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Diet-Acne Study

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#41 evigrex

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Posted 21 July 2004 - 11:22 AM

QUOTE(SweetJade1980 @ Jul 21 2004, 12:12 AM)
Evigrex,
    Whether you want to call it an Anti-androgen or a DHT Inhibitor is up to you.  I'm under the impression that an anti-androgen blocks the effects of DHT or Testosterone by preventing them from binding to androgen receptors.  Where as a DHT Inhibitor prevents the actual production of DHT by reducing/inhibiting the neccessary enzymes.  OK, so based on those studies it shows that accutane may just be....both.  Do you really want to argue over this? 


QUOTE
Isotretinoin, used to treat severe acne, has been shown to induce hormonal changes, especially to reduce 5 alpha-reductase in the production of the tissue-derived dihydrotestosterone (DHT) metabolite 3 alpha-Adiol G........  After 12 weeks of therapy, there was a decrease in the levels of the precursor androgens androstenedione, testosterone and 3 alpha-Adiol G in 6/9 patients. Acne improved after 4.5 months in all but 2 male patients, who had very low serum hormone binding globulins (SHBG) and a high free androgen index (FAI).


See, again males CAN have too much Free Testosterone.


QUOTE
The decrease in skin androgen receptor levels (this study) and the recently reported suppression of skin 5 alpha-dihydrotestosterone production by isotretinoin treatment appeared consistent with the involvement of androgen receptor and 5 alpha-dihydrotestosterone in the pathogenesis of acne. Indeed, sebum production is under androgen control, and an abnormal response of the pilosebaceous unit to androgens appears to be implicated in the pathogenesis of acne. These observations were consistent with the absence of sebum in complete androgen-insensitive patients and normal sebum production in male pseudohermaphrodites.



QUOTE
Dihydrotestosterone is a peripheral paracrine hormone
R. Horton
Department of Medicine, University of Southern California, Los Angeles 90033.

Androgen action in sexual tissues, especially skin and the prostate, is expressed by dihydrotestosterone (DHT) acting at the nuclear level. Dihydrotestosterone in the circulation and target tissues is almost solely derived from the peripheral conversion of secreted testosterone (T) in men and androstenedione in women. The general pathway is testosterone----DHT in equilibrium with androstanediol (3 alpha diol). However, a number of studies suggest that blood DHT or 3 alpha diol are not reliable indicators of peripheral DHT formation. This is particularly suggested by discrepancies in the specific activity of DHT in blood and urine following infusion of labeled DHT, suggesting that total body DHT formation is not reflected by blood levels. Thus, DHT should be thought of as a paracrine hormone formed and acting primarily in target tissues. 3 alpha androstanediol glucuronide (3 alpha diol G) is a major metabolite of DHT. An important site of its formation is the skin. Levels in blood and urine are increased in hirsutism and acne, and blood levels closely parallel pubertal development. 3 alpha diol G levels are especially increased in adrenal disorders of androgenicity such as andrenogenital syndrome; it is also a good marker of response to therapy. Levels are reduced in various forms of male pseudohermaphroditism. 3 alpha androstanediol glucuronide appears to be the best marker available of DHT formation in target tissues such as skin.
http://www.andrology...bstract/13/1/23



It seems to me that what you are arguing the most for is that accutane affects DHT levels in the skin only, right? Yet from what I've read, DHT is only produced when it interacts with androgen receptors on it's target tissues (prostate, skin, muscle) so that's a given. As such, it also has the ability to affect people's prostate or muscles postively, or negatively, depending on your outlook in regards to DHT inhbition and/or tissue growth. So, I don't know what to say except, it's still a DHT Inhibitor or ...anti-androgen.


Nighty Night

Let me spell it out: 5 alpha reductase inhibitors lowers or blocks the amount of a sex hormone produced by the pituitary. Spironolactone does this (anti androgen). Proscar, propecia and avodart do this (5ar inhibitors.). They block the production of sex hormones within the body - with accutane this is not the case.

#42 evigrex

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Posted 21 July 2004 - 11:36 AM

QUOTE(aaa @ Jul 21 2004, 01:11 AM)
High insulin may be a contributing factor in acne, nearsightedness, male pattern balding, as well as many other things.

Hyperinsulinemic diseases of civilization: more than just Syndrome X.

Source:
Comp Biochem Physiol A Mol Integr Physiol (Comparative biochemistry and physiology. Part A, Molecular & integrative physiology.) 2003 Sep; 136(1): 95-112
Additional Info: United States

Standard No:
ISSN: 1095-6433; 1531-4332; NLM Unique Journal Identifier: 9806096

Language:
English

Abstract:
Compensatory hyperinsulinemia stemming from peripheral insulin resistance is a well-recognized metabolic disturbance that is at the root cause of diseases and maladies of Syndrome X (hypertension, type 2 diabetes, dyslipidemia, coronary artery disease, obesity, abnormal glucose tolerance). Abnormalities of fibrinolysis and hyperuricemia also appear to be members of the cluster of illnesses comprising Syndrome X. Insulin is a well-established growth-promoting hormone, and recent evidence indicates that hyperinsulinemia causes a shift in a number of endocrine pathways that may favor unregulated tissue growth leading to additional illnesses. Specifically, hyperinsulinemia elevates serum concentrations of free insulin-like growth factor-1 (IGF-1) and androgens, while simultaneously reducing insulin-like growth factor-binding protein 3 (IGFBP-3) and sex hormone-binding globulin (SHBG). Since IGFBP-3 is a ligand for the nuclear retinoid X receptor alpha, insulin-mediated reductions in IGFBP-3 may also influence transcription of anti-proliferative genes normally activated by the body's endogenous retinoids. These endocrine shifts alter cellular proliferation and growth in a variety of tissues, the clinical course of which may promote acne, early menarche, certain epithelial cell carcinomas, increased stature, myopia, cutaneous papillomas (skin tags), acanthosis nigricans, polycystic ovary syndrome (PCOS) and male vertex balding. Consequently, these illnesses and conditions may, in part, have hyperinsulinemia at their root cause and therefore should be classified among the diseases of Syndrome X.

So according to this study, only overweight, insulin resistant people should worry about acne. Yes, there is a link between obesity and insulin resisntance.

The signs of insulin sensitivity are clear: Weight gain in the lower abdominal area only, little weight gain in peripheral areas (leading to a pear shape), slow metabolism, and a hard time losing weight regardless of the amount of exercise or caloric intake. Also, insulin resistance results in elevated blood glucose levels above 95 ng/dl after fasting for 12 hours. 126ng/dl or above after fasting would quality as a full blown diabetic. SO who here has been tested and qualifies as above?

So what you guys are saying is that only insulin resistant people have a link between diet and acne.....right. Normal healthy folk do not have a diet-acne link...?

