Page needing exploring about how accutane works and what else it's doing to you.
I wish I could copy and paste the higher level board topics and their summaries. Topics like: " Significant Irriversible Hormone Antagonism" and "Affected neurotransmitters and parts of the brain". Unfortunately, in addition to some good content, there's a lot of placeholders and a hell of a lot of spam.
What accutane does. Not light reading.
Isotretinoin and FOX01
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3219165/#__abstractid984712title
about FOX01 obviously, but also PPARy, IGF-1, Innate & aquired immune response, and many more mechanisms. including those that least to adverse affects like causing muscle pain, bone density, dry mucosa, hair loss, etc. ( I have the dry eyes/nasal passages (and mouth but it didn't mention mouth) and maybe the muscle ache. ) )
Here's one people should like. Marijuana for acne.
Cannabidiol exerts sebostatic and antiinflammatory effects on human sebocytes
Cannabidiol is one of the compounds most studied for medicinal use. http://www.leafscience.com/2014/02/23/5-must-know-facts-cannabidiol-cbd/
The thing to look into is the content in Hemp or Hemp seed/oil.
Beta carotene, UV exposure and Retinoic Acid
Trying to follow up on a theory by autonomousone
acne may be a genetic defect in vitamin a metabolism particularly with the pathway that creates retinoic acid in the skin. iv</strong>e read studies that suggest retinoic acid could be rendered inactive in our bodies so we may have ultra low levels of it, sending our skin and sebum cells into chaos.
BETA CAROTENE is derived from plants only and enters the body as ~60% beta carotene and 40 % retinal . the body can then turn retinal into retinol as needed and the body can store large amounts of beta carotene with no known overdose. So the true source of retinol is beta carotene ...
one other interesting fact to consider is that our skin stores a lot of our beta carotene intake thats why eating too many carrots can turn your skin orange. i also find it interesting that acne mainly occurs on the face and the back and these are places that are otherwise exposed to the sun when walking outside, <strong>and ive read a study that proves uv rays cause beta carotene to stimulate retinoic acid production</strong>. Interestng thoughts hey!!
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We are lacking/have too much of/have a mutation in the CYP26AI enzyme/gene in involved in the metabolism of retinoic acid in our skin?? And UV involvement in stimulating retinoic acid production could be one way many people's skin clears when they get more sun exposure
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>Polymorphisms in the human cytochrome P-450 1A1 gene (CYP1A1) as a factor for developing acne.
Paraskevaidis A, Drakoulis N, Roots I, Orfanos CE, Zouboulis CC.
Department of Dermatology, University Medical Center Benjamin Franklin, Free University of Berlin, Germany.
Cytochromes P-450 are a supergene family of enzymes involved in the metabolism of a wide range of endogenous and foreign compounds. The existing genetic variations of the distinct isozymes lead to interindividually different metabolic capacity. Since vitamin A, endogenous retinoids and their natural metabolites are morphogenic for the sebaceous gland, we investigated the polymorphisms of cytochrome P-450 1A1, as being one of the most active isozymes involved in their interconversion. From the known mutations, two were investigated; an additional cleavage site for MspI in the 3'-flanking region identified as a thymine-to-cytosine transition 1,194 bp downstream of exon 7 (m1) and an adenine-to-guanine transition at position 4889 in exon 7 (m2). We studied 96 acne patients for m1 and m2 mutations by restriction fragment length polymorphism and allele-specific polymerase chain reaction, respectively, and compared the results with 408 reference individuals. No statistically significant difference was found in the distribution of m2 alleles; the frequency was 3.13 and 3.06% of the alleles, respectively (odds ratio = 1.02, confidence limits 0.41-2.52, p = 0.96). In contrast,a trend to an overrepresentation of m1 alleles in acne patients was observed; allele frequency was 8.33 in the patients and 6.99% in the control subjects, respectively (odds ratio 1.21, 95% confidence limits 0.68-2.16, p = 0.52). As the m1 mutation might define a marker for alterations on regulatory sites, the biological efficacy of natural retinoids could be greatly impaired by their rapid metabolism to inactive compounds. The resulting deficit of active natural retinoids may lead to abnormal sebocyte differentiation and hyperkeratinization of the follicular canal implicating the development of acne in some patients.
