@Yetanotheraccutanevictim

I have so many of the same symptoms as you and others being Accucrapped on, that I am not even sure that I have SIBO. It may have been a false positive as most of the GI doctors tell me since the numerous antibiotics did absolutely nothing. Or I may have SIBO, but the drug destroyed my body so much that I cannot fight the overgrowth. I will try again to see if there is any improvement with the SIBO diet and then may add in the antibacterial supplements for a month.

 

When I eat raw vegetables like spinach or kale, I notice the next morning my skin usually has a yellowish tint to it (instead of being the usual pale it is these years), but the yellowish tint goes away within a couple hours. I have told the doctors about it, but they just tell me well, you dont look yellow now. I hope your liver is just fine. I dont know if you have had any abdominal imaging done to look at your liver, spleen, etc, but it might be worth it just to make sure everything is okay. I really think something is wrong with my liver, despite normal liver enzymes and normal images of it. These past 5 years, I drank alcohol maybe three or four times. Those times that I drank something, which was very little, I would wake up in the morning with pain where the liver is located. Also, the surgeon gave me some pain pills after my gallbladder surgery, and I took one and I woke up in the middle of the night in pain in that area. When I tried acupuncture, she told me that people who are under extreme stress feel pain there. I dont know about this, but hopefully our livers are just fine. She also told me that the gallbladder is the angry organ, but now that I dont have one anymore, I am still angry, oh I may be even angrier now!

 

Thanks again for your help.

I know that accutane ruins your immune system due to retinoic acid toxicity and vit A deficiency. So perhaps it is true that you can't fight off the overgrowth.

Extremely strange that your skin turns yellow after ingesting green leafy vegetables. If you are eating fat with those vegetables then that could explain it. But your liver shouldn't struggle if you are just eating plain vegetables. One possible way it could be screwing with you is that the fiber from the vegetables is feeding your overgrowth. Perhaps the translocation of bacterial endotoxins such as lipopolysaccharides to your liver is making your phase I and II detox sluggish and possibly backing up your liver. Do you have high LDL particles? Those will be elevated to try to capture and neutralize those endotoxins. Also, if you aren't already taking an ox bile supplement, I HIGHLY recommend it. Anyone without a gallbladder should be taking exogenous bile with every fatty meal. And you do need to be eating plenty of fats to support your hormonal system.

*I would always cook your vegetables. I know that I cannot digest raw vegetables. They are harder on my digestion than meat protein. I always cook them or blend them in a Vitamix. Cooking will destroy some nutrients but it will actually increase bioavailability of others so it actually balances out. Btw, I have had an abdominal MRI with contrast and they did not see any abnormalities. However, I bet they wouldn't notice anything unless there was a softball sized tumor stuck in the side of my liver. I've noticed that conventional doctors only look for horrible diseases that have progressed to extreme levels. They are terrible at diagnosing other "under the hood" problems. I'm very hesitant about even giving the Mayo clinic a shot. We'll see. Giving liver flushing another chance. Just my 2nd flush yesterday, actually. Got out 50-100 bile blobs (some were very dark green/black). Hopefully they are filled with accugunk.

Doesn't surprise me about the alcohol or the pill you took. It's very likely your liver is messed up. I haven't had a sip of alcohol or a single processed food in over two years. I'm too scared. I've also heard that certain organs can cause emotional distress when poorly functioning. I heard the liver will cause anger if dysfunctional.

I don't think the SIBO can be beaten without doing the diet AND the herbs simultaneously. That seems to be the message that Dr. Siebecker gives.

My derm who prescribed me accutane was also on that list of docs being paid by big pharma. He only got paid $26, though - it was for Zenatane.

Stay strong peeps

EDIT:

I'd love it if others would post their entire list of accutane symptoms in order of severity. Perhaps you guys could put it in your signature or something. Always interesting to compare

do you have trouble gaining mass? i seem to be having that too. can't gain a lick

Yes, gaining mass is hard. Accutane sort of pushes the developing body towards atrophy, meaning more complete adult like muscles, but no real sustenance. With cellular division at a snail pace, and at the expense of weakened joints, one can make minimal gains, but it's really tough.

 

do you have trouble gaining mass? i seem to be having that too. can't gain a lick

 

Yes, gaining mass is hard. Accutane sort of pushes the developing body towards atrophy, meaning more complete adult like muscles, but no real sustenance. With cellular division at a snail pace, and at the expense of weakened joints, one can make minimal gains, but it's really tough.

any tips you can give me? supplements? gaining volume was never this hard.