#43 ritzvin

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Posted 21 July 2004 - 12:58 PM

QUOTE(Chloe646 @ Jul 20 2004, 08:09 PM)
Anyway, docs are not very good at making those connections and often remain ignorant to what could be glaring epidemiological evidence. Hard core scinetific researchers are much more openminded than docs about diet,

I know a lot of people going the medical school route, and I have to agree with that. Because of how the curriculum is, those that excel in medical school are those that are skilled in rote memorization first and foremost. Logical thinking and making connections isn't a utilized skil set, unfortunately. Anything that wasn't specifically mentioned in their (old) textbooks are often disregarded by them.

#44 evigrex

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Posted 21 July 2004 - 01:03 PM

QUOTE(aaa @ Jul 21 2004, 10:06 AM)
Yeah... I wish I would have known about myopia and carbs BEFORE I had to get glasses.  My vision has not gotten any worse in the last couple years, so I guess I can't complain.
   I think the palieodiet is interesting... I do something more geared toward bodybuilding though.  It's based on a book called Natural Hormone Enhancement (NHE)  Basicaly I eat very low carb everyday (around 20 grams, all from veggies) and two nights a week (Sun., & Wed.) I have a high carb meal (100 grams + ) right before bed.  The carb meals are supposed to refill glycogen stores and help with weight training.  I would recommend against the carb ups if a person was not lifting weights regularly.
   I started doing NHE recently, but I did Atkins strict for a month before that.  Anyway, my skin cleared up about 2 weeks after I started eating low carb... It's not perfect, but much better.

How could bodybuilders possibly go low carb aside from contest prep? Insulin is what shuttles amino acids to the muscles so they can grow, so carbs are pretty much necessary. Unless one is taking a bucketfull of steroids as well....and then they will gain muscle but not nearly as much as they would, had they eaten a proper amount of carbohydrate.

Besides....carbs aren't evil....its all dependant on the type of carbohydrate. There's a big difference between a sugar laden piece of cake than a bowl of plain oats.

#45 ritzvin

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Posted 21 July 2004 - 01:08 PM

QUOTE(SweetJade1980 @ Jul 21 2004, 02:12 AM)
I recall definately having a steady diet of junk food as early as age 3 in school (life a.k.a. memory for me begins at this age).  I recall having Tues and Thursday our "fun" days at the private school because we got to order fast food.

The funny thing is that the school lunches were much healthier (still not really healthy by my standards today) at the "ghetto" schools I went to when I was younger than the wealthy suburban school I went to for high school. The suburban school served hamburgers pretty much every day, and some other (usually even more disgusting item) and/or pizza. The poor city elementary school I went to served government packaged lunches that comprised a sandwich or hot food item and either juice or fruit and milk (and was cheaper).

#46 Dices15

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Posted 21 July 2004 - 01:09 PM

It's just a theroy you would have to stest every single person on the planet to say the is true. Everyones diffrent. I personally do think that acne in affected by diet..

#47 evigrex

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Posted 21 July 2004 - 03:38 PM

The argument presented is that insulin resistance leads to acne. So, why isn't the insulin resistant population suffering from acne more than those with normal glucose tolerance.

#48 SweetJade1980

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Posted 22 July 2004 - 03:29 AM

QUOTE(evigrex @ Jul 21 2004, 03:25 PM)
The argument presented is that insulin resistance leads to acne.   So, why isn't the insulin resistant population suffering from acne more than those with normal glucose tolerance.


Evigrex,
LOL, I truly enjoy this about you. ;-) I honestly wish that the others would debate with as much energy and passion as you put forth. While I answered your diabetes, Insulin resistance question already on Page 1, I will clarify a "few" things.

First of all, you are forgetting to account for the fact that most Diabetics (90%) are Type II Diabetics. Type II Diabetes is very strongly thought to be brought on from Insulin Resistance. Insulin Resistance leads to Type II Diabetes, which if prolonged & severe enough, Type I Diabetes can result. Of course, people are born with Type I Diabetes and require insulin injections (they don't overproduce), and as such, my initial impression is that no, I wouldn't expect most of these individuals to be hyperandrogenic or obese, let alone have acne. They lack certain things that Type IIs and the "normal" population have and it will affect them in many ways. After glimpsing at a few studies theys were more in favor of Erectile dysfunction for "Diabetics" or Type I Diabetics but said that Type IIs had a greater chance the longer they went untreated (slower becoming Type I?).
http://www.ncbi.nlm....t_uids=11431598

http://www.ncbi.nlm....t_uids=10869326


Once again, I have had 2 Glucose Tolerance Tests run since April 2001, and while I don't have copies of all the results my doctor repeatedly said I was "either Insulin Resistant or PCOS" Every 3 or 4 months, he continually tested my hormone levels for cholesterol (normal), glucose (normal), several of the androgens, adrenal hormones, liver enzymes, etc. He not only checked my hematocrit (normal), but he also checked me for several anemias, a gluten intolerance, and other hormonal disorders which all came out negative. Yet, Diabetes Type II has hit a few members of my fathers side, most are borderline so I know I'm susceptible and fall into one of those groups and since IR leads to PCOS, I just say that I'm IR. Furthermore, the proof is in the results from using the medication for over a year. However I am no longer taking it because dietary changes were more effective for me.

Now, my personal defination of Hyperandrogenism is when you produce Too Much Total Testosterone, when you produce Too much Free Androgen, When you produce Too Much DHEA, etc. However, some people can be sensitive to androgens that fall on the end of the High-Normal Range and behave as if they are hyperandrogenic. Not to mention, that there are Book definitions that actually include Hyperinsulinemia as leading to Hyperandrogenism, so I didn't come up with this all on my own. http://sharedjourney...es/insulin.html

I personally produce too much DHEA and Free Testosterone (in the normal male ranges), yet my DHEA-S and Total Testosterones are normal. My Thyroid, Cortisol, 17OHA Progesterone, Progesterone, LH, FSH are normal, and my estrogen is on the low-normal side. I do not fit the classic mold of what was once thought of as Insulin Resistance. My former endocrinologist would tease me about that. When I spoke to a nutritonist at school, she qouted the same "Classic Characteristics" that you did, and looked at me as if I was nuts. ;-)

Despite whatever she or you or the world is ready to accept, Insulin Resistance SYNDROME means that not everyone will have ALL the SAME symptoms. There are over 2 dozen symptoms or disorders associated with this syndrome and I'm grateful I don't have them all. Thus, no, not everyone that is Insulin Resistant will have acne and I have NEVER said otherwise.


I'm sorry if you are soo anti-androgen that you can't fathom the fact that you used an anti-androgen to get clear. I'm sorry if you can't deal with that, but I would just laugh it off and learn from it. Not all DHT Inhibitors or Anti-Androgens have the same side effects, nor do they all affect the same enzymes or pathways. In that respect I throw in Dietary Changes (particularly lowering carbs) as an anti-androgen method. I throw in Insulin Sensitizers as an Anti-Androgen method. Believe it or not, there are studies that have shown that this is in fact occurring.

