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    Old 11-16-2004, 07:57 PM   #76
    SweetJade1
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    Re: Sugar Sugar!

    Quote:
    Originally Posted by DiselPower4
    Hey SweetJade is Coke and Pepsi bad for acne?
    Disel,
    Well that depends on what type of sweetner is found in them. Considering that most are sweetened with High Fructose Corn Syrup, I would say it's not only bad for acne, but also for anyone concerned with gaining weight (some gain 10 - 12lbs from sodas & non-100% fruit juice), or high cholesterol.

    Then there are artificially sweetened sodas & juices and well, aside from how bady the taste for some of us, they aren't likely to give you acne, but could cause you other health/neurological problems.

    So if you personally enjoy sodas, and don't have a problem with caffeine (can increase IGF-1) , you can always try fruit juice or cane juice sweetened sodas. These will be found in a health food store, but do not be taken in by "naturally sweetened" claims on the cans. Make sure you read the label to ensure it is not sweetend with corn syrup or HFCS.

    If you have noticed that sodas give you acne you can test drinking organic sodas such as Wild Oats or Blue Sky Organic and/or drinking decaffeinated sodas to see if either play a role on your skin. Oh and there's even a sparkling 100% juice type carbonated breverage from Knudsens that doesn't add any sugar to their product!

    Now, personally HFCS & corn syrup give me cysts while table sugar & evaporated cane syrup/juice just give me a few whiteheads. So depending on your personal severity to refined & added sugars, still drinking "natural sodas" may be worth a gamble to you ;-)

    Take care


    Psst...if you are just missing variety, purchase (organic) kool-aid packets (they don't have sugar) or no sugar added flavorings, add to water, and then sweeten with xylitol (or perferred alternative). =)

    Last edited by SweetJade1; 11-16-2004 at 08:11 PM.

     
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    Old 11-16-2004, 09:47 PM   #77
    SweetJade1
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    Re: Sugar Sugar!

    Quote:
    Originally Posted by Katrinamp
    aaahh.. finally, there is that study mentioning the chocolate. we were waiting for that one from you...

    Can we please hear your argument based on a study that:
    1. Has a much larger sample size than 77 (this small number is not sufficient enough to get an accurate sample of the population)
    2. Experimented this type of experiment on people who have the acne gene to begin with (as we have been talking about this entire time), so that they could see whether acne-prone people are affected by fluctuating sugar levels
    and
    3. EXPERIMENTS WITH THE INSULIN/SUGAR LEVELS. NOT CHOCOLATE LEVELS. COCOA DOES NOT HAVE INFLAMMATORY PROPERTIES. THE SUGAR ADDED TO CHOCOLATE BARS DOES.

    Katrina,
    Perhaps below is a sufficient reason why we don't get acne duriing childhood, although it may also explain why in some of my baby pictures I did have a few "bumps" on my face.

    So, according to the the American Academy of Family Physicians, Dr. John J. Russell, M.D. of Templo University School of Medicine, Philly wrote something to the effect saying "Pilosebaceous units are present and active at birth as a reaction to maternal hormones. Therefore, newborns can have clinical symptoms of acne. While the pilosebaceous units atrophy during childhood, under the influence of androgens, they reemerge during adolescence."

    Fascinating, isn't it?

    Last edited by SweetJade1; 11-16-2004 at 09:49 PM.

     
    Old 11-17-2004, 05:46 AM   #78
    openseason
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    Re: Sugar Sugar!

    Acne inflamation is thousands of dead skin cells which have clogged the oil gland. Hormones alone do not clog the pore. Oil itself does not clog the pore. This is another myth. The pore is clogged by retained skin cells called "retention hyperkeratosis" first published by Dr. Albert Kligman University of Pennsylvania. Then the oil glands continue to pump oil into a closed oil follicle. The specific defect either enzyme or structural defect has not been discovered so far, although the research in Paris France may have found it. Diet has nothing to do with how the oil gland operates. Acne is a disease passed genetically, not through food. Think of how sebaceous glands mature. First the glands in the nose and forehead, then cheeks, then jawline then shoulders, then lower back. This is the sequence acne appears in puberty. So that is genetic programming not diet.

