Posted 29 March 2012 - 03:14 PM
Posted 30 March 2012 - 09:18 AM
i thought raw was healthy.
Try to understand this. It applies to most things in life. Very few things are black and white, all or nothing.
And if you are planning on eating all raw, then you better learn which foods you cannot eat raw because they contain toxins.
Edited by alternativista, 30 March 2012 - 09:20 AM.
Posted 08 April 2012 - 01:14 PM
It looks like a pretty good blog on nutrients and health.
And in those mice/rat studies, they found that resveratrol and/or the sirtuin enzyme promote energy/stamina and fat loss. The mice on resveratrol where much faster on the treadmill and more active on the wheel than those that weren't. Even when they fattened the mice up before starting the resveratol. And of course, resveratrol mice were thinner and fitter than the non-resveratrol mice.
This is a polyphenol, one of the most fascinating and most studied, due to its ability to mimic caloric-restriction (CR) through the sirtuin pathway [[/font][/color]5,6] and by stimulating AMP kinase [7,8]. Sirtuins are a class of proteins that may have been evolutionarily conserved in order to protect life during challenging times .
Caloric restriction itself is mediated through the sirtuin pathway. Sirtuin overexpression increases lifespan, in flies, mice, and nematodes. In nematodes, and flies, the sirtuin of relevance is SIR2, but in humans the equivalent, or orthologue, is SIRT1. Resveratrol indirectly activates sirtuins. When animals without the sirtuin protein are given resveratrol, or caloric restriction regimens, their lifespans do not increase. When resveratrol is combined with caloric restriction, no extra effect is seen, because the protein cannot be expressed anymore , whereas if they occurred via two independent pathways some synergistic effect may have been seen. If you want the awesome details, check out this article and this one.
Other chemicals such as the flavonoid quercetin also stimulate SIRT1, although about 2.5 times less with quercetin. This compound is found in dark berries such as blueberries and bilberries, so probably is found in mulberries as well, in addition to in black and green tea, apples, tomatoes, red onions, and many other plants. This flavonoid is just another reason why fruit and vegetables are good for ya.
It is difficult to tell how much of these compounds is needed to see a significant effect on lifespan though. First of all, these scientists use a single chemical. The chemical in addition to the whole food will probably have a more significant effect on the independent variable than just the single chemical. It's a complete fallacy when you hear people say, "oh well you need X g of this to see a clinically relevant benefit, and you only get Y g in the food." Too bad the whole food is not studied often, or ever, to validate a statement like that.
Also it's not easy to come up with a way to detect how much of these proteins are being acetylated or what not. The first study I talked about just studies one pathway of life extension, when there are other mediators, such as AMP kinase (AMPK).
There does seem to be evidence though that even at low doses, resveratrol has the ability to ward of some cancers. I think David Sinclair (one of the leading researcherson sirtuins, along with his former mentor Guarente) and Joseph Baur summed it up well in this review article: 
"The efficacy of low doses (for example, 200 g per kg (body weight) daily in a rat model of colon carcinogenesis15) suggests that even the concentration of resveratrol obtained from dietary sources, such as red wine, could be therapeutic in some cases. At higher, but pharmacologically achievable doses, protective effects of resveratrol are more frequently observed, and the results are more dramatic. For example, a daily dose of 40 mg per kg (body weight) increased the survival of mice with subcutaneous neuroblastomas from 0% to 70%16. Although most in vivo studies strongly support a chemopreventive effect of resveratrol, there are notable exceptions in which no benefit has been observed. For example, administration of 1–5 mg per kg (body weight) daily of resveratrol failed to affect the growth or metastasis of breast cancer in mice, despite promising in vitro results17. Dosage, delivery method, tumour origin and other components of the diet could all contribute to the efficacy of resveratrol treatment."
Resveratrol, who we'll nickname Rtrol (are-trol) is cardioprotective , neuroprotective , due to activation of AMPK, and burns fat  from SIR2 activation, which we talked about earlier being essential for producing lifespan extension.
