
-Papillary dermis.
This is a thin, superficial layer of loose areolar connective tissue with type III collagen and elastic fibers that also contains dermal papillae (finger-like projections that interlock with the epidermis’s rete ridges).
Its main functions are to supply nutrients to the epidermis via capillary loops, houses sensory nerve endings for touch and pain and supports immune surveillance.
Its components include capillary loops that deliver oxygen and nutrients to the epidermis and regulate temperature, meissner’s corpuscles that are mechanoreceptors for light touch sensation and free nerve endings that detect pain, temperature, and itch.
This region also provides a vascular supply for granulation tissue formation during the proliferation phase of wound healing.
-Reticular dermis.
This is a thicker, deeper layer of dense irregular connective tissue with type I collagen and elastic fibers arranged in a network, giving it a fibrous texture.
Its main functions are to provide tensile strength and elasticity to resist mechanical stress.
Its components include blood vessels that are larger arteries and veins for systemic circulation and thermoregulation, lymphatic vessels that drain excess fluid and support immune responses, pacinian corpuscles that ar emechanoreceptors for deep pressure and vibration, ruffini endings that detect skin stretch and tension, plus skin appendages such asair follicles, sebaceous glands (secrete sebum), eccrine sweat glands (thermoregulation), and apocrine sweat glands (scented sweat).
Thus region also serves as a reservoir for fibroblasts and ECM components during wound healing, contributing to collagen deposition and scar formation in the remodeling phase.
The dermis is separated from the epidermis by a basement membrane, a thin layer of collagen IV, laminin, and proteoglycans that anchors the epidermis via hemidesmosomes and anchoring fibrils, facilitating nutrient diffusion and structural stability.
3. The hypodermis (the innermost layer of the skin (some do not consider as part of the skin)).
The hypodermis, also known as the subcutaneous layer, sits beneath the dermis and is a layer of mainly adipocytes whose primary role is to store triglycerides, provide thermal insulation, and cushion against mechanical trauma, some fibroblasts that produce collagen and elastic fibers with the purpose of maintaining structural integrity and flexibility, macrophages (variable), which clear debris and pathogens, supporting immune defense and a few mast cells (sparse), which contribute to inflammation and immune responses.
Its overall purpose is to “anchor” the skin to things such as the muscles and bones while providing insulation and cushioning.
It is composed of the following regions:
-Adipose tissue layer.
As stated, this is the primary component, consisting of lobules of adipocytes (fat cells) separated by fibrous septae made of collagen and elastic fibers.
The adipose tissue is highly vascularized to support metabolic demands, stores energy as triglycerides, insulates the body to conserve heat, and cushions underlying structures against mechanical stress.
Its main components are blood vessels that are once again large arteries and veins supply the hypodermis and connect to the dermal vasculature, sensory nerves such as Pacinian corpuscles for pressure and autonomic nerves that regulate blood flow and adipose metabolism and lymphatic vessels that drain interstitial fluid to prevent edema.
-Loose connective tissue layer.
This is a thinner layer of loose areolar connective tissue with collagen and elastic fibers, blending with the reticular dermis above and deep fascia below and anchors the skin to muscles or bones which allows mobility while also maintaining stability.
Its main components are fibrous septae (collagen-rich bands that compartmentalize adipose lobules and anchor the hypodermis and bursa in some areas).
The hypodermis, also known as the subcutaneous layer, sits beneath the dermis and is a layer of mainly adipocytes whose primary role is to store triglycerides, provide thermal insulation, and cushion against mechanical trauma, some fibroblasts that produce collagen and elastic fibers with the purpose of maintaining structural integrity and flexibility, macrophages (variable), which clear debris and pathogens, supporting immune defense and a few mast cells (sparse), which contribute to inflammation and immune responses.
Its overall purpose is to “anchor” the skin to things such as the muscles and bones while providing insulation and cushioning.
It is composed of the following regions:
-Adipose tissue layer.