Dermatology. 1998;196(1):171-5. Related Articles, Links
Promotes keratinocyte differentiation and apoptosis:
"Combination of betaC-promoted keratinocyte differentiation with the cellular "UV response" caused synergistic induction of cell cycle arrest and apoptosis." <a href=" http://www.ncbi.nlm.nih.gov/pubmed/15675964?dopt=Abstrac t" class="bbc_url" title="External link" rel="nofollow external"> http://www.ncbi.nlm....4?dopt=Abstract</a>
"UV-induced cell death by apoptosis is considered to be a natural protective mechanism that removes damaged keratinocytes and circumvents the risk of malignant transformation." <a href=" http://www.ncbi.nlm.nih.gov/pubmed/1596469 2" class="bbc_url" title="External link" rel="nofollow external"> http://www.ncbi.nlm....pubmed/15964692</a>
About the skin's ability to metabolize retinoic acid from beta carotene:
Skin retinoid concentrations are modulated by CYP26AI expression restricted to basal keratinocytes in normal human skin and differentiated 3D skin models.
<a href=" http://www.ncbi.nlm.nih.gov/pubmed/16778795?dopt=Abstrac t" class="bbc_url" title="External link" rel="nofollow external"> http://www.ncbi.nlm....5?dopt=Abstract</a>concludes<em><strong> '
strong constitutive expression of CYP26AI in vivo and in organotypic culture was found to be restricted to basal epidermal keratinocytes, as well as eccrine sweat glands and sebaceous glands. These studies verify the capacity of human skin to metabolize RA, although substantial differences exist in CYP expression between normal skin and 3D skin models compared to monolayer cultures. Complex metabolic processes that maintain retinoid homeostasis may therefore be better studied in model systems more closely resembling in vivo skin. In light of our prior studies documenting the functional activity of RA metabolites, expression of CYP26 in the sebaceous gland epithelium supports the suggestion that <strong>altered RA metabolism may be involved in the pathogenesis of acne
Biogenesis of retinoic acid from beta-carotene. Differences between the metabolism of beta-carotene and retinal.
<a href=" http://www.ncbi.nlm.nih.gov/pubmed/3182850?dopt=Abstrac t" class="bbc_url" title="External link" rel="nofollow external"> http://www.ncbi.nlm....0?dopt=Abstract</a>
Expression and function of cytochrome p450-dependent enzymes in human skin cells.
<a href=" http://www.ncbi.nlm.nih.gov/pubmed/1878194 7" class="bbc_url" title="External link" rel="nofollow external"> http://www.ncbi.nlm....pubmed/18781947</a></strong>
"human skin cells express various CYP enzymes, including </span></span></p><strong>CYP26AI which is responsible for the metabolism of retinoic acid in skin cells"
Good report with sources for research:
Cytochrome P450: A Target for Drug Development for Skin Diseases
;<a href=" http://www.nature.com/jid/journal/v123/n3/full/5602457a.htm l" class="bbc_url" title="External link" rel="nofollow external"> http://www.nature.co...l/5602457a.html</a>
The special interest for CYP enzymes in skin is evident by the fact that most, if not all, drugs used by the practicing dermatologist are either substrate or inducer, or inhibitor of this enzyme family (<a href=" http://www.nature.com/jid/journal/v123/n3/full/5602457a.html#tbl 1" class="bbc_url" title="External link" rel="nofollow external">Table I</a>. It is important to mention here that CYP enzymes act on many endogenous substrates including vitamin D and vitamin A, which are widely used in clinical practice for treating a variety of dermatological disorders....
Liarozole, which is an imidazole-containing compound, is known to inhibit the CYP-mediated metabolism of t-RA resulting in an increase of the retinoid in skin and plasma ( <a href=" http://www.nature.com/jid/journal/v123/n3/full/5602457a.html#bib8 1" class="bbc_url" title="External link" rel="nofollow external">VanWauwe and Janssen, 1989</a>; <a href=" http://www.nature.com/jid/journal/v123/n3/full/5602457a.html#bib2 1" class="bbc_url" title="External link" rel="nofollow external">Dockx <em>et al</em>, 1995</a></sup>
Cyp enzymes also affect vitamin D production:
Based on several studies, it is now clear that the active form of vitamin D and its analogs suppress growth and stimulate the terminal differentiation of keratinocytes ( <a href=" http://www.nature.com/jid/journal/v123/n3/full/5602457a.html#bib3 9" class="bbc_url" title="External link" rel="nofollow external">Kira <em>et al</em>, 2003</a>
It is also known that in psoriatic lesions, epidermal keratinocytes exhibit hyper-proliferation and impaired differentiation triggered by inflammation. Therefore, it is quite reasonable to assume that vitamin D is effective on psoriasis.
