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Diet/Lifestyle has 100 percent effect on acne

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#21 SweetJade1980

SweetJade1980

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Posted 25 October 2004 - 01:29 AM

QUOTE(apple49 @ Oct 24 2004, 11:40 AM)
SJ,
You know I totally respect your dedication to holistic living and science.But, I have done the diets, the pills, the vitamins too.All I'm saying is that genetics play a really big role. So MB's assertion that diet=oily skin is bunk.I do live a healthy lifestyle, but I would hate someone to think that if they just found the right diet all their problems would be solved.And to the person who asked about siblings without acne.Check out acnebook.com. Dr. Fulton, the most influential acne researcher of our time, has a much analysis of the genetic data than I can duplicate here.

PS. Why do the refs never call penalties on the Vikings??? eusa_sick.gif  I just watched them spear and no call as usual. Enjoy your Sunday wink.gif

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Apple,
I'm not saying that diet will work for everyone 100%, nothing does ;-) However, I suppose I should clarify myself a bit as I view the genetic role of acne differently from others around here. So, regarding acne, all "genetics" is is a way to express a problem that our body has. In other words acne is a phenotypic (physical) expression of our genes' reaction to something abnormal going on.

- It's like getting a rash from poison ivy, are we really meant to always have that rash???? Remove the poison ivy and what happens to the rash?

- It's like the person who gains weight from eating the same foods, that myself wouldn't gain a pound from. Are we saying that the type & quality of food they are eating hasn't contributed in some way? Add in some exercise and change their diet properly and what usually happens?

- It's like most acne sufferers saying that they can eat all they want, and still be thin, but can they really? What if all they are doing is just eating all they want and getting all the acne they "want"??? That's how it is for myself and others...

- It's like coming down with a viral or bacterial infection, are we really meant to have the chicken pox, that runny nose, or that cough forever? Once the infection has gone away, don't those symptoms?


So were are all the above signs & symptoms something we were all BORN with, or was it due to something else going on at the time??? I've never read anywhere about anyone just "having acne", it's always been associated with a disease induced by microorganisms, toxins, deficiencies, allergies, intolerances, tumors, hormonal imbalance, and/or health problems.

I think that part of the problem is that a majority truly believe that it is genetic only, and that there's nothing that can be done to change this. Myself and many others have proven otherwise through changing our diets (when other methods failed or weren’t effective enough). Others have proven otherwise by correcting their nutrient deficiencies or eliminating their toxins. Others have proved otherwise by taking the right medications to heal or suppress their problems.

I think that most people around here are wishing and hoping that doctors will find that "acne gene", but acne isn't formed by just one thing, it's a combination of factors that produces acne. So, if there's a gene specifically for those factors, at this time, it would be known as “Androgen�. Androgens are what induces the development of sebum glands, thus sebum, skin cell proliferation (IGF-1 helps), and Hyperkertinization (IGF-1) that all help form a blocked pore where microorganisms are free to grow and possibly release inflammatory cytokines. Yet, just because you may have hyperandrogenisim, it doesn't guarantee that you'll have acne. Nope you may have, hirstuism, menstrual & fertility problems, obesity, rheumatoid arthritis, eczema, and/or even seborrhea..

So maybe a better way to look at this is in terms of having a Skin Androgen Receptor Defect. This is actually supposed to be the cause of acne for 90% of the cases (the others have serum hyperandrogenisim). In which case, you produce normal androgens, but once they reach your sebaceous glands, you start producing more DHT than normal. In this case, medications seem like the best option and this is probably why antiandrogen retinoids: topical (retina, azelex, isotrex) & oral (accutane), birth control, and spironolactone can get most people clear. Of course, altering your diet in order to reduce your Insulin production (or your inflammatory prostaglandins) will also reduce your overall sex hormone production. Through the use of diet you can reduce your hormones enough that the receptor defect doesn’t matter or in conjunction with prescription anti-androgens, you can block the additional formation or activity of DHT.

So I guess in that respect the receptor defect could be the genetic problem regarding acne formation and at that point there is some sort of trigger/switch (gene) that "decides" whether it should be expressed as androgenic alopecia, hirstuism, eczema, seborrhea, and/or acne. Yet, should we really be so focused on what it is, instead of WHY it is (all those other factors that preceded that decision)?

Regardless of WHAT participates in acne formation in the skin, if one has chronic health or hormonal problems that initiated the events leading to acne, that’s not going to go away just because something was used to suppress or maybe even fix the skins sensitivity to androgens. You will still be overproducing or underproducing something…. If not taken care of early enough (?) that something is capable of coming back and haunting us in the form of a NEW and probably worse health problem.