As stated, this is the primary component, consisting of lobules of adipocytes (fat cells) separated by fibrous septae made of collagen and elastic fibers.
The adipose tissue is highly vascularized to support metabolic demands, stores energy as triglycerides, insulates the body to conserve heat, and cushions underlying structures against mechanical stress.
Its main components are blood vessels that are once again large arteries and veins supply the hypodermis and connect to the dermal vasculature, sensory nerves such as Pacinian corpuscles for pressure and autonomic nerves that regulate blood flow and adipose metabolism and lymphatic vessels that drain interstitial fluid to prevent edema.
-Loose connective tissue layer.
This is a thinner layer of loose areolar connective tissue with collagen and elastic fibers, blending with the reticular dermis above and deep fascia below and anchors the skin to muscles or bones which allows mobility while also maintaining stability.
Its main components are fibrous septae (collagen-rich bands that compartmentalize adipose lobules and anchor the hypodermis and bursa in some areas).
Let’s talk about the skin microbiome.
This term refers to the diverse community of microorganisms that form a complex ecosystem on the skin’s surface and within its layers such as the hair follicles and sweat glands.
So this ecosystem hosts a variety of bacteria, some beneficial and others potentially harmful, depending on their balance and context.
The main list of beneficial bacteria includes, staphylococcus epidermidis, corynebacterium spp. and micrococcus luteus.
These perform several key functions such as protecting us against pathogens like S. aureus or Streptococcus pyogenes with the help of commensal bacteria like S. epidermidis that produce antimicrobial peptides, some of these like S. epidermidis and certain Cutibacterium strains (note, while beneficial in small amounts, overgrowth in clogged pores can trigger acne) produce short-chain fatty acids such as propionic acid and thus exert anit-inflammatory effects, immune system modulation where these commensals interact with dendritic cells and T-cells in the dermis, promoting balanced immune responses by basically “training” the immune system, some of them also enhance NMF production and thus support stratum corneum integrity while also promoting keratinocyte proliferation and collagen deposition, accelerating re-epithelialization during the proliferation phase of wound healing.
The main list of potentially harmful bacteria (these can become problematic under certain conditions, such as overgrowth, skin barrier disruption or immune suppression) includes staphylococcus aureus, cutibacterium acnes, pseudomonas aeruginosa and streptococcus pyogenes.
These can cause infections like impetigo, cellulitis, or abscesses when it penetrates the skin or overgrows.
So once again, just like any other ecosystem, balance is critical.
This term refers to the diverse community of microorganisms that form a complex ecosystem on the skin’s surface and within its layers such as the hair follicles and sweat glands.
So this ecosystem hosts a variety of bacteria, some beneficial and others potentially harmful, depending on their balance and context.
The main list of beneficial bacteria includes, staphylococcus epidermidis, corynebacterium spp. and micrococcus luteus.
These perform several key functions such as protecting us against pathogens like S. aureus or Streptococcus pyogenes with the help of commensal bacteria like S. epidermidis that produce antimicrobial peptides, some of these like S. epidermidis and certain Cutibacterium strains (note, while beneficial in small amounts, overgrowth in clogged pores can trigger acne) produce short-chain fatty acids such as propionic acid and thus exert anit-inflammatory effects, immune system modulation where these commensals interact with dendritic cells and T-cells in the dermis, promoting balanced immune responses by basically “training” the immune system, some of them also enhance NMF production and thus support stratum corneum integrity while also promoting keratinocyte proliferation and collagen deposition, accelerating re-epithelialization during the proliferation phase of wound healing.
The main list of potentially harmful bacteria (these can become problematic under certain conditions, such as overgrowth, skin barrier disruption or immune suppression) includes staphylococcus aureus, cutibacterium acnes, pseudomonas aeruginosa and streptococcus pyogenes.
These can cause infections like impetigo, cellulitis, or abscesses when it penetrates the skin or overgrows.
So once again, just like any other ecosystem, balance is critical.
Now here’s a practical example when it comes to why the things that were just mentioned are worth knowing.