From this on hirsutism and PCOS <a href=" http://www.fastbleep.com/medical-notes/o-g-and-paeds/17/39/25 1" class="bbc_url" title="External link" rel="nofollow external"> http://www.fastbleep...paeds/17/39/251</a>
Spironolactone: An aldosterone antagonist. Reduces Hitsutism through competitive inhibition of DHT, reduces CYP enzyme and increases peripheral aromatisation of testosterone and inhibition of skin 5 alpha reductase.
Vitamin A and its natural and synthetic metabolites ( retinoids) affect growth and differentiation of human skin and among the genes affected by retinoids in epidermis are keratin genes. <a href=" http://www.ncbi.nlm.nih.gov/pubmed/2211077 3" class="bbc_url" title="External link" rel="nofollow external"> http://www.ncbi.nlm....pubmed/22110773</a>
"Vitamin A and its natural and synthetic metabolites (retinoids) affect growth and differentiation of human skin and among the genes affected by retinoids in epidermis are keratin genes."</p>
Retinoids might also help by being anti-inflammatory: Inflammation resolved by retinoid X receptor-mediated inactivation of leukotriene signaling pathways (Such as by acting PPARs.)
"Leukotrienes are implicated in the pathogenesis of diverse, inflammation-driven diseases.... Retinoids affect numerous signaling pathways in human skin (36) <a href=" http://www.fasebj.org/content/22/2/538.full#B3 6" class="bbc_url" title="External link" rel="nofollow external"><img src=" http://www.fasebj.org/icons/ref-arrow.gi f" alt="Posted Image" class="bbc_img"></a><span style="color: #403838"> .
Their antiinflammatory, prodifferentiating, and chemopreventative properties are efficacious toward diverse disorders including psoriasis, acne, ichthyosis, photoaging, cancer, emphysema, and bronchopulmonary dysplasia in newborns (38</span><a href=" http://www.fasebj.org/content/22/2/538.full#B3 8" class="bbc_url" title="External link" rel="nofollow external"><img src=" http://www.fasebj.org/icons/ref-arrow.gi f" alt="Posted Image" class="bbc_img"></a><span style="color: #403838"> 39</span><a href=" http://www.fasebj.org/content/22/2/538.full#B3 9" class="bbc_url" title="External link" rel="nofollow external"><img src=" http://www.fasebj.org/icons/ref-arrow.gi f" alt="Posted Image" class="bbc_img"></a><span style="color: #403838"> 40</span><a href=" http://www.fasebj.org/content/22/2/538.full#B4 0" class="bbc_url" title="External link" rel="nofollow external"><img src=" http://www.fasebj.org/icons/ref-arrow.gi f" alt="Posted Image" class="bbc_img"></a><span style="color: #403838"> 41)</span><a href=" http://www.fasebj.org/content/22/2/538.full#B4 1" class="bbc_url" title="External link" rel="nofollow external"><img src=" http://www.fasebj.org/icons/ref-arrow.gi f" alt="Posted Image" class="bbc_img"></a><span style="color: #403838"> . We present evidence that retinoids up-regulate a proresolving pathway in human epidermal keratinocytes by mechanisms involving RXR-mediated </span><em>CYP4F</em><span style="color: #403838">transcriptional activation (</span><strong>Fig. 6</strong><a href=" http://www.fasebj.org/content/22/2/538.full#F 6" class="bbc_url" title="External link" rel="nofollow external"><img src=" http://www.fasebj.org/icons/ref-arrow.gi f" alt="Posted Image" class="bbc_img"></a><span style="color: #403838"> ). One result is increased epithelial capacity to metabolically inactivate leukotrienes produced by infiltrating neutrophils, thereby antagonizing LTB4 signaling and further neutrophil recruitment. This CYP4F-dependent pathway functions as a physiological stop signal for epithelial inflammation, facilitating the switch to tissue repair and wound healing. </span><span style="color: #403838">" There's talk of celiac disease near the end of the full text..</span>
<a href=" http://www.fasebj.org/content/22/2/538.ful l" class="bbc_url" title="External link" rel="nofollow external"> http://www.fasebj.or...t/22/2/538.full</a>
Caratenoids and how they protect us from UVA damage with a comparison of beta carotene, Astaxanthin, and canthaxanthin
<a href=" http://www.ncbi.nlm.nih.gov/pubmed/1880365 8" class="bbc_url" title="External link" rel="nofollow external"> http://www.ncbi.nlm....pubmed/18803658</a>
Carotenoids and other phytonutrients protect from photodamage
<a href=" http://www.ncbi.nlm.nih.gov/pubmed/2225406 2" class="bbc_url" title="External link" rel="nofollow external"> http://www.ncbi.nlm....pubmed/22254062</a><p></p>
1: Biochem Biophys Res Commun. 1987 Aug 31;147(1):25-30. Links
Interference of retinoic acid binding to its binding protein by omega-6 fatty acids.Sani BP, Allen RD, Moorer CM, McGee BW.
