98 replies to this topic

[SweetJade1980]

Hi All,

OK, I've heard ya...well most of ya. Some, or would it be most of you, just don't seem to (fully) understand how diet can play a role in acne development, is this correct?

OK, I know that some of you get confused or bored when some of us start talking in scientify terms (I like that "word") and while we could make it simpler, it doesn't empower you for us to always do so. Why? When we use a term like Insulin-like Growth Factor-1 (IGF-1), this makes what we say seem almost credible or valid. Now if you take that term and put it into pubmed or some other (full-text) journal database and combine it with "acne" and "diet", "food", "wheat", or "trans fat" or some other combinations of other dietary components, you will discover for yourself (how awesome is that) what we are talking about.

Yes, I also know that you get bored, tired, overwhelmed, or lost when members, such as myself, make loooooong posts. I do apologize for this as I never know how long it will take me to respond to someone's question. Some people a paragraph is sufficient, but for others, yes it can take as much as 5 pages....to explain the same thing

Now below is a list of events that contribute to the development of acne and if I forgot one please mention it. Everyone is welcome to chime in on what they feel is the biggest contributor and why, but I will try to explain the process of each of them from a diet perspective in parts (seperate posts) in hopes of making things a bit simpler.


How Can Diet Influence (not in any specific order):

1) Hormonal balance, increase hormones, or increase androgens?
2) Sebum production?
3) Hypercornification or microcomedone formation?
4) Bacteria, candida, & other overgrowth of normal flora?
5) Hyperproliferation or skin cell overgrowth?
6) Hyperkeritinization or thickening of skin cells?
7) Hypodesquamation or poor skin cell shedding?
8) Development of Inflammation?
9) Different anti-acne regimens or why aren't there universal pro-acne foods?
10) Our genetic makeup?



Furthermore, below is a list of various forms of acne. Reason? Acne is not just Acne. There are specific types (acneforms), specific locations, specific irritators/stimuli, and sometimes specific treatments for each. In fact, some of us, I know I do, probably have more than one type. So, if we take these different types into consideration, perhaps it will be a bit easier to understand why one person's solution, wasn't yours or vice versa.

ACNE:

Aestivalis
Chloracne
Comedonica
Congloblata
Cosmetica
Cystica
Detergicans
Excoriee
Fulminans
Infantum
Inversa
Mechanica
Neonatorum
Papulopustulosa
Pustulosa
Rosacea(has subtypes)
Venenata
Vulgaris
etc.
[can you tell the cause by the name?]

http://www.dermis.net/doia/abrowser.asp?zu...cne&type=search (pictures)
http://atlases.muni.cz/atl_en/main+nenadory+vlas.html (pictures)
http://www.skincarephysicians.com/acnenet/acne.html (descriptions)
http://www.acnegroup.org/aboutacne.php4 (description)

Of course, what I hope we all learn from this is that while the above events seem seperate, they tend to utilize the some of the same "ingredients" (proper names later) and as such, you may find that there's some repetition in the process for each. For those interested, this should further aid you in understanding those scientify terms as well as further expanding your comprehension of the diet-acne connection. Otherwise, I'll start with either #1 or #3 tomorrow as I really need to get some sleep.

G'night

[Baby Blue]

Okay smart guy, that was a ton of info! I found that very interesting; I guess that might be why beer breaks me out. My poor liver Anyway, I am curious if you believe that food allergies can cause acne? I read that the reason some people break out and others do not, can be due to an allergic reaction to food. Kind of like some people are allergic to poison ivy and others aren't. I do believe acne is a sign of serious internal problems. You did leave off the improper shedding of skin cells. At least I believe this is another cause of acne because that is what I think caused my acne. What helped me tremendously was SA and bp. I would like to hear thoughts on this.

Baby Blue

[SweetJade1980]

Sound like anyone you know?

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[SweetJade1980]

Delta force,

In order to gain some perspective, let's define toxic & toxin:

Webster's Dictionary http://www.m-w.com/cgi-bin/dictionary

Main Entry: 1tox·ic
Pronunciation: 'täk-sik
Function: adjective
Etymology: Late Latin toxicus, from Latin toxicum poison, from Greek toxikon arrow poison, from neuter of toxikos of a bow, from toxon bow, arrow
1 : of, relating to, or caused by a poison or toxin
2 : affected by a poison or toxin <toxic pregnant women>
3 : POISONOUS
- tox·ic·i·ty  /täk-'si-s&-tE/ noun

Main Entry: tox·in
Pronunciation: 'täk-s&n
Function: noun
Etymology: International Scientific Vocabulary
: a poisonous substance that is a specific product of the metabolic activities of a living organism and is usually very unstable, notably toxic when introduced into the tissues, and typically capable of inducing antibody formation

WordNet 2.0 http://wordnet.princeton.edu/cgi-bin/webwn...ge=1&word=toxin