Myself and others tried “diet� several times before we hit the jackpot, yet my plight isn’t about convincing you or anyone else to do the same, especially if you don’t want to. This is about hopefully getting others to realize that acne isn’t some curse, that while there may be a gene at play, it’s NOT the “I was born to have acne all my life gene� and to also make others more aware of what their treatment options are. Since I read that you’ve had acne for 30 years (???) and have health problems, you are definitely a good candidate for altering your environmental influences. This just doesn’t mean diet or supplements, but also taking medications. So, do you mind sharing what exactly you did change diet & supplement wise? Also, I’m assuming you’ve been to an Endocrinologist and if so, what did you find out? If not, considering how you feel about your acne, why haven’t you gone?
These are not steps, but stages some people progress through when going from conventional to holistic medicine. Stage 2 is how I became 99%+ Clear, eliminated my dysmennorhea, significantly reduced my sebum & pore size, etc & is my predominant method.

Stage 1 (Treatment):
* (Daily) Isocare Skin Control Cleanser, Dream Products Customized Natural Face Lotion & Coppertone Sport Spray Sunscreen (mixed)
* (Sporadically) spot treat w/ anti-inflammatory (neosporin, hydrocortisone, salicylic acid) or a skin lightener (post-inflammatory pigmentation) to treat stubborn cystic/nodular acne that appears due to unknowingly or knowingly ingesting a food/ingredient that breaks me out (I do my best to avoid these foods). If you cover treated area w/ a bandaid, it makes product more effective.

Stage 2 (Prevention): "cheapest" method ~ Since Aug. 2002
* Follow a Gluten-Free, Trans-Fat Free, Dairy-Free and No Added Sugar diet for my Insulin Resistance/Hyperandrogenism (Silent Chronic Inflammatory Syndrome)
* Avoid ALL types of nuts and the Genus Prunus (almonds, plums, peaches, nectarines, apricots, cherries), Bananas, Pineapples, Cottonseed oil, Artificial Sweetners.

Stage 3 (Correction):
* 1/18/08 Ultimate Colon Cleanse (30 day program)

Research:
* Developing functional foods for those with acne & other special needs (assuming there's a defficiency).
* Developing good & "safe" formulas for various hormonal issues for women. Correction stage may resolve this for some.

#22 SweetJade1980

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Posted 25 October 2004 - 02:24 AM

Ooops, gotta back up what I say ;-)


Possible Explanations

A)
QUOTE
Clin Endocrinol Metab. 1986 May;15(2):341-62. Related Articles, Links 


Pilosebaceous physiology in relation to hirsutism and acne.

Rosenfield RL.

PSAs, with few exceptions, consist of a piliary and a sebaceous component. In androgen-sensitive areas, each has the capacity to develop into either a terminal hair follicle or a sebaceous follicle depending upon its location. Without androgen, there is no development of the sexual hair follicle or sebaceous gland. Androgens appear to promote sexual hair growth by recruiting a population of PSAs that have preset genetic sensitivity to initiate the production of terminal hairs. The site of action of androgens within the PSA is unclear. There are indications that androgens may act at more than one site in a system that requires two-way reciprocal interaction between dermal and epithelial cells for the generation of hair growth. Growth hormone appears to exert an important synergism with androgen in affecting the PSA, seemingly through the mediation of insulin-like growth factors. Hirsutism is due to an increased density of growing terminal hairs. The majority of cases of moderately severe hirsutism in women are due to hyperandrogenaemia, as are half the cases of mild hirsutism and about one-quarter of the cases of mild acne vulgaris. We advocate reserving the term idiopathic hirsutism or idiopathic acne for those patients in whom excessive growth of terminal hair or acne is not explained by androgen excess. We believe that highly variable sensitivity to androgen within the population explains both idiopathic hirsutism and cryptic hyperandrogenaemia; that is, these disorders lie at opposite ends of the normal spectrum of sensitivity to androgen. The biological basis for the variations in responsiveness of PSAs to androgens is unknown. The regression of hirsutism induced by antiandrogen treatment is characterized by the growth of hairs that are more vellus in character, i.e. smaller and less medullated.

http://www.ncbi.nlm....st_uids=2941189 ]



B)
QUOTE
Z Hautkr. 1978 Nov 1;53(21):759-65. Related Articles, Links 


[Dermatologic indications for anti-androgenic treatment]

[Article in German]

Zaun H, Ludwig E.

In spite of remarkable therapeutic results obtained by gestagens with antiandrogenic activity, usually combined with estrogen, in oily seborrhea, acne, Fox-Fordyce disease, androgenetic alopecia and hirsutism many dermatologist still hesitate to treat the named disorders by hormones. The reason for their hesitation appears to be the erroneous belief, that the named disturbances represent hormonal disorders the treatment of which does not belong to dermatology. After a survey on the mechanism of action of antiandrogens the basic difference between androgen dependent skin disorders and endocrinopathies with manifestation on the skin and its appendages is explained. Androgen dependent skin disorders, like oily seborrhea and most cases of acne are not the result of endocrine disturbances in the sense of an pathologically increased or decreased production of sexual hormons. Administering sexual hormons the physician takes advantage of the sebosuppressive effect of female sexual hormons as he does of the antiallergic activity of the hormon cortisol (and related compounds) in the treatment of eczemas. The antiandrogenic treatment of androgenetic alopecia, hirsutism and androgenetic acne--with their underlying hormonal disturbance, consisting in an increased production of androgens, represents an quasi etiological therapy. As in these cases the hormonal disturbances finds its expression mainly or exclusively in disorders of the skin or hair growth, the dermatologist, preferentially in cooperation with endocrinogists and/or gynacologists remains entitled to take over the treatment. The available drugs are discussed and suggestions are made for their appropriate use.