The other thing I've noticed is that you seem to focus on one area of a study, but you aren't really comprehending what the study is saying in terms of androgen expression, not that I claim to know ALL of the vocabulary either (but I will look it up). I know that the majority of initial studies (hence the conflicting data) are far from perfect. I know that they don't control for everything that you, I, and the rest of the acne community, would like in a perfect diet-acne study, but over time they are getting more specific. I think that the Full Text articles would help us see just how much fat, what types of carbs, or what doses were used to get these results, as that is VERY important to know. However these studies do something better and that's show how a variety of environmental factors play a role in hormone expression or suppression. If you understand what each hormone is, and what glands, hormones, proteins, nutrients & receptors regulate it, then you can understand one aspect of the diet-acne connection.

Again, I don't begin to claim to understand all the complexities of the human body, but based on what I've learned, read, and observed 5-alpha reductase is the enzyme used for DHT production. Apparently DHT is produced mainly through a reduction interaction with the Androgen Receptors. So if somehow Accutane suppresses this enzyme, it will suppress DHT Production. If accutane binds to the androgen receptors (studies show that it doesn’t) so that androgen/DHT can’t, then it would have an anti-androgenic effect. Now, if Roche, the manufacturer of Accutane, is posting articles on their website that claim it to be a DHT Inhibitor, WHY can't you accept that???

You mentioned something about "normal healthy folk" and well, it's almost laughable because what is healthy? I thought I was healthy because I didn't get sick, had normal cholesterol levels, normal blood pressure, but I was underweight, and other than having mild asthma for a few years, my BIGGEST fight has been the Symptoms of my Hormonal Imbalance = PCOS, Insulin Resistance, or Metabolic Syndrome. Insulin Resistance doesn't have to have external symptoms it can all be internal and asymptomatic so just how many "normal" people do you think really DO have Insulin Resistance? Heck, I thought I was normal enough, I never would have thought of IR ;-)

Again, when I think about it, I'm soo grateful because if I hadn't finally found a GOOD Endocrinologist to test me for so many disorders and retest me, I wouldn't have gotten a Diagnosis and I would have just gotten worse. If I didn't have that diagnosis, and if I didn't see how well Avandia had worked for me, I probably never would have thought to follow some form of a Low Carbohydrate Diet. From there I would have never thought to break it down more and see what other foods affect us.

I recall one time when everyone raved about milk having bad hormones and when I initially researched it 2 years ago, it was on a superficial level and discounted that it was significant enough. LOL, 3 years ago I was so naive that I thought that since I had the medication, I didn't need to change my diet, especially since I didn't need to lose weight....well I know better now. When I realized the difference it made in several areas, I took the above info I had learned about Insulin Resistance and started throwing it (researching) at all kinds of foods, supplements, prescriptions, & topicals and some "Hit a Home Run," I guess you could say, and others didn't. This is the stuff that theories, medications, protocols, etc are based on, yet there are an increasing number of studies that suggest that most of this is MORE than just a theory. I'm glad, because this nation is not getting "healthier."

#49 SweetJade1980

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Posted 22 July 2004 - 03:54 AM

Hmm... Evigrex, I don't want to do your homework for you, but here:

QUOTE
Regulation of testosterone levels is governed by two factors: the total amount of testosterone in the blood, and the binding capacity of the plasma proteins [SHBG]. Obviously, as binding capacity goes up blood levels of free testosterone go down. Not surprisingly, certain drugs (anabolic-androgenic steroids, insulin, etc.) and perhaps nutritional supplements (like avena sativa, urtica dioica, etc.) can reduce the binding capacity of the blood and result in higher free-testosterone levels. [Editors' Note: Nutrition is also a factor in testosterone regulation; see our March discussion on this topic in Experiments vs. Experience.] ….

…..Of the "free" testosterone that interacts at the tissue level, much of it is converted within the cells to DHT - a more potent androgen - by the enzyme 5-alpha reductase. In the prostate, for example, this conversion is thought to be necessary for physiologic effects. Other tissues (like the epididymis, vas deferens, seminal vesicles, skeletal muscle, and bone) lack the 5-alpha reductase enzyme and therefore are thought to respond to testosterone directly.  http://www.bodybuild...om/fun/vm12.htm


This is just to establish that my concern is not with all Androgens but in EXCESS Androgens (beyond referance ranges) and Free Testosterone (unbound) and SHBG regulates this amount. FSH & Estrogen raises SHBG, while LH & Insulin lowers SHBG. So yeah, its definitely possible that due to negative feedback inhibition, normally or drug induced (side effect), that the pituitary will produce less tropic hormones, which can work positively or negatively for both males and females.

QUOTE
"[Acne in the male resistant to isotretinoin and responsibility of androgens: 9 cases, therapeutic implications]

[Article in French]

Chaspoux C, Lehucher-Ceyrac D, Morel P, Lefrancq H, Boudou P, Fiet J, Vexiau P.

Service d'Endocrinologie, Hopital Saint-Louis, Paris.

INTRODUCTION: Treatment failures with isotretinoin in female patients are frequently related to endocrinological dysfunctions. Such a concept has never been discussed in male patients. CASE REPORTS: An extensive endocrinological work-up has been performed in nine male patients who presented with an acne refractory to conventional treatment and to isotretinoin. Adrenal dysfunction was found in four patients and isolated 5-alpha reductase hyperactivity in 2 cases. Three work-ups were normal. A suppressive treatment in three patients with adrenal dysfunction provided immediate efficacy. COMMENTS: These results would provide insight into the mechanism of refractory acne in men." http://www.ncbi.nlm....t_uids=10095884


http://www.pubmedcen...gi?artid=370187

Dang I know women can be screwed endocrinologically, and I know that men can be too as some of these studies show, but I too would love to know just how screwed males are in this dept. wouldn't you?


QUOTE
Interactions of retinoic acid and androgens in human prostatic tissue.

Jutley JK, Reaney S, Kelleher J, Whelan P.

Department of Medicine, St. James's University Hospital, Leeds, England.

The effect of retinoic acid (RA) on testosterone metabolic pathway was investigated in hyperplastic and neoplastic human prostatic tissues, and also the effects of steroids on RA binding to its receptor. Steroids only had a minimal effect on the binding of RA by its receptor. The conversion of testosterone to DHT by 5 alpha-reductase was reduced in the presence of retinoic acid. The inhibition was probably due to competition with NADPH for enzyme binding sites. The degree of inhibition found with retinoic acid at a concentration of 10(-4)M was greater for hyperplastic (41%) than that for neoplastic tissue (24%). The inhibition of 5 alpha-reductase by retinoic acid was dose-dependent. The activity of 5 alpha-reductase is significantly less in neoplastic compared with hyperplastic tissue.
http://www.ncbi.nlm....st_uids=1695368


This is a rather old study, 1990, but it was one of the few that actually looked for a correlation among Prostate, DHT and Retinoids. However, we've both posted studies that were more recent that said the same thing about 13-cis retinoic acid specifically, and it's DHT suppression abilities. Who knows, maybe accutane requires higher doses to play such a role on the prostate that it does on the skin. As such, it's not widely used for more things because it's just better] at treating specific types of skin disorders and cancers. Not to mention, the side effects...


