Acne
This article does NOT constitute medical advice.
Consult with your physician before making any changes to your medical plan.
Consult with your physician before making any changes to your medical plan.
These are my notes from discussion with a friend.
Let’s write a definition of “acne” so we know what we’re up against.
Acne Definition: A chronic inflammatory and autoimmune disorder involving dysregulation of follicular epithelial differentiation, sebaceous gland activity, skin microbiome ecology, and innate and adaptive immune responses.
Now let’s break down that definition so we understand what each part really means as it relates to acne.
Inflammation: An increase in distance between the proteins of the electron transport chain on the inner mitochondrial membrane which results in leaking of the 30 million volt/meter potential and the increased production of reactive oxygen species. This then initiates the immune cascade of cytokines, histamines, prostaglandins, leukotrienes, etc. This ties right into all the things related to mitochondrial health that we’ve both been learning about.
Autoimmune disorder: In the context of acne this means a chronic, immune-mediated disease where the body's immune system triggers an inflammatory response that goes beyond simply fighting bacteria. Ok, so we need to figure out how to calm and modulate the innate and adaptive immune systems. We’ll look at the below.
Follicular epithelial differentiation: Thyroid hormones regulate epidermal cell proliferation, differentiation, and turnover, impacting the skin's barrier function and sebaceous gland activity. While not a direct primary cause of acne, autoimmune thyroiditis (AIT) is associated with severe acne, suggesting that abnormal thyroid function influences follicular keratinization and sebum production, particularly in cases involving autoantibodies. Hmmm….well that’s really interesting. I had no idea that the thyroid gland was so involved in acne. Iodine supplementation could really help. Get some 2% Lugol’s iodine and go watch Dr. David Brownstein videos, and while you listen to him think about acne as a cyst in the context of iodine. Strict ketosis is really helpful for thyroid recovery.
Sebaceous gland activity: Overactive sebaceous glands, often driven by hormones like androgens, produce excessive sebum (oil), which mixes with dead skin cells to clog hair follicles. This blockage creates an anaerobic, oily environment that triggers the rapid growth of Cutibacterium acnes bacteria, leading to inflammation, red pimples, and cystic acne. Again, really interesting because androgens (testosterone and DHEA) are controlled by the suprachiasmatic nucleus (SCN), come from cholesterol, and CANNOT be optimally produced without proper circadian light signaling. Poor sex steroid hormone function is causing the overproduction of sebum. I also find it interesting that the blockage creates an “anaerobic” microbiome environment which leads into the next part of our “acne” definition, skin microbiome environment. Ok, so morning sun and eating lots of cholesterol.
Skin microbiome ecology: Acne develops when the skin microbiome shifts from a balanced state to dysbiosis, characterized by a loss of microbial diversity and the overproliferation of specific Cutibacterium acnes () strains of bacteria. Excess sebum provides nutrients for to overgrow, triggering inflammation, weakening the skin barrier, and causing acne lesions. Since the blockage of sebaceous glands creates an anaerobic environment, I would think that using make-up (foundation) would also block oxygen from the skin and further exacerbate the growth of harmful anaerobic Cutibacterium acnes. Perhaps consider leaving the skin exposed to the natural air and consider a topical form of Lactobacillus rhamnosus, L. plantarum, and Streptococcus thermophilus to push out Cutibacterium acnes..
Innate and adaptive immune responses: The innate immune system triggers initial inflammation via TLR-2/TLR-4 activation and NLRP3 inflammasomes, while the adaptive system (CD4+ T-cells) amplifies it, forming pustules and papules. Well, this ties right into POMC. Both the innate and adaptive immune systems require beta and gamma MSH which only come from the POMC pathway. How do you drive POMC? In winter the only way is cold plunging, so consider bumping up to every day and slowly strive toward the 50-55 degree temperature. In summer you can drive POMC with UV-B sunlight.
Other things we need to consider: The microbiome of the gut.
Let’s write a definition of “acne” so we know what we’re up against.
Acne Definition: A chronic inflammatory and autoimmune disorder involving dysregulation of follicular epithelial differentiation, sebaceous gland activity, skin microbiome ecology, and innate and adaptive immune responses.
Now let’s break down that definition so we understand what each part really means as it relates to acne.
Inflammation: An increase in distance between the proteins of the electron transport chain on the inner mitochondrial membrane which results in leaking of the 30 million volt/meter potential and the increased production of reactive oxygen species. This then initiates the immune cascade of cytokines, histamines, prostaglandins, leukotrienes, etc. This ties right into all the things related to mitochondrial health that we’ve both been learning about.
Autoimmune disorder: In the context of acne this means a chronic, immune-mediated disease where the body's immune system triggers an inflammatory response that goes beyond simply fighting bacteria. Ok, so we need to figure out how to calm and modulate the innate and adaptive immune systems. We’ll look at the below.
Follicular epithelial differentiation: Thyroid hormones regulate epidermal cell proliferation, differentiation, and turnover, impacting the skin's barrier function and sebaceous gland activity. While not a direct primary cause of acne, autoimmune thyroiditis (AIT) is associated with severe acne, suggesting that abnormal thyroid function influences follicular keratinization and sebum production, particularly in cases involving autoantibodies. Hmmm….well that’s really interesting. I had no idea that the thyroid gland was so involved in acne. Iodine supplementation could really help. Get some 2% Lugol’s iodine and go watch Dr. David Brownstein videos, and while you listen to him think about acne as a cyst in the context of iodine. Strict ketosis is really helpful for thyroid recovery.
Sebaceous gland activity: Overactive sebaceous glands, often driven by hormones like androgens, produce excessive sebum (oil), which mixes with dead skin cells to clog hair follicles. This blockage creates an anaerobic, oily environment that triggers the rapid growth of Cutibacterium acnes bacteria, leading to inflammation, red pimples, and cystic acne. Again, really interesting because androgens (testosterone and DHEA) are controlled by the suprachiasmatic nucleus (SCN), come from cholesterol, and CANNOT be optimally produced without proper circadian light signaling. Poor sex steroid hormone function is causing the overproduction of sebum. I also find it interesting that the blockage creates an “anaerobic” microbiome environment which leads into the next part of our “acne” definition, skin microbiome environment. Ok, so morning sun and eating lots of cholesterol.
Skin microbiome ecology: Acne develops when the skin microbiome shifts from a balanced state to dysbiosis, characterized by a loss of microbial diversity and the overproliferation of specific Cutibacterium acnes () strains of bacteria. Excess sebum provides nutrients for to overgrow, triggering inflammation, weakening the skin barrier, and causing acne lesions. Since the blockage of sebaceous glands creates an anaerobic environment, I would think that using make-up (foundation) would also block oxygen from the skin and further exacerbate the growth of harmful anaerobic Cutibacterium acnes. Perhaps consider leaving the skin exposed to the natural air and consider a topical form of Lactobacillus rhamnosus, L. plantarum, and Streptococcus thermophilus to push out Cutibacterium acnes..
Innate and adaptive immune responses: The innate immune system triggers initial inflammation via TLR-2/TLR-4 activation and NLRP3 inflammasomes, while the adaptive system (CD4+ T-cells) amplifies it, forming pustules and papules. Well, this ties right into POMC. Both the innate and adaptive immune systems require beta and gamma MSH which only come from the POMC pathway. How do you drive POMC? In winter the only way is cold plunging, so consider bumping up to every day and slowly strive toward the 50-55 degree temperature. In summer you can drive POMC with UV-B sunlight.
Other things we need to consider: The microbiome of the gut.