Good sign that i am still getting a pump? and still getting sore? just not as much.

it's hard to gain mass without eating loads of shit, but with accutane you need to watch the diet, so its a catch 22.

 

do you have trouble gaining mass? i seem to be having that too. can't gain a lick

 

Yes, gaining mass is hard. Accutane sort of pushes the developing body towards atrophy, meaning more complete adult like muscles, but no real sustenance. With cellular division at a snail pace, and at the expense of weakened joints, one can make minimal gains, but it's really tough.

any tips you can give me? supplements? gaining volume was never this hard.

Good sign that i am still getting a pump? and still getting sore? just not as much.

it's hard to gain mass without eating loads of shit, but with accutane you need to watch the diet, so its a catch 22.

Yup, you've got it figured out as much as me, we're in the same boat. I dunno, its hard. The pump is there but it doesn't last as long. And you're right about the soreness. The only time I get that good feeling muscle breaking down soreness is if I take a couple weeks or month off and then get back into lifting (and now its painful). I think this lack of lactic acid sensation plays a part in all of this, both the pump and d.o.m.s (delayed onset muscle soreness)

I can't imagine that this is beneficial in any way, other than hyper adaptability, I think by exercising we're just treading water somewhere in between muscle wasting and development. Just a theory though, but it explains why its so painful to workout after only a month break, and continued exercise only makes minimal gains.

I just take basic whey (isopure) along with my standard supps for health and joints (ginseng, hyaluron, flax, vitamins) I have to stay away from creatine and other hardcore supplements as it is extremely stressful on the pancreas and our digestive organs.

I do see increase in volume size and I get a lot of complements, but it's definitely not to our full potential. Doesn't feel like it anways. There are reports I read years ago about isotretinoin and its side effects on DOMS. I would start searching there.

Oh how I do find it interesting that many think that us damaged by Accutane do nothing with our lives. I have obtained a degree, married, raised a child that will be 18 in the fall and going off to college. I have worked and dedicated my life also to help those who have suffered at the hands of this poison! Not sure though if I have really been able to help anyone recover!

For the person that asked what problems, symptoms one has obtained from Accutane....Well I feel fortunate and unfortunate in that department! Fortunate to have answers that took about 4yrs I am about 8yrs out now! However, unfortunate of what it left me with! Bone loss, loss of height, low egg reserve, Type 1 diabetes ( yes there is a difference between type 1 and type 2) Which is a 24hr disease, thyroid disorder.

the other fortunate thing is I meet a lot of people and even in person like Patti, which helped knowing your not alone in this fight!

By the way thought the 2nd ragforum never replaced the original as of July 8th it was taken down due to inactivity! spammers took over and well almost 8 yrs ago Dave had a nervous breakdown. it still had some good info though!

Well, I hope you are all doing well! For you newcomers hang in there it is a long road, but your life can go on, some things may get better, some may come and go and some my be there for life! You have to get out and live. You have one life. I personally have a list and am making sure it's accomplished as I have no clue when my life will be cut short due to the damage!

I hope where you are my friends you are enjoying your day smile

Oli Girl

I hope all of you are doing well!

Hey everyone! Been awhile. I'm curious for those who were looking at zinc or copper deficiencies and how that worked out.

Also, for the older members who were experimenting with methyl donors such as TMG and folate, etc. How is that program working out and what kind of time have u committed and what results. Hope everyone is well. Live life to the fullest. Hope all are well.

Im praying for you guys

Belive in god s power he is with you and he can heal every wound! He gave you life (first miracle in your existente) he can give you your health back! You know deep down it s true!

I would really apreciate if you guys starting to look at this org group as a group to United our faith in god too ! God is love and its the most powerful thing in the universo!!

So every post here could HAVe a religious sentence in the end to affirm that , wouldn't it be nice? Together se can make our healing geiki dama! ) its coll also to break the depressive aura around here.

So ill start : remeber that every day trillions of cells are working to keep you working well , you got your own universe within yourself ,made of atoms and quarks and mol©culas , everyday god makes little miracles in your life !!!! Just believe and ser biggers coming!!!

if there was a god, he/she wouldn't have done this and let it continue to happen to people that chime in on this thread experiencing the same shit. accutane would no longer be on shelves across the world, generic or not generic. lawsuits would be successful, and questions will be answered.

don't tell me to have a "religious sentence" in ending my posts. that is nonsensical drivel. I have faith in people like Dubya and Modea and literally everyone else busting their non-working nuts off trying to figure out something. i don't have faith in god, and i won't be told to.

