68 replies to this topic

[bber]

Lately I've been clearing out almost completely. The doc has suggested that I might be outgrowing my acne. But I think its related to something else. A few weeks ago I upped my fish oil intake to 10g a day from supplementation as part of my bulk. I also received a REZ-V bottle(300mg resveratrol) from biotest. My skin has been comfortably dry all this time, and my skin is usually oily to the point that if i touch my face my fingers are covered in oil.

I've read some research suggesting that fish oil and resveratrol _might possibly, maybe_ help control sebum production. So what I ask is, is anyone else willing to try this out and report back if it worked for them? Maybe its a coincidence but maybe I stumbled on to something that could help some people.

[anony.]

whats resveratrol?

and are you taking 10 1000mg fish oil pills? how many mg of EPA and DHA do you get per pill?

[Legend]

Resveratrol is the anti-fungal substance that plants create to protect their fruit. It's found in red grape's peel, peanuts.

Lately scientists from highly regarded places (such as Harvard) have been finding that high doses of resveratrol has insane health benefits. We're talking about actually decreasing the rate of aging by as much as half, increasing athletic performance, decreasing the risk of heart disease.

The problem is that the amount used in studies is equivalent to like 100 bottles of red wine a day, so you've got to supplement.

http://www.news.harvard.edu/gazette/2003/0...-antiaging.html

I don't think Harvard has completed one of their studies because it involves rats. Rats have an average lifspan of about 2 years. The study isn't complete because the rats are around 3 years old and just won't die.


I've been supplementing with Biotest's REV-Z. I've noticed a minor improvement in inflammation. But that's not why I started taking the stuff.

Edit: I need to video tape myself. I'm afraid that I have schizo and that I am actually bber, lol.

[Case N]

Edit: I need to video tape myself. I'm afraid that I have schizo and that I am actually bber, lol.

2nd'd

[blackbirdbeatle]

Ya some people say resveratrol is the holy grail in terms of aging and a link to extremely long life. In those animal studies they didn't take into account differences between how mice and use process the stuff. We need a lot less per kg. Although that still ends up at like 500mg a day, which is a lot. Just not the grams and grams needed to replicate the studies(Although they do sell it in bulk now and for about 80.00 a month you can take severl grams a day and theoretically live for a very long time).

Also the trans form is the one that's valuable and unfortunately it's only found in a few products.

And I think that melatonin is a far more potent antioxidant and life extender if you will. In mice studies, they lived even longer on Melatonin than the megadoses of resveratrol. I take Melatonin every day. I'll let you know in 100 years if it works.

[xtr3m]

Uhh, according to the BioTest description REZ-V's main purpose is testosterone increase -- isn't that the last thing an acne sufferer needs?

[bber]

whats resveratrol?

and are you taking 10 1000mg fish oil pills? how many mg of EPA and DHA do you get per pill?

Should have been more specific, I actually take in 24 1g pills, which turns out to be around 10g EPA and DHA.

[bber]

Uhh, according to the BioTest description REZ-V's main purpose is testosterone increase -- isn't that the last thing an acne sufferer needs?

I don't have an answer to that question. I believe--and I could very well be wrong--that testosterone itself isnt the enemy, but rather that high levels of testosterone could stimulate the sebaceous glands into producing more oil. However, both res and fish oil can lead to an increase in testosterone levels. If these compounds also help down regulate sebum production then theres gotta be something we are missing.

[blackbirdbeatle]

It also increases healthy sperm counts. I've seen studies that showed it as a phytoestrogen in some respects. I've also seen studies that show that it modulates not only estrogen but testosterone and other androgens as well.

And I saw another study that actually gave rats 1000x the amount a 70kg adult taking 1.4grams per day is taking. With no adverse effects. Of course with melatonin they gave adults several thousand times more than the averge pill worth for a long period with no adverse effects. Although their jetlag would have probaly been impossible to overcome.

Sucks for people here but peanuts are a great source of this as well.