From here with sources:
Red Wine and Red Grapes
Red wine contains high amounts of resveratrol, depending on the grape. The resveratrol is found in the grape skins. This is why white wine has less resveratrol than red wine - because red wine is fermented with the skins and white wine is not. An ounce of red wine may contain as much as 1,000 micrograms of resveratrol.[/left][/size][/font][/color]
Peanuts and Peanut Butter
Peanuts and peanut butter are a great source of resveratrol.[/left][/size][/font][/color]
Cocoa Powder and Dark Chocolate
Cocoa powder and dark chocolate have the second highest amount of resveratrol after red wine.
The mulberry fruit is a good source of resveratrol. There are resveratrol supplements available that contain this fruit. Mulberries are also sold dried in many health food stores.[/left][/size][/font][/color]
Blueberries are also a great source of resveratrol. Eat them after dinner alongside some dark chocolate and you'll have a healthy, resveratrol rich dessert![/left][/size][/font][/color]
Note: mulberries might be growing as weedy trees and shrubs near you. Especially near waterways. And they ripen early, before other berries. I've been picking tons since discovering them along the bayou where I walk my dog. Funny I'd never heard of them except in that nursery rhyme or song until last year. And now I discover they are everywhere.
And I've been wondering about Grappa - a liquor made from the grape skins left over from wine making.
Edited by alternativista, 09 April 2012 - 08:10 AM.
Posted 10 April 2012 - 08:53 AM
Trying to follow up on a theory by autonomousone
acne may be a genetic defect in vitamin a metabolism particularly with the pathway that creates retinoic acid in the skin. ive read studies that suggest retinoic acid could be rendered inactive in our bodies so we may have ultra low levels of it, sending our skin and sebum cells into chaos....
BETA CAROTENE is derived from plants only and enters the body as ~60% beta carotene and 40 % retinal . the body can then turn retinal into retinol as needed and the body can store large amounts of beta carotene with no known overdose. So the true source of retinol is beta carotene ...
one other interesting fact to consider is that our skin stores a lot of our beta carotene intake thats why eating too many carrots can turn your skin orange. i also find it interesting that acne mainly occurs on the face and the back and these are places that are otherwise exposed to the sun when walking outside, and ive read a study that proves uv rays cause beta carotene to stimulate retinoic acid production. Interestng thoughts hey!!
Perhaps we are lacking/or have too much of the CYP26AI enzyme involved in the metabolism of retinoic acid in our skin?? And UV involvement in stimulating retinoic acid production could be one way many people's skin clears when they get more sun exposure.
Promotes keratinocyte differentiation and apoptosis:
"Combination of betaC-promoted keratinocyte differentiation with the cellular "UV response" caused synergistic induction of cell cycle arrest and apoptosis."http://www.ncbi.nlm....4?dopt=Abstract
"UV-induced cell death by apoptosis is considered to be a natural protective mechanism that removes damaged keratinocytes and circumvents the risk of malignant transformation."http://www.ncbi.nlm....pubmed/15964692
About the skin's ability to metabolize retinoic acid from beta carotene:
Skin retinoid concentrations are modulated by CYP26AI expression restricted to basal keratinocytes in normal human skin and differentiated 3D skin models.
strong constitutive expression of CYP26AI in vivo and in organotypic culture was found to be restricted to basal epidermal keratinocytes, as well as eccrine sweat glands and sebaceous glands. These studies verify the capacity of human skin to metabolize RA, although substantial differences exist in CYP expression between normal skin and 3D skin models compared to monolayer cultures. Complex metabolic processes that maintain retinoid homeostasis may therefore be better studied in model systems more closely resembling in vivo skin. In light of our prior studies documenting the functional activity of RA metabolites, expression of CYP26 in the sebaceous gland epithelium supports the suggestion thataltered RA metabolism may be involved in the pathogenesis of acne
Biogenesis of retinoic acid from beta-carotene. Differences between the metabolism of beta-carotene and retinal.http://www.ncbi.nlm....0?dopt=Abstract
Expression and function of cytochrome p450-dependent enzymes in human skin cells.