Cellular retinoic acid-binding protein (CRABP) is the putative mediator of the biological effects of retinoic acid in the control of epithelial differentiation and tumorigenesis. Omega-6 fatty acids such as linoleic acid and arachidonic acid, precursors of prostaglandin synthesis, caused inhibition of retinoic acid binding to CRABP. These fatty acids, however, possessed lower affinity than retinoic acid for the binding protein. Omega-3 fatty acids, such as eicosapentaenoic acid and docosohexaenoic acid, did not cause such inhibition in the binding of retinoic acid. Whereas retinoic acid was a potent modulator of differentiation of F9 embryonal carcinoma cells, neither omega-3 nor omega-6 fatty acids showed any significant differentiation potential. Competition by omega-6 fatty acids with retinoic acid for CRABP may neutralize the binding protein-mediated biological functions of retinoic acid, and could thereby enhance tumor production.
Cordain may have said something about insulin surges can also lowering retinoic acid binding protien. (along with other factors like sex hormone binding globulin.
It's has been awhile since I posted on this site but I wanted to report a partial success I had with Vitamin A. This theory about UV light definetly holds some truth. I noticed that after taking Vitamin A in the form of 10,000 IU of retinol (the animal source, not beta carotene) and exposing my face and body to the sun every other day for an adequate amount of time, I could manage my acne to an extent. Now this didn't "cure" or completely cure my condition but it helped tremendously. I must note that during this time I was eating very healthy and also consumed many sources of plant sourced Beta-carotene from spinach, carrots, sweet potatoes, butternut squash, etc. Although I suggest only using retinol at first (since it is already converted to the active Vitamin A form whereas the conversion rate of beta-carotene is very low) beta-carotene could have still played a factor since I know that beta carotene is deposited in the surface skin and acts as an fat soluble antioxidant, and an electron acceptor from the sun.
This further supports the evolutionary biology approach to acne. At my worst points, I experienced severe acne on my face, and tops of my back and chest, the areas on the body that would be exposed most to the sun when we lived primitively. I believe we evolved a higher density of retinoic acid receptors in these areas of the skin so that more sun light was needed to produce a normal amount of retinoic acid. Now, our traditional american diets are low in Vitamin A, and antioxidants/pigments (zeaxanthin, astaxanthin, lutein, beta-carotene, lycopene) and we are being told to avoid the sun at all cost. My theory is that the sun and its "harmful" UV's do NOT cause skin cancer, but our lack of internal protection allow us to be susceptible to cancer. Please don't quote me saying that vitamin a cures skin cancer, this is just a theory on acne and the skin. And again I must stress that acne is multifactorial and this is just on of the ways it can "get" you, not including omega 3:6 ratio, hormone imbalace, etc...
