Sugar-acne is true?

[SweetJade1]

I'm really tired, but I thought I'd start of this little debate with examples of skin disorders that aren't purely cosmetic, genetic or fungal based:

Skinmed. 2004 Mar-Apr;3(2):83-91. Related Articles, Links


Comment in:
Skinmed. 2004 Mar-Apr;3(2):73-4.

Foods, diet, and skin diseases.

Lo Schiavo A, Aurilia A, Guerrera V.

Department of Dermatology, School of Medicine and Surgery, Second University of Naples, Via S. Pansini no. 5, 80131 Naples, Italy.

Human skin is continuously exposed to internal and external influences that may alter its condition and functioning. As a consequence, the skin may undergo alterations leading to immune dysfunction, imbalanced epidermal homeostasis, or other skin disorders. New theories are developing that link food intake and health. The objective of this review is to evaluate current knowledge about the interrelation of food and skin, particularly the effect of nutrients on some cutaneous immune disorders and therapeutic actions of nutrients in skin disorders.

[url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15010633[/url]

[url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11994143[/url]

MMW Munch Med Wochenschr. 1976 Feb 6;118(6):155-60. Related Articles, Links


[The problem of vitamin B6/B12 acne. A contribution on acne medicamentosa (author's transl)]

[Article in German]

Braun-Falco O, Lincke H.

Deterioration of acne vulgaris or eruption of an acneiform exanthema could be established during treatment with vitamin B6 and/or vitamin B12 in 14 patients. Females were by far the more frequently affected. The appearance of skin symptoms, even outside the age groups typically affected by acne vulgaris is characteristic. The clinical appearance of acneiform exanthema occurring during treatment with vitamin B6 or B12 consists of loosely disseminated small papules or papulopustules on the face (especially on the forehead and chin), on the upper parts of the back and chest and spreading to the upper arm. The pathogensis of the change is not yet certain. The acneiform rash generally fades within a short time after vitamin B6 or vitamin B12 treatment has been stopped.

[url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=130553[/url]

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, Phila******a, Pennsylvania 19107, USA.

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..

[url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12688837[/url]

Those in bold are the ones that I'm aware of that can have acne as a symptom.

Horm Res. 2000;54(5-6):230-42. Related Articles, Links


Human skin: an independent peripheral endocrine organ.

Zouboulis CC.

Department of Dermatology, University Medical Center Benjamin Franklin, The Free University of Berlin, Berlin, Germany.

The historical picture of the endocrine system as a set of discrete hormone-producing organs has been substituted by organs regarded as organized communities in which the cells emit, receive and coordinate molecular signals from established endocrine organs, other distant sources, their neighbors, and themselves. In this wide sense, the human skin and its tissues are targets as well as producers of hormones. Although the role of hormones in the development of human skin and its capacity to produce and release hormones are well established, little attention has been drawn to the ability of human skin to fulfil the requirements of a classic endocrine organ. Indeed, human skin cells produce insulin-like growth factors and -binding proteins, propiomelanocortin derivatives, catecholamines, steroid hormones and vitamin D from cholesterol, retinoids from diet carotenoids, and eicosanoids from fatty acids. Hormones exert their biological effects on the skin through interaction with high-affinity receptors, such as receptors for peptide hormones, neurotransmitters, steroid hormones and thyroid hormones. In addition, the human skin is able to metabolize hormones and to activate and inactivate them. These steps are overtaken in most cases by different skin cell populations in a coordinated way indicating the endocrine autonomy of the skin. Characteristic examples are the metabolic pathways of the corticotropin-releasing hormone/propiomelanocortin axis, steroidogenesis, vitamin D, and retinoids. Hormones exhibit a wide range of biological activities on the skin, with major effects caused by growth hormone/insulin-like growth factor-1, neuropeptides, sex steroids, glucocorticoids, retinoids, vitamin D, peroxisome proliferator-activated receptor ligands, and eicosanoids. At last, human skin produces hormones which are released in the circulation and are important for functions of the entire organism, such as sex hormones, especially in aged individuals, and insulin-like growth factor-binding proteins. Therefore, the human skin fulfils all requirements for being the largest, independent peripheral endocrine organ. Copyright 2001 S. Karger AG, Basel

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11595811

Suggestion: Look up the keywords in there, particularly those bolded in relation to diet as well as the topicals & prescription drugs used to treat or cure acne and tell me if there isn't a connection.

J Assoc Physicians India. 1994 Jul;42(7):529-30. Related Articles, Links


Endocrine profiles in six patients with acanthosis nigricans.

Kapasi A, Varthakavi PK, Khopkar U, Wadhwa SL, Nihalani KD.

Department of Dermatology, TN Medical College & B Y L Nair Charitable Hospital, Bombay.

Six women (age range 17-38 years), who presented to the dermatology services with biopsy-proven acanthosis nigricans of variable duration were evaluated to rule out endocrine diseases. Menstrual abnormalities (5/6 patients), pallid striae (4/6 patients), hirsutism (4/6 patients) and acne vulgaris (2/6 patients) were found on physical examination. All the patients had body mass indices in the obese (> 27 kg/m2) range, and in association we found ovarian hyperthecosis, PCOD, premature ovarian failure, glucose intolerance and hyperprolactinaemia in the above six patients. The importance of appropriate endocrinal evaluation in patients with biopsy-proven acanthosis nigricans is emphasized

[SweetJade1]

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.

