It seems that resveratrol, green tea, chlorophyll and other phytonutrients all seem to have some overlapping properties. If I recall correctly, green tea is an antioxidant, cox/lox inhibitor, dht inhibitor etc etc. I agree that PPAR's are probably at the forefront of the acne problem. PPAR's are responsible for lipid metabolism in the body as well as sebaceous control in the skin. IT is clear that sesamin and fish oil have some effect on the ppar's. Both generally active ppar alpha which tends to be affiliated with its anti-inflammatory effects. I noticed that when I took fish oil and sesamin (on separate occasions) both DEFINATALY made me oilier. Which makes sense since ppar agonists increase sebum production. Also, artificial ppar agonists like Avandia for diabetes are also known to increase sebum production. So then why do some people improve on fish oil and sesamin and dry up while others get worse? I don't know. My best guess is that in acne patients, there is either an imbalance to the ppar's expressed. Perhaps an overactive or over expressed ppar gamma, or even beta delta is to blame. Ppar gamma tends to get activated by proinflammatory ligands and oxidized fats. Perhaps naturally occurring proimflammaytory ligands are enough to cause a greater response in acne patients than non sufferers. Perhaps some acne patients have ppar gamma upregulated due to exposure to some sort of allergen or toxin. What is known is that our body tends to balance out the expression of ppars, so by increasing the expression of antimflammatory ppar alpha through supplements, that mighe be enough to downregulate ppar gamma? Maybe for some people this "imbalance" is worse than others which might explain why some people get oiler at first or get an initial breakout. The supplements are activating and upregulating ppar alpha before our body can slowly downregulate the other ppars?
I'm personally believe that accutane resets the ppars to zero. That is why people stay clear at least temporarily after a course even in the presense of foods, allergens or toxins that make them breakout. It is only over the course of weeks/months that our body slowly upregulates the proinflammatory receptors and causes our acne to remerge. So perhaps taking a ppar alpha agonist after a course of accutane would be the most practical way to keep acne at bay? Or perhaps taking enough fish oil/sesamin for long enough at the right dosage might be enough to slowly change our receptors over the passing months?
This is only a general hypothesis based on what I have observed. I am not a scientist, doctor and anyone in any position to be giving medical advice. Please, feel free to correct me, disprove me make fun of me, whatever.
p.s. sorry for changing the topic
That is very interesting Jemini.
But I still can't understand then, why people outgrow acne. Do these PPARs naturally stabilize? Some people on accutane, I believe 50% are cured after one course! Obviously after discontinuing isotretinoin, it will leave you're system. Do you think that, taking those dosages at extended periods of time cause a permanent change in these receptors?
Autonomous noted that the alpha receptor is responsible for creating a "carrier" that collects fat which is brought to the liver to be broken down. So there are conflicting ideas about the actual function of these receptors regarding sebum. I wonder what would happen if you shut down these receptors.
I forgot to add, but a while back I had clear skin. I played football, and with full gear, specifically head gear, pressing on your forehead, temples, and chin, added with sweat and bacteria, my skin still was clear. It was until I started experimenting with testosterone boosters, which made me break out horribly.
Another thing that has been knawing at my ankle. What about hyperkeratinization? I've come across numerous posts where people have oily skin but no acne. Whats the deal?
Here's a quote:
"While any hormonal excess can promote acne, the male hormones (which are present in both males and females, only in differing amounts) are particularly notorious for stimulating the cells in the hair follicle to produce more keratin (a hard protein that forms hair, skin and nails)."
Also, check this link: http://www.blackwell-synergy.com/doi/abs/1...1997.d01-1162.x
From personal experience and research, PPARs and androgens MUST be what is causing acne. There cannot be acne if there is no improper shedding of skin cells. Then again, it maybe sebum composition that affects keratinization.
I would also like to add, that, although some people with acne have normal levels of androgens in their bloodstream, they have a higher amount of it in the local area of the sebaceous glands.