[AutonomousOne1980]

resveratrol is a potent 5 lipo oxygenase and cyclo oxygenase inhibitor http://content.febsjournal.org/cgi/content/full/265/1/27

5-lipo oxygenase is the enzyme that converts efas specifically arachinodic acid into pro-inflammatory leukotrines
http://en.wikipedia.org/wiki/Lipoxygenase#...enase_.285LO.29

it is believed by some that the production of these pro inflammatory luekotrines especially ltb4 can stimulate sebaceous glands and could be a possible cause for acne in some people
J Mol Med. 2006 Jan;84(1):75-87. Epub 2005 Dec 31.Links
Enzymes involved in the biosynthesis of leukotriene B4 and prostaglandin E2 are active in sebaceous glands.

Department of Dermatology, Charite Universitaetsmedizin Berlin, Campus Benjamin Franklin, Fabeckstrasse 60-62, 14195 Berlin, Germany.
The expression of enzymes involved in leukotriene and prostaglandin signalling pathways, of interleukins 6 and 8 and of peroxisome proliferator-activated receptors in sebaceous glands of acne-involved facial skin was compared with those of non-involved skin of acne patients and of healthy individuals. Moreover, 5-lipoxygenase and leukotriene A(4) hydrolase were expressed at mRNA and protein levels in vivo and in SZ95 sebocytes in vitro (leukotriene A(4) hydrolase > 5-lipoxygenase), while 15-lipoxygenase-1 was only detected in cultured sebocytes. Cyclooxygenase-1 and cyclooxygenase-2 were also present. Peroxisome proliferator-activated receptors were constitutively expressed. Enhanced 5-lipoxygenase, cyclooxygenase 2 and interleukin 6 expression was detected in acne-involved facial skin. Arachidonic acid stimulated leukotriene B(4) and interleukin 6 release as well as prostaglandin E(2) biosynthesis in SZ95 sebocytes, induced abundant increase in neutral lipids and down-regulated peroxisome proliferator-activated receptor-alpha, but not receptor-gamma1 mRNA levels, which were the predominant peroxisome proliferator-activated receptor isotypes in SZ95 sebocytes. In conclusion, human sebocytes possess the enzyme machinery for functional leukotriene and prostaglandin pathways. A comprehensive link between inflammation and sebaceous lipid synthesis is provided.

in that last study it proved that arachidonic acid it downregulated ppar alpha and stimulated ltb4 and il-6

so that means that arachidonic acid has a direct control over ppars which are agonist(influencer) for the rxr receptor just like accutane does.
http://en.wikipedia.org/wiki/PPAR

here is another study that say ppars can control sebum production(just like accutane)
1: J Invest Dermatol. 2006 Sep;126(9):2002-9. Epub 2006 May 4. Links
Peroxisome proliferator-activated receptors increase human sebum production.Trivedi NR, Cong Z, Nelson AM, Albert AJ, Rosamilia LL, Sivarajah S, Gilliland KL, Liu W, Mauger DT, Gabbay RA, Thiboutot DM.
The Jake Gittlen Cancer Research Institute, Hershey, Pennsylvania 17033, USA.

Sebum production is key in the pathophysiology of acne, an extremely common condition, which when severe, may require treatment with isotretinoin, a known teratogen. Apart from isotretinoin and hormonal therapy, no agents are available to reduce sebum. Increasing our understanding of the regulation of sebum production is a milestone in identifying alternative therapeutic targets. Studies in sebocytes and human sebaceous glands indicate that agonists of peroxisome proliferator-activated receptors (PPARs) alter sebaceous lipid production. The goal of this study is to verify the expression and activity of PPARs in human skin and SEB-1 sebocytes and to assess the effects of PPAR ligands on sebum production in patients. To investigate the contribution of each receptor subtype to sebum production, lipogenesis assays were performed in SEB-1 sebocytes that were treated with PPAR ligands and isotretinoin. Isotretinoin significantly decreased lipogenesis, while the PPARalpha agonist-GW7647, PPARdelta agonist-GW0742, PPARalpha/delta agonist-GW2433, PPARgamma agonist rosiglitazone, and the pan-agonist-GW4148, increased lipogenesis. Patients treated with thiazolidinediones or fibrates had significant increases in sebum production (37 and 77%, respectively) when compared to age-, disease-, and sex-matched controls. These data indicate that PPARs play a role in regulating sebum production and that selective modulation of their activity may represent a novel therapeutic strategy for the treatment of acne.


notice that the name ppar has proliferater in it, denoting control over proliferation.