http://www.ncbi.nlm....list_uids=82309



C)
QUOTE
J Invest Dermatol. 2002 Dec;119(6):1317-22. Related Articles, Links 

 
The influence of genetics and environmental factors in the pathogenesis of acne: a twin study of acne in women.

Bataille V, Snieder H, MacGregor AJ, Sasieni P, Spector TD.

Twin Research and Genetic Epidemiology Unit, St Thomas' Hospital, London, UK. vbataille@twin-research.ac.uk

Acne is common and often leads to significant psychologic and physical morbidity. From clinical experience, acne appears to run in families; however, very few studies have investigated the genetic basis of this very common skin disease. A large twin study based on 458 pairs of monozygotic and 1099 pairs of dizygotic twins, all women with a mean age of 46 y was performed to investigate the relative contribution of genetic and environmental factors on the liability to acne. In addition, potential risk factors were assessed in twins with and without acne in a nested cross-sectional design. Fourteen percent of the twins reported a history of acne. Genetic modeling using acne scores showed that 81% (95% confidence interval 73-87%) of the variance of the disease was attributable to additive genetic effects. The remaining 19% was attributed to unique (i.e., unshared) environmental factors. Of the potential risk factors tested in 400 acne twins and 2414 unaffected twins, only apolipoprotein A1 serum levels were significantly lower in acne twins even after adjusting for age and weight. Family history of acne was also significantly associated with an increased risk. No significant differences were found between acne twins and nonacne twins for weight, body mass index, height, birth weight, hair thinning, reproductive factors as well as cholesterol, triglycerides, high-density lipoprotein, and glucose levels. The lower serum levels of apolipoprotein A1 in acne twins were also confirmed when analyzing acne discordant twin pairs. The evidence of a major genetic influence on acne should stimulate the search for potential genes that may lead to new therapeutic approaches.

http://www.ncbi.nlm....t_uids=12485434


Keep in mind that Apoplipoprotein A1 is a component of HDL. HDL is something this is found to be lower in people that have Insulin Resistance Syndrome, Heart Disease, etc. So while this shows a greater genetic contribution, reduction or avoidance of environmental factors that will further lower your HDL, thus raising your LDL (bad cholesterol), would also help.



D)
QUOTE
West Afr J Med. 2004 Jan-Mar;23(1):65-8. Related Articles, Links 

Pattern of skin surface lipids in some south-western Nigerians with acne vulgaris.
Ikaraocha CI, Taylor GO, Anetor JI, Onuegbu JA.

Department of Chemical Pathology, College of Medicine, University of Ibadan, Nigeria.

Unanswered questions still exist regarding pathophysiology of acne vulgaris generally and particularly in this environment. METHODS: Skin surface lipid (SSL) samples were collected by the heptane sponge technique from faces of 20 Nigerians with facial acne vulgaris and 25 controls. The subjects were classified into mild and moderately severe acne groups. Total cholesterol and triglycerides were determined and expressed in percentage (%) while Undetermined Skin Surface Lipids (USSL) (free fatty acids + squalene + wax ester + diglycerides) were computed. RESULTS: Triglycerides and total cholesterol levels were significantly higher in subjects with acne vulgaris compared with controls (p < 0.001 and p < 0.029 respectively). There was a progressively significant increase in triglycerides from control, though mild to moderately severe acne vulgaris subjects (P < 0.01) in all cases. In contrast there was a significant progressive decrease in USSL among the three groups (P < 0.001) in all cases. No significant difference was evident for all the values on comparison of female subjects with male subjects. There were however, significant increases in triglycerides and significant decreases in USSL levels for both male and female subjects with acne vulgaris compared with their respective controls (P < 0.02, P < 0.01, P < 0.03 and P < 0.014). CONCLUSION: Alterations in composition of SSL may in part be the pathophysiological basis of inflammatory acne vulgaris. Severity of the disorder appears to parallel triglyceride level but there was no association with sex. Triglycerides and total cholesterol levels are lower in SSL in this environment compared with hotter climates.
http://www.ncbi.nlm....t_uids=15171531


E)
QUOTE

Metabolism. 2001 May;50(5):505-11. Related Articles, Links 

Postprandial changes in sex hormones after meals of different composition.

Habito RC, Ball MJ.

School of Biomedical Sciences, University of Tasmania, Launcastor, Australia.