Each skin-related condition affects the skin’s layers differently.
Psoriasis and eczema for example are epidermal disorders and acne is primarily a dermal disorder.
So knowing what the epidermis and dermis are on a fundamental level is quite useful as a first step.
Each skin-related condition affects the skin’s layers differently.
Psoriasis and eczema for example are epidermal disorders and acne is primarily a dermal disorder.
So knowing what the epidermis and dermis are on a fundamental level is quite useful as a first step.
Now let’s dive in the causes and mechanisms behind skin issues like acne, psoriasis, and eczema (all disrupt the skin’s anatomy, regeneration, and microbiome, often involving inflammation, barrier dysfunction, and microbial dysbiosis).
1. Acne
Main causes:
-Excess sebum: The sebaceous glands in the dermis, stimulated mainly by hormonal releases, produce excessive sebum (oil), which clogs things such as the hair follicles and overall promoting bacterial growth.
-Follicular hyperkeratinization: Overproliferating keratinocytes block follicles, forming comedones and trapping sebum and bacteria.
-Bacterial proliferation: Cutibacterium acnes thrives in sebum-rich follicles, triggering inflammation (it metabolizes sebum, releasing pro-inflammatory byproducts)
-Inflammation: Cytokines such as IL-1 and TNF-α cause redness and pustules.
1. Acne
Main causes:
-Excess sebum: The sebaceous glands in the dermis, stimulated mainly by hormonal releases, produce excessive sebum (oil), which clogs things such as the hair follicles and overall promoting bacterial growth.
-Follicular hyperkeratinization: Overproliferating keratinocytes block follicles, forming comedones and trapping sebum and bacteria.
-Bacterial proliferation: Cutibacterium acnes thrives in sebum-rich follicles, triggering inflammation (it metabolizes sebum, releasing pro-inflammatory byproducts)
-Inflammation: Cytokines such as IL-1 and TNF-α cause redness and pustules.
Biggest ROI steps/tools you can use for addressing acne:
-Getting a hormonal panel done that includes androgens, cortisol, DHEA, DHEA-S, estrogens and IGF-1.
Based on these results, you will know which diet suits you the best.
If your IGF-1 for example, is very high, this makes high-glycemic foods and dairy a no go for example.
-Avoid highly processed foods, histamine-rich foods, foods that will negatively affect the state of your gut such as wheat for example and monitor your linoleic acid intake.
-Use the sauna but hop in the shower right after.
-Go measure your vitamin D levels.
-Sulfur soap.
-Consider the following gut-related tests: Urea breath test, stool antigen test for H. pylori antigens, breath tests that measure hydrogen, methane, or hydrogen sulfide after lactulose/glucose ingestion, a stool analysis for candida, fungal culture, CHROMagar Candida.
-Provide enough whole food vitamin C, E, B5, selenium and zinc all of which are crucial for the health of the skin and helping our bodies deal with inflammation.
-Use non-comedogenic, oil-free skin care products.
-Use a shower filter and follow basic hygiene rules.
Now someone might ask: what if i have for example, both a gut issue and hormonal imbalances?
A basic answer to this is: Focus on the most compromised area while using relatively safe tools for the other one.
If your gut is the most compromised area for example but you also have elevated estrogen, then focus on the gut while trying to lower your body weight in case you are overweight for example since one of the most effective things you can do in order to manage aromatase.
-Getting a hormonal panel done that includes androgens, cortisol, DHEA, DHEA-S, estrogens and IGF-1.
Based on these results, you will know which diet suits you the best.
If your IGF-1 for example, is very high, this makes high-glycemic foods and dairy a no go for example.
-Avoid highly processed foods, histamine-rich foods, foods that will negatively affect the state of your gut such as wheat for example and monitor your linoleic acid intake.
-Use the sauna but hop in the shower right after.
-Go measure your vitamin D levels.
-Sulfur soap.