QUOTE
Effect of oral isotretinoin treatment on skin androgen receptor levels in male acneic patients.

Boudou P, Soliman H, Chivot M, Villette JM, Vexiau P, Belanger A, Fiet J.

Department of Hormonal Biology, St. Louis University Hospital, Paris, France.

An oral daily dose (mean +/- SD, 0.75 +/- 0.05 mg/kg) of isotretinoin was administered for 3 months to six male patients with acne (scores of 4 and 5 according to Rosenfield). The therapy resulted in complete resolution of acne in four patients and improved acne significantly (score 1) in two patients. In accordance with recent findings, no change in serum testosterone and significant decreases in 5 alpha-dihydrotestosterone, 5 alpha-androstane-3 alpha,17 beta-diol glucosiduronate, and androsterone glucosiduronate levels were observed after treatment. Androgen receptor status was investigated in back skin biopsies obtained in acne areas before and after 3 months of isotretinoin treatment. The treatment did not modify the binding affinity constant of skin androgen receptor (0.44 vs. 0.32 nmol/L), but it did induce a 2.6-fold decrease in its binding capacity constant (62 vs. 24 fmol/mg cytosolic protein), as assessed by Scatchard plot and confirmed immunologically by Western blot analysis. These data clearly showed that skin androgen receptor was sensitive to oral isotretinoin administration in acneic patients. The decrease in skin androgen receptor levels (this study) and the recently reported suppression of skin 5 alpha-dihydrotestosterone production by isotretinoin treatment appeared consistent with the involvement of androgen receptor and 5 alpha-dihydrotestosterone in the pathogenesis of acne. Indeed, sebum production is under androgen control, and an abnormal response of the pilosebaceous unit to androgens appears to be implicated in the pathogenesis of acne. These observations were consistent with the absence of sebum in complete androgen-insensitive patients and normal sebum production in male pseudohermaphrodites.


http://www.ncbi.nlm....st_uids=9298137

These were both studies I posted earlier. Apparently all DHT Inhibitors or anti-androgens will eventually affect the levels of select steroid hormones, but the question is to what degree and severity of effects to the individual.


QUOTE
The most pronounced effect was observed in skin biopsies, which lost 80% of their ability to form 5 alpha-dihydrotestosterone (P < 0.001). It is concluded that 13-cis-RA therapy in men with severe nodulocystic acne did not alter gonadal or adrenal functions, but it did induce 1) a highly significant decrease in 5 alpha-dihydrotestosterone formation by skin biopsies; 2) significant decreases in serum 5 alpha-dihydrotestosterone, androsterone glucosiduronate, and 5 alpha-androstan-3 alpha, 17 beta-diol glucosiduronate; and, finally, 3) deviation of the liver androgen 5 alpha- to 5 beta-reduction pathway. The effect of 13-cis-RA treatment on severe acne is consistent with the dramatic decrease in androgen 5 alpha-reduction observed mainly in the skin. http://www.ncbi.nlm....st_uids=8175961


Please note the bolded areas


QUOTE
13-cis-retinoic acid competitively inhibits 3 alpha-hydroxysteroid oxidation by retinol dehydrogenase RoDH-4: a mechanism for its anti-androgenic effects in sebaceous glands?

Karlsson T, Vahlquist A, Kedishvili N, Torma H.

Department of Medical Sciences/Dermatology and Venereology, University Hospital, Uppsala, Sweden.

Retinol dehydrogenase-4 (RoDH-4) converts retinol and 13-cis-retinol to corresponding aldehydes in human liver and skin in the presence of NAD(+). RoDH-4 also converts 3 alpha-androstanediol and androsterone into dihydrotestosterone and androstanedione, which may stimulate sebum secretion. This oxidative 3 alpha-hydroxysteroid dehydrogenase (3 alpha-HSD) activity of RoDH-4 is competitively inhibited by retinol and 13-cis-retinol. Here, we further examine the substrate specificity of RoDH-4 and the inhibition of its 3 alpha-HSD activity by retinoids. Recombinant RoDH-4 oxidized 3,4-didehydroretinol-a major form of vitamin A in the skin-to its corresponding aldehyde. 13-cis-retinoic acid (isotretinoin), 3,4-didehydroretinoic acid, and 3,4-didehydroretinol, but not all-trans-retinoic acid or the synthetic retinoids acitretin and adapalene, were potent competitive inhibitors of the oxidative 3 alpha-HSD activity of RoDH-4, i.e., reduced the formation of dihydrotestosterone and androstandione in vitro. Extrapolated to the in vivo situation, this effect might explain the unique sebosuppressive effect of isotretinoin when treating acne.

http://www.ncbi.nlm....t_uids=12646198


The above article may be the most recent findings (published in 2003) and yet another one that I had already posted for you on another thread (soy thread). If we didn't already know, DHEA and other Androgens can be converted into DHT which is most acne sufferers’ concern. Thanks to the accutane articles we know that DHT can be converted into 3 alpha-diol glucuronide (3 alpha diol-G)) in target tissues, such as the skin. As such, some studies have mentioned that this is considered a marker for androgen or DHT actions in the skin and regarding acne. Of course, some of these androgens love to revert back to weaker forms and so the pathways below are a bit more complicated than what is depicted, but hopefully it will help us visualize things:

(Insulin) --- Cholesterol – (LH or ISCH) --- Pregnenolone --- Progesterone --- DHEA --- Androstenedione --- [estrogen or] < = > Testosterone --- Estrogen


AND


(Insulin) --- Cholesterol --- (LH or ISCH) -- Pregnenolone --- Progesterone -- DHEA --- Androstenedione and/or Androstenediol < = > Testosterone ---.DHT < = > 3-alpha Androstenediol Glucuronide (or other metabolites)


Now, Androstenedione, Androstenediol, 3alpha diol-G, and DHT are blamed for acne, hirsutism, and androgenic alopecia problems. They all are androgen hormones and apparently some of them can convert back and forth to their weaker or more active forms. Since DHT is further metabolized in the skin, perhaps the way that 13-cis retinoic acid affects 3alpha diol-G is by inhibiting 5alpha reductase which of course prevents DHT formation (see article on page 3). If there’s a reduced amount of DHT, then this would reduce the amount of 3alpha diol-G androgens that are produced from DHT. So based on the above studies, accutane inhibits not only DHT, but several of it’s corresponding androgenic metabolites. Thus accutane is not only good at reducing IGF-1, in the case of cancers and cell proliferation, including sebum growth, but it also directly inhibitis the enzyme, Retinol dehydrogenase-4 which consequently reduces/inhibits the liver enzymes 5 alpha reductase, 3 alpha HSD, etc responsible for DHT production.

http://secure.dslabs...un02_flyers.pdf
http://www.estetik.c...le_hormones.htm

It sounds like a DHT Inhibitor to me, what do you think?