One more interesting study on androgens and sebum + hyperkeratinization:
http://www.dms.moph.go.th/inderm/Journal/C...20no2%20p92.pdf
While I'm no expert on nuclear biology or ppars, I can offer my opinion. In all honesty, I don't think accutane cures acne, but merely buys a person time for their hormones/ppars or whatever is out of whack in their system to return to normal. It clears most people the first time, since most people take it during puberty, a time of insulin resistance when acne is more likely to be prevelent. The accutane would buy them time until they grow out of puberty. Permanent remission rates in adulthood tend not to be so good. If puberty related insulin resistance isn't the cause, then accutane probably won't "buy you time" until your body fixes yourself.
I also remember reading a study, though I don't have the link that ppar's have been linked to skin's keritinization functions. Though I couldn't tell you how. All I can suggest is that you google ppar's and just try to suck up as much information as you can about them from different studies. The problem is even still, ppar's remain at the cutting edge of research and no one is able to tell the full story on what they do, how they work, and how they play with each other and other receptors.
My guess with hormones is that they must play some sort of indirect role. Androgens (namely testosterone) binding to the AR must affect ppar binding or expressivity. I do know that ppars do form dimers with other nuclear receptors, so the expression and binding of those receptors may also have an effect. Its problems like these that make nuclear biology so hard and why there still isn't any cure for acne. I don't believe in any of those pharmaceutical conspiracies people rave about on this site, and I also believe in the good nature of most scientists. If a scientist came across a cure, I believe they would share it with the world. And though there is alot of money in treatment of acne, if someone comes up with a cure, not only would that company become EXTREMELY rich, it would also help to put rival companies out of business.
As people have said before, acne is a symptom of an underlying cause. There could be many different causes. Only a few years ago, acne was thought to be caused by bacteria, which was found rarely to be the case. It turns out antibiotics worked coincidentally because they also exerted antinflammtory effects on specific enzymes. That is why low dose antibiotics (below bacteriocidal concentrations) are being researched for acne too. Check out the drug incyclinide. http://rosacea-support.org/incyclinide-col...x-gets-nih.html
Its a drug in development that has tetracycline like antimflammatory effect, but does not kill the bacteria, so there is no risk of immune strains, or kill of the probiotics in the gut and other problems associated with antibiotic therapy. I believe you'll be hearing alot about this drug in the next few years.
Anyway, I forgot what I was talking about. I'll save the ranting for another time
I know I probably stated this before, but on wikipedia it says:
"All PPARs dimerize with the retinoid X receptor (RXR) and bind to specific regions on the DNA of target genes."
Correct me if I am wrong, but doesn't isotretinoin affect the RXR? If so, it leaves PPARs unable to dimerize with anything, and thats why accutane works?
It just puzzles me that every sign points to androgens, as the real culprit of acne. I mean Kids don't have acne. They touch their face with greasy hands, eat horrible food, but have clear skin! It is only when they hit puberty and hormones surge through their bodies that acne beings to show up. Likewise, many people outgrow acne, relatively close to when puberty ends.
Also, although the key could be, to find something to bind to these receptors, we are unsure of what it would do. There is a possibility it would increase/decrease sebum.
Androgens MUST play a role in PPAR dimerization.
It seems that resveratrol, green tea, chlorophyll and other phytonutrients all seem to have some overlapping properties. If I recall correctly, green tea is an antioxidant, cox/lox inhibitor, dht inhibitor etc etc. I agree that PPAR's are probably at the forefront of the acne problem. PPAR's are responsible for lipid metabolism in the body as well as sebaceous control in the skin. IT is clear that sesamin and fish oil have some effect on the ppar's. Both generally active ppar alpha which tends to be affiliated with its anti-inflammatory effects. I noticed that when I took fish oil and sesamin (on separate occasions) both DEFINATALY made me oilier. Which makes sense since ppar agonists increase sebum production. Also, artificial ppar agonists like Avandia for diabetes are also known to increase sebum production. So then why do some people improve on fish oil and sesamin and dry up while others get worse? I don't know. My best guess is that in acne patients, there is either an imbalance to the ppar's expressed. Perhaps an overactive or over expressed ppar gamma, or even beta delta is to blame. Ppar gamma tends to get activated by proinflammatory ligands and oxidized fats. Perhaps naturally occurring proimflammaytory ligands are enough to cause a greater response in acne patients than non sufferers. Perhaps some acne patients have ppar gamma upregulated due to exposure to some sort of allergen or toxin. What is known is that our body tends to balance out the expression of ppars, so by increasing the expression of antimflammatory ppar alpha through supplements, that mighe be enough to downregulate ppar gamma? Maybe for some people this "imbalance" is worse than others which might explain why some people get oiler at first or get an initial breakout. The supplements are activating and upregulating ppar alpha before our body can slowly downregulate the other ppars?