-Consider the following gut-related tests: Urea breath test, stool antigen test for H. pylori antigens, breath tests that measure hydrogen, methane, or hydrogen sulfide after lactulose/glucose ingestion, a stool analysis for candida, fungal culture, CHROMagar Candida.
-Provide enough whole food vitamin C, E, B5, selenium and zinc all of which are crucial for the health of the skin and helping our bodies deal with inflammation.
-Use non-comedogenic, oil-free skin care products.
-Use a shower filter and follow basic hygiene rules.
Now someone might ask: what if i have for example, both a gut issue and hormonal imbalances?
A basic answer to this is: Focus on the most compromised area while using relatively safe tools for the other one.
If your gut is the most compromised area for example but you also have elevated estrogen, then focus on the gut while trying to lower your body weight in case you are overweight for example since one of the most effective things you can do in order to manage aromatase.
2. Psoriasis
Main causes:
-Immune dysregulation: Overactive T-cells (Th1/Th17) release cytokines (IL-17, IL-23, TNF-α), stimulating keratinocyte proliferation and the normal 28–30 day epidermal turnover cycle is reduced to 3–5 days, leading to an accumulation of immature keratinocytes in the stratum corneum (parakeratosis), forming thick plaques.
-Epidermal hyperproliferation: Overstimulated keratinocytes produce excess keratin, but nuclei are retained in the stratum corneum (unlike normal keratinization).
-Angiogenesis through cytokines.
-Genetics (common (up to 50% of patients): PSORS1 mutations increase susceptibility by altering immune signaling (HLA-Cw6 variant).
Main causes:
-Immune dysregulation: Overactive T-cells (Th1/Th17) release cytokines (IL-17, IL-23, TNF-α), stimulating keratinocyte proliferation and the normal 28–30 day epidermal turnover cycle is reduced to 3–5 days, leading to an accumulation of immature keratinocytes in the stratum corneum (parakeratosis), forming thick plaques.
-Epidermal hyperproliferation: Overstimulated keratinocytes produce excess keratin, but nuclei are retained in the stratum corneum (unlike normal keratinization).
-Angiogenesis through cytokines.
-Genetics (common (up to 50% of patients): PSORS1 mutations increase susceptibility by altering immune signaling (HLA-Cw6 variant).
Biggest ROI steps/tools you can use for addressing psoriasis:
-Stabilizing mast cells in case you have symptoms of histamine intolerance.
-Relaxing, avoiding alcohol, stimulants, B5, zinc, selenium, C, B6 and magnesium deficiencies and in general anything that activates the hypothalamic-pituitary-adrenal axis to an excess.
-Measure your vitamin D levels (from 50% all the way up to 80% of psoriasis patients have insufficient serum vitamin D levels (<20 ng/mL))
-Testing for mycotoxins/mold toxicity and heavy metals.
-Stop smoking and using nicotine, both increase oxidative stress and VEGF expression.
-Managing your weight, excess adipose tissue produces cytokines (IL-6, TNF-α), exacerbating T-cell-driven inflammation.
-Unaddressed food allergies.
-Get full-spectrum sunlight (also remember that vitamin D regulates keratinocyte growth).
-Focus on optimizing your gut and sleep since gut dysbiosis and lack of sleep are the fastest ways to disrupt immune regulation.
-Stabilizing mast cells in case you have symptoms of histamine intolerance.
-Relaxing, avoiding alcohol, stimulants, B5, zinc, selenium, C, B6 and magnesium deficiencies and in general anything that activates the hypothalamic-pituitary-adrenal axis to an excess.
-Measure your vitamin D levels (from 50% all the way up to 80% of psoriasis patients have insufficient serum vitamin D levels (<20 ng/mL))
-Testing for mycotoxins/mold toxicity and heavy metals.
-Stop smoking and using nicotine, both increase oxidative stress and VEGF expression.
-Managing your weight, excess adipose tissue produces cytokines (IL-6, TNF-α), exacerbating T-cell-driven inflammation.
-Unaddressed food allergies.
-Get full-spectrum sunlight (also remember that vitamin D regulates keratinocyte growth).