#50 thebignosebandit

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Posted 22 July 2004 - 11:20 PM

I personally feel that diet and acne have no link.....BUT

I can CONCLUDE indefinately that diet does NOT CAUSE acne........

If this were the case, acne would occur in young children, and senior citizens. The fact of the matter is a 6 year old, even a 6 year old with acne prone genes and parents who have a history of acne, can eat steak everyday, drink a gallon of milk everyday, and eat 2 snickers bars a day and not get a single zit. Nor will this 6 year old experience oily skin, or clogged pores......same goes for the senior citizen, so what can we conclude? diet itself is not the direct cause of acne, diet itself is not responsible for acne.....

now some may argue that diet AGGRAVATES their acne, i don't agree, however, some swear it does, so i say, to each their own.

i personally believe that many people who feel they suffer worse breakouts due to diet are only being fooled by a mere coincidence.

I read about the paleo diet article, researched the sources, and found that the source that stated an Alaskan community who once never experienced acne only until they switched to the western diet to be a false source.

Many argue that in africa acne prevalence is low, however, in america, blacks have acne. The truth is, african americans are genetically composed of whites, native american, genes through interracial breeding, thus, acne genes may be brought into the mix.

again, diabitics, type 1 and 2, show no correlation with acne suffering.

The acne equation consits of - Sebum overproduction, Cell shedding, Bacteria = clogged pores inflamed by bacteria. Diet has no significant effect on any part of this equation.

#51 SweetJade1980

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Posted 22 July 2004 - 11:45 PM

QUOTE
The acne equation consits of - Sebum overproduction, Cell shedding, Bacteria = clogged pores inflamed by bacteria. Diet has no significant effect on any part of this equation.


Then you have not investigated thoroughly enough ;-)

#52 Chloe646

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Posted 22 July 2004 - 11:55 PM

I strongly disagree Sensitivities/allergies to food/how one is affected by environmental causes isn't cut and dry as in, for example six year olds don't have acne even if they ate junk. Diet can affect hormones in the body which IN TURN could effect or cause acne. "If diet caused acne six year olds would have it" is not a strong argument.

Not everyone who eats a lot is fat..i eat more than some really big guys and I'm very slim. I could eat ice cream all day and still be very thin. BUT, that doesn't mean somone who's suscptible to being fat can't lose weight. Also, one type of food will cause one person to gain weight while another will lose weight on it. Most people don't know what's healthy for them in terms of diet. Diet definitely afected my skin because i have the blood tests showing affected hormone levels due to diet to prove it.

if you say diet can't affect skin, then you also must believe foods don't cause allergic skin reactions, cholesterol is not affected by food, blah blah blah. the skin is an organ like any other, it really makes MUCH LESS SENSE that one would conclude diet has no effect. accutane is derived from vitamin a, also if a person doesn't get enough vit. c they get scurvy, or not enuf a, blindness which can be treated by diet. the same can and IS true for acne. While some may coose to eat candy and cake and bitch about their pimples while they apply more cream, I'll gladly nix the dairy and eat my paleo diet without so much as a tiny pimple cropping up for months and months.

#53 flipside

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Posted 23 July 2004 - 12:23 AM

well said chloe!

diet does affect acne, along with every other aspect of our health.

its just a question of how and to what extent.

#54 SweetJade1980

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Posted 23 July 2004 - 01:35 PM

Chloe & Flipside,
LOL, indeed some people's arguments for why there is not connection makes absolutely zero sense. Most of them like to throw back to us that it's a placebo effect, but how can there be an effect if you never altered your diet or took a specific medication with the hopes of thinking it would clear you?

Furthermore, perhaps a better point than that is, how we've also noticed improvements in other problems we have that some people may not have associated with an allergy, intolerance, chemical sensitivity, or hormonal symptom. Now how is that a placebo effect?

Not only did it improve my skin by 99%, but it slightly improved my vision, and I felt less bloated & tired after eating. Not to mention, my pores shrank, produced less oil, and the biggest one of all was that it eliminated my horrible crying on the floor menstrual cramps!!!! That was the last thing I was thinking of it doing for me and I tried to find that Insulin connection with it and prostaglandins, but I didn't have much luck. Then a few weeks ago, I was reading something on another board, and bam, I found the connection. I tell you for that alone, I would stay on this diet forever ;-)


Take care

#55 flipside

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Posted 23 July 2004 - 09:18 PM

hi sweetjade,

im just curious, what type of diet are you on? i assume its low carb with lots of fruits and veggies.

i stopped drinking milk and ive mostly been eating lots of fruits and veggies and nuts. sometimes i dip wheat bread in olive oil or avocado oil.

im a little worried about getting enough protein. i only eat meat (fish or chicken) a few times per week. most of my other protein comes from peanut butter (the healthy kind)

#56 evigrex

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Posted 23 July 2004 - 09:28 PM

Hmm... Evigrex, I don't want to do your homework for you, but here:

Regulation of testosterone levels is governed by two factors: the total amount of testosterone in the blood, and the binding capacity of the plasma proteins [SHBG]. Obviously, as binding capacity goes up blood levels of free testosterone go down. Not surprisingly, certain drugs (anabolic-androgenic steroids, insulin, etc.) and perhaps nutritional supplements (like avena sativa, urtica dioica, etc.) can reduce the binding capacity of the blood and result in higher free-testosterone levels. [Editors' Note: Nutrition is also a factor in testosterone regulation; see our March discussion on this topic in Experiments vs. Experience.] ….

Bodybuilding.com, now there's a credible source of information. I can find a wealth of misinformation over there - what leads you to believe this is any different.

…..Of the "free" testosterone that interacts at the tissue level, much of it is converted within the cells to DHT - a more potent androgen - by the enzyme 5-alpha reductase. In the prostate, for example, this conversion is thought to be necessary for physiologic effects. Other tissues (like the epididymis, vas deferens, seminal vesicles, skeletal muscle, and bone) lack the 5-alpha reductase enzyme and therefore are thought to respond to testosterone directly. http://www.bodybuild...om/fun/vm12.htm


Bodybuilding.com, now there's a credible source of information. I can find a wealth of misinformation over there - what leads you to believe this is any different.