I'm personally believe that accutane resets the ppars to zero. That is why people stay clear at least temporarily after a course even in the presense of foods, allergens or toxins that make them breakout. It is only over the course of weeks/months that our body slowly upregulates the proinflammatory receptors and causes our acne to remerge. So perhaps taking a ppar alpha agonist after a course of accutane would be the most practical way to keep acne at bay? Or perhaps taking enough fish oil/sesamin for long enough at the right dosage might be enough to slowly change our receptors over the passing months?
This is only a general hypothesis based on what I have observed. I am not a scientist, doctor and anyone in any position to be giving medical advice. Please, feel free to correct me, disprove me make fun of me, whatever.
p.s. sorry for changing the topic
While I'm no expert on nuclear biology or ppars, I can offer my opinion. In all honesty, I don't think accutane cures acne, but merely buys a person time for their hormones/ppars or whatever is out of whack in their system to return to normal. It clears most people the first time, since most people take it during puberty, a time of insulin resistance when acne is more likely to be prevelent. The accutane would buy them time until they grow out of puberty. Permanent remission rates in adulthood tend not to be so good. If puberty related insulin resistance isn't the cause, then accutane probably won't "buy you time" until your body fixes yourself.
I also remember reading a study, though I don't have the link that ppar's have been linked to skin's keritinization functions. Though I couldn't tell you how. All I can suggest is that you google ppar's and just try to suck up as much information as you can about them from different studies. The problem is even still, ppar's remain at the cutting edge of research and no one is able to tell the full story on what they do, how they work, and how they play with each other and other receptors.
My guess with hormones is that they must play some sort of indirect role. Androgens (namely testosterone) binding to the AR must affect ppar binding or expressivity. I do know that ppars do form dimers with other nuclear receptors, so the expression and binding of those receptors may also have an effect. Its problems like these that make nuclear biology so hard and why there still isn't any cure for acne. I don't believe in any of those pharmaceutical conspiracies people rave about on this site, and I also believe in the good nature of most scientists. If a scientist came across a cure, I believe they would share it with the world. And though there is alot of money in treatment of acne, if someone comes up with a cure, not only would that company become EXTREMELY rich, it would also help to put rival companies out of business.
As people have said before, acne is a symptom of an underlying cause. There could be many different causes. Only a few years ago, acne was thought to be caused by bacteria, which was found rarely to be the case. It turns out antibiotics worked coincidentally because they also exerted antinflammtory effects on specific enzymes. That is why low dose antibiotics (below bacteriocidal concentrations) are being researched for acne too. Check out the drug incyclinide. http://rosacea-support.org/incyclinide-col...x-gets-nih.html
Its a drug in development that has tetracycline like antimflammatory effect, but does not kill the bacteria, so there is no risk of immune strains, or kill of the probiotics in the gut and other problems associated with antibiotic therapy. I believe you'll be hearing alot about this drug in the next few years.
Anyway, I forgot what I was talking about. I'll save the ranting for another time
Autonomous,
That we will never know. I am just speaking from anecdotal experiences. My friend for example, had very bad acne for about 2-3 years of high school. All of a sudden, when he hit 18 and so forth, his acne started clearing up drastically. I am just guessing his hormones calmed down and his acne subsided. To this day, he will still get the occasional pimple, but nothing severe like before.