     
    Old 11-17-2004, 02:58 PM   #79
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    Angry Re: Sugar Sugar!

    To everyone arguing with Open- He will never, ever get it. He keeps repeating his argument that food doesn't cause acne but has not once responded to our research and arguments that inflammatory foods enhance the propensity and inflammatory properties of acne breakouts. He is one person, we might as well just let him dwell in his greasy extra-cheese pizza and 2 liter pepsi and let his face continue to break out.

    Open- My boyfriend and I are raising a puppy who is overly nippy. Our trainer said that when he does that, we should ignore him and leave him alone and he will stop. I am joining the other girls when I say I am no longer responding to your claims and stubborn, close-minded, snotty, self-righteous comments that have nothing to do with what we are saying and have no solid research behind them. I am begginning to think you get off on it.

    To all of the rest of you out there- Don't let what Open has said get you down. Don't lose hope because of it (my main worry). A change in diet HAS helped thousands of people who suffer from acne, and you should always give it a try if it feels right to you. There is an answer out there for all of us, it just takes us some time to find the right one.

    Last edited by Katrina; 11-17-2004 at 02:59 PM. Reason: spelling error

     
    Old 11-17-2004, 05:05 PM   #80
    openseason
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    Re: Sugar Sugar!

    I am only repeating what dermatologists tell me who certainly have studied the problem in depth. The food cause is a holdover from the 1950s. Soda pop does not make acne worse, although it will make you fat. Greasy foods fill the blood with grease that makes sense. A pepperoni pizza looks like acne so it must cause acne, that makes sense also. As I have stated acne is an ancient disease and existed when people ate only whole natural foods and drank pure water.

     
    Old 11-17-2004, 05:12 PM   #81
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    Re: Sugar Sugar!

    Your pop psychology is interesting. I did not say anything could not be done for acne. I am saying food has nothing to do with it, just talk to some dermatologists and acne researchers.

     
    Old 11-17-2004, 08:12 PM   #82
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    Re: Sugar Sugar!

    A whole foods diet basically cured my acne. I don't know how I could have ever been so blind to food and what I've been putting in my body. Now I read all the ingredients before hand. I guess it is because we are constantly told from a young age that you can eat whatever you want and it won't matter until you are 50 or it might not matter at all...but it mattered for me. Our bodies are biological organisms. It matters what we eat.

     
    Old 11-18-2004, 04:19 AM   #83
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    Re: Sugar Sugar!

    When food trials are conducted and people are given diets which they claim make acne, the results are the diet makes no difference. For instance someone will claim tomatos make them break out with pimples. They take these people and feed them lots of tomatos, and the reult is no acne. Doctors have not been able to replicate the food hysteria. Acne has been around long before there were cheeseburgers, fried food hershey bars, pizza or soft drinks. Just do a search for food trials and acne. You are reading a list of ingredients on your food. A whole food does not have a list of ingredients. A whole food is a vegetable. There are no other ingredients. So you prove my point. You are eating processed foods and you still have clear skin.

    Last edited by openseason; 11-18-2004 at 04:23 AM. Reason: forgot something

     
    Old 11-18-2004, 08:46 AM   #84
    SweetJade1
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    Re: Sugar Sugar!

    For those interested, there have been several editorials and comments regarding Loren Cordains observations which he published under two studies, one of which I posted on earlier titled: Hyperinsulinemic Diseases of Civilization: More Than Just Syndrome X (2002)

    While most are in favor, this is one posted by a female dermatologist that I think goes over both sides of the issue and in the end:

    Quote:
    Diet and Acne Revisited

    Arch Dermatol. 2002;138:1591-1592.

    THE ARTICLE by Cordain et al1 in this issue of the ARCHIVES represents an interesting departure for a contemporary, peer-reviewed medical journal. While the present-day emphasis is on controlled, double-blinded clinical studies that pass the muster for evidence-based medicine, the report by Cordain et al is observational, and the only control is the dietary limitations characteristic of 2 isolated nonwesternized populations.