-Focus on optimizing your gut and sleep since gut dysbiosis and lack of sleep are the fastest ways to disrupt immune regulation.
3. Eczema / atopic dermatitis
Main causes:
-Mutations in the FLG gene (encoding filaggrin, a protein in the stratum corneum) reduce the production of natural moisturizing factors (NMFs) and lipids (ceramides).
And it’s unfortunately quite common with up to 50% of patients having it (but there are also natural tools that can help you with it (keep reading)).
-Immune system dysregulation: A skewed Th2 immune response in the dermis releases cytokines such as IL-4, IL-13, IL-31 thus promoting inflammation and itchiness.
-Microbial dysbiosis: Reduced antimicrobial peptides such as cathelicidin due to barrier defects allow overgrowth of Staphylococcus aureus on the skin surface.
-Toxin accumulation (related to the immune system and Th2)/liver dysfunction.
Main causes:
-Mutations in the FLG gene (encoding filaggrin, a protein in the stratum corneum) reduce the production of natural moisturizing factors (NMFs) and lipids (ceramides).
And it’s unfortunately quite common with up to 50% of patients having it (but there are also natural tools that can help you with it (keep reading)).
-Immune system dysregulation: A skewed Th2 immune response in the dermis releases cytokines such as IL-4, IL-13, IL-31 thus promoting inflammation and itchiness.
-Microbial dysbiosis: Reduced antimicrobial peptides such as cathelicidin due to barrier defects allow overgrowth of Staphylococcus aureus on the skin surface.
-Toxin accumulation (related to the immune system and Th2)/liver dysfunction.
Biggest ROI steps/tools you can use for addressing eczema:
-Stabilizing mast cells in case you have symptoms of histamine intolerance.
-Getting enough vitamin E, B5, zinc, selenium, C, B6 and magnesium.
-Measuring your vitamin D levels (from 50% all the way up to 80% of psoriasis patients have insufficient serum vitamin D levels (<20 ng/mL))
-Testing for mycotoxins/mold toxicity and heavy metals.
-Stop smoking and using nicotine, both increase oxidative stress and VEGF expression.
-Managing your weight, excess adipose tissue produces cytokines such as IL-6 and TNF-α, exacerbating T-cell-driven inflammation.
-Unaddressed food allergies.
-Get full spectrum sunlight since insufficient natural sunlight (e.g., in winter or northern regions) reduces vitamin D synthesis, which normally regulates keratinocyte growth.
-Focus on optimizing your gut and sleep since gut dysbiosis and lack of sleep are the fastest ways to disrupt immune regulation.
-Natural IL-4/IL-13 inhibitors such as (pick one, don’t use all of these) luteolin, fisetin, quercetin, EGCG and apigenin.
-Stabilizing mast cells in case you have symptoms of histamine intolerance.
-Getting enough vitamin E, B5, zinc, selenium, C, B6 and magnesium.
-Measuring your vitamin D levels (from 50% all the way up to 80% of psoriasis patients have insufficient serum vitamin D levels (<20 ng/mL))
-Testing for mycotoxins/mold toxicity and heavy metals.
-Stop smoking and using nicotine, both increase oxidative stress and VEGF expression.
-Managing your weight, excess adipose tissue produces cytokines such as IL-6 and TNF-α, exacerbating T-cell-driven inflammation.
-Unaddressed food allergies.
-Get full spectrum sunlight since insufficient natural sunlight (e.g., in winter or northern regions) reduces vitamin D synthesis, which normally regulates keratinocyte growth.
-Focus on optimizing your gut and sleep since gut dysbiosis and lack of sleep are the fastest ways to disrupt immune regulation.
-Natural IL-4/IL-13 inhibitors such as (pick one, don’t use all of these) luteolin, fisetin, quercetin, EGCG and apigenin.
4. Rosacea
Main causes:
-Vascular dysfunction: Abnormalities in the dermal blood vessels lead to excessive vasodilation and increased blood flow, causing flushing and persistent redness.