J Steroid Biochem Mol Biol. 2002 Nov;82(4-5):393-400. Links
Inhibitors of the arachidonic acid pathway and peroxisome proliferator-activated receptor ligands have superadditive effects on lung cancer growth inhibition.
Intervention Section, Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA.
Arachidonic acid (AA) metabolizing enzymes and peroxisome proliferator-activated receptors (PPARs) have been shown to regulate the growth of epithelial cells. We have previously reported that exposure to the 5-lipoxygenase activating protein-directed inhibitor MK886 but not the cyclooxygenase inhibitor, indomethacin, reduced growth, increased apoptosis, and up-regulated PPARalpha and gamma expression in breast cancer cell lines. In the present study, we explore approaches to maximizing the proapoptotic effects of PPARgamma on lung cancer cell lines. Non-small-cell cancer cell line A549 revealed dose-dependent PPARgamma reporter activity after treatment with MK886. The addition of indomethacin in combination with MK886 further increases reporter activity. We also show increased growth inhibition and up-regulation of apoptosis after exposure to MK886 alone, or in combination with indomethacin and the PPAR ligand, 15-deoxy-Delta12,14-prostaglandin J2 compared with single drug exposures on the adenocarcinoma cell line A549 and small-cell cancer cell lines H345, N417, and H510. Real-time PCR analyses showed increased PPAR mRNA and retinoid X receptor (RXR)alpha mRNA expression after exposure to MK886 and indomethacin in a time-dependent fashion. The results suggest that the principal proapoptotic effect of these drugs may be mediated through the known antiproliferative effects of the PPARgamma-RXR interaction. We therefore explored a three-drug approach to attempt to maximize this effect. The combination of low-dose MK886, ciglitazone, and 13-cis-retinoic acid interacted at least in a superadditive fashion to inhibit the growth of lung cancer cell lines A549 and H1299, suggesting that targeting PPARgamma and AA action is a promising approach to lung cancer growth with a favorable therapeutic index.

The ligands for the PPARs are free fatty acids and eicosanoids. PPARγ is activated by PGJ2 (a prostaglandin). In contrast, PPARα is activated by leukotriene B4. so eicosanoids influence ppars.

eicosaniods are made from efas http://en.wikipedia.org/wiki/Eicosanoids

here is a chart for how efas are made into eicosanoids http://en.wikipedia.org/wiki/Image:EFA_to_Eicosanoids.svg

by analyzing this chart you can see that an over balance of arachidonic acid leads to the production of pro-inflammatory eicosanoids
and most detrimentally to the production of ltb4 and pge2 which alter ppar ligands and can control sebum secretion.

if this is all in fact true, it is now easy to see why there is a prevelance of acne in industrialized nations due to a diet too high in omega 6s in relation to omega 3s. although there is a main underlying genetic component to this disease this is why some people probably dont get acne, but they will probably get cancer or heart disease somewhere down the line.

From all the research ive been doing lately ive learned alot and have tons upon tons of studys that can easliy prove this theory as a cause for most acne. as the sebum could be controlled in a few ways there are still a few different factors the developing the disease but this could easliy explain aboiut 90% of the cases for acne.

my theory is that sebum secretion is basicly your bodys way to get rid of excess omega 6s and in fact could be a very good survival function to keep you alive by not keeping all that bad fat in your blood and causing cancer or heart disease or a heart attack. in a way our bodys could be alot stronger then most others.