human skin cells express various CYP enzymes, including
CYP26AI which is responsible for the metabolism of retinoic acid in skin cells
Good report with sources for research:
Cytochrome P450: A Target for Drug Development for Skin Diseases
The special interest for CYP enzymes in skin is evident by the fact that most, if not all, drugs used by the practicing dermatologist are either substrate or inducer, or inhibitor of this enzyme family (Table I. It is important to mention here that CYP enzymes act on many endogenous substrates including vitamin D and vitamin A, which are widely used in clinical practice for treating a variety of dermatological disorders....
Liarozole, which is an imidazole-containing compound, is known to inhibit the CYP-mediated metabolism of t-RA resulting in an increase of the retinoid in skin and plasma (VanWauwe and Janssen, 1989; Dockx et al, 1995).
Cyp enzymes also affect vitamin D production:
Based on several studies, it is now clear that the active form of vitamin D and its analogs suppress growth and stimulate the terminal differentiation of keratinocytes Kira et al, 2003
It is also known that in psoriatic lesions, epidermal keratinocytes exhibit hyper-proliferation and impaired differentiation triggered by inflammation. Therefore, it is quite reasonable to assume that vitamin D is effective on psoriasis.
From this on hirsutism and PCOS
Spironolactone: An aldosterone antagonist. Reduces Hitsutism through competitive inhibition of DHT, reduces CYP enzyme and increases peripheral aromatisation of testosterone and inhibition of skin 5 alpha reductase.
Vitamin A and its natural and synthetic metabolites (retinoids) affect growth and differentiation of human skin a
nd among the genes affected by retinoids in epidermis are keratin genes.http://www.ncbi.nlm....pubmed/22110773
Retinoids might also help by being anti-inflammatory:Inflammation resolved by retinoid X receptor-mediated inactivation of leukotriene signaling pathways
"Leukotrienes are implicated in the pathogenesis of diverse, inflammation-driven diseases....Retinoids affect numerous signaling pathways in human skin (36) . Their antiinflammatory, prodifferentiating, and chemopreventative properties are efficacious toward diverse disorders including psoriasis, acne, ichthyosis, photoaging, cancer, emphysema, and bronchopulmonary dysplasia in newborns (38 39 40 41) . We present evidence that retinoids up-regulate a proresolving pathway in human epidermal keratinocytes by mechanisms involving RXR-mediated CYP4Ftranscriptional activation (Fig. 6 ). One result is increased epithelial capacity to metabolically inactivate leukotrienes produced by infiltrating neutrophils, thereby antagonizing LTB4 signaling and further neutrophil recruitment. This CYP4F-dependent pathway functions as a physiological stop signal for epithelial inflammation, facilitating the switch to tissue repair and wound healing. " There's talk of celiac disease near the end of the full text..
Caratenoids and how they protect us from UVA damage with a comparison of beta carotene,
Astaxanthin, and canthaxanthin
Carotenoids and other phytonutrients protect from photodamage:
Edited by alternativista, 20 April 2012 - 10:46 AM.
Posted 16 April 2012 - 10:07 AM
(I'm looking to focus on betacarotene/sunlight in production of retinoids, linoleic acid, chlrorophyll, resveraterol and other nutrients to activate PPAR alpha/gamma. Because acne prone people may have an impaired ability to metabolize retinoids, are deficient in linoleic acid, have Fewer llamelar granulars that contain the desquammation enzymes and lipids (which improved by linoleic acid)
-PPARS - peroxisome proliferator-activated receptors PPAR alpha receptor is involved in regulating the sebaceous glands, is yet another thing impacted by insulin, therefore blood sugar stabilizing diet habits. PPAR's are responsible for lipid metabolism in the body as well as sebaceous control in the skin. see resveratrol link, also this discussion
PPAR beta and delta cells increase sebum production
PPAR alpha and gamma cells reduce sebum production
An imbalance between receptors can cause acne.