-Immune activation: Overactive innate immunity, particularly via toll-like receptor 2 (TLR2), responds to environmental triggers such as UV light or microbes such as demodex mites.
-Microbial contribution: Demodex mites are known to proliferate excessively in rosacea-prone skin, triggering TLR2 activation.
-Barrier dysfunction: Here, the stratum corneum’s lipid matrix is compromised, increasing transepidermal water loss and sensitivity to irritants.
Main causes:
-Vascular dysfunction: Abnormalities in the dermal blood vessels lead to excessive vasodilation and increased blood flow, causing flushing and persistent redness.
-Immune activation: Overactive innate immunity, particularly via toll-like receptor 2 (TLR2), responds to environmental triggers such as UV light or microbes such as demodex mites.
-Microbial contribution: Demodex mites are known to proliferate excessively in rosacea-prone skin, triggering TLR2 activation.
-Barrier dysfunction: Here, the stratum corneum’s lipid matrix is compromised, increasing transepidermal water loss and sensitivity to irritants.
Biggest ROI steps/tools you can use for addressing rosacea:
-Topical ivermectin.
-Stabilizing mast cells in case you have symptoms of histamine intolerance.
-Stop smoking and using nicotine, both increase oxidative stress and VEGF expression.
-Consider the following gut-related tests: Urea breath test, stool antigen test for H. pylori antigens, breath tests that measure hydrogen, methane, or hydrogen sulfide after lactulose/glucose ingestion, a stool analysis for candida, fungal culture, CHROMagar Candida.
If you only do one, do H. Pylori if you don’t have symptoms of IBS and breath tests if you do.
-Try your very best to stick to a 1:2 O3:O6 ratio in your diet
-Get enough zinc, selenium and vitamin E (zinc alone has been shown to reduce rosacea severity in 30–50% of patients after just 8 weeks for example).
-Topical ivermectin.
-Stabilizing mast cells in case you have symptoms of histamine intolerance.
-Stop smoking and using nicotine, both increase oxidative stress and VEGF expression.
-Consider the following gut-related tests: Urea breath test, stool antigen test for H. pylori antigens, breath tests that measure hydrogen, methane, or hydrogen sulfide after lactulose/glucose ingestion, a stool analysis for candida, fungal culture, CHROMagar Candida.
If you only do one, do H. Pylori if you don’t have symptoms of IBS and breath tests if you do.
-Try your very best to stick to a 1:2 O3:O6 ratio in your diet
-Get enough zinc, selenium and vitamin E (zinc alone has been shown to reduce rosacea severity in 30–50% of patients after just 8 weeks for example).
5. Vitiligo
Main causes:
-Autoimmune issues: Cytotoxic T-cells and autoantibodies target melanocytes in the stratum basale driven by cytokines such as IFN-γ and TNF-α which trigger apoptosis of melanocytes.
-Oxidative stress: Reactive oxygen species (ROS) accumulate in melanocytes due to defective antioxidant defenses such as reduced catalase for example.
This damages melanocyte membranes and DNA, sensitizing them to immune attack.
-Genetics: Variants in genes like NLRP1, TYR, or PTPN22 increase susceptibility to autoimmune responses or melanocyte dysfunction.
Biggest ROI steps/tools you can use for addressing vitiligo:
-Avoid night shifts and anything that dysregulates the circadian rhythm.
-Managing stress (it can reduce alpha-MSH production by 25% in animal models)
-Cold exposure (in mice it can increase POMC expression by even 25%).
-Getting enough tyrosine, vitamin C, zinc and copper to enhance prohormone convertase activity.
-Natural janus kinase (JAK) inhibitors might also help (curcumin, resveratrol, quercetin, berberine, ginger, EGCG).
Main causes:
-Autoimmune issues: Cytotoxic T-cells and autoantibodies target melanocytes in the stratum basale driven by cytokines such as IFN-γ and TNF-α which trigger apoptosis of melanocytes.