Again, I can't answer why you're acne got worse. But like you said maybe the root cause of you're acne is different since you are way past puberty.
When you say the androgen levels in those males are normal, are you speaking about the levels in the bloodstream or in the local area of the sebaceous glands. There are studies where testosterone levels were the same in bloodstream, but people with acne had a more considerable amount in the local area of acne. Just a thought though.
BTW, I am only 17 years old. I am still in that growing stage of my life. That, and the fact that I experimented with testosterone boosters earlier. (Broke me out pretty bad)
Hey Guys,
I came across this very interesting study on acne and androgens.
It is a very long read, but well worth it.
crazy shit about chlorophyll i didnt expect to find
Mol Biol Cell. 1996 Aug;7(8):1153-66. Links
Phytol metabolites are circulating dietary factors that activate the nuclear receptor RXR.Kitareewan S, Burka LT, Tomer KB, Parker CE, Deterding LJ, Stevens RD, Forman BM, Mais DE, Heyman RA, McMorris T, Weinberger C.
Orphan Receptor Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.
RXR is a nuclear receptor that plays a central role in cell signaling by pairing with a host of other receptors. Previously, 9-cis-retinoic acid (9cRA) was defined as a potent RXR activator. Here we describe a unique RXR effector identified from organic extracts of bovine serum by following RXR-dependent transcriptional activity. Structural analyses of material in active fractions pointed to the saturated diterpenoid phytanic acid, which induced RXR-dependent transcription at concentrations between 4 and 64 microM. Although 200 times more potent than phytanic acid, 9cRA was undetectable in equivalent amounts of extract and cannot be present at a concentration that could account for the activity. Phytanic acid, another phytol metabolite, was synthesized and stimulated RXR with a potency and efficacy similar to phytanic acid. These metabolites specifically displaced [3H]-9cRA from RXR with Ki values of 4 microM, indicating that their transcriptional effects are mediated by direct receptor interactions. Phytol metabolites are compelling candidates for physiological effectors, because their RXR binding affinities and activation potencies match their micromolar circulating concentrations. Given their exclusive dietary origin, these chlorophyll metabolites may represent essential nutrients that coordinate cellular metabolism through RXR-dependent signaling pathways.
could this actually be the dietary natural equivelant to accutane?
when i first discovered phytanic acid and its ability to affect ppar alpha, i thought it was peculiar that it was derived from the green pigment in plants, when you think of this pigment it is pretty much the universal color of life like in spring when everything turns green again you see everything coming back to life, i was thinking to myself why our creator made this pigment so abundant? well of course i know that chlorophyll helps plants convert sunlight into energy but now even to learn that it may also affect rxr receptors directly as well as through ppar pathway is just cool.
As we know through studying retinoids that when 13-cis retinoic acid binds to rxr it restores the cell to homeostasis or makes the cell stable by inducing apoptosis or cell death, an organism that is alive and well is basically a collection of cells that are in homeostasis and is a stable organism, so life=homeostasis and death=uncontrolled proliferation such as cancers that kill most people and also similar to the uncontrolled proliferation of keratinocytes and sebaceous glands, so acne could be one step closer to death since their is a lack of homeostasis, its as though phytanic acid or phytol or chlorophyll could be natures way of stabilizing life on planet earth, as rxr agonists are also used for many cancers as well as acne and psoriasis which are all cell that have lost homeostasis and all are conditions that are treated very well with retinoids.
Autonomous,
That is indeed very interesting!
"Structural analyses of material in active fractions pointed to the saturated diterpenoid phytanic acid, which induced RXR-dependent transcription at concentrations between 4 and 64 microM. Although 200 times more potent than phytanic acid"
What exactly does this mean??
You also stated:
"13-cis retinoic acid binds to rxr it restores the cell to homeostasis or makes the cell stable by inducing apoptosis or cell death. To my understanding isotretinoin helps acne, so why would it induce cell death, which as you stated, is "uncontrolled proliferation"?