And this study: http://www.acne.org/...dpost&p=2740146 that indicates that 'PPAR-beta/delta activation stimulates keratinocyte differentiation, is anti-inflammatory, improves barrier homeostasis, and stimulates TG accumulation in keratinocytes.'
Accutane (or other retinoids) binds to the retinoid X receptor (RXR)- blocking PPAR. That's how it works.
- the PPAR situation is improved by linoleic acid and derivatives, sesamin, chloropyll, fish oil and resveratrol (see the resveratrol thread. Seriously. Read it!) and is affected by insulin/insulin sentitivity:
From a sweetjade post on healthboards http://www.healthboa...255-post43.html
Follicular keratinocytes fail to differentiate by apoptosis and produce hypergranulosis similar to the impermeable skin outer layer, resulting in the formation of microcomedones." and this is a result of something called Peroxisome Proliferator-Activated Receptor Cells (mentioned in a prior article about acne). These are genes that can be upregulated (turned on) or downregulated (turned off) by our diets (or supplements) and they also happen to interact/bind with the retinoid X receptors!
In fact Avandia, an Insulin Sensitizer binds to PPAR-gamma to help our bodies become more insulin sensitive, thus decreasing our insulin resistance. Yet if we eat foods that support insulin resistance we can increase our production of PPAR-beta/delta receptors cells that are responsible for 95% sebum production, inflammation, as well as hyperkeritinization. Yet if we eat in a way that decreases Insulin Resistance we can also upregulate PPAR-alpha & PPAR-gamma (oppose PPAR-beta/delta) and the cells will differentiate normally!
Ascetic acid (vinegar) also improves the PPAR balance, but that could be all about the insulin sensitivity. http://www.acne.org/messageboard/index.php/topic/165897-resveratrol/page__view__findpost__p__3044527
Acne and other problem-prone skin is deficient in Linoleic acid: http://www.acne.org/...cneskin-health/
Stuff from an old thread on resveraterol: http://www.acne.org/...97-resveratrol/
"Resveratrol is a potent 5 lipoxygenase inhibitor. 5 lipoyxgenase converts arachinodic acid into pro-inflammatory leukotrines. According to the studies posted by autonomous, these leukotrines can stimulate the sebaceous glands. Arachinodic downregulates PPARs, which affect rxr receptors, just like how accutane works!
"resveratrol is a CYP1A1 enzyme inhibior. CYP1A1 is an ezyme that encourages the breakdown of retinoic acid which maybe be the reason why the cells in our skins begin to disfunction, resulting in hyperkeratinization." And mutations of this gene have been found in acne prone people. http://www.acne.org/...is-information/
"I agree that PPAR's are probably at the forefront of the acne problem. PPAR's are responsible for lipid metabolism in the body as well as sebaceous control in the skin. IT is clear that sesamin and fish oil have some effect on the ppar's. Both generally active ppar alpha which tends to be affiliated with its anti-inflammatory effects. I noticed that when I took fish oil and sesamin (on separate occasions) both DEFINATALY made me oilier. Which makes sense since ppar agonists increase sebum production. Also, artificial ppar agonists like Avandia for diabetes are also known to increase sebum production. So then why do some people improve on fish oil and sesamin and dry up while others get worse? I don't know. My best guess is that in acne patients, there is either an imbalance to the ppar's expressed. Perhaps an overactive or over expressed ppar gamma, or even beta delta is to blame. Ppar gamma tends to get activated by proinflammatory ligands and oxidized fats. Perhaps naturally occurring proimflammaytory ligands are enough to cause a greater response in acne patients than non sufferers. Perhaps some acne patients have ppar gamma upregulated due to exposure to some sort of allergen or toxin. What is known is that our body tends to balance out the expression of ppars, so by increasing the expression of antimflammatory ppar alpha through supplements, that mighe be enough to downregulate ppar gamma? Maybe for some people this "imbalance" is worse than others which might explain why some people get oiler at first or get an initial breakout. The supplements are activating and upregulating ppar alpha before our body can slowly downregulate the other ppars?