Hi guys I'm 22 years old male and I have the typical side effects. The worst one is erectile dysfunction. I was by doctors nobody has helped me. They think that ist psychological Problems (Bullshit). / years ago I took my first accutane pill. So now my hormones are fucked up here the results: Very high (over the normal range) SHBG, very low free Testosterone, high estradiol:testosterone Ratio. And very high ( twice over normal range) DHEAS. Accutane lowers 5 Alpha reductase type 1. The main inducer of type 1 is IGF-1 accutane lowers this too. Low 5 Alpha reductase means more aromatase (Enzyme that converts testo to estrogen) More estradiol means higher SHBG and lower IGF-1... If you fuck with one Hormone you fuck with all others too. The high DHEAS I think ist the cause of low Steroid sulfatase in the Skin (Steroid sulfatase converts DHEAS to ist free from DHEA and other androgens to there more potent forms. So our Problem is not only 5 Alpha reductase. The last androgen Hormone (and the most potent that causes acne is DHT) I think the best drug to restore sebum and erectile heaslth would be proviron (a dht Derivate but where to get it Greetings to all of you.

all in one i think you should activate androgen receptors and increasse free Testosteron and dht.

SHBG: Things that increase it: Estrogens / Things that lower it: Insulin, IGF-1 (also stimulates 5 Alpha reductase), low estrogen and active DHT.

I know that accutane ruins your immune system due to retinoic acid toxicity and vit A deficiency. So perhaps it is true that you can't fight off the overgrowth.

Extremely strange that your skin turns yellow after ingesting green leafy vegetables. If you are eating fat with those vegetables then that could explain it. But your liver shouldn't struggle if you are just eating plain vegetables. One possible way it could be screwing with you is that the fiber from the vegetables is feeding your overgrowth. Perhaps the translocation of bacterial endotoxins such as lipopolysaccharides to your liver is making your phase I and II detox sluggish and possibly backing up your liver. Do you have high LDL particles? Those will be elevated to try to capture and neutralize those endotoxins. Also, if you aren't already taking an ox bile supplement, I HIGHLY recommend it. Anyone without a gallbladder should be taking exogenous bile with every fatty meal. And you do need to be eating plenty of fats to support your hormonal system.

*I would always cook your vegetables. I know that I cannot digest raw vegetables. They are harder on my digestion than meat protein. I always cook them or blend them in a Vitamix. Cooking will destroy some nutrients but it will actually increase bioavailability of others so it actually balances out. Btw, I have had an abdominal MRI with contrast and they did not see any abnormalities. However, I bet they wouldn't notice anything unless there was a softball sized tumor stuck in the side of my liver. I've noticed that conventional doctors only look for horrible diseases that have progressed to extreme levels. They are terrible at diagnosing other "under the hood" problems. I'm very hesitant about even giving the Mayo clinic a shot. We'll see. Giving liver flushing another chance. Just my 2nd flush yesterday, actually. Got out 50-100 bile blobs (some were very dark green/black). Hopefully they are filled with accugunk.

 

Doesn't surprise me about the alcohol or the pill you took. It's very likely your liver is messed up. I haven't had a sip of alcohol or a single processed food in over two years. I'm too scared. I've also heard that certain organs can cause emotional distress when poorly functioning. I heard the liver will cause anger if dysfunctional.

 

I don't think the SIBO can be beaten without doing the diet AND the herbs simultaneously. That seems to be the message that Dr. Siebecker gives.

 

My derm who prescribed me accutane was also on that list of docs being paid by big pharma. He only got paid $26, though - it was for Zenatane.

 

Stay strong peeps

 

EDIT:

I'd love it if others would post their entire list of accutane symptoms in order of severity. Perhaps you guys could put it in your signature or something. Always interesting to compare

Retinoic acid toxicity and vitamin A deficiency. Is this what is going on? Is it because some vitamin A receptors have been damaged and some have not, therefore we get symptoms of deficiency where the receptors have been damaged and symptoms of overdose where the receptors are still functioning properly? I dunno. Is it the effects that retinoic acid has on gene expression is upregulating or downregulating cellular differentiation, proliferation, and apoptosis of certain cells at abnormal rates? I still dunno. Is there a decrease in the expression of genes where there is a 'perceived vitamin A deficiency' by the body and an increase in the expression of genes where there is 'hypervitaminosis A?' Ugh, I dunno. All I really know is I hate Accucrap. I can't even say the name of the drug.

