Acne.org Products
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.
Some anti-aging stuff on resveratrol and the sirtuin enzyme it activates that is anti-aging. calorie restriction and intermittent fasting also promote this enzyme. There's also good info on other phyto-nutrients in mulberries such as anthocyanins, carotenoids,
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.
Resveratrol:
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 [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 [5].
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 [5], 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: [9]
"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 15 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 [10], neuroprotective [7], due to activation of AMPK, and burns fat [11] from SIR2 activation, which we talked about earlier being essential for producing lifespan extension.
From here with sources:
http://therawhigh.bl...rry-part-2.html
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.
Peanuts and Peanut Butter
Peanuts and peanut butter are a great source of resveratrol.
Cocoa Powder and Dark Chocolate
Cocoa powder and dark chocolate have the second highest amount of resveratrol after red wine.
Mulberries
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.
Blueberries
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!
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.
Beta carotene, UV exposure and Retinoic Acid
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!!
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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.
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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.
http://www.ncbi.nlm....5?dopt=Abstract
concludes '
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 that
altered 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.
http://www.ncbi.nlm....pubmed/18781947
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
http://www.nature.co...l/5602457a.html
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 (
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
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
http://www.fastbleep...paeds/17/39/251
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..
http://www.fasebj.or...t/22/2/538.full
Caratenoids and how they protect us from UVA damage with a comparison of beta carotene,
Astaxanthin, and canthaxanthin
http://www.ncbi.nlm....pubmed/18803658
Carotenoids and other phytonutrients protect from photodamage:
About PPARs
(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:
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!
From a sweetjade post on healthboards http://www.healthboa...255-post43.html
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/
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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- (PPAR)- and liver X receptor- (LXr)-mediated lipogenesis, -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/
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"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. "
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.[16][17] 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.[18]
- Cathepsin E.[19]another factor affecting differentiation. Cathepsin D is involved in desquamation.
Stuff about Inflammatory processes being at the root of acne formation:
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.
Added a link to the linoleic acid thread to the Sebum Quality thread. And for those that missed it, acne and other problem prone skin has been found to be deficient in linoleic acid. topically applied oils high in linoleic acid have been found to improve skin. http://www.acne.org/messageboard/index.php/topic/314390-acne-prone-skinsebum-deficient-in-linoleic-acid-possible-topical-solution/
About CoQ10 Synthesis:
Biosynthesis
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.
http://lpi.oregonstate.edu/infocenter/othernuts/coq10/#deficiency
Some studies posted on Healthboards by Sweetjade in this thread: http://www.healthboards.com/boards/acne/254590-sugar-acne-true-7.html
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:
http://www.healthboards.com/boards/1516235-post32.html
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=130553
Those in bold are the ones that I'm aware of that can have acne as a symptom.
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.
Last edited by SweetJade1; 02-25-2005 at 12:44 AM.
Links to some parasite and detox stuff. Whether or not everything they claim is true, parasites are real and cause health problems. These should all have info on home remedies as that was what I was looking for.
http://www.o3center.org/Articles/TheOwnersManualForTheHumanBody.html -
http://leowei.blogspot.com/2009/02/human-intestinal-parasites-worms.html
http://www.joyfullivingservices.com/parasitesandpeople.html
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.
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.
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.
Thanks!
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.
Thanks!
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.
"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.com/product/3854/10858/Skincare/Daily-Essentials/Exfoliators/Modern-Friction/Natures-gentle-dermabrasion/index.tmpl
"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.
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.
About FoxO1
Paper by researchers that theorize that FoxO1
FoxO1 plays a pivotal role in the regulation of androgen receptor (ARs), cell proliferation, cell survival, apoptosis, lipid
and glucose metabolism, oxidative stress and innate immunity all important factors in acne pathogenesis (Fig. 1).
2
Nuclear FoxO1 is predominantly regulated by the activity of the phosphoinositol-3 kinase Akt pathway. Increased growth factor
signalling in puberty (insulin-like growth factor-1, IGF-1) and an insulinotropic Western diet, especially by high-glycaemic load diets (insulin) and increased consumption of insulinotropic dairy products (insulin IGF-1), may play a fundamental role in the reduction of the nuclear content of FoxO1.
Oxidative stress is AKA inflammation.
But elsewhere there's this statement:
If a substantial body of evidence accumulates showing that FoxO1 levels are different in patients with acne compared with
patients without acne, then the discussion can be elevated to that of a theory.
So as of 2010 when this was written, it hasn't been demonstrated that acne prone patients are any more deficient in FoxO1 than anyone else. However, I've found some info on the use of linoleic acid
This site is a data mining site for 'for previously unknown relations between genes and phenotypes, and improved gene prioritisation catching non-obvious disease causing genes.'
http://biograph.be/project/project And apparently there is a known relationship between the FoxO1 gene and linoleic acid. There's an interactive chart that 'provides putative functional links between FOXO1 gene (context) and trans-10,cis-12-conjugated linoleic acid (target)'
And here's a paper on the 'Role of FoxO1 in FFA-induced oxidative stress in adipocytes' FFA = free fatty acids, but as far as I can tell, they don't say which FFAs.
http://ajpendo.physi...1/E159.full.pdf
And here's one on resveraterol. I don't know if it's already in the resveraterol or linoleic acid thread:
Conjugated linoleic acid-mediated inflammation and insulin resistance in human adipocytes are attenuated by resveratrol*
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Several studies on the benefits of topical green tea:
Skin photoprotection by green tea: antioxidant and immunomodulatory effects
Green tea polyphenolic antioxidants and skin photoprotection (Review)
And some on topical lotions. Some of these may be duplicates.