I'm personally believe that accutane resets the ppars to zero. That is why people stay clear at least temporarily after a course even in the presense of foods, allergens or toxins that make them breakout. It is only over the course of weeks/months that our body slowly upregulates the proinflammatory receptors and causes our acne to remerge. " http://www.acne.org/...ost__p__1996356
FoxO1 - FoxOs play a pivotal role in the regulation of androgen receptor transactivation, insulin/insulin like growth factor-1 (IGF-1)-signaling, peroxisome proliferator-activated receptor-γ (PPARγ)- and liver X receptor-α (LXrα)-mediated lipogenesis, β-catenin signaling, cell proliferation, apoptosis, reactive oxygene homeostasis... Retinoids work by upregulating FOX01 http://www.ncbi.nlm....pubmed/22110774
Fox01 key to acne pathogenesis thread: http://www.acne.org/...herapy-of-acne/
"stimulating the cells in the hair follicle to produce more keratin (a hard protein that forms hair, skin and nails)."
sex hormones allow for enhanced cellular growth and affects sebaceous glands, but who is to say that if you did not enter puberty, your acne wouldnt have continued to get worse due to other inlfuences on sebaceous glands, and the fact you were going through puberty, was just another reason your acne was really bad."
"accutane upregulates rxr receptors and makes your skin more sensitive to natural retinoic acid created intercellularly allowing the cells to return to a normal controlled growth cycle. "
[b]Keratinocyte is the predominant cell type in the epidermis, the outermost layer of the skin,
- Vitamin D3 (cholecalciferol) regulates keratinocyte proliferation and differentiation mostly by modulating calcium concentrations and regulating the expression of genesinvolved in keratinocytes differentiation. Keratinocytes are the only cells in the body with the entire vitamin D metabolic pathway from vitamin D production tocatabolism and Vitamin D receptor expression.
- Cathepsin E. another factor affecting differentiation. Cathepsin D is involved in desquamation.
Edited by alternativista, 20 April 2012 - 10:42 AM.
Posted 16 April 2012 - 10:59 AM
Peroxidated squalene induces the production of inflammatory mediators in HaCaT keratinocytes: a possible role in acne vulgaris.
In order to investigate whether products derived from the oxidation of sebum can be responsible for the induction of inflammatory processes, HaCaT keratinocytes were treated with peroxidated squalene. NF-kappaB activation, secretion, and expression of IL-6, as well as peroxisome proliferator-activated receptor alpha (PPARalpha) mRNA and protein levels, were measured at the end of the treatment and after 24 and 48 hours of recovery. Squalene peroxidation products were administered in amounts able to elicit significant hyperproliferation and to induce lipoxygenase (LOX) activity. The results showed an early activation of NF-kappaB followed by an increase in PPARalpha mRNA and protein levels. Moreover, squalene peroxides induced an initial upregulation of IL-6 production and secretion that was counteracted by PPARalpha activation, as suggested by the subsequent decrease of NF-kappaB nuclear translocation and IL-6 levels. Inflammatory processes play an important role in the development of acne vulgaris. In combination with our own previous findings, which indicated an association between LOX stimulation and increased percentage of proinflammatory lipids in acne as well as a correlation between increased cytokine levels in the infundibulum, pilosebaceous duct hyperkeratinization, and augmented sebogenesis, the present data further support the involvement of lipid peroxides, in particular squalene peroxides, in establishing an inflammatory process in acne.
DHT increases inflammatory processes
Effect of dihydrotestosterone on the upregulation of inflammatory cytokines in cultured sebocytes.