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.

[url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11686547[/url]

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.

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.

[url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14764747[/url]

Again, those in bold are disorders that I'm aware of that can have acne as a symptom.

Ann Dermatol Venereol. 1999 Jan;126(1):17-9. Related Articles, Links


Comment in:
Ann Dermatol Venereol. 1999 Jan;126(1):9-10.

[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.

[url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10095884[/url]

Lancet. 1999 Aug 28;354(9180):739-40. Related Articles, Links


Acne fulminans in late-onset congenital adrenal hyperplasia.

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

Acne may be the only clinical sign of androgen excess in men. We report a boy with acne fulminans and androgen excess due to late-onset congenital adrenal hyperplasia.

[url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10475188[/url]

Late-onset congenital adrenal hyperplasia (LOCAH) is the same as Non-classical congenital adrenal hyperlasia (NCCAH) and there's actually 5 possible enzyme defects for this!

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 60637-1470, USA. [email]ddeplews@peds.bsd.uchicago.edu[/email]

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.

[url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10950157[/url]

FYI: This is just so you can understand a bit more how complicated the pathway is for the development of acne. Sometimes all one needs is to intercept one of these and the problem is solved. Do you know how many of these are affected by one's diet?


Considering that the Diet-Acne connection is a bit less straightforward and needs to be pieced together with the knowledge of how the human body & diet work together to influence acne formation in order to see it, I'll stop here. I will not repeatedly piece this together again for someone that probably doesn't even care, but if you do care to see those studies & explanations, try a search under my name.

Nighty night.

[Zenfish]

.

Thanks.

But what I really want to know is, if I eat too much of something that influences a bunch of those internal biological/chemical reactions, will I aggravate my acne? Yes, or No?

.

[SweetJade1]

Originally Posted by Zenfish

.

Thanks.

But what I really want to know is, if I eat too much of something that influences a bunch of those internal biological/chemical reactions, will I aggravate my acne? Yes, or No?

.

All of that wasn't for you, but yes. =) You alrealdy know this based on your experiences here vs. in Japan, so why aren't you assured by that? In fact, you explained it beautifully right here:

Saying "sugar does not cause acne," is like saying "gasoline does not cause mobility." True, by itself sugar does not cause acne, nor does gasoline cause mobility.

But put sugar into your body, where it interacts with and disrupts your hormones, causes chemical imbalances and stress, and you definitely get acne. But sugar alone doesn't cause it.

It's true, sugar alone doesn't cause acne, ask any Type I Diabetic. These individuals have way too much sugar in their blood stream, due to lacking in (enough) Insulin, which is the pro-hormone that's giving some of us that follow these diets problems (others its food allergies or food intolerances or combination) a variety of issues (hyperandrogenism, increased inflammtoary products, hyperkeritinization). If you do study the chemistry of a Type I Diabetic, you'll see how likely it really is that it's micoorganisms that causing your acne as well.

Of course micoorganisms can contribute, but when you actually think about why there's an overgrowth of naturally occuring micoorganisms on your skin, its usually becase they are trapped in a clogged pore. It the pore wasn't clogged, they wouldn't be overgrowing and possibly contributing to the problem by further irritating our skin. A Type I Diabetic, before they're diagnosed, doesn't even make enough growth hormones, androgens, etc to develop normally sometimes, notice that they are thin and not usually overwieght, so they don't have enough of the neccessary products to produce the reactions neccessary for acne to develop. That's not to say that no one with Type I Diabetes has acne, it's just that they are far less likely to have it then someone that is a Type II Diabetic or Insulin Resistant (regarding glucose intolerance issues).

You know this and when the time come for your daughter, the sooner the better for her, you will teach her I'm sure. If not, I guess it's just what young people do. Acne started for me when I was 10 and by the time I was 12 I was seeking out natural solutions. Never could get it right, despite dietary changes (avoided soda & chocolate for 10 years), because the doctors hadn't diagnosed me yet (HAIR-AN synderome subtype of PCOS). Once I got the diagnosis (at 20) I still didn't understand why I should follow a low or moderate carb diet as I was already thin and wanted to gain weight not loose it. I thought taking the medication (avandia) would solve my problem, but it was only a bit more effective than birth control was. That's when I started reading more and more into the diets of an acne sufferer on these boards and why things like bread can cause acne for us. I swiched my diet before I fully understood it and since then I have learned how the diets we eat have a HUGE involvement in the development of acne, as well as other "preventable" diseases on the rise today such as Type II Diabetes (90% of cases), Obesity, Hyperlipidemia, and even certan cancers.

With health care costs rising along with the rate of "preventable" health problems, we are all much wiser to do what we can through diet, exercise, and proper sleep (all can contribute to or increase insulin resistance) habits as it will cost us far too much in the long run if we do not. Thankfully, you figured this out and I wish you the best with your helping your daughter through this. ;-)

[yelps]

So now we learn that acne is a complicated interaction of gland functions and hormones. To conclude that diet is the aggravating factor is not accurate.