You're theory makes a lot of sense though. I wonder how much chlorophyll would need to be ingested to have a noticeable effect.
Here's something else I found of Chlorophyll and acne:
Chlorophyll and lemon
Chlorophyll is one of the best ways to detoxify the colon fast. Your colon needs to be detoxified constantly to prevent toxins from getting into your blood and seeping into your facial skin where they can create acne. It also helps the skin keep healthy by acting as an
* antioxidant
* anti-inflammatory
* anti-microbial agent
* absorber of heavy metals in the colon
Here are some of the benefits you will get from drinking chlorophyll,
* Heals open wounds inside your body
* Increases re-growth of tissues
* Helps to heal sores in your mouth
* Acts as a antiseptic
* Destroys bacteria
* Brings more oxygen to your cells
* Give protection from low levels of radiation such as TV, computers, microwaves, and hospital equipment
* Reduces toxins in the colon and body
* Helps to purify the liver
* Helps sores heal faster
* Reduces pain from inflammation
Ahhh alright, thanks for clarifying that up a bit.
Just to be straight, when 13 cis retinoic acid binds to RXR, the cells become stable and the life and death cycle is returned to normal?
I came across this website:
http://www.leaddiscovery.co.uk/target-disc...Med-030306.html
"Since RXR forms heterodimers with both PPARalpha and PPARgamma blocking RXR may produce a phenotype that shares some similarities with PPARalpha deletion and others with PPARgamma deletion. Since therapeutic candidates that target PPAR may confer most benefit in the context of diabetes and obesity if they activate PPARalpha and/or block PPARgamma it is conceivable that RXRalpha antagonists may be of use if they are selective for RXR:PPARgamma heterodimers and fail to impede RXR:PPARalpha mediated effects. This is supported in part by recent research showing that the dual antagonism of RXR and PPARgamma decreases triglyceride content, potentiates leptin's effects and increased fatty acid combustion and energy dissipation, thereby ameliorating diet-induced obesity and insulin resistance. Molecules that block RXR:PPARgamma and stimulate RXR:PPARalpha dimers may represent an even better approach."
Looks like PPARs and RXRs go hand in hand. Isotretinoin binds to RXR and does not allow PPARs to form dimers?
So basically we need to upregulate PPAR alpha? What are the roles of delta and gamma?
That was a very informative and sorta fun watch! Thanks for sharing.
I went to Vitaminshoppe today to pick up some Cholorophyll and ended up getting something called the Cholor-Combo.
It contains:
Amount Per
Serving
Sodium (An Electrolyte)
Chlorophyll (Sodium Copper Chlorophyllins)(From Alfalfa Leaves)(Medicago Sativa)
CAPE ALOE (WHOLE)(ALOE SOLCATA)
ALLANTOIN
HERBAL COMPLEX BLEND PEPPERMINT LEAVES (MENTHA PIPERITA), FENNEL SEED (FOENICULUM VULGARE), GINGER ROOT (ZINGIBER OFFICINATE), RED RASPBERRY LEAVES (RUBUS STRIGOSUS)
....
Allantoin from Wiki:
"Manufacturers cite several beneficial effects for allantoin as an active ingredient in over-the-counter cosmetics: a moisturizing and keratolytic effect, increasing the water content of the extracellular matrix and enhancing the desquamation of upper layers of dead skin cells, increasing the smoothness of the skin; promotion of cell proliferation and wound healing; and a soothing, anti-irritant, and skin protectant effect by forming complexes with irritant and sensitizing agents."
Lets see how this works out!