The postprandial effects of different meals on serum testosterone, serum sex hormone-binding globulin (SHBG), and free androgen index were sequentially evaluated in 15 healthy men. The isocaloric meals contained different proteins and different quantities and type of fat as a mixed meal. Four test meals were given to subjects in random order: a lean meat meal, a tofu meal (both containing approximately 20% energy from fat), and meat meals with added animal fat or safflower oil (both 54% energy from fat). Blood samples were obtained at baseline and at 2, 3, and 6 hours after each meal. There was a significant decrease in testosterone and free androgen index after both tofu and lean meat meals. The 2-hour serum testosterone and the decremental area under the curve were significantly more negative after the lean meat meal than the meat meal with added animal fat. The testosterone area under the curve was least for the high animal fat meal indicating little change from baseline. As men are postprandial for a significant proportion of the day, the lower sex hormone values after a low animal fat meal may provide long-term benefits in reducing the risk of diseases, such as prostate cancer, which appear to be sex hormone-dependent. Copyright 2001 by W.B. Saunders Company
http://www.ncbi.nlm....t_uids=11319710



F)
QUOTE
J Clin Endocrinol Metab. 2004 Aug;89(8):4053-61. Related Articles, Links 

 
Gender differences of adiponectin levels develop during the progression of puberty and are related to serum androgen levels.

Bottner A, Kratzsch J, Muller G, Kapellen TM, Bluher S, Keller E, Bluher M, Kiess W.

Research Laboratory, University Hospital for Children and Adolescents, University of Leipzig, Oststrasse 21-25, 04317 Leipzig, Germany. antje.boettner@medizin.uni-leipzig.de

Adiponectin is an adipocytokine with profound antidiabetic and antiatherogenic effects that is decreased in obesity. With the increasing prevalence of obesity and the emergence of related disorders, including type 2 diabetes in children, the regulation of adiponectin and its relationship to childhood obesity is of great interest. In this study we aimed to elucidate the impact of gender, pubertal development, and obesity on adiponectin levels in children. We investigated two phenotypically characterized cohorts of 200 normal weight and 135 obese children and adolescents covering a wide range of age (3.4-17.9 yr) and body mass index (-2.1 to +4.8 sd score). In healthy lean boys, adiponectin levels significantly declined in parallel with physical and pubertal development, subsequently leading to significantly reduced adiponectin levels in adolescent boys compared with girls (5.6 +/- 0.5 vs. 7.1 +/- 0.5 mg/liter; P = 0.03). This decline was inversely related to testosterone (r = -0.42; P < 0.0001) and dehydroepiandrosterone sulfate (r = -0.20; P = 0.0068) serum concentrations and may account for the gender differences seen in adults. Using a stepwise forward multiple regression model, pubertal stage was the strongest independent predictor of adiponectin (r(2) = 0.206; P < 0.0001), with additional influences of body mass index sd score and testosterone. Adiponectin levels were decreased in obese children and adolescents compared with lean peers of corresponding age and pubertal stage (5.18 vs. 7.13 mg/liter; P = 0.015). In obese children, adiponectin levels were closely associated with parameters related to the metabolic syndrome, such as insulin resistance, hyperinsulinemia, blood pressure, and uric acid, in univariate and multivariate analyses, with the insulin sensitivity index being the strongest independent parameter identified by stepwise forward multiple regression (r(2) = 0.226; P < 0.0001). Hence, there is a strong association of adiponectin serum concentrations with obesity, pubertal development, and metabolic parameters in children indicating epidemiological and pathophysiological relevance already in childhood.
http://www.ncbi.nlm....t_uids=15292348





These are not steps, but stages some people progress through when going from conventional to holistic medicine. Stage 2 is how I became 99%+ Clear, eliminated my dysmennorhea, significantly reduced my sebum & pore size, etc & is my predominant method.

Stage 1 (Treatment):
* (Daily) Isocare Skin Control Cleanser, Dream Products Customized Natural Face Lotion & Coppertone Sport Spray Sunscreen (mixed)
* (Sporadically) spot treat w/ anti-inflammatory (neosporin, hydrocortisone, salicylic acid) or a skin lightener (post-inflammatory pigmentation) to treat stubborn cystic/nodular acne that appears due to unknowingly or knowingly ingesting a food/ingredient that breaks me out (I do my best to avoid these foods). If you cover treated area w/ a bandaid, it makes product more effective.

Stage 2 (Prevention): "cheapest" method ~ Since Aug. 2002
* Follow a Gluten-Free, Trans-Fat Free, Dairy-Free and No Added Sugar diet for my Insulin Resistance/Hyperandrogenism (Silent Chronic Inflammatory Syndrome)
* Avoid ALL types of nuts and the Genus Prunus (almonds, plums, peaches, nectarines, apricots, cherries), Bananas, Pineapples, Cottonseed oil, Artificial Sweetners.

Stage 3 (Correction):
* 1/18/08 Ultimate Colon Cleanse (30 day program)

Research:
* Developing functional foods for those with acne & other special needs (assuming there's a defficiency).
* Developing good & "safe" formulas for various hormonal issues for women. Correction stage may resolve this for some.