    These authors suggest that the absence of acne in more than 1300 subjects in 2 nonwesternized societies—the Kitavan Islanders of Papua New Guinea and Aché hunter-gatherers of Paraguay—is attributable to their diets, which have a substantially lower glycemic index than a Western diet. In addition, these people are more physically active than Westerners. They do not demonstrate insulin resistance, nor do they have obesity, hypertension, diabetes, or heart disease. Their genetic background is similar to other Pacific Islanders and South American Indians, respectively, yet their incidence of acne is lower than that of members of these same groups who have incorporated elements of a Western diet.

    Isolated observations and case reports suggest that acne can develop in groups not generally susceptible to this disorder when a highly glycemic diet is adopted, which can induce acute or chronic hyperinsulinemia, as in the case of Eskimos who adopted a Western diet.2 One of us (J.S.S.) has also heard many young Irish women report that they had no acne until they immigrated to the New England area from rural Ireland. However, no systematic studies are available to fully support or refute these observations. Of course, the study by Cordain et al1 would have benefited from the opportunity to provide the subjects with a diet containing highly glycemic foods to determine if acne occurred, but this was not possible.

    The relationship of acne to foods is certainly not new. The "big three" US textbooks of dermatology3-5 popular in the early 1950s when one of us (J.S.S.) was in training all contained elaborate prose regarding specific foods to avoid. The admonition to avoid chocolate, fats, sweets, and carbonated beverages was commonly given to patients as part of acne therapy. But all of this dietary advice was removed from standard texts, and it has been many years since restriction of specific foods has been recommended in managing acne. Nonetheless, few of us feel compelled to argue strongly with the occasional patient who insists that his or her acne is exacerbated by a certain food item. It should be noted, however, that it was reported in an article published only last year6 that 30% of medical students surveyed in Australia believed that acne was influenced by diet.

    Cordain et al1 suggest that diet-induced hyperinsulinemia elicits endocrine responses that may affect the development of acne through mediators such as androgens, insulinlike growth factor (IGF) 1, IGF binding protein 3, and retinoid signaling pathways. The role of diet in endocrine activity is supported by the observation that improvements in nutrition have been linked to an earlier onset of sexual maturation and the development of acne in young girls and boys. Numerous studies have shown that improvements in general nutrition in girls have led to an earlier onset of menses and that menses is delayed in girls with low body fat such as athletes and ballet dancers.7 In 1970, the mean age of onset of menarche in the United States was 12 years compared with age 16 years for girls in 1835.8 Of interest is the observation that the mean age of onset of menarche in the Kitavan population is 16 years, which is significantly older than girls in westernized societies. In a 5-year longitudinal cohort study of 439 black girls and 432 white girls in Cincinnati, Ohio, Lucky et al9 demonstrated that those with severe comedonal acne had a significantly earlier age of onset of menarche and higher serum levels of dehydroepiandrosterone than girls with mild comedonal acne. This study demonstrated that the early development of comedonal acne might be one of the best predictors of later, more severe disease. In a similar 5-year longitudinal study of 219 black and 249 white early adolescent boys in Cincinnati, black boys had higher pubertal maturation scores than white boys of the same age.10 The prevalence and severity of acne correlated well with advancing pubertal maturation. Is the late onset of menarche in Kitavan girls "protective" against the development of acne or severe acne? Although Cordain et al do not present data regarding the age of sexual maturation of the Kitavan or Aché boys, is it also possible that their relative lack of acne might relate to a later age of pubertal maturation and sebaceous gland exposure to higher circulating levels of androgen?