Regarding my LDL particles, I am not sure what that number is, but my LDL cholesterol is 107 mg/dl (normal < 100), so it is a little high, but my HDL is 59 mg/dl (normal > 39), so my risk ratio LDL/HDL is good (1.81, normal < 3.22). I do have ox bile and cholacol, but as usual, I react bad to these supplements as well. I may try again, if my digestive system gets better. I do have some olive oil with my vegetables (salad), but I really think it is just the vegetables making me turn yellow. When I tried juice fasting for a short time, my skin turned yellow and my eyes were bloodshot red. Symptoms of vitamin A overdose? Maybe. Bacterial endotoxins? Possibly. I cook most of my veggies now, but sometimes I have raw veggies and it does just seem to sit in my stomach, rotting away. For the past few weeks, I have been staying away from all veggies (not good probably), and my skin has amazingly stopped peeling.

I hope that you feel better after liver flushing. Please, please no pictures though! I may try another water fast again, but I don't think my body can make it long enough to experience any possible benefits from it. When i tried it 4 years ago, I had to stop because I kept blacking out and my blood sugar level was 20-something.

 

I know that accutane ruins your immune system due to retinoic acid toxicity and vit A deficiency. So perhaps it is true that you can't fight off the overgrowth.

Extremely strange that your skin turns yellow after ingesting green leafy vegetables. If you are eating fat with those vegetables then that could explain it. But your liver shouldn't struggle if you are just eating plain vegetables. One possible way it could be screwing with you is that the fiber from the vegetables is feeding your overgrowth. Perhaps the translocation of bacterial endotoxins such as lipopolysaccharides to your liver is making your phase I and II detox sluggish and possibly backing up your liver. Do you have high LDL particles? Those will be elevated to try to capture and neutralize those endotoxins. Also, if you aren't already taking an ox bile supplement, I HIGHLY recommend it. Anyone without a gallbladder should be taking exogenous bile with every fatty meal. And you do need to be eating plenty of fats to support your hormonal system.

*I would always cook your vegetables. I know that I cannot digest raw vegetables. They are harder on my digestion than meat protein. I always cook them or blend them in a Vitamix. Cooking will destroy some nutrients but it will actually increase bioavailability of others so it actually balances out. Btw, I have had an abdominal MRI with contrast and they did not see any abnormalities. However, I bet they wouldn't notice anything unless there was a softball sized tumor stuck in the side of my liver. I've noticed that conventional doctors only look for horrible diseases that have progressed to extreme levels. They are terrible at diagnosing other "under the hood" problems. I'm very hesitant about even giving the Mayo clinic a shot. We'll see. Giving liver flushing another chance. Just my 2nd flush yesterday, actually. Got out 50-100 bile blobs (some were very dark green/black). Hopefully they are filled with accugunk.

 

Doesn't surprise me about the alcohol or the pill you took. It's very likely your liver is messed up. I haven't had a sip of alcohol or a single processed food in over two years. I'm too scared. I've also heard that certain organs can cause emotional distress when poorly functioning. I heard the liver will cause anger if dysfunctional.

 

I don't think the SIBO can be beaten without doing the diet AND the herbs simultaneously. That seems to be the message that Dr. Siebecker gives.

 

My derm who prescribed me accutane was also on that list of docs being paid by big pharma. He only got paid $26, though - it was for Zenatane.

 

Stay strong peeps

 

EDIT:

I'd love it if others would post their entire list of accutane symptoms in order of severity. Perhaps you guys could put it in your signature or something. Always interesting to compare

Retinoic acid toxicity and vitamin A deficiency. Is this what is going on? Is it because some vitamin A receptors have been damaged and some have not, therefore we get symptoms of deficiency where the receptors have been damaged and symptoms of overdose where the receptors are still functioning properly? I dunno. Is it the effects that retinoic acid has on gene expression is upregulating or downregulating cellular differentiation, proliferation, and apoptosis of certain cells at abnormal rates? I still dunno. Is there a decrease in the expression of genes where there is a 'perceived vitamin A deficiency' by the body and an increase in the expression of genes where there is 'hypervitaminosis A?' Ugh, I dunno. All I really know is I hate Accucrap. I can't even say the name of the drug.