Im also intrigued by how accutane has a tendancy to raise serum(blood) cholesterol levels while you are on the drug, indicating that they cannot escape via the sebum glands and now they are released into the blood instead.

check out these other threads they may interest you
http://www.acne.org/messageboard/index.php?showtopic=140133

http://www.acne.org/messageboard/index.php?showtopic=140399

http://www.acne.org/messageboard/index.php...&hl=evening

[bber]

resveratrol is a potent 5 lipo oxygenase and cyclo oxygenase inhibitor http://content.febsjournal.org/cgi/content/full/265/1/27

5-lipo oxygenase is the enzyme that converts efas specifically arachinodic acid into pro-inflammatory leukotrines
http://en.wikipedia.org/wiki/Lipoxygenase#...enase_.285LO.29

it is believed by some that the production of these pro inflammatory luekotrines especially ltb4 can stimulate sebaceous glands and could be a possible cause for acne in some people
J Mol Med. 2006 Jan;84(1):75-87. Epub 2005 Dec 31.Links
Enzymes involved in the biosynthesis of leukotriene B4 and prostaglandin E2 are active in sebaceous glands.

Department of Dermatology, Charite Universitaetsmedizin Berlin, Campus Benjamin Franklin, Fabeckstrasse 60-62, 14195 Berlin, Germany.
The expression of enzymes involved in leukotriene and prostaglandin signalling pathways, of interleukins 6 and 8 and of peroxisome proliferator-activated receptors in sebaceous glands of acne-involved facial skin was compared with those of non-involved skin of acne patients and of healthy individuals. Moreover, 5-lipoxygenase and leukotriene A(4) hydrolase were expressed at mRNA and protein levels in vivo and in SZ95 sebocytes in vitro (leukotriene A(4) hydrolase > 5-lipoxygenase), while 15-lipoxygenase-1 was only detected in cultured sebocytes. Cyclooxygenase-1 and cyclooxygenase-2 were also present. Peroxisome proliferator-activated receptors were constitutively expressed. Enhanced 5-lipoxygenase, cyclooxygenase 2 and interleukin 6 expression was detected in acne-involved facial skin. Arachidonic acid stimulated leukotriene B(4) and interleukin 6 release as well as prostaglandin E(2) biosynthesis in SZ95 sebocytes, induced abundant increase in neutral lipids and down-regulated peroxisome proliferator-activated receptor-alpha, but not receptor-gamma1 mRNA levels, which were the predominant peroxisome proliferator-activated receptor isotypes in SZ95 sebocytes. In conclusion, human sebocytes possess the enzyme machinery for functional leukotriene and prostaglandin pathways. A comprehensive link between inflammation and sebaceous lipid synthesis is provided.

in that last study it proved that arachidonic acid it downregulated ppar alpha and stimulated ltb4 and il-6

so that means that arachidonic acid has a direct control over ppars which are agonist(influencer) for the rxr receptor just like accutane does.
http://en.wikipedia.org/wiki/PPAR

here is another study that say ppars can control sebum production(just like accutane)
1: J Invest Dermatol. 2006 Sep;126(9):2002-9. Epub 2006 May 4. Links
Peroxisome proliferator-activated receptors increase human sebum production.Trivedi NR, Cong Z, Nelson AM, Albert AJ, Rosamilia LL, Sivarajah S, Gilliland KL, Liu W, Mauger DT, Gabbay RA, Thiboutot DM.
The Jake Gittlen Cancer Research Institute, Hershey, Pennsylvania 17033, USA.

Sebum production is key in the pathophysiology of acne, an extremely common condition, which when severe, may require treatment with isotretinoin, a known teratogen. Apart from isotretinoin and hormonal therapy, no agents are available to reduce sebum. Increasing our understanding of the regulation of sebum production is a milestone in identifying alternative therapeutic targets. Studies in sebocytes and human sebaceous glands indicate that agonists of peroxisome proliferator-activated receptors (PPARs) alter sebaceous lipid production. The goal of this study is to verify the expression and activity of PPARs in human skin and SEB-1 sebocytes and to assess the effects of PPAR ligands on sebum production in patients. To investigate the contribution of each receptor subtype to sebum production, lipogenesis assays were performed in SEB-1 sebocytes that were treated with PPAR ligands and isotretinoin. Isotretinoin significantly decreased lipogenesis, while the PPARalpha agonist-GW7647, PPARdelta agonist-GW0742, PPARalpha/delta agonist-GW2433, PPARgamma agonist rosiglitazone, and the pan-agonist-GW4148, increased lipogenesis. Patients treated with thiazolidinediones or fibrates had significant increases in sebum production (37 and 77%, respectively) when compared to age-, disease-, and sex-matched controls. These data indicate that PPARs play a role in regulating sebum production and that selective modulation of their activity may represent a novel therapeutic strategy for the treatment of acne.