    If acne results from hyperinsulinemia, as proposed by Cordain et al,1 one would expect that obese individuals, who are relatively chronically insulin resistant, would have a higher prevalence of acne. Bourne and Jacobs11 evaluated 2720 military recruits for obesity and the presence of acne and noted an association between the 2 in the older recruits (ages 20-40 years) but not in those in the age range of 15 to 19 years. This observation suggests that the presence of acne in a younger population may be associated with factors other than obesity or insulin resistance. In fact, serum levels of IGF-1 are highest during periods of the adolescent growth spurt and taper off in the 20s, which coincides with the pattern in the peak incidence of acne.12 Insulinlike growth factor 1 functions similarly to insulin in that it can promote the growth of keratinocytes and sebaceous glands. It is possible that that the effects of the hyperinsulinemia on acne in obese adolescents may be overshadowed by the effects of high levels of circulating IGF-1. As pointed out by Cordain et al, acne has been associated with elevated serum levels of IGF-1 in adult women with acne.13 All adolescents, including the Kitavan and Aché, would experience increases in IGF-1 during adolescence, so increases in IGF-1 alone cannot explain the presence of acne.

    Within the past few years, tremendous advances have been made in our understanding of the molecular mechanisms of obesity, insulin resistance, diabetes, and hyperandrogenism. For example, the association of hyperandrogenism and acne in women with conditions such as polycystic ovarian syndrome (PCOS) has been clearly established. In women with PCOS, insulin resistance can lead to hyperandrogenism, which then can lead to the exacerbation of acne. The treatment of PCOS now includes drugs such as thiazolidinediones and metformin, which are aimed at increasing insulin sensitivity. The reduction in serum insulin concentration has been linked to a reduction in the level of serum androgens and improvement in fertility.14 Whether this reduction in serum insulin and androgen levels equates with an improvement in acne remains to be determined.

    Interestingly, not all women with PCOS are obese. Hyperandrogenism, insulin resistance, and acne still occur in lean women with this disorder. If hyperinsulinemia rather than hyperandrogenism exacerbated acne, we would expect to see much more acne in obese men and women with diabetes, hyperinsulinemia, and insulin resistance. This does not appear to be the case. On the other hand, type 2 diabetes is generally a disease of adults, who have lower serum levels of IGF-1 and growth hormone than adolescents. Perhaps the increasing levels of growth hormone, IGF-1, and androgens in the adolescent sets the stage for susceptibility to diet-induced hyperinsulinemia as a trigger for the development of acne.

    Last edited by SweetJade1; 11-18-2004 at 08:48 AM.

     
    Old 11-18-2004, 08:48 AM   #85
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    Re: Sugar Sugar!

    (continuation)

    Quote:
    Although Cordain et al1 make a strong argument for the role of diet in acne, we believe that it is difficult to dissociate environmental factors such as diet from genetic factors in their study. The Aché and Kitavan people live in closely knit communities, and therefore genetic factors may play a role in the relative lack of acne in these populations. Several studies point to an association of genetic factors with acne, including studies that demonstrate variations in the prevalence of acne among ethnic groups and the high degree of concordance of acne in twins.15-19

    In fact, numerous studies have failed to demonstrate significant differences in sebum composition between subjects with and without acne, suggesting that overall sebum production and not sebum composition is more important in the development of acne. During periods of starvation, when total caloric consumption is greatly reduced, sebum production is decreased by about 40%,20-21 which could certainly improve acne. However, this reduction occurred with extreme caloric restriction (<100 calories/d [<418 J/d]), a circumstance that is not practical to apply as a therapy, to say the least. In each of these studies, changes in the quantity and quality of sebum were reversed after a normal diet was resumed. Biochemical studies clearly demonstrate that the sebaceous gland can make lipids (cholesterol, squalene, triglycerides, wax esters, and cholesterol esters) from a variety of substrates (including acetate, glucose, and fatty acids) that serve to donate 2 carbon fragments.22-23 The starvation studies indicate that a dietary source of substrates is needed to produce sebaceous lipids. The type of food from which substrates are derived may not be important in overall sebum production.