Linking diet to acne metabolomics, inflammation, and comedogenesis: an update
Bodo C Melnik
Department of Dermatology, Environmental Medicine and Health Theory, University of Osnabruck, Germany
Abstract: Acne vulgaris, an epidemic inflammatory skin disease of adolescence, is closely related to Western diet. Three major food classes that promote acne are: 1) hyperglycemic carbohydrates, 2) milk and dairy products, 3) saturated fats including trans-fats and deficient -3 polyunsaturated fatty acids (PUFAs). Diet-induced insulin/insulin-like growth factor (IGF-1)-signaling is superimposed on elevated IGF-1 levels during puberty, thereby unmasking the impact of aberrant nutrigenomics on sebaceous gland homeostasis. Western diet provides abundant branched-chain amino acids (BCAAs), glutamine, and palmitic acid. Insulin and IGF-1 suppress the activity of the metabolic transcription factor forkhead box O1 (FoxO1). Insulin, IGF-1, BCAAs, glutamine, and palmitate activate the nutrient-sensitive kinase mechanistic target of rapamycin complex 1 (mTORC1), the key regulator of anabolism and lipogenesis. FoxO1 is a negative coregulator of androgen receptor, peroxisome proliferator-activated receptor- (PPAR), liver X receptor-, and sterol response element binding protein-1c (SREBP-1c), crucial transcription factors of sebaceous lipogenesis. mTORC1 stimulates the expression of PPAR and SREBP-1c, promoting sebum production. SREBP-1c upregulates stearoyl-CoA- and 6-desaturase, enhancing the proportion of monounsaturated fatty acids in sebum triglycerides. Diet-mediated aberrations in sebum quantity (hyperseborrhea) and composition (dysseborrhea) promote Propionibacterium acnes overgrowth and biofilm formation with overexpression of the virulence factor triglyceride lipase increasing follicular levels of free palmitate and oleate. Free palmitate functions as a danger signal, stimulating toll-like receptor-2-mediated inflammasome activation with interleukin-1 release, Th17 differentiation, and interleukin-17-mediated keratinocyte proliferation. Oleate stimulates P. acnes adhesion, keratinocyte proliferation, and comedogenesis via interleukin-1 release. Thus, diet-induced metabolomic alterations promote the visible sebofollicular inflammasomopathy acne vulgaris. Nutrition therapy of acne has to increase FoxO1 and to attenuate mTORC1/SREBP-1c signaling. Patients should balance total calorie uptake and restrict refined carbohydrates, milk, dairy protein supplements, saturated fats, and trans-fats. A paleolithic-like diet enriched in vegetables and fish is recommended. Plant-derived mTORC1 inhibitors and -3-PUFAs are promising dietary supplements supporting nutrition therapy of acne vulgaris.
Keywords: acne, comedogenesis, diet, inflammasome, metabolomics, quorum sensing
Potential role of FoxO1 and mTORC1 in the pathogenesis of Westerndiet-inducedacne.
Acne in adolescents of developed countries is an epidemic skin disease and has currently been linked to the Western diet (WD). It is the intention of this viewpoint to discuss the possible impact of WD-mediated nutrient signalling in the pathogenesis of acne. High glycaemic load and dairy protein consumption both increase insulin/insulin-like growth factor-1 (IGF-1) signalling (IIS) that is superimposed on elevated IGF-1 signalling of puberty. The cell's nutritional status is primarily sensed by the forkhead box transcription factor O1 (FoxO1) and the serine/threonine kinase mammalian target of rapamycin complex 1 (mTORC1). Increased IIS extrudes FoxO1 into the cytoplasm, whereas nuclear FoxO1 suppresses hepatic IGF-1 synthesis and thus impairs somatic growth. FoxO1 attenuates androgen signalling, interacts with regulatory proteins important for sebaceous lipogenesis, regulates the activity of innate and adaptive immunity, antagonizes oxidative stress and most importantly functions as a rheostat of mTORC1, the master regulator of cell growth, proliferation and metabolic homoeostasis. Thus, FoxO1 links nutrient availability to mTORC1-driven processes: increased protein and lipid synthesis, cell proliferation, cell differentiation including hyperproliferation of acroinfundibular keratinocytes, sebaceous gland hyperplasia, increased sebaceous lipogenesis, insulin resistance and increased body mass index. Enhanced androgen, TNF- and IGF-1 signalling due to genetic polymorphisms promoting the risk of acne all converge in mTORC1 activation, which is further enhanced by nutrient signalling of WD. Deeper insights into the molecular interplay of FoxO1/mTORC1-mediated nutrient signalling are thus of critical importance to understand the impact of WD on the promotion of epidemic acne and more serious mTORC1-driven diseases of civilization.
2013 John Wiley & Sons A/S.
Dietary intervention in acne: Attenuation of increased mTORC1 signaling promoted by Westerndiet.