notice that the name ppar has proliferater in it, denoting control over proliferation.

J Steroid Biochem Mol Biol. 2002 Nov;82(4-5):393-400. Links
Inhibitors of the arachidonic acid pathway and peroxisome proliferator-activated receptor ligands have superadditive effects on lung cancer growth inhibition.
Intervention Section, Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA.
Arachidonic acid (AA) metabolizing enzymes and peroxisome proliferator-activated receptors (PPARs) have been shown to regulate the growth of epithelial cells. We have previously reported that exposure to the 5-lipoxygenase activating protein-directed inhibitor MK886 but not the cyclooxygenase inhibitor, indomethacin, reduced growth, increased apoptosis, and up-regulated PPARalpha and gamma expression in breast cancer cell lines. In the present study, we explore approaches to maximizing the proapoptotic effects of PPARgamma on lung cancer cell lines. Non-small-cell cancer cell line A549 revealed dose-dependent PPARgamma reporter activity after treatment with MK886. The addition of indomethacin in combination with MK886 further increases reporter activity. We also show increased growth inhibition and up-regulation of apoptosis after exposure to MK886 alone, or in combination with indomethacin and the PPAR ligand, 15-deoxy-Delta12,14-prostaglandin J2 compared with single drug exposures on the adenocarcinoma cell line A549 and small-cell cancer cell lines H345, N417, and H510. Real-time PCR analyses showed increased PPAR mRNA and retinoid X receptor (RXR)alpha mRNA expression after exposure to MK886 and indomethacin in a time-dependent fashion. The results suggest that the principal proapoptotic effect of these drugs may be mediated through the known antiproliferative effects of the PPARgamma-RXR interaction. We therefore explored a three-drug approach to attempt to maximize this effect. The combination of low-dose MK886, ciglitazone, and 13-cis-retinoic acid interacted at least in a superadditive fashion to inhibit the growth of lung cancer cell lines A549 and H1299, suggesting that targeting PPARgamma and AA action is a promising approach to lung cancer growth with a favorable therapeutic index.

The ligands for the PPARs are free fatty acids and eicosanoids. PPARγ is activated by PGJ2 (a prostaglandin). In contrast, PPARα is activated by leukotriene B4. so eicosanoids influence ppars.

eicosaniods are made from efas http://en.wikipedia.org/wiki/Eicosanoids

here is a chart for how efas are made into eicosanoids http://en.wikipedia.org/wiki/Image:EFA_to_Eicosanoids.svg

by analyzing this chart you can see that an over balance of arachidonic acid leads to the production of pro-inflammatory eicosanoids
and most detrimentally to the production of ltb4 and pge2 which alter ppar ligands and can control sebum secretion.

if this is all in fact true, it is now easy to see why there is a prevelance of acne in industrialized nations due to a diet too high in omega 6s in relation to omega 3s. although there is a main underlying genetic component to this disease this is why some people probably dont get acne, but they will probably get cancer or heart disease somewhere down the line.

From all the research ive been doing lately ive learned alot and have tons upon tons of studys that can easliy prove this theory as a cause for most acne. as the sebum could be controlled in a few ways there are still a few different factors the developing the disease but this could easliy explain aboiut 90% of the cases for acne.

my theory is that sebum secretion is basicly your bodys way to get rid of excess omega 6s and in fact could be a very good survival function to keep you alive by not keeping all that bad fat in your blood and causing cancer or heart disease or a heart attack. in a way our bodys could be alot stronger then most others.