 

Regarding my LDL particles, I am not sure what that number is, but my LDL cholesterol is 107 mg/dl (normal < 100), so it is a little high, but my HDL is 59 mg/dl (normal > 39), so my risk ratio LDL/HDL is good (1.81, normal < 3.22). I do have ox bile and cholacol, but as usual, I react bad to these supplements as well. I may try again, if my digestive system gets better. I do have some olive oil with my vegetables (salad), but I really think it is just the vegetables making me turn yellow. When I tried juice fasting for a short time, my skin turned yellow and my eyes were bloodshot red. Symptoms of vitamin A overdose? Maybe. Bacterial endotoxins? Possibly. I cook most of my veggies now, but sometimes I have raw veggies and it does just seem to sit in my stomach, rotting away. For the past few weeks, I have been staying away from all veggies (not good probably), and my skin has amazingly stopped peeling.

 

I hope that you feel better after liver flushing. Please, please no pictures though! I may try another water fast again, but I don't think my body can make it long enough to experience any possible benefits from it. When i tried it 4 years ago, I had to stop because I kept blacking out and my blood sugar level was 20-something.

I took Roaccutane for 1 month in September 2014 (I live in the UK btw), expecting side effects would only be temporary. Before I took this drug, my world was a bright and happy place but now I wake up everyday miserable. Looking back at my life there was nothing I would have changed, it was perfect. Roaccutane has caused permanent impotence,depression, suicidal ideation, mood swings and sometimes I start crying for no reason. These side effects all persisted even upon discontinuation of Roaccutane. I don't understand how this stuff can still be in my system 9 months later? it just doesn't make any sense. The fact I took it for such a short period makes it even more unusual. I don't deserve this, I can't continue to live my life this way. Its not fair.

 

my name is Ed btw, feel free to add me on facebook and talk about this stuff

 

 

www.facebook.com/ed.henthorn.77

 

^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^

9 months lol.... try 20+ years here

We need a PPAR-a inducer!?

We hypothesize that a competition for common catabolic pathways activated by PPAR- may explain, at least in part, the interference between dietary CLA and tissue retinoid metabolism. Preliminary data from our laboratories seem to support this possibility. Feeding wild-type mice with WY-14,643 (0.01%), a potent synthetic PPAR- inducer [58], dramatically decreased liver retinol and retinyl esters content (Table 1), possibly due to an increased PPAR--mediated CYP activity, even though we cannot rule out that the decrease may be related to other causes, such as decreased dietary uptake and/or increased mobilization to extrahepatic tissues.

SCD1 converts saturated fatty acids into monounsaturated fatty acids using palmitoyl- and stearoyl-CoA as preferred substrates to generate palmitoleic (9-16:1) and oleic acid (9-18:1), respectively. Both are essential components of triglycerides and more complex lipids found in lipoproteins and eukaryotic membranes

Interestingly, SCD1 deficiency leads to disruption of the epidermal lipid barrier most likely caused by the strong reduction of epidermis-specific ceramides, one of the crucial lipid fraction in mammalian skin.⁶The dramatic phenotype seen in SCD1 mutants highlights the importance of unsaturated fatty acids for sebaceous gland formation and functional skin barrier

http://www.ncbi.nlm.nih.gov/pubmed/22211892

Through the generation of various mouse models of SCD1 deficiency, we have come to understand that SCD1 plays a role, directly or indirectly, in diverse metabolic processes, including lipogenesis, fatty acid oxidation, insulin signaling, thermogenesis, and inflammation

...... so wouldnt taking palmitoleic (9-16:1) and oleic acid (9-18:1) bypass the downregulated SCD1??

 

The funny thing about vitamin A deficiency and toxicity as it relates to accutane is that accutane isn't true vit A. Its chemical structure is different. We are toxic in the synthetic, non-usable form and deficient in the true, usable form. So our genetics are epigenetically altered in both aspects. Now, if we were to be genetically altered for life, I would think that some form of the accutane would have to still be in our bodies.

So, basically the drug interferes with normal Vitamin A metabolism and maybe vitamin D metabolism, as well as many, many other things in the body. I will try the sweet potato test later when I get the guts (pun intended). Just started adding in the veggies for the past two days, and sure enough, skin started peeling today.