This is just to establish that my concern is not with all Androgens but in EXCESS Androgens (beyond referance ranges) and Free Testosterone (unbound) and SHBG regulates this amount. FSH & Estrogen raises SHBG, while LH & Insulin lowers SHBG. So yeah, its definitely possible that due to negative feedback inhibition, normally or drug induced (side effect), that the pituitary will produce less tropic hormones, which can work positively or negatively for both males and females.

I have not seen any studies indicating that having higher free testosterone will have any type of effect on other androgens - and just about everyone, I mean everyone has SHBG at around 2%.


QUOTE

INTRODUCTION: Treatment failures with isotretinoin in female patients are frequently related to endocrinological dysfunctions. Such a concept has never been discussed in male patients. CASE REPORTS: An extensive endocrinological work-up has been performed in nine male patients who presented with an acne refractory to conventional treatment and to isotretinoin. Adrenal dysfunction was found in four patients and isolated 5-alpha reductase hyperactivity in 2 cases. Three work-ups were normal. A suppressive treatment in three patients with adrenal dysfunction provided immediate efficacy. COMMENTS: These results would provide insight into the mechanism of refractory acne in men."

Whats your point here? I know that adrenal hyperactivity or hypoactivity can potentially cause or aggravate acne. Cortosol, norepinephrine and epheniphrine are all KNOWN to increase sebum production. How is this possibly linked to androgen prodution? Androgens /=/ Adrenal hormones.



http://www.pubmedcen...gi?artid=370187

Dang I know women can be screwed endocrinologically, and I know that men can be too as some of these studies show, but I too would love to know just how screwed males are in this dept. wouldn't you?

Yeah, I thought we were talking about ANDROGENS, right?



QUOTE
Interactions of retinoic acid and androgens in human prostatic tissue.

Jutley JK, Reaney S, Kelleher J, Whelan P.

Department of Medicine, St. James's University Hospital, Leeds, England.

The effect of retinoic acid (RA) on testosterone metabolic pathway was investigated in hyperplastic and neoplastic human prostatic tissues, and also the effects of steroids on RA binding to its receptor. Steroids only had a minimal effect on the binding of RA by its receptor. The conversion of testosterone to DHT by 5 alpha-reductase was reduced in the presence of retinoic acid. The inhibition was probably due to competition with NADPH for enzyme binding sites. The degree of inhibition found with retinoic acid at a concentration of 10(-4)M was greater for hyperplastic (41%) than that for neoplastic tissue (24%). The inhibition of 5 alpha-reductase by retinoic acid was dose-dependent. The activity of 5 alpha-reductase is significantly less in neoplastic compared with hyperplastic tissue.
http://www.ncbi.nlm....st_uids=1695368

Uh, accutane is an artificial derivative of RA : 13-cis-RA. Not the same thing.



This is a rather old study, 1990, but it was one of the few that actually looked for a correlation among Prostate, DHT and Retinoids. However, we've both posted studies that were more recent that said the same thing about 13-cis retinoic acid specifically, and it's DHT suppression abilities. Who knows, maybe accutane requires higher doses to play such a role on the prostate that it does on the skin. As such, it's not widely used for more things because it's just better] at treating specific types of skin disorders and cancers. Not to mention, the side effects...

My entire point is that whatever you define DHT surpression as, accutane does not have an effect on the production of male sex hormones *by the pituitary*. Period, end of story. There are too many studies on this to even suggest otherwise.


QUOTE
Effect of oral isotretinoin treatment on skin androgen receptor levels in male acneic patients.

Boudou P, Soliman H, Chivot M, Villette JM, Vexiau P, Belanger A, Fiet J.

Department of Hormonal Biology, St. Louis University Hospital, Paris, France.

An oral daily dose (mean +/- SD, 0.75 +/- 0.05 mg/kg) of isotretinoin was administered for 3 months to six male patients with acne (scores of 4 and 5 according to Rosenfield). The therapy resulted in complete resolution of acne in four patients and improved acne significantly (score 1) in two patients. In accordance with recent findings, no change in serum testosterone and significant decreases in 5 alpha-dihydrotestosterone, 5 alpha-androstane-3 alpha,17 beta-diol glucosiduronate, and androsterone glucosiduronate levels were observed after treatment. Androgen receptor status was investigated in back skin biopsies obtained in acne areas before and after 3 months of isotretinoin treatment. The treatment did not modify the binding affinity constant of skin androgen receptor (0.44 vs. 0.32 nmol/L), but it did induce a 2.6-fold decrease in its binding capacity constant (62 vs. 24 fmol/mg cytosolic protein), as assessed by Scatchard plot and confirmed immunologically by Western blot analysis. These data clearly showed that skin androgen receptor was sensitive to oral isotretinoin administration in acneic patients. The decrease in skin androgen receptor levels (this study) and the recently reported suppression of skin 5 alpha-dihydrotestosterone production by isotretinoin treatment appeared consistent with the involvement of androgen receptor and 5 alpha-dihydrotestosterone in the pathogenesis of acne. Indeed, sebum production is under androgen control, and an abnormal response of the pilosebaceous unit to androgens appears to be implicated in the pathogenesis of acne. These observations were consistent with the absence of sebum in complete androgen-insensitive patients and normal sebum production in male pseudohermaphrodites.

Again, what does this have to do with endogenous production of androgens by the pitutary. Be my guest to do a search of pubmed for "accutane testosterone", there are several studies showing no change in sex hormone production during and after treatment.


QUOTE
The most pronounced effect was observed in skin biopsies, which lost 80% of their ability to form 5 alpha-dihydrotestosterone (P < 0.001). It is concluded that 13-cis-RA therapy in men with severe nodulocystic acne did not alter gonadal or adrenal functions, but it did induce 1) a highly significant decrease in 5 alpha-dihydrotestosterone formation by skin biopsies; 2) significant decreases in serum 5 alpha-dihydrotestosterone, androsterone glucosiduronate, and 5 alpha-androstan-3 alpha, 17 beta-diol glucosiduronate; and, finally, 3) deviation of the liver androgen 5 alpha- to 5 beta-reduction pathway. The effect of 13-cis-RA treatment on severe acne is consistent with the dramatic decrease in androgen 5 alpha-reduction observed mainly in the skin. http://www.ncbi.nlm....st_uids=8175961

But it doesn't inhibit 5AR produced by the pitutary. How many times do I have to say it? Accutane has this action in the skin, but it doesn't inhibit the production of hormones by the pituitary.



Please note the bolded areas



QUOTE
13-cis-retinoic acid competitively inhibits 3 alpha-hydroxysteroid oxidation by retinol dehydrogenase RoDH-4: a mechanism for its anti-androgenic effects in sebaceous glands?

Karlsson T, Vahlquist A, Kedishvili N, Torma H.

Department of Medical Sciences/Dermatology and Venereology, University Hospital, Uppsala, Sweden.