Acne is a complex, chronic and common skin disorder of pilosebaceous units. Hyperkeratinization of keratinocytes, increased sebum excretion from sebocytes via androgen stimulation and inflammatory cytokines are the major factors involved in the pathophysiology of acne. In addition, it is known that keratinocytes play an important role in acne synthesizing a number of inflammatory cytokines. However, the nature of the association between inflammatory cytokines and sebocytes in acne remains unclear. Culture of sebocytes provides a new insight into the participation of dihydrotestosterone (DHT) in the production of inflammatory cytokines in acne. To examine the possible involvement of DHT in the production of inflammatory cytokines in the cultured sebocytes, we used immunohistochemistry and RT-PCR to compare the expression of interleukin-1 (IL-1), IL-6, tumor necrosis factor-alpha (TNF-alpha). Upregulation of IL-6 and TNF-alpha in immunohistochemistry, and increase in RNA amplification for IL-6 and TNF-alpha were observed after addition of DHT compared with the control. This study suggests that DHT may not only be involved in sebum production but also in production of proinflammatory cytokines in acne. PMID: 20043171 [PubMed - indexed for MEDLINE]
Skin surface lipid
(SSL) film is a mixture of sebum and keratinocyte membrane lipids, protecting skin from environment.
One of the reasons for the increase in acne, besides lack of nutrients and screwed up hormones, could be the increased exposure to free radicals causing oxidative damage to skin lipids.
Antioxidant activity, lipid peroxidation and skin diseases. What's new.
Due to its interface function between the body and the environment, the skin is chronically exposed to both endogenous and environmental pro-oxidant agents, leading to the harmful generation of reactive oxygen species (ROS). There is compelling evidence that oxidative stress is involved in the damage of cellular constituents, such as DNA, cell membrane lipids or proteins. To protect the skin against the over-load of oxidant species, it contains a well-organised system of both chemical and enzymatic antioxidant which are able to work in a synergistic manner. Skin antioxidant network protects cells against oxidative injury and prevent the production of oxidation products, such as 4-hydroxy-2-nonenal or malonaldehyde, which are able to induce protein damage, apoptosis or release of pro-inflammatory mediators, such as cytokines. When oxidative stress overwhelms the skin antioxidant capacity the subsequent modification of cellular redox apparatus leads to an alteration of cell homeostasis and a generation of degenerative processes. Topical application or oral administration of antioxidants has been recently suggested as preventive therapy for skin photoaging and UV-induced cancer. The recognition that ROS can act as second messengers in the induction of several biological responses, such as the activation of NF-kB or AP-1, the generation of cytokines, the modulation of signalling pathways, etc., has led many researchers to focus on the possible effects of antioxidants in many pathological processes. The recent demonstration that the peroxisome proliferators-activated receptors, whose natural ligands are polyunsaturated fatty acids and theirs oxidation products, have a central role in the induction of some skin diseases, such as psoriasis or acne, has indicated new links between free radicals and skin inflammation. Based on these findings, the review summarises the possible correlations between antioxidant imbalance, lipid oxidative breakage and skin diseases, from both a pathological and therapeutic points of view. http://www.ncbi.nlm....pubmed/14761133
Posted 24 April 2012 - 06:41 PM
Posted 10 May 2012 - 04:46 PM
Coenzyme Q10 is synthesized in most human tissues. The biosynthesis of coenzyme Q10 involves three major steps: (1) synthesis of the benzoquinone structure from either tyrosine or phenylalanine, two amino acids; (2) synthesis of the isoprene side chain from acetyl-coenzyme A (CoA) via the mevalonate pathway; and (3) the joining or condensation of these two structures. The enzyme hydroxymethylglutaryl (HMG)-CoA reductase plays a critical role in the regulation of coenzyme Q10synthesis, as well as the regulation of cholesterol synthesis (1,6).
The first step in benzoquinone biosynthesis (the conversion of tyrosine to 4-hydroxyphenylpyruvic acid) requires vitamin B6 in the form of pyridoxal 5'-phosphate. Thus, adequate vitamin B6nutrition is essential for coenzyme Q10 biosynthesis. A pilot study in 29 patients and healthy volunteers found significant positive correlations between blood levels of coenzyme Q10 and measures of vitamin B6 nutritional status (91). However, further research is required to determine the clinical significance of this association.