The more I research the drug, the more I wonder how do people NOT get affected in some way by it. It just seems to have the potential to do so much harm to the body. I just keep hoping that there is some way to reverse it.

here ya go. these are the available PPAR-a Activators that dramatically reduce retinoic acid stores in the liver.

Fenofibrate is a common heart drug.

http://www.scbt.com/chemicals-table-ppar_alpha_activators.html

http://www.pnas.org/content/90/6/2160.full.pdf

look at this link, and see if you can figure this out.

The cannabinoids influences on PPARs consist of considerable theoretical and therapeutic significances. Although many effects of cannabinoids can be explained though their action on membrane-associated G protein-coupled receptors CB1/CB2 and related downstream signalling cascades; nuclear receptors PPARs provide an additional mechanism for cannabinoids regulation of gene transcription which may associate with their long-term exposure consequences. Many therapeutic effects of cannabinoids including management of glaucoma, rebel of inflammatory and neuropathic pain, amelioration of certain types of cancer, and various kinds of motor dysfunction associated with multiple sclerosis, spinal cord injury, and ischemic stroke can be connected with PPARs as well (Pertwee [45]). In summary, there is strong evidence to suggest that some cannabinoids can act on PPARs through either direct or indirect pathways. These discoveries not only broaden the promising usage of cannabinoids as therapeutic agents, but also support PPARs as new targets for some neuroprotective treatment.

D-limonene a natural PPAR agonist? Read the first few paragraphs on PPAR and LXR

D-Limonene has been shown to clear the gall bladder and get the bile flow moving as well. It also activates phase I and II detoxification enzymes.

http://www.researchgate.net/publication/248383875_Preventive_and_ameliorating_effects_of_citrus_d-limonene_on_dyslipidemia_and_hyperglycemia_in_mice_with_high-fat_diet-Induced_obesity

re

On 7/17/2015 at 6:06 AM, Modeaa said:

On 7/17/2015 at 4:32 AM, tryingtohelp2014 said:

SCD1 converts saturated fatty acids into monounsaturated fatty acids using palmitoyl- and stearoyl-CoA as preferred substrates to generate palmitoleic (9-16:1) and oleic acid (9-18:1), respectively. Both are essential components of triglycerides and more complex lipids found in lipoproteins and eukaryotic membranes

Interestingly, SCD1 deficiency leads to disruption of the epidermal lipid barrier most likely caused by the strong reduction of epidermis-specific ceramides, one of the crucial lipid fraction in mammalian skin.⁶The dramatic phenotype seen in SCD1 mutants highlights the importance of unsaturated fatty acids for sebaceous gland formation and functional skin barrier

http://www.ncbi.nlm.nih.gov/pubmed/22211892

Through the generation of various mouse models of SCD1 deficiency, we have come to understand that SCD1 plays a role, directly or indirectly, in diverse metabolic processes, including lipogenesis, fatty acid oxidation, insulin signaling, thermogenesis, and inflammation

...... so wouldnt taking palmitoleic (9-16:1) and oleic acid (9-18:1) bypass the downregulated SCD1??

maybe. see thia regurding oleic acid

http://www.ncbi.nlm....pubmed/15066988

acording to this fructose alone help, but more when oleic is added.

about palmitoleic - from an earlier post i mad,

[Edited link out]

he had a problem of dry eyes which he atribue to accutane,

read also his update from 2015, the fact that he speaks about an increased oil production from all of his oil glands(not just the eyes) and increased acne is interesting. is it somehow reverese an accutane dammage to the oil glands/sebaceous glands?

from the science aspect-the importent molucela might be ''Palmitoleic acid, or (9Z)-hexadec-9-enoic acid, is an

he used seabuckthorn oil which has one of the highest sources of Palmitoleic acid, but also other fatty acids which mighe block the action a bit?? isolated palmitoleic acid is also available, but it worried me more cause the fact that it is isolated one nutrient, who know,

anyaway, the seabuckthorn oil worked for that guy, and other one post there that he used macademia oil which is the other highest natural source of palmitoleic acid acording to wilki, it he sais he see a big improvements.

seabuckthorn oil i think is high in beta carotene and or Vitamin A.

CLA might be a blessing and a curse, in that it helps our body absorb Vitamin A, but it also activates the enzymes needed for oxidation.... i think our body shuts down as a protective measure, in order to stop absorbing excess Vitamin A that is constantly there post accutane.