    In summary, as proposed by Cordain et al,1 it remains possible that adolescents in westernized societies may be repeatedly acutely hyperinsulinemic due to their highly glycemic diet. Hyperinsulinemia in turn may initiate an endocrine cascade that affects the sebaceous gland and follicular keratinization and involves IGF, IGF binding protein 3, androgens, and retinoid signaling pathways. Whether adherence to a diet with a low glycemic load can alter acne in other populations is unknown.
    [url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12472347[/url]

    Now what I liked is that this author didn't assume to know everything and just toss aside information because it didn't fit 100% with someone else's theory. This was written in 2002 and since then there have been additional studies to further support that:

    Insulin Resistance is necessary for growth during Puberty, hence the increase in IGF-1 for all adolescence

    Androgens are responsible for the development (with IGF-1) of sebaceous glands and sebum production

    IGF-1 is responsible for the stimulation, growth of sebaceous glands, sebum production, skin cell hyperproliferation (overgrowth), and hyperkeritinization (thick skin).

    Hyperandrogenism can lead to a variety of factors including acne, hirsutism, rheumatoid arthritis, obesity, seborrhea, heart disease, etc. The question is how many of these disease are actually a result of Hyperinsulinemia induced Hyperandrogenism (as there are overlapping signs)?

    That Insulin Resistance is "asymptomatic" for many many years and if left untreated Diabetes Type II results. Therefore it makes sense that Type II Diabetes wouldn't be present until someone's 30s or 40s, but it is slowly becoming more prevelant in younger generations. Asymptomatic means that you won't show any outward signs of a problem...until it worsens or it's too late. However, acanthosis nigricans (another skin disorder) is one sign of Insulin Resistance and I'm betting acne is yet another sign they haven't officially declared yet.

    Insulin Resistance also leads to the production of higher LDL (bad) cholesterol levels and lower HDL (good) cholesterol levels and this has been found in acne sufferers and acneic twins. In fact acneic twins were found to be deficient in a component that's apart of HDL called Apolipoprotiein A1. Furthermore because LDL is higher that means you have higher trigylcerides and free fatty acids, which have the option to not only produce cholesterol (needed for steriod hormone synthesis, like androgens), but also PGE1 (good) and PGE2 (bad, inflammatory) prostaglandins.

    Now, based on the above, sebum alone was discounted as being the only culprit, IGF-1 was discounted as being the only culprit, hyperinsulinemia was discounted as being the only culprit, furthermore, microorganisms were discounted as being the only culprit, & hyperandrogenism has also been discounted as being the only culprit. What's my point? Obviously the reason that these factors are present in several types of related diseases, but doesn't ALWAYS produce the same symptoms, has to do with our genetic makeup. You do not have to have high androgen levels to produce acne, but you DO need to have defective or sensitized androgen receptors of the skin!

    So, just because the above is true, it doesn't mean that the foods you consume aren't a huge part of the equation. It's like saying "sugar isn't my enemy because I have Diabetes (type I), it's because I don't produce enough insulin." Riiiight, but if you don't produce enough insulin, it's best if you dont consume a whole lot sugar unless you can supply your body with that insulin...otherwise health complications & death results. Same goes with Insulin Resistance or Type II Diabetes, you must either improve the cells insulin utilization (sensitivity), reduce insulin secretion and/or reduce the foods that promote a higher insulin output. Furthermore, when you look at people that do have the obesity gene, it doesn't mean that they can keep eating foods that have been show to ALSO support the incidence of obesity & associated health problems because it's "genetic", they still need to REDUCE their risk.

    In that respect, if anyone noticed, you can't produce sebum without androgens. You can't produce the products of sebum & steriod hormones without fats in your diet (good or bad). You can't induce cell uptake of fats without insulin (& lipoproteins, LDL) anymore than can induce the uptake of glucose without insulin. You can't initiate sebum production & skin cell growth without IGF-1, which is also present as a result of the insulin in your blood stream (to reduce Insulin). Yet insulin has the ability to inhibit IGFBP-3 and SHBG production which are neccessary to bind/inhibit & reduce the presence of IGF-1 and Free Androgens. Therefore, when IGF-1 is present, if long enough or in high enough concentrations, pro-inflammatory cytokines will also be present (to reduce IGF-1). Let's not for get that our bodies have the ability to produce anti-inflammatory (PGE1) or inflammatory prostaglandins (PGE2) based on the foods & nutrients we supply. Thus, if you eat a certain way, you will favor inflammatory prostaglandins, such as archiadonic acid, which the presence of pro-inflammatory cytokines encourage the production of!