Posted 11 May 2012 - 11:12 AM
See also this post from that thread which has several studies about thryoid and adrenal health as well as retinoid/PPAR receptors, accutane and other hormones:
Quote: Skinmed. 2004 Mar-Apr;3(2):83-91. Related Articles, Links
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.
Quote: 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.
Quote: Am J Clin Dermatol. 2003;4(5):315-31. Related Articles, Links
Cutaneous manifestations of endocrine disorders: a guide for dermatologists.
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 withhypothyroidism, 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 ofCushing 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 ofdiabetes mellitus include necrobiosis lipoidica diabeticorum, diabetic dermopathy, scleredema adultorum and acanthosis nigricans..
Those in bold are the ones that I'm aware of that can have acne as a symptom.
Quote: Horm Res. 2000;54(5-6):230-42. Related Articles, Links
Human skin: an independent peripheral endocrine organ.
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
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.
Quote: 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
Last edited by SweetJade1; 02-25-2005 at 12:44 AM.
Posted 15 May 2012 - 02:23 PM
Posted 17 May 2012 - 12:37 PM
Posted 17 May 2012 - 05:17 PM
Hey I have a question, I know if you have bad acne and eat McDonalds or something like that you will get a bad breakout, but as you're getting better and better lets say you acne is like 50% better, does this mean that if you eat McDonalds your breakout will only be 50% as bad now because you've gotten rid of some of the acne already? And the better your face is the less the breakout will be, and vice versa? I've noticed that at the peak of my acne, food affected me a whole lot, while before when my acne wasn't as bad food didn't affect me as much.
sorry. I can't tell you what exactly happens to you as a result of the food you eat. Too many variables. But if you mostly eat very well, you should be able to have some less healthy foods once in a while.
Posted 22 May 2012 - 08:06 PM
Posted 24 May 2012 - 09:02 AM
Hi alternavista. I totally agree with you that diet affects acne - I had food allergies that I never knew about that turned out to be a trigger - but I'm wondering why you say gluten is bad for you. I've heard mixed things about it, and I'm wondering what effect you think it has internally and what sources you might have for that.
See the ZAG enzyme thread linked to several times in the first page of this thread. Or clink on the links that would be right there where ever you read my comments on gluten.
Edited by alternativista, 24 May 2012 - 09:03 AM.
Posted 04 June 2012 - 12:52 PM
So should we acne-prone people exfoliate? Whats the least harmful way to do this? I dont want to irritate the skin too much... I have this product at home: http://www.origins.c...sion/index.tmpl
Posted 05 June 2012 - 12:46 PM
"Acne-prone skin produces more dead skin cells than is typical, and these cells aren't properly shed. This condition, called retention hyperkeratosis, is the reason regular exfoliation is so important for acne prone skin types. In normal functioning skin, excess dead skin cells are constantly being sloughed away naturally. In acne-prone skin, dead cells remain stuck on the skin's surface and within the follicle, creating a clog (impaction). This plug of cellular debris and excess oil forms a blackhead or, if bacteria invade, an inflamed blemish."
So should we acne-prone people exfoliate? Whats the least harmful way to do this? I dont want to irritate the skin too much... I have this product at home: http://www.origins.c...sion/index.tmpl
Do it gently with a soft cloth, oil cleansing, or BHA/AHAs. And take steps to reduce the tendency towards hyperkeratinization, improve sebum quality, etc.
Posted 08 June 2012 - 12:36 AM
Posted 09 June 2012 - 02:14 PM
Posted 09 June 2012 - 03:35 PM
Man this is SO helpful but how on Earth am I supposed to take all these supplements or preferably consume foods with all of these vitamins in them? EEK!
By eating primarily real, whole nutrient dense foods in place of all the near empty calories in all the processed foods that make up the typical diet.
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