Limonene doesnt have any Vitamin A in it, doesnt seem to help absorb Vitamin A ( it isnt a fat), and it also seems to activate the PPAR and LXR?

Cannabinoids, Ketogenic Diets, Holy Basil, And The Ppar Connection

http://michiganmedicalmarijuana.org/blog/587/entry-1090-cannabinoids-ketogenic-diets-holy-basil-and-the-ppar-connection/

There's a large number of natural compounds that are PPAR agonists [14]. These include, but aren't limited to: cannabinoids, terpenes, flavonoids, and saturated fats [15, 16]. This is one example of a commonality shared between the use of cannabinoids, ketogenic diets, and Tulsi (holy basil) in the treatment of epilepsy. They all contain PPAR agonists, and in turn modulate gene expression [1, 2, 3].

As an example: d-limonene is not only a PPAR alpha agonist, but it can also increase the bioavailability of non water soluble lipids, like cannabinoids [27, 28].

remember that one guy said he cured is accutane side effects in a video using a ketogenic diet?!

Ketogenic Diet

This paper won't delve into the physiological mechanisms that are suspected to be involved with ketogenic diets, in relation to epilepsy, other than to point out that it's believed to involve the activation of PPAR alpha [1].

Ocimum sanctum, or Tulsi (holy basil), has a wide variety of chemotypes. However, it's possible to find essential oils from one particular chemotype that may be of particular interest. Ocimum sanctum ct eugenol has two main constituents with implications to epilepsy. The primary constituent is eugenol. Eugenol is a PPAR gamma agonist

I remember feeling better when i added cloves (highest in eugenol and manganese) to my soup. macadamia nuts 180% manganese heh

remember that other guy who actually put grape seed oil on his arm and said it cured him?

[Edited link out]

Thanks man, I guess I'm going to shoot myself in the head now

Peroxisome proliferator-activated receptors increase human sebum production. http://www.ncbi.nlm.nih.gov/pubmed/16675962

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.

going with d-limonene, a PPAR-a agonist

http://suppversity.blogspot.com/2012/12/seabuckthorn-leaves-increase-ppar-alpha.html

Seabuckthorn Leaves Increase PPAR-Alpha & PPAR-Gamma Expression, Keep the Liver Fat Free and Fatty Oxidation Up. Plus: PPARs

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3090422/

seems we have to downregulate LCN2 and upregulate SCD1

One of the most well-studied retinoid drugs is isotretinoin (13-cis retinoic acid), which likely acts as a prodrug that becomes selectively activated in the sebocyte possibly after isomerization to tretinoin (all-transretinoic acid) [72]. Isotretinoin treatment causes apoptosis and reduced size of the sebaceous gland, and the sebocytes appear undifferentiatied and have decreased lipid accumulation [2], [73]. We propose that the elevated levels of all-trans retinoic acid in the skin of SKO mice leads to sebaceous gland dysfunction. As previously suggested by Sundberg et al., the sebaceous gland dynsfunction due to Scd1-deficiency impairs the degradation of the inner root sheath causing restraint and destruction of the hair follicle, inducing an inflammatory reaction, epidermal hyperplasia and scarring alopecia [8].

Skin biopsies taken from patients treated with isotretinoin also showed high expression of LCN2 (lipocalin-2)[57], [73]. Additionally, isotretinoin treatment of SEB-1 human sebocyte cultures causes cell cycle arrest and apoptosis concomitant with increased expression of LCN2 [72], [74]. SEB-1 cells were rescued from isotretinoin-induced apoptosis upon siRNA knockdown of LCN2 [57]. The LCN2 promoter has binding sites for both RAR and retinoid-X-receptor (RXR), suggesting that the toxic effect of retinoic acid on sebocytes is occurring via a lipocalin-2-mediated mechanism [57]. Since we observed a robust 27.7-fold elevation ofLcn2 in the skin of SKO mice, it is possible that the primary disturbance in the skin of SKO mice is retinoic acid-induced Lcn2 leading to sebocyte dysfunction and sebaceous gland hypoplasia. However, Lcn2 is also increased in lesional compared to non-lesional skin samples from psoriasis patients, as well as increased in the skin of a murine model of PPAR hyperactivation with a psoriasis-like condition [41]. Therefore, the increased Lcn2 in SKO mice may be influenced not only by retinoic acid, but also by the secondary effects of inflammation [75]. Alternatively, decreased expression of fatty acid metabolizing enzymes and key transcription factors involved in lipid synthesis in SKO mice may also contribute to sebaceous gland hypoplasia. Future studies are required to ascertain which of these potential mechanisms is responsible for the skin phenotype of the SKO mice.