    Therefore as you can see, while the defect for the formation of acne is probably in the skin's androgen receptors, if you eat a certain way that favors the production of the above contributors, knowingly or unknowingly, you are solely or further encouraging the production of acne.

    Believe me I've thought of the solution, permanent inhibition or suppression of (some of) the skin's androgen receptors. Unfortunately gene therapy is a looong way off and if they ever do this, it will probably initally target ALL androgen receptors of the body and that's not a good thing whatsoever. This is why currently the only effective solutions are topical or oral/internal anti-inflammatories and/or anti-androgens. As these two, inflammatory products & androgens, are responsible for the events that lead to the production of acne. Therefore until gene therapy has figured it out, our best bet, especially for chronic acne sufferers, are to find solutions to the above, such as (natural or prescription) Anti-inflammatories, Insulin Sensitizers, Glucocorticoids, Antiandrogens, DHT Inhibitors & Anti-inflammatory or Hormone Balancing Diets, as these are currently our strongest & most effective options.

    Last edited by SweetJade1; 11-18-2004 at 10:27 AM.

     
    Old 11-18-2004, 11:45 AM   #86
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    Re: Sugar Sugar!

    The fact is no one knows what causes the retention of dead skin cells which then block the oil gland. But,since you are so sure Jade it has something to do with sugar, I think you should publish your findings and the proof in a medical journal.

     
    Old 11-18-2004, 12:22 PM   #87
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    Re: Sugar Sugar!

    Quote:
    When food trials are conducted and people are given diets which they claim make acne, the results are the diet makes no difference. For instance someone will claim tomatos make them break out with pimples. They take these people and feed them lots of tomatos, and the reult is no acne. Doctors have not been able to replicate the food hysteria. Acne has been around long before there were cheeseburgers, fried food hershey bars, pizza or soft drinks. Just do a search for food trials and acne. You are reading a list of ingredients on your food. A whole food does not have a list of ingredients. A whole food is a vegetable. There are no other ingredients. So you prove my point. You are eating processed foods and you still have clear skin.
    Diet made all the difference for me. I have been lucky to find out what was causing my acne and yes if I eat something that is precooked or packaged (for you "processed") I have to read the ingredients and (for me) whole foods doesn't negate everything cooked or packaged. So actually I can see how confusion can occur. Yes you could say I eat "processed foods" when I cook at home too (because cooking is a process) and I have clear skin..but someone else may construe this to mean they can eat cheese doodles and it doesn't affect them because they are both "processed". This isn't good logic. Maybe they can..maybe they can't. You can argue that all day. I am lucky to have found out what I can and can't eat and it has made ALL the difference. Granted, reading the ingredients can be inconveniencing but hey this small inconvenience is nothing compared to having acne. I am so glad I found the diet connection.

    Last edited by Mehtab; 11-18-2004 at 12:24 PM.

     
    Old 11-18-2004, 01:02 PM   #88
    SweetJade1
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    Re: Sugar Sugar!

    Mehtab,
    I'm so glad things are working wonderfully for you. Some people don't understand that even "whole" foods contain nutrients, hormones, enzyme inhibitors, etc that can affect our health just as processed food contain ingredients that can do the same. The important thing is that WE know this and we are much better off because of it. =)

    Best wishes!

     
    Old 11-18-2004, 01:56 PM   #89
    SweetJade1
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    Re: Sugar Sugar!

    Hmm... give a normal or acne free person IGF-1 and what happens?

    Quote:
    Clin Endocrinol (Oxf). 1998 Jan;48(1):81-7. Related Articles, Links


    Development of hyperandrogenism during treatment with insulin-like growth factor-I (IGF-I) in female patients with Laron syndrome.

    Klinger B, Anin S, Silbergeld A, Eshet R, Laron Z.

    Endocrinology and Diabetes Research Unit, Schneider Children's Medical Center of Israel, Tel Aviv.