Here's a little tidbit about androgens and ppars
http://www.medscape.com/viewarticle/460988_5
Sebocyte Glands
Activation of PPARgamma and PPARalpha by their respective specific ligands, thiazolidinedione, rosiglitazone and the fibrate, WY-14643, were found to stimulate lipid droplet accumulation in cultured immature sebocytes, but not in keratinocytes, as assessed histochemically using Oil Red O staining in cells cultured under high calcium conditions.[46,47] When dihydrotestosterone (DHT) was added with PPAR activators, an additive effect on lipid droplet formation in sebocytes was only seen with the combination of DHT and PPARgamma activator. This suggests that PPARgamma influences a step in sebocyte differentiation that is related but distinct from that influenced by androgen.[48]
Because increased sebum production is an important element in the pathogenesis of acne vulgaris, development of PPAR antagonists that can interfere selectively with sebum formation may have implications for the treatment of acne.
Yeah, the video pretty much summed up how they work in a nutshell.
"Since RXR forms heterodimers with both PPARalpha and PPARgamma blocking RXR may produce a phenotype that shares some similarities with PPARalpha deletion and others with PPARgamma deletion. Since therapeutic candidates that target PPAR may confer most benefit in the context of diabetes and obesity if they activate PPARalpha and/or block PPARgamma it is conceivable that RXRalpha antagonists may be of use if they are selective for RXR:PPARgamma heterodimers and fail to impede RXR:PPARalpha mediated effects. This is supported in part by recent research showing that the dual antagonism of RXR and PPARgamma decreases triglyceride content, potentiates leptin's effects and increased fatty acid combustion and energy dissipation, thereby ameliorating diet-induced obesity and insulin resistance. Molecules that block RXR:PPARgamma and stimulate RXR:PPARalpha dimers may represent an even better approach."
Looks like PPARs and RXRs go hand in hand. Isotretinoin binds to RXR and does not allow PPARs to form dimers?
So basically we need to upregulate PPAR alpha? What are the roles of delta and gamma?
Yes, basically isotretinoin (or much more likely its metabolites since isotretinoin actually has a low affinity for the rxr receptor) binds very tightly to rxr, thus preventing other molecules to stimulate/activate ppar alpha and gamma. My HYPOTHESIS on accutane is as follows. I feel that among other things, acne for many people is caused by overactivation of ppar gamma, or an increased transcription of the dna ppar gamma activates due to seemingly "normal" levels of natural ligands in the body (could be a genetic factor here). Anecdotal reports say that Sesamin, a known ppar alpha activator used as a weight loss supplement seemingly clears acne. How exactly is anyones guess. A few possibilities include that binding a ligand binding with ppar alpha (presumably by also forming a dimer with rxr maybe?) prevents the "bad" over activation of ppar gamma. Perhaps some of the transcription products of ppar alpha counter the negative effects of ppar gamma. Whatever the case may be, it is my best guess that tilting the ratio of in favor of ppar alpha versus gamma is probably a good thing, at least for acne. My belief is that when accutane binds to rxr and shuts off both ppar gamma and alpha in the skin, these receptors overtime become downregulated (body produces less receptors). This might be why the effects of accutane and other retinoids persist, even after treatment has stopped.
What I can tell you from personal experience is that sesamin definitely made me oiler, though acne remained approximately the same. My guess is that ppar's have some overlapping functions, sebum function being one of them. Maybe if i stuck with it long enough, over time it might have corrected the imbalance between ppar alpha and gamma. This could take months to see results, or it could not work at all if a) the activating effects of sesamin (or fish oil) aren't powerful enough to "override" the genetic programming in the expression of ppar gamma, or b) I'm completely wrong. Judging from accutanes effects, it could take months or longer to get this downregulation to finally occur.
There is also some anecodotal evidence that ppar gamma antagonism might work as well. I know of 2 examples, which hint at this correlation. First, there is Zileuton, a 5-lox inhibitor. It is used as an asthma medication, but was believed to be the next breakthrough in acne treatment. 5-lox produces inflammatory ligands which among other things, bind to ppar gamma. One study showed it dried up oil as much as low dose accutane (google it if you don't believe me). The actual clinical trial was less than breakthrough. After a few months (I think 3) the level of acne between placebo group and medicated group was about the same. However, the full study revealed that in the medicated group, the level of imflammatory acne decreased. What does this mean? Obviously, further testing is required but perhaps if the trial was run for longer the results would have been better. Also, Zileuton isn't the best 5-lox inhibitor since it has to be taken I think 4 times a day since it gets metabolized so fast (it was designed with asthma in mind). So perhaps a better drug based on this principle would have been better. Also, ppar gamma ligands may be produced by other pathways as well. The point is that inhibiting ppar gamma ligands did have a beneficial effect on acne. Perhaps a drug which targeted ppar gamma directly and efficiently would yield much better results.