The purpose of this paper is to highlight the endocrine signaling of Western diet, a fundamental environmental factor involved in the pathogenesis of epidemic acne. Western nutrition is characterized by high calorie uptake, high glycemic load, high fat and meat intake, as well as increased consumption of insulin- and IGF-1-level elevating dairy proteins. Metabolic signals of Western diet are sensed by the nutrient-sensitive kinase, mammalian target of rapamycin complex 1 (mTORC1), which integrates signals of cellular energy, growth factors (insulin, IGF-1) and protein-derived signals, predominantly leucine, provided in high amounts by milk proteins and meat. mTORC1 activates SREBP, the master transcription factor of lipogenesis. Leucine stimulates mTORC1-SREBP signaling and leucine is directly converted by sebocytes into fatty acids and sterols for sebaceous lipid synthesis. Over-activated mTORC1 increases androgen hormone secretion and most likely amplifies androgen-driven mTORC1 signaling of sebaceous follicles. Testosterone directly activates mTORC1. Future research should investigate the effects of isotretinoin on sebocyte mTORC1 activity. It is conceivable that isotretinoin may downregulate mTORC1 in sebocytes by upregulation of nuclear levels of FoxO1. The role of Western diet in acne can only be fully appreciated when all stimulatory inputs for maximal mTORC1 activation, i.e., glucose, insulin, IGF-1 and leucine, are adequately considered. Epidemic acne has to be recognized as an mTORC1-driven disease of civilization like obesity, type 2 diabetes, cancer and neurodegenerative diseases. These new insights into Western diet-mediated mTORC1-hyperactivity provide a rational basis for dietary intervention in acne by attenuating mTORC1 signaling by reducing (1) total energy intake, (2) hyperglycemic carbohydrates, (3) insulinotropic dairy proteins and (4) leucine-rich meat and dairy proteins. The necessary dietary changes are opposed to the evolution of industrialized food and fast food distribution of Westernized countries. An attenuation of mTORC1 signaling is only possible by increasing the consumption of vegetables and fruit, the major components of vegan or Paleolithic diets. The dermatologist bears a tremendous responsibility for his young acne patients who should be advised to modify their dietary habits in order to reduce activating stimuli of mTORC1, not only to improve acne but to prevent the harmful and expensive march to other mTORC1-related chronic diseases later in life.
FoxO, IGF-1, Western diet, acne, androgen, insulin, leucine, mTORC1, nutrition, prevention
Turning acne on/off via mTORC1.
Over the past 10 years, the increase in comprehension of the mechanisms behind acne has been truly exponential. Starting with the ethnological work of Cordain, accelerated by the epidemiological work of Adebamowo, supported by the clinical trials of Smith and Mann, Kwon, DiLandro and others, the interface of diet and acne is coming into focus. Melnik now presents an exceptional pair of papers that illustrate for dermatologists what translational research is all about. The Western diet, the role of dairy, FoxO1 and mTORC1, the interplay of agonists and antagonists, therapeutics present and future - the jigsaw puzzle is coming together.
2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
Full article: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3746129/
http://www.landesbio..._full_text=true
http://www.lipidworl.../content/8/1/25
These papers on mTor & acne areexcellent summaries of all the known factors involved in acne formation and most of the research into cause and intervention from big pharma like isotretinoin, BP and metformin to EGCG and resveraterol. And of course diet, especially the western diet.
And I wish to point out that they citeover one hundred scientific studies into these factors and how nutrients and diet habits affect those factors and thus acne. And yet people keep claiming there's no scientific evidence that diet affects acne. I guess it's like climate change deniers. No amount of evidence will change their minds.
Epigallocatechin-3-Gallate Improves Acne in Humans by Modulating Intracellular Molecular Targets and InhibitingP. acnes http://www.jidonline.org/article/S0022-202X(15)36111-X/fulltext#s0010
As in Green tea. I skimmed but didn't see if they were testing it topically or orally. Full text is available. And we knew it usually helped. Make a toner with a little ACV diluted with green tea.
Modulators of UDP-glucose ceramide glucosyltransferase for treating acne or hyperkeratinization - diagram, schematic, and image 08
@alternativistaHi, would love to hear more from you about recent advances. I track pubmed regularly, and sometimes also ClinicalTrials.gov.
The number of articles on acne is growing each year which is great. But for long time there are no major discoverieson acne which is sad.
Recent clinical trial going on is the testing ofApremilast on acne (conglobata). I'm really looking forward to check the results in a year or so.
This is a disease of the immune system, so the final solution I expect to be in the form of immunomodulatory drug.