Im also intrigued by how accutane has a tendancy to raise serum(blood) cholesterol levels while you are on the drug, indicating that they cannot escape via the sebum glands and now they are released into the blood instead.

check out these other threads they may interest you
http://www.acne.org/messageboard/index.php?showtopic=140133

http://www.acne.org/messageboard/index.php?showtopic=140399

http://www.acne.org/messageboard/index.php...&hl=evening

Thanks for the heads up AutonomousOne, I really appreciate it.
All that research is very interesting, im going to keep this up and see if the change in sebum production i have seen in my skin is permanent while on this regimen. As far as the omega 6 to omega 3 ratio I agree that the vast amounts of omega 6 in our diet compared to the small amount of omega 3s is a cause for many problems. Maybe megadosing on fish oil is helping restore that balance to healthy levels. I'll keep you guys posted. If anyone else who has moderate to severe acne wants to give this a try and report back that'd be great. That way we can have a greater sample.

[Legend]

It also increases healthy sperm counts. I've seen studies that showed it as a phytoestrogen in some respects. I've also seen studies that show that it modulates not only estrogen but testosterone and other androgens as well.

And I saw another study that actually gave rats 1000x the amount a 70kg adult taking 1.4grams per day is taking. With no adverse effects. Of course with melatonin they gave adults several thousand times more than the averge pill worth for a long period with no adverse effects. Although their jetlag would have probaly been impossible to overcome.

Sucks for people here but peanuts are a great source of this as well.

Yes, it is a phytoestrogen. But unlike other phytoestrogens, like genistein in soy, this one doesn't seem to fight testosterone. It only seems to share the characteristic of estrogen when it comes to circulatory health.

I don't think women should take 300 mg of this stuff because that's the dose Biotest recommends to overload estrogen receptors, and that's probably not good for female health.

[Legend]

Uhh, according to the BioTest description REZ-V's main purpose is testosterone increase -- isn't that the last thing an acne sufferer needs?

I don't think it's that simple. Ever seen pictures of ripped body builders, like Arnold in his prime. Ridiculously unnatural levels of testosterone, but the guy didn't have any acne at all.

[Axelhack]

I take fish oil, not pills, the actual oil... I notice if i don't take it because my nails and the skin on my hands starts to die.

[xtr3m]

The issue with testosterone when it comes to acne is not about elevated levels, which usually are pretty normal, but an increased sensitivity of sebaceous glands to the hormone.

Having said that, the number one side effect of steroids is acne.

[bber]

The issue with testosterone when it comes to acne is not about elevated levels, which usually are pretty normal, but an increased sensitivity of sebaceous glands to the hormone.

Having said that, the number one side effect of steroids is acne.

#2, #1 is water retention. A lot of people don't get acne while on juice.

[BLASK5420]

if your juicing it is actually the DHT that makes your bodies oil glands go on overdrive. DHT is produced by excessive testosterone in the body(a little more complicated, but in simple terms). if you take
Finasteride it will prevent your body from turning the extra test into dht therefor stopping any steroid induced acne.

[overman]

so from what i am hearin I should up the ante on my fish oil pop ins? and buy that rez-v?

[Legend]

so from what i am hearin I should up the ante on my fish oil pop ins? and buy that rez-v?

I don't think REZ-V is that important in regards to acne. I'm taking it for the major health benefits...

Careful with the fish oil. When I took more walmart caps, my nose would bleed easily. It thins your blood. I don't know what the exact reason for that, but I don't think it's DHA. I'm taking the Biotest fish oil complex, which has 2200 mg of DHA per 4 caps (daily dose), without any reaction. Either there's something different to the formula, or Biotest is scamming me.

[overman]

so from what i am hearin I should up the ante on my fish oil pop ins? and buy that rez-v?

I don't think REZ-V is that important in regards to acne. I'm taking it for the major health benefits...

Do you think it would help with blood circulation and me going to the gym?