Retinol dehydrogenase-4 (RoDH-4) converts retinol and 13-cis-retinol to corresponding aldehydes in human liver and skin in the presence of NAD(+). RoDH-4 also converts 3 alpha-androstanediol and androsterone into dihydrotestosterone and androstanedione, which may stimulate sebum secretion. This oxidative 3 alpha-hydroxysteroid dehydrogenase (3 alpha-HSD) activity of RoDH-4 is competitively inhibited by retinol and 13-cis-retinol. Here, we further examine the substrate specificity of RoDH-4 and the inhibition of its 3 alpha-HSD activity by retinoids. Recombinant RoDH-4 oxidized 3,4-didehydroretinol-a major form of vitamin A in the skin-to its corresponding aldehyde. 13-cis-retinoic acid (isotretinoin), 3,4-didehydroretinoic acid, and 3,4-didehydroretinol, but not all-trans-retinoic acid or the synthetic retinoids acitretin and adapalene, were potent competitive inhibitors of the oxidative 3 alpha-HSD activity of RoDH-4, i.e., reduced the formation of dihydrotestosterone and androstandione in vitro. Extrapolated to the in vivo situation, this effect might explain the unique sebosuppressive effect of isotretinoin when treating acne.

Beating a dead horse. I am talking about androgens produced by the pituitary! Christ. Again, there are studies showing no change in testosterone, DHEA, DHT, etc production by the male pitutary gland.


http://www.ncbi.nlm....t_uids=12646198


The above article may be the most recent findings (published in 2003) and yet another one that I had already posted for you on another thread (soy thread). If we didn't already know, DHEA and other Androgens can be converted into DHT which is most acne sufferers’ concern. Thanks to the accutane articles we know that DHT can be converted into 3 alpha-diol glucuronide (3 alpha diol-G)) in target tissues, such as the skin. As such, some studies have mentioned that this is considered a marker for androgen or DHT actions in the skin and regarding acne. Of course, some of these androgens love to revert back to weaker forms and so the pathways below are a bit more complicated than what is depicted, but hopefully it will help us visualize things:

(Insulin) --- Cholesterol – (LH or ISCH) --- Pregnenolone --- Progesterone --- DHEA --- Androstenedione --- [estrogen or] < = > Testosterone --- Estrogen


AND


(Insulin) --- Cholesterol --- (LH or ISCH) -- Pregnenolone --- Progesterone -- DHEA --- Androstenedione and/or Androstenediol < = > Testosterone ---.DHT < = > 3-alpha Androstenediol Glucuronide (or other metabolites)


Now, Androstenedione, Androstenediol, 3alpha diol-G, and DHT are blamed for acne, hirsutism, and androgenic alopecia problems. They all are androgen hormones and apparently some of them can convert back and forth to their weaker or more active forms. Since DHT is further metabolized in the skin, perhaps the way that 13-cis retinoic acid affects 3alpha diol-G is by inhibiting 5alpha reductase which of course prevents DHT formation (see article on page 3). If there’s a reduced amount of DHT, then this would reduce the amount of 3alpha diol-G androgens that are produced from DHT. So based on the above studies, accutane inhibits not only DHT, but several of it’s corresponding androgenic metabolites. Thus accutane is not only good at reducing IGF-1, in the case of cancers and cell proliferation, including sebum growth, but it also directly inhibitis the enzyme, Retinol dehydrogenase-4 which consequently reduces/inhibits the liver enzymes 5 alpha reductase, 3 alpha HSD, etc responsible for DHT production.

http://secure.dslabs...un02_flyers.pdf
http://www.estetik.c...le_hormones.htm

It sounds like a DHT Inhibitor to me, what do you think?

I think your definition of "DHT inhibitor" is vastly different than what most of the medical community thinks of the term as. Accutane does not inhibit the enzyme 5AR in the endocrine system, and hence, does not lower the conversion of testosterone to DHT. Feel free to search pubmed for proof.

Yeah, it has an action in the skin..but whatever.


#57 evigrex

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Posted 23 July 2004 - 09:37 PM

Reading a few studies, it seems that accutane may increase a dht derivative in females - not males. All the studies i've seen (and bloodwork i've seen myself) shows no change in FAI in males taking accutane. A DHT "inhibitor" would cause a drastic *increase* in testosterone and E2 due to the inability of testosterone to convert to DHT via the 5AR enzyme. This is definitely not the case with accutane.

Either way, calling accutane a DHT inhibitor is outright wrong, because there are too many studies demonstrating no change in hormone production by the pituitary in males. It does inhibit receptor affinity for androgens in the skin, but that is far different than being a full blown dht inhibitor like finasteride or dutasteride.

#58 SweetJade1980

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Posted 23 July 2004 - 11:01 PM

Evigrex,

Accutane, 13-Cis Retinoic Acid, and Isotretinion are all the same things.

LOL, I know that a body building site isn't the most accurate source, but majority of that information was correct, and of course who knows better about the effects of testosterone then they...or the hormonally imbalanced, like myself.

If you don't want to believe those studies, so be it, but males and females are capable of being hyperandrogenic. Usually there is a decrese in SHBG as a result of having too much androgens; they are each others antagonist. A decrease in SHBG is also considered to be a greater marker for Insulin Resistance, than IGF-1 (something accutane also inhibits).

Furthermore, certain adrenal abnormalities resulting in production of too much or too little cortisol, have also lead to an overproduction of male steriod hormones. This process works similarly along the lines of how Insulin Resistance Syndrome is thought to produce excess androgens....overcompensation or rather, overstimulation. See NCCAH / LOCAH, Cushings, Hypercortisolism, etc

Yes, I too found some studies that showed a change over time in most or all male steriod hormone levels and some studies said "there was no change". These numbers also varied depending on not just gender but wether the subjects were obese, which is why most recent studies are more preferred. However there were recent studies that showed that DHT production was affected in both males and females in the skin or other target tissues (as is where most DHT is produced, not in the blood stream). Also, since various DHT Inhibitor, Anti-Androgen, Insulin Sensitizing medications, etc. don't affect the same pathways, I would expect to see a variance here as well. I''ve never been the one to argue about that with you.

The Pituary gland does not produce nor directly affect enzyme production, the LIVER, pancreas, and other digestive organs do. Therefore, no I wouldn't expect to see a change in 5 Alpha Reductase or any other androgenic enzyme as the liver produces these. The liver also produces 13-cis retinoic acid via a CYP450 enzyme, but this pathway can be defective as well.

Now, as for the Pituitary gland:

QUOTE
The anterior pituitary secretes four tropic hormones and two regular hormones  

Here are the hormones, starting with the tropic hormones, and finishing with the regular ones:

1. TSH-- thyroid stimulating hormoneThis hormone influences thyroid gland secretion of hormones.

2. ACTH-- adrenocorticotropic hormoneDo you see the "tropic" in its name?  Good!  It works on the adrenal cortex (adrenocortico-).