Green tea extract which seems to be popular on this board is also known to be a 5-lox inhibitor among other things. And for some people, it seems to take the imflammation out of acne.
I'm not saying ppars are the only factor in acne formation. i'm willing to bet that many of the nuclear receptors have some sort of moderating effect on each other, this may explain why androgen and thyroid disorders may cause acne as well.
I am currently on my second course of accutane at 30 mg's a day for 8 months. I am about 2 months in and still suffering from the IB. Knowing my past history, I should see a turn around in a few weeks. I might consider a little self experimentation. I would continue my accutane course until clear, maybe at even a lower dosage. Accutane has the ability to clear acne at low dosages around 5-10mg a day, but is prescribed higher due to a better chance of remission. I am 22, almost 23 and my gut instinct is that accutane this time around won't clear me for good, just buy me more time. I am considering taking accutane until clear, then dropping the accutane and picking up the sesamin and fish oil again. Perhaps, once my ppar's are "reset" so to speak, these supplements might be able to maintain IF my theory is right. If the acne returns, then I'll just hop back on the accutrain.
I apologize for rambling, hijacking the thread, telling my life story and once again being an asshole in general.
Jemini,
Thats some real interesting thinking!
What exactly are the metabolites of isotretinoin? Would taking something with a higher affinity for the RXR receptors have the saem effect as accutane?
It's interesting that you mention weight loss, because alot of bodybuilders who obviously have high amounts of testosterone have no acne. I know they take supplements to shed the fat, and maybe that plays a role in acne as well? I mean maybe fat loss regimens affect lipogensis?
Perhaps you are correct about, sticking to it longer. Some people on accutane get oiler for a couple weeks and then they get dry. Keep in mind that this is megadosing on 13 cis retinoic acid. The effects of "regular" supplementing with sesamin. Kinda like B5. It looks like you need to mega dose on something to see results.
Off topic, women usually start to break out during period, when hormones are in flux. There must be something going on when there are hormonal shifts. Whether it be with the PPARs or the ARs themselves.
If you read the study I posted early on in this thread, there was a study that showed 95% of people have significant success with topical resveratrol. Resveratrol is a 5 lipoxygenase inhibtor. If memory serves correct (there are so many things, I get confused), 4 Lipoxygenase is responsible for anachinodic acid, which in turn makes leukotrines, which can stimulate the sebaceous glands. Resveratrol also inhibits CYP1A1, an enzyme that could break down retinoic acid quicker than it can be used. Just things to think about.
My mom has hypthyroidism. I'm not sure if I have it because:
1) I don't have any of the symptoms for it
2) I have alot of my dad's genes. I look like him, built like him and everything.
Check out the studies about the chlorophyll too! Its very interesting that its derivatives affect PPARs. Like Autonomous said, look at all the green around, the algae which has survived for 2.5 billion years, and is abundant in chlorophyll. As an added benefits, its very effective in cleansing the entire body. Always a plus if you're acne is produced by toxins that may affect the up/downregulation of certain PPARs
Today was the third time I took Chlorophyll. (Chloro Combo)
I mix it with orange juice and drink 1 cup in the morning and 1 cup at night. It really helps with bowel movements and it feels like everything comes out.
There are alot of benefits with cholorphyll, aside from the possibility it may upregulate ppar alpha.
As for phytanic acid, no I don't think they have that as a supplement. The chlorophyll you buy in stores is actually chlorophyllins, and theyre suppose be have more benefits that chlorophyll itself.
I know my previous post was for Jemini, but does anyone else have any thoughts?
Thanks!