#23 SweetJade1980

SweetJade1980

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Posted 25 October 2004 - 02:37 AM

Other Conditions (just a few):


A)
QUOTE
Int J Epidemiol. 1993 Dec;22(6):1000-9. Related Articles, Links 


Erratum in:
Int J Epidemiol 1994 Dec;23(6):1330.

The influence of medical conditions associated with hormones on the risk of breast cancer.

Moseson M, Koenig KL, Shore RE, Pasternack BS.

Department of Environmental Medicine, NYU Medical Center, NY 10010-2598.

Medical conditions related to hormonal abnormalities were investigated in a case-control study of breast cancer among women who attended a screening centre. Information was obtained by telephone interview regarding physician-diagnosed medical conditions such as thyroid or liver diseases, diabetes, and hypertension, as well as hirsutism, acne, galactorrhoea, and reproductive, menstrual, and gynaecological factors. Results are presented for 354 cases and 747 controls. Women with fertility problems who never succeeded in becoming pregnant were at significantly increased breast cancer risk (adjusted odds ratio [OR] = 3.5; 95% confidence interval [CI]:1.1-10.9). An elevated cancer risk was also associated with having excess body hair (OR = 1.5; 95% CI:1.0-2.3), or having excess body hair in addition to persistent adult acne (OR = 6.8; 95% CI:1.7-27.1). Recurrent amenorrhea (OR = 3.5; 95% CI:1.1-11.5), and a treated hyperthyroid condition (OR = 2.2; 95% CI:1.1-4.4) were significantly associated with risk. A non-significant elevation of risk was present for endometrial hyperplasia (OR = 1.8; 95% CI: 0.8-4.0). There was a suggestion of an association between a history of galactorrhoea and breast cancer risk (OR = 2.0; 95% CI:0.8-4.9) among premenopausal women. No associations were found with other medical or gynaecological factors. The possibility that some of these findings are due to chance cannot be excluded because of the problem of multiple comparisons
http://www.ncbi.nlm....st_uids=8144280



B)
QUOTE
J Endocrinol Invest. 2001 Sep;24(8):628-38. Related Articles, Links 


Skin disorders and thyroid diseases.

Niepomniszcze H, Amad RH.

Division of Endocrinology, Hospital de Clinicas Jose de San Martin, University of Buenos Aires, Argentina. hniepom@elsitio.net

Thyroid disorders have a high prevalence in medical practice; they are associated with a wide range of diseases with which they may or may not share etiological factors. One of the organs which best show this wide range of clinical signs is the skin. This review is an attempt to approach most of the dermopathies reflecting several degrees of harmfulness, coming directly or indirectly from thyroid abnormalities, as well as to update current knowledge on the relationship between the thyroid and skin. We have proposed a primary classification of skin disorders, regarding thyroid involvement, into two main groups: 1) dermopathies associated with thyroid abnormalities, mainly with autoimmune thyroid diseases, like melasma, vitiligo, Sjogren's syndrome, alopecia, idiopathic hirsutism, pre-menstrual acne, bullous diseases, connective tissue diseases, hamartoma syndrome, atopy, leprosy and DiGeorge anomaly; and 2) dermopathies depending on the nature of the thyroid disorder, in which the evolution and outcome of the skin disorder depend on the thyroidal treatment in most cases, such as trophism and skin blood flow, myxedema, alopecia, onychodystrophy, hypo- and hyperhidrosis, xanthomas, intraepidermal bullae, carotenodermia, pruritus, flushing, pyodermitis, palmoplantar keratoderma, ecchymosis, etc. In some other cases, the skin disease which developed as a consequence of the thyroid abnormality can remain unaltered despite functional treatment of the thyroid problem, such as pretibial myxedema, thyroid acropachy and some cutaneous manifestations of multiple endocrine neoplasia types 2A and 2B.
http://www.ncbi.nlm....t_uids=11686547



C)
QUOTE
Br J Dermatol. 2003 Jun;148(6):1263-6. Related Articles, Links 

 
Congenital adrenal hyperplasia and acne in male patients.

Degitz K, Placzek M, Arnold B, Schmidt H, Plewig G.

Department of Dermatology, Ludwig-Maximilian-University, Munchen, Germany. klaus.degitz@lrz.uni-muenchen.de

Seborrhoea is one pathogenic factor for acne. Androgens induce sebum production, and excess androgen may provoke or aggravate acne. In women an androgen disorder is frequently suspected when acne is accompanied by hirsutism or menstrual irregularities. In men acne may be the only symptom of androgen excess. We report three male acne patients in whom hormonal screening revealed irregularities of androgen metabolism suggestive of late-onset congenital adrenal hyperplasia and who benefitted from low-dose glucocorticoids. Disorders of androgen metabolism may influence acne not only in women, but also in men, and these patients may benefit from low-dose glucocorticoid therapy.
http://www.ncbi.nlm....t_uids=12828760



D)
QUOTE
Am J Clin Dermatol. 2003;4(5):315-31. Related Articles, Links 


Cutaneous manifestations of endocrine disorders: a guide for dermatologists.