    OBJECTIVE: Patients with Laron syndrome (LS) can now be treated with recombinant IGF-I. We describe the development of androgenization during IGF-I treatment of female LS patients. PATIENTS: Six female patients with LS--two clinically prepubertal (11.6 and 13.8 years of age) and four young adults (30 to 39 years old)--underwent long-term replacement treatment with recombinant IGF-I. The daily doses were 150 micrograms/kg/day by subcutaneous (s.c.) injection in the girls and 120 micrograms/kg/day in the adult women. METHODS: Testosterone, delta 4-androstenedione, LH, FSH, insulin and IGF-I were determined by radioimmunoassay. Blood samples were obtained after an overnight fast before the IGF-I injection. Serum IGF-I was also determined 4 hours after the s.c. injections. RESULTS: During IGF-I treatment, four out of the six patients (two girls and two adults) developed progressive clinical symptoms and signs of hyperandrogenism (oligo/amenorrhoea and acne). Laboratory determinations showed a significant elevation in serum testosterone, delta 4-androstenedione and LH/FSH ratio. The hyperandrogenism occurred concomitantly with an increase in IGF-I serum and a decrease in serum insulin concentrations. Reduction in IGF-I dose or interruption in IGF-I treatment restored androgen levels to normal values. At the same time, the acne and oligomenorrhoea resolved. CONCLUSIONS: Overdosage of IGF-I can lead to androgenization, a previously undescribed undesirable effect of IGF-I. Long-term IGF-I treatment necessitates progressive adjustment of the IGF-I dose to avoid overtreatment.
    [url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9509072[/url]

    Quote:
    Endocr Rev. 2000 Aug;21(4):363-92. Related Articles, Links


    Role of hormones in pilosebaceous unit development.
    Deplewski D, Rosenfield RL.

    Department of Medicine and Pediatrics, The University of Chicago Pritzker School of Medicine, Illinois

    Androgens are required for sexual hair and sebaceous gland development. However, pilosebaceous unit (PSU) growth and differentiation require the interaction of androgen with numerous other biological factors. The pattern of PSU responsiveness to androgen is determined in the embryo. Hair follicle growth involves close reciprocal epithelial-stromal interactions that recapitulate ontogeny; these interactions are necessary for optimal hair growth in culture. Peroxisome proliferator-activated receptors (PPARs) and retinoids have recently been found to specifically affect sebaceous cell growth and differentiation. Many other hormones such as GH, insulin-like growth factors, insulin, glucocorticoids, estrogen, and thyroid hormone play important roles in PSU growth and development. The biological and endocrinological basis of PSU development and the hormonal treatment of the PSU disorders hirsutism, acne vulgaris, and pattern alopecia are reviewed. Improved understanding of the multiplicity of factors involved in normal PSU growth and differentiation will be necessary to provide optimal treatment approaches for these disorders.
    (Full Text Available...maybe someone should read it)
    [url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10950157[/url]




    Quote:
    Acta Derm Venereol. 1997 Sep;77(5):394-6. Related Articles, Links


    Isotretinoin, tetracycline and circulating hormones in acne.

    Palatsi R, Ruokonen A, Oikarinen A.

    Department of Dermatology, University Central Hospital, Oulu, Finland.

    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. However, the effects of isotretinoin on other pituitary, adrenal or gonadal hormones have not been thoroughly elucidated. In the present study, isotretinoin administered at a dose of 0.5 mg/kg/day for 4 weeks caused no marked changes in the serum levels of pituitary, adrenal or gonadal hormones or 3 alpha-Adiol G in patients with severe papulopustulotic acne (n = 19). 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). Isotretinoin did not affect the elevated LH/FSH ratio in a patient with the polycystic ovarian syndrome (PCOS); nor did it change the high FAI or low SHBG in the male patients. For comparison, tetracycline had no effects on the serum hormonal levels of patients with mild acne (n = 19) after 7 days of treatment. This study confirms that the effects of isotretinoin on the serum hormone levels are small and unlikely to be of relevance for the resolution of acne or the suppression of sebum excretion.
    [url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9298137[/url]

    There's studies dating back to 1988 discussing retinoids antiproliferative effects (accutane was originally used to treat cancer) so above may explain why antiandrogenic retinoids such as Isotretinoin AKA 13-cis Retinoic Acid AKA Accutane, don't permanently work for everyone (not strong enough or cease of treatment?).