-Oxidative stress: Reactive oxygen species (ROS) accumulate in melanocytes due to defective antioxidant defenses such as reduced catalase for example.
This damages melanocyte membranes and DNA, sensitizing them to immune attack.
-Genetics: Variants in genes like NLRP1, TYR, or PTPN22 increase susceptibility to autoimmune responses or melanocyte dysfunction.
Biggest ROI steps/tools you can use for addressing vitiligo:
-Avoid night shifts and anything that dysregulates the circadian rhythm.
-Managing stress (it can reduce alpha-MSH production by 25% in animal models)
-Cold exposure (in mice it can increase POMC expression by even 25%).
-Getting enough tyrosine, vitamin C, zinc and copper to enhance prohormone convertase activity.
-Natural janus kinase (JAK) inhibitors might also help (curcumin, resveratrol, quercetin, berberine, ginger, EGCG).
6. Seborrheic dermatitis.
Main causes:
-Sebum overproduction.
-Fungal overgrowth: Usually a malassezia yeast overgrowth and its byproducts trigger an immune response via TLRs.
-Immune system dysregulation: Overactive innate immunity releases cytokines (IL-1, IL-8), recruiting neutrophils and macrophages.
-Inflammation: It weakens the stratum corneum’s lipid matrix, increasing TEWL and irritant penetration.
Main causes:
-Sebum overproduction.
-Fungal overgrowth: Usually a malassezia yeast overgrowth and its byproducts trigger an immune response via TLRs.
-Immune system dysregulation: Overactive innate immunity releases cytokines (IL-1, IL-8), recruiting neutrophils and macrophages.
-Inflammation: It weakens the stratum corneum’s lipid matrix, increasing TEWL and irritant penetration.
Biggest ROI steps/tools you can use for addressing it:
-Getting a hormonal panel done that includes androgens, cortisol, estrogens and IGF-1.
-Ketoconazole (it needs cycling every 2 weeks, you can use zinc pyrithione in between)
-Get enough zinc, selenium, B1, B5 and vitamin E.
-Full spectum sunlight and measure your vitamin D levels.
-Consider the following gut-related tests: Urea breath test, stool antigen test for H. pylori antigens, breath tests that measure hydrogen, methane, or hydrogen sulfide after lactulose/glucose ingestion, a stool analysis for candida, fungal culture, CHROMagar Candida.
-Getting a hormonal panel done that includes androgens, cortisol, estrogens and IGF-1.
-Ketoconazole (it needs cycling every 2 weeks, you can use zinc pyrithione in between)
-Get enough zinc, selenium, B1, B5 and vitamin E.
-Full spectum sunlight and measure your vitamin D levels.
-Consider the following gut-related tests: Urea breath test, stool antigen test for H. pylori antigens, breath tests that measure hydrogen, methane, or hydrogen sulfide after lactulose/glucose ingestion, a stool analysis for candida, fungal culture, CHROMagar Candida.
That's all.
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https://x.com/Helios_Movement/status/1941799246983790943
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#1. Detox handbook:
fitandball.gumroad.com/l/detox2/4th
#2. Gut health handbook:
fitandball.gumroad.com/l/uftii/4th
#3. Supplement handbook:
fitandball.gumroad.com/l/Supplements2……
#4. Histamine intolerance and MCAS handbook:
fitandball.gumroad.com/l/histamine25/…
#5. Nutritional library:
fitandball.gumroad.com/l/nutritionall…
#6. The system:
fitandball.gumroad.com/l/georgesystem…
#1. Detox handbook:
fitandball.gumroad.com/l/detox2/4th
#2. Gut health handbook:
fitandball.gumroad.com/l/uftii/4th
#3. Supplement handbook:
fitandball.gumroad.com/l/Supplements2……
#4. Histamine intolerance and MCAS handbook:
fitandball.gumroad.com/l/histamine25/…
#5. Nutritional library:
fitandball.gumroad.com/l/nutritionall…
#6. The system:
fitandball.gumroad.com/l/georgesystem…
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