Jabbour SA.

Division of Endocrinology, Diabetes and Metabolism, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. serge.jabbour@mail.tju.edu

Dermatologists may commonly see skin lesions that reflect an underlying endocrine disorder. Identifying the endocrinopathy is very important, so that patients can receive corrective rather than symptomatic treatment. Skin diseases with underlying endocrine pathology include: thyrotoxicosis; hypothyroidism; Cushing syndrome; Addison disease; acromegaly; hyperandrogenism; hypopituitarism; primary hyperparathyroidism; hypoparathyroidism; pseudohypoparathyroidism and manifestations of diabetes mellitus. Thyrotoxicosis may lead to multiple cutaneous manifestations, including hair loss, pretibial myxedema, onycholysis and acropachy. In patients with hypothyroidism, there is hair loss, the skin is cold and pale, with myxedematous changes, mainly in the hands and in the periorbital region.The striking features of Cushing syndrome are centripetal obesity, moon facies, buffalo hump, supraclavicular fat pads, and abdominal striae. In Addison disease, the skin is hyperpigmented, mostly on the face, neck and back of the hands.Virtually all patients with acromegaly have acral and soft tissue overgrowth, with characteristic findings, like macrognathia and enlarged hands and feet. The skin is thickened, and facial features are coarser.Conditions leading to hyperandrogenism in females present as acne, hirsutism and signs of virilization (temporal balding, clitoromegaly).A prominent feature of hypopituitarism is a pallor of the skin with a yellowish tinge. The skin is also thinner, resulting in fine wrinkling around the eyes and mouth, making the patient look older.Primary hyperparathyroidism is rarely associated with pruritus and chronic urticaria. In hypoparathyroidism, the skin is dry, scaly and puffy. Nails become brittle and hair is coarse and sparse. Pseudohypoparathyroidism may have a special somatic phenotype known as Albright osteodystrophy. This consists of short stature, short neck, brachydactyly and subcutaneous calcifications.Some of the cutaneous manifestations of diabetes mellitus include necrobiosis lipoidica diabeticorum, diabetic dermopathy, scleredema adultorum and acanthosis nigricans.
http://www.ncbi.nlm....t_uids=12688837



E)
QUOTE
J Clin Endocrinol Metab. 2004 Feb;89(2):453-62. Related Articles, Links 

 
Androgen excess in women: experience with over 1000 consecutive patients.

Azziz R, Sanchez LA, Knochenhauer ES, Moran C, Lazenby J, Stephens KC, Taylor K, Boots LR.

Departments of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, Alabama 35233, USA. azzizr@cshs.org

The objective of the present study was to estimate the prevalence of the different pathological conditions causing clinically evident androgen excess and to document the degree of long-term success of suppressive and/or antiandrogen hormonal therapy in a large consecutive population of patients. All patients presenting for evaluation of symptoms potentially related to androgen excess between October 1987 and June 2002 were evaluated, and the data were maintained prospectively in a computerized database. For the assessment of therapeutic response, a retrospective review of the medical chart was performed, after the exclusion of those patients seeking fertility therapy only, or with inadequate follow-up or poor compliance. A total of 1281 consecutive patients were seen during the study period. Excluded from analysis were 408 patients in whom we were unable to evaluate hormonal status, determine ovulatory status, or find any evidence of androgen excess. In the remaining population of 873 patients, the unbiased prevalence of androgen-secreting neoplasms was 0.2%, 21-hydroxylase-deficient classic adrenal hyperplasia (CAH) was 0.6%, 21-hydroxylase-deficient nonclassic adrenal hyperplasia (NCAH) was 1.6%, hyperandrogenic insulin-resistant acanthosis nigricans (HAIRAN) syndrome was 3.1%, idiopathic hirsutism was 4.7%, and polycystic ovary syndrome (PCOS) was 82.0%. Fifty-nine (6.75%) patients had elevated androgen levels and hirsutism but normal ovulation. A total of 257 patients were included in the assessment of the response to hormonal therapy. The mean duration of follow-up was 33.5 months (range, 6-155). Hirsutism improved in 86%, menstrual dysfunction in 80%, acne in 81%, and hair loss in 33% of patients. The major side effects noted were irregular vaginal bleeding (16.1%), nausea (13.0%), and headaches (12.6%); only 36.6% of patients never complained of side effects. In this large study of consecutive patients presenting with clinically evident androgen excess, specific identifiable disorders (NCAH, CAH, HAIRAN syndrome, and androgen-secreting neoplasms) were observed in approximately 7% of subjects, whereas functional androgen excess, principally PCOS, was observed in the remainder. Hirsutism, menstrual dysfunction, or acne, but not alopecia, improved in the majority of patients treated with a combination suppressive therapy; although more than 60% experienced side effects.

http://www.ncbi.nlm....t_uids=14764747



F)
QUOTE
Comp Biochem Physiol A Mol Integr Physiol. 2003 Sep;136(1):95-112. Related Articles, Links 

 
Hyperinsulinemic diseases of civilization: more than just Syndrome X.