    Last edited by SweetJade1; 11-18-2004 at 02:34 PM.

     
    Old 11-18-2004, 02:35 PM   #90
    SweetJade1
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    Re: Sugar Sugar!

    Introduce IL-1 (pro-inflammatory cytokine) and what happens?

    Quote:
    J Invest Dermatol. 1996 Jan;106(1):176-82. Related Articles, Links


    Modeling acne in vitro.

    Guy R, Green MR, Kealey T.

    Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, U.K.

    To help elucidate the factors responsible for the infundibular changes seen in acne, the human sebaceous pilosebaceous infundibulum was isolated by microdissection and maintained for 7 d in keratinocyte serum-free medium supplemented with 50 micrograms/ml bovine pituitary extract, 100 units/ml penicillin and streptomycin, 2.5 micrograms/ml amphotericin B and CaCl2(10H2O) to give a final Ca2+ concentration of 2 mM. Infundibular structure was maintained over 7 d in this medium; the pattern of cell division mimicked that in vivo. The rate of cell division was significantly higher than previously described for infundibula maintained in supplemented William's E medium, and moreover did not fall over 7 d. The addition of 1 ng/ml interleukin-1 alpha (IL-1 alpha) caused hypercornification of the infundibulum similar to that seen in comedones; this could be blocked by 1000 ng/ml interleukin-1 receptor antagonist (IL-1ra). In about 20% of subjects there was spontaneous hypercornification of the infundibulum that could be blocked by 1000 ng/ml IL-1ra, suggesting that the infundibulum is capable of synthesising IL-1 alpha. The addition of 5 ng/ml epidermal growth factor or 5 ng/ml transforming growth factor-alpha to the medium caused a disorganisation of the keratinocytes of the infundibulum that resulted in rupturing similar to that seen in the more severe, purulent grades of acne. The addition of 1 microM 13-cis retinoic acid caused a significant reduction in the rate of DNA synthesis and apparent parakeratosis. We are now, therefore, able to model histologically the major infundibular changes in acne.
    [url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8592071[/url]



    Barring the fact that the article below didn't mention pro-inflammatory cytokines from other diseases (thyroiditis, hyperinsulinemia, etc) you can't get anymore recent than this!
    Quote:
    Cutis. 2004 Aug;74(2):92-7. Related Articles, Links


    The pathophysiology of acne vulgaris in children and adolescents, Part 1.

    Bergfeld WF.

    Department of Dermatology, Cleveland Clinic, Ohio

    Microcomedones, the earliest lesions of acne, appear at adrenarche, which typically occurs at about 8 years of age when androgens of adrenal origin begin to stimulate follicular hyperkeratosis and sebaceous hyperplasia in pilosebaceous units on the face. Comedones appear about 2 years later, when androgens of gonadal origin are produced and colonization of follicles by Propionibacterium acnes increases. Inflammatory lesions, such as pustules, papules, and nodules, are the result of the host's immune responses to P acnes; the proinflammatory cytokines are released by immunocompetent leukocytes that are recruited in response to this bacterium and its metabolic by-products. Androgens also affect the barrier function of the skin, and disturbances of barrier function may stimulate epidermal DNA synthesis. This leads to epidermal hyperplasia, which may also contribute to follicular hyperkeratosis in acne. Optimal treatment for this disorder will address these various pathophysiologic factors
    [url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15379361[/url]


    Obviously there's plenty of scientists, doctors, endocrinologists, nutritionists, science & medical students, etc around the world that understand what's going on....to bad some people don't. You can't "grow" properly without growth hormone and associated growth factors. It just can not be done. Hmm... maybe the barrier is that some people just don't understand what skin cell proliferation, hyperkeritinization or follicular hyperkeratosis or hypercornification means. Mediical Dictionary anyone?

    Last edited by SweetJade1; 11-18-2004 at 02:39 PM.

     
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