3. LH-- luteinizing hormone – [or ISCH stimulates testosterone production]

4. FSH-- follicle stimulating hormone – [stimulates progesterone & estrogen production]

These last two together are often termed "gonadotropins" because they exert a tropic hormone effect on the gonads, influencing gonadal secretion of sex hormones.


5. PRL-- prolactin

6. GH-- growth hormone [stimulates IGF-1 production in the liver]

The functions of the last two merit a bit more description.  PRL is pretty straightforward in females, promoting milk production by the mammary glands.  In males, PRL has the function of actually decreasing LH secretion.  Therefore, in males, PRL actually acts like a tropic hormone, more specifically as an inhibitory tropic hormone.   

GH stimulates cells to grow in size, speed up their mitotic cycle (dividing faster), increases protein synthesis, and more.  These functions of GH lead to growth!  Because its effects are so dramatic, problems in GH secretion are also dramatic.  For example, dwarfism and acromegaly are both cases of altered GH secretion.  Take a look at your book and the PowerPoint presentation for more on this.
http://distance.stcc...ne/hypothal.htm


However, the pituitary gland can indirectly affect enzyme production through negative feedback inhibition as well as when it's tropic hormones are released to act upon the ovaries, testes, or adrenal glands in order to produce steriod hormones, etc.

HTH

#59 SweetJade1980

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Posted 23 July 2004 - 11:45 PM

QUOTE(flipside @ Jul 23 2004, 09:05 PM)
hi sweetjade,

im just curious, what type of diet are you on?  i assume its low carb with lots of fruits and veggies.

i stopped drinking milk and ive mostly been eating lots of fruits and veggies and nuts.  sometimes i dip wheat bread in olive oil or avocado oil.

im a little worried about getting enough protein.  i only eat meat (fish or chicken) a few times per week.  most of my other protein comes from peanut butter (the healthy kind)

Flipside,
LOL, plenty of vegetables, yeah right. Wow imagine how clear I would be if I did eat enough veggies...hmm. Anyway, I tend to eat more fruits than I do veggies. I've heard that we should eat 2 - 3 vegetables for every 1 fruit, well, I'm unfortunately doing the opposite. ;-)

I avoid Gluten & usually most grains, only consuming (white) rice & corn grains. As such, occassionally I will have GF Pasta (I like brown rice pastas best) w/ organic sauce. I consume practically every time of protein, such as poultry, beef, pork, seafood, certain nuts, and occassionally beans. My goal here is to increase my EFA content through more seafood (I love salmon), and I rarely consume eggs, but I do love them scrambled or omelet style.

I usually eat watermelon, honey dew melon, cantaloupe, pears (asian pears are so good), apples, and grapes. While I'm still learning how to pick them and use them quickly, I really do love veggies and tend to crave certain ones when I haven't eaten them in a while (like now). I eat most types of vegetables, including potatos, brocolli, cauliflower, romaine lettuce, greens, green string beans, spinach, cabbage, cucumbers, squash, carrots, etc. I try to avoid peas & sweet potatos and severely dislike brussel sprouts...yuck!

I also avoid Dairy, peanuts, cashews, pistachios, bananas, and (decaffinated) sodas as these break me out. I chose to also avoid non-100% fruit juice, and usually most refined foods & sugars, bad preservatives, and trans fats.

As a result of my dietary changes, I drink water at least 90% of the time otherwise its usually diluted (with water) 100% juice. When I drink tea I now sweeten it with Xylitol (it feels like I'm "cheating"). I munch on almonds, hazlenuts, brazil nuts, macademias, sunflower seeds, pumpkin seeds, sesame seeds, and most dried fruit through the day (I try to avoid sulphured ones). While, I've also never been a big fan of beens, but that's another source of protien for you if you and your body can tolerate them.

I also consume a nice bit of "junk" food such as rice cakes, beef jerky (if I can find the right ingredients), (organic) potato chips, popcorn (non hydrogenated oils), natural (flavored) applesauce. Rarely do I consume candy, instead I may pop a xylitol mint or chew some xylitol gum. Of course there's others, but I usually have to order Gluten Free Substitute products as the local ones have too many ingredients that I'm avoiding.

As for oils, I rarely use salad dressing, but when I do I make sure it doesn't have the ingredients that I'm avoiding. When I cook I use olive oil or applesauce depending on what the food is. When my parents cook it's more than likely vegetable oil (soy) or canola oil as "olive oil is expensive". When a recipe calls for butter, we now use Smart Balance.

Since I have 1% of acne left my goals now are to improve my diet by upping my fiber (brown rice) and Green Vegetable intake. As well as removing Cottonseed oil and corn syrup from my diet.

I've been doing this for almost 2 years and have been happy as a peach until now. The more things you eliminate the more you realize you have to cook foods yourself or purchase natural or organic products. It's a bit fit frustrating sometimes because while I rarely use them, most condiments in my house have Corn syrup or High Fructose Corn syrup in them and I can't always control what my parents will use to cook with. I feel like throwing it all away, but of course that means I have to replace it all, which I intend to do as soon as I hit my only organic healthfood store, Sun Harvest.

So, why aren't you eating more protein? Is it because it's not organic or does non-organic cause you problems? If you want you could try consuming Brown Rice Protein Powder (search for a list). It's not only hypoallergenic, but also helps balance insulin levels, etc.

Bye for now =)

P.S. If I didn't mention a fruit it's probably because I don't know what to think of them yet. I'm either naturally avoiding them or limiting my consumpton because some happen to be in the same family of the nuts that I'm avoiding.

#60 Chloe646

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Posted 24 July 2004 - 12:30 AM

Hey, in this months glamour magazine, a doctor is quoted as saying that eating too many refined carbs CAUSES ACNE:::::::there go the arguments for people waiting with baited breath for a prescious med figure to say diet can cause acne:

Hey SweetJade:

yeah, what a lot of people see as a strict diet is just a diet that is natural and devoid of crap..damn, it's easier to eat healthy in poor rural countries than the US!!!!! I eat lots of bananas, they seem not to affect my skin...but upping the veggie intake, whoa does that make a diff obviously cause you're upping the vitamins you're eating. a lot of veggies contain plenty of Vit. C>people seem to only think fruits are the best source of that.....ANYWAY, are you using any topicals? Witch hazel is fantastic....these changes have literally made my pores look like they've disappeared in some places! and the best part, you don't have to deal with flakiness and red skin from too much topical. the changes are so apparent sometimes I run over and over to a mirror checking under lights that shine DOWN (the worst angle, unless your a six year old haha) and yup diet did ALL that in a few weeks. Woo woo : )

Also, Corn is a grain, I actually don't feel too great when i eat it even tho it doesn't make me break out. have you tried buckwheat? that tastes pretty good. And are you taking supplements?I take selenium and coQ10 (anti oxidants)