Cordain L, Eades MR, Eades MD.

Department of Health and Exercise Science, Colorado State University, Fort Collins, CO 80523, USA. cordain@cahs.colostate.edu

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 http://www.ncbi.nlm....t_uids=14527633



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QUOTE
ScientificWorldJournal. 2004 Jul 08;4:507-11. Related Articles, Links 

Clinical profiles, occurrence, and management of adolescent patients with HAIR-AN syndrome.

Omar HA, Logsdon S, Richards J.

Section of Adolescent Medicine, Department of Pediatrics, University of Kentucky, Lexington, KY 40536-0284, USA. haomar2@uky.edu

The syndrome of hyperandrogenism, insulin resistance, and acanthosis nigricans (HAIR-AN) is a subphenotype of the polycystic ovary syndrome. It is one of the most common causes of menstrual problems, hyperandrogenic symptoms, and insulin resistance among young women. Review of clinical data in an outpatient adolescent clinic showed that of the 1,002 young women (ages 10-21 years) attending the clinic over a 2-year period, 50 (5%) were diagnosed with HAIR-AN syndrome. Mean age of the patients was 15.5, initial mean weight at diagnosis was 94.5 kg, and the mean BMI was 33.33 kg/m2. Patients were treated with a weight-stabilization and -reduction program, oral contraceptive pills, and in most cases metformin. Of the patients, 80% were compliant with the follow-up and treatment regimen, 60% maintained or reduced their weight, 95% had regular menstrual cycles, and in most patients, the acne and/or hirsutism were the same or better than at the start of treatment. We conclude that HAIR-AN syndrome is a common disease in young women and multifaceted, aggressive treatment appears to be effective in reducing the severity of symptoms and preventing further consequences. http://www.ncbi.nlm....t_uids=15258677


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QUOTE
Obes Rev. 2002 Nov;3(4):303-8. Related Articles, Links 

 
Prostate cancer: another aspect of the insulin-resistance syndrome?
Barnard RJ, Aronson WJ, Tymchuk CN, Ngo TH.

jbarnard@physci.ucla.edu

Insulin resistance and compensatory hyperinsulinaemia are thought to be the underlying factors in the metabolic or insulin-resistance syndrome and can be controlled by diet and exercise. Hyperinsulinaemia has been shown to have a direct effect on the live, suppressing the production of sex hormone-binding globulin (SHBG) and insulin-like growth factor-binding proteins 1 and 2 (IGFBP-1, -2) while stimulating the production of insulin-like growth factor 1 (IGF-1). These factors have been proposed to be important modulators of hormone-related cancers, such as prostate cancer. Men adopting a low-fat diet and daily exercise reduced their levels of serum insulin and IGF-1, while increasing their levels of IGFBP-1 and sex hormone-binding globulin (SHBG). Cell-culture studies with LNCaP prostate cancer cells showed apoptosis of tumour cells and a reduction in serum-stimulated cell growth in the post diet and exercise serum. These results suggest that prostate cancer may be another aspect of the insulin-resistance syndrome and that adopting a low-fat diet combined with regular exercise may reduce the risk for prostate and other hormone-related cancers. This needs to be tested with prospective studies. http://www.ncbi.nlm....t_uids=12458975

These are not steps, but stages some people progress through when going from conventional to holistic medicine. Stage 2 is how I became 99%+ Clear, eliminated my dysmennorhea, significantly reduced my sebum & pore size, etc & is my predominant method.

Stage 1 (Treatment):
* (Daily) Isocare Skin Control Cleanser, Dream Products Customized Natural Face Lotion & Coppertone Sport Spray Sunscreen (mixed)
* (Sporadically) spot treat w/ anti-inflammatory (neosporin, hydrocortisone, salicylic acid) or a skin lightener (post-inflammatory pigmentation) to treat stubborn cystic/nodular acne that appears due to unknowingly or knowingly ingesting a food/ingredient that breaks me out (I do my best to avoid these foods). If you cover treated area w/ a bandaid, it makes product more effective.

Stage 2 (Prevention): "cheapest" method ~ Since Aug. 2002
* Follow a Gluten-Free, Trans-Fat Free, Dairy-Free and No Added Sugar diet for my Insulin Resistance/Hyperandrogenism (Silent Chronic Inflammatory Syndrome)
* Avoid ALL types of nuts and the Genus Prunus (almonds, plums, peaches, nectarines, apricots, cherries), Bananas, Pineapples, Cottonseed oil, Artificial Sweetners.

Stage 3 (Correction):
* 1/18/08 Ultimate Colon Cleanse (30 day program)

Research:
* Developing functional foods for those with acne & other special needs (assuming there's a defficiency).
* Developing good & "safe" formulas for various hormonal issues for women. Correction stage may resolve this for some.