Topical therapy of acne vulgaris using 2% tea lotion in comparison with 5% zinc sulphate solution
The efficacy of topical 2% green tea lotion in mild-to-moderate acne vulgaris
Treatment of acne vulgaris with 2% topical tea lotion
Outcomes of 3% green tea emulsion on skin sebum production in male volunteers
I will most definately be following your blog. All this information really makes you think about how wrong we all have it. I feel like we could be living forever if it was possible to do everything in this thread.
About FoxO1
Paper by researchers that theorize that FoxO1
FoxO1 plays a pivotal role in the regulation of androgen receptor (ARs), cell proliferation, cell survival, apoptosis, lipid
and glucose metabolism, oxidative stress and innate immunity all important factors in acne pathogenesis (Fig. 1).
2
Nuclear FoxO1 is predominantly regulated by the activity of the phosphoinositol-3 kinase Akt pathway. Increased growth factor
signalling in puberty (insulin-like growth factor-1, IGF-1) and an insulinotropic Western diet, especially by high-glycaemic load diets (insulin) and increased consumption of insulinotropic dairy products (insulin IGF-1), may play a fundamental role in the reduction of the nuclear content of FoxO1.
Oxidative stress is AKA inflammation.
But elsewhere there's this statement:
If a substantial body of evidence accumulates showing that FoxO1 levels are different in patients with acne compared with
patients without acne, then the discussion can be elevated to that of a theory.
So as of 2010 when this was written, it hasn't been demonstrated that acne prone patients are any more deficient in FoxO1 than anyone else. However, I've found some info on the use of linoleic acid
This site is a data mining site for 'for previously unknown relations between genes and phenotypes, and improved gene prioritisation catching non-obvious disease causing genes.'
http://biograph.be/project/project And apparently there is a known relationship between the FoxO1 gene and linoleic acid. There's an interactive chart that 'provides putative functional links between FOXO1 gene (context) and trans-10,cis-12-conjugated linoleic acid (target)'
And here's a paper on the 'Role of FoxO1 in FFA-induced oxidative stress in adipocytes' FFA = free fatty acids, but as far as I can tell, they don't say which FFAs.
http://ajpendo.physi...1/E159.full.pdf
And here's one on resveraterol. I don't know if it's already in the resveraterol or linoleic acid thread:
Conjugated linoleic acid-mediated inflammation and insulin resistance in human adipocytes are attenuated by resveratrol*
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Several studies on the benefits of topical green tea:
Skin photoprotection by green tea: antioxidant and immunomodulatory effects
Green tea polyphenolic antioxidants and skin photoprotection (Review)
And some on topical lotions. Some of these may be duplicates.
Topical therapy of acne vulgaris using 2% tea lotion in comparison with 5% zinc sulphate solution
The efficacy of topical 2% green tea lotion in mild-to-moderate acne vulgaris
Treatment of acne vulgaris with 2% topical tea lotion
Outcomes of 3% green tea emulsion on skin sebum production in male volunteers
Hey there Alternativista,
Firstly, I just would like to tell you how much I admire your contributions to this board. They have taught me alot, and I will most certainly be checking out your blog. Your posts have inspired me to make quite a few changes to my diet. I was on a low-glycemic diet to shed the "puff" I carry on the sides of my waist and hips for a few months before even coming across your posts, but the research that some of your posts contain has inspired me to try a Paleo diet, and abstain from gluten and most dairy to see if it helps me not to have the little pustules I get once in a while.
But I have a question for you; how exactly could changing my diet make a real impact on my hormonal acne? I know my cystic acne that I got beginning around 21, and lasting until 24 was linked to my hormones. The lifestyle choices I made at the time were of no help, either. I am nearly convinced they made my acne worse. I guess what I'm saying to you is that I don't quite understand the connection between diet and hormones. Of course I get that humans should not eat any junk they want, because it can affect the internal organs (my mom quit drinking diet Dr. Pepper, because she realized that it was causing pains to her liver for nearly a year), but what I want to know is how can eating a Paleo-type diet clear one's skin if the problems with one's skin are related to the hormones?
I am trying to do a Paleo-diet because I think it's worth a shot. Also, I just plain feel better when I eat low-glyemic, or Paleo-type foods. My body looks healthier. It's not bloated anymore, and that's always a plus! But I would just absolutely love it if you would take the time to explain the correlation between a healthier diet and hormonal acne.
Thanks so much,
Cherry
Page listing the diet makeup of the various primates include those in the genus homo: http://tolweb.org/treehouses/?treehouse_id=4446 . Thought it would be handy to refer to next time we argue about how much we are adapted to eating meat.
Tree of Life
The Tree of Life Web Project (ToL) is a collaborative effort of biologists and nature enthusiasts from around the world. On more than 10,000 World Wide Web pages, the project provides information about biodiversity, the characteristics of different groups of organisms, and their evolutionary history (phylogeny).
alternativista, do you think that having white rice on a daily basis is bad? Rice is a staple in my country so it is hard for me not to have it since I am already on gluten, diary, wheat-free diet. Can't stop drinking coffee though because I am kinda "slow" without it. I also think that it is bad to consume meat everyday.
It would be best if you could "Long story cut short".
I did. It's there in the first post.
alternativista, do you think that having white rice on a daily basis is bad? Rice is a staple in my country so it is hard for me not to have it since I am already on gluten, diary, wheat-free diet. Can't stop drinking coffee though because I am kinda "slow" without it. I also think that it is bad to consume meat everyday.
It's individual how bad consuming that empty carb is for you because it depends on what else you do, your lean muscle mass, insulin sensitivity that may vary due to genetics, etc. . But regardless, white rice is an empty carb that could be taking the place of much more nutrient dense foods. And have you tried drinking teas for a lower dose of caffeine?