In summary, we have shown that SCD1 is essential for normal retinoid homeostasis in the skin. Lack of skin SCD1 causes an elevation in skin levels of retinol and retinoic acid, which in turn activates the transcription of retinoic acid-induced genes. We speculate that one of these elevated retinoic acid-induced genes, Lcn2(lipocalin-2) results in sebocyte dysfunction and sebaceous gland hypoplasia in the SKO mice. Additionally, lack of SCD1 causes decreased fatty acid synthesis gene expression in the skin concomitant with elevated cholesterol synthesis. This pattern suggests a state of disturbed lipid metabolism that may also contribute to the skin phenotype. The disturbed retinol metabolism and inflammatory gene expression is also evident at 23 days postnatal, highlighting that Scd1 is essential for early events in sebocyte development and normal hair cycling.Since our studies are performed in whole-skin, the retinyl esters, retinol and retinoic acid might all be compartmentalized in different places. The accumulated retinol in the skin of SKO mice may be localized to a compartment that is inaccessible to LRAT, and subsequently converted to retinoic acid. Furthermore, the accumulated retinoic acid could possibly diffuse out and upregulate LRAT-mediated retinyl ester formation in different cells. Alternatively, retinyl ester hydrolase(s) may become active, resulting in a futile cycle where retinyl esters are made and then hydrolyzed. The persistent elevation in skin retinoic acid levels could also be due to decreased retinoic acid catabolism. We observed robust suppression of Cyp2e1 and Cyp1a1, which encode two cytochrome P450 enzymes that can catalyze retinoic acid 4-hydroxylase activity in murine skin[51], [52].

Despite reducing liver retinol stores by more than 400-fold with a RD diet intervention in both Lox and SKO mice, we were unable to normalize skin retinoic acid levels and normal hair growth in SKO mice. In contrast, studies by Shih et al. in Dgat1-deficient mice were able to normalize skin retinoic acid levels and hair growth with a similar intervention [48]. This may indicate that lack of Scd1 causes a more pronounced alteration in retinoic acid metabolism. Consistent with this notion, the skin phenotype elicited by Scd1 deficiency is more severe than that observed due to Dgat1 deficiency [48]. Alternatively, non-retinoid pathways may also be contributing to the skin phenotype. MUFAs are also important for cellular cholesterol ester synthesis [11] and SKO mice have elevated levels of skin free cholesterol [18]. Thus, a decrease in MUFA availability may affect both cholesterol and retinol homeostasis, in addition to triglyceride synthesis.

vitamin D

http://www.pubfacts.com/detail/24939880/Chemopreventive-and-chemotherapeutic-effect-of-dietary-supplementation-of-vitamin-D-on-cholangiocarc

Intrahepatic cholangiocarcinoma (ICC) is an aggressive cancer. Vitamin D, a pro-hormone, is getting popular due to its hormone-like functions after converted to its active form, 1,25(OH)2D3. Here, we show that dietary supplementation with 6 IU/g of vitamin D greatly suppressed ICC initiation and progression without apparent toxicity in a chemically induced rat model. Microarray analysis of rat ICC tissues showed vitamin D supplementation modulated the expressions of several unique genes, including lipocalin 2 (Lcn2), confirmed by RT-qPCR and immunohistochemical (IHC) staining. Further, 53 of 80 human ICC specimens (66%) exhibited high LCN2 expression and LCN2 knockdown in SNU308 cells decreased cell growth and migration, suggesting LCN2 be an oncogene in human ICC. As human ICC SNU1079 cells were treated by 1,25(OH)2D3, LCN2 expression and cell proliferation were attenuated. The downregulation of LCN2 expression was blunted when vitamin D receptor (VDR) was knocked down, implicating that the in vivo Lcn2 downregulation is a direct consequence of vitamin D supplementation Our results support the prevailing concept that vitamin D status is negatively associated with cancer incidence and mortality and suggest LCN2 may be a potential target against ICC. Further studies of application of vitamin D or its analog against ICC are warranted.