#24 Ben16

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Posted 25 October 2004 - 06:46 AM

The reason why people act so ignorant on the acne food matter is simply because they can not handle the fact that in the end, a drastic change must be done in order to clear up completely.They'd rather spend money on moisturizers, cleansers, soaps instead of actually going to the health food store for some organic veggies, fruits or even supplements. So instead of pitying yourself, go on a DIET FOR A FEW WEEKS AND LEAVE OUT ALL TOPICALS and come back with your results. Sorry, I'm just a bit frustrated about how stupid people can be. Just because your doctor or your derm says CHOCOLATE DOES NOT CAUSE ACNE DOES NOT MEAN HE'S RIGHT.Do your own research or even ask SJ for help and you'll discover so many new things, overwhelming at first but pieces by pieces you'll come to realize what a fool you been for not believing any acne food related messages.
"We are not enemies, but friends. We must not be enemies. Though passion may have strained, it must not break our bonds of affection. The mystic cords of memory will swell when again touched as surely they will be by the better angels of our nature."

#25 apple49

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Posted 26 October 2004 - 10:39 PM

Without a long treatise, I have had tests and tests between 1998 and 2001. My hormones are right as rain.During my three year medical saga where I nearly died twice, I had so much misinformation from well meaning friends, coworkers, and family.I will take a doctor over self diagnosis any day. If I would have tried to heal my medical problems through diets and not surgery and medicines I would not be here to debate with all of you.With acne, do what works,and for some diet isn't going to get the results while other methods can. For me, topical mandelic acid is the key, and I'm looking great.

#26 BenKweller

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Posted 26 October 2004 - 11:57 PM

We aren't against diet/acne connections because we're afraid of change. We're against it because people like you turn everyone with a few zits into paranoid animals regulating every calorie they intake.

#27 SweetJade1980

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Posted 27 October 2004 - 08:26 AM

Apple,
Oh wow, I love hearing stuff like that. I'm glad mandelic acid worked for you. I keep hearing about it and Maya loves this stuff, but I've yet to try it. Just because the right dietary changes worked for me, I'm still susceptible to the "wrong" skin care products. So when I hear the words "marine complex" I get a bit concerned and since there's no ingredient list anywhere (emailed nucelle last night), I won't purchase products without knowing what's in it first.

My main interest is in finding a gentle exfoilant that will help with what's left of my hyperpigmentation and I've heard it's good for this, yet did you have an initial breakout like they say??? Anyway, I also discovered that it's not just a gentle exfoilant but it's also an antibiotic so now wonder it's so good for acne. I'll definately add it to my topical suggestion list.

Thanxs
These are not steps, but stages some people progress through when going from conventional to holistic medicine. Stage 2 is how I became 99%+ Clear, eliminated my dysmennorhea, significantly reduced my sebum & pore size, etc & is my predominant method.

Stage 1 (Treatment):
* (Daily) Isocare Skin Control Cleanser, Dream Products Customized Natural Face Lotion & Coppertone Sport Spray Sunscreen (mixed)
* (Sporadically) spot treat w/ anti-inflammatory (neosporin, hydrocortisone, salicylic acid) or a skin lightener (post-inflammatory pigmentation) to treat stubborn cystic/nodular acne that appears due to unknowingly or knowingly ingesting a food/ingredient that breaks me out (I do my best to avoid these foods). If you cover treated area w/ a bandaid, it makes product more effective.

Stage 2 (Prevention): "cheapest" method ~ Since Aug. 2002
* Follow a Gluten-Free, Trans-Fat Free, Dairy-Free and No Added Sugar diet for my Insulin Resistance/Hyperandrogenism (Silent Chronic Inflammatory Syndrome)
* Avoid ALL types of nuts and the Genus Prunus (almonds, plums, peaches, nectarines, apricots, cherries), Bananas, Pineapples, Cottonseed oil, Artificial Sweetners.

Stage 3 (Correction):
* 1/18/08 Ultimate Colon Cleanse (30 day program)

Research:
* Developing functional foods for those with acne & other special needs (assuming there's a defficiency).
* Developing good & "safe" formulas for various hormonal issues for women. Correction stage may resolve this for some.

#28 blackbirdbeatle

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Posted 27 October 2004 - 09:31 AM

I haven't looked for a while but when I did there were two mandelic brands, both the same strength. One didn't have all that marine stuff that was breaking everyone out.

#29 apple49

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Posted 27 October 2004 - 11:20 AM

I did not have an initial breakout with Nucelle.I saw on acnebook.com that Dr. Fulton has a mandelic acid serum also.He also advocates BP cleanser with mandelic acid.Fulton's serum is a bit more expensive and he only has the 15% strength, which is pretty potent.Even with my pretty tough skin, I alternate between 10% in the am and 15% at night.There is a gal I have spoken to at Nucelle, Charlene Poitras, who is very helpful. Her number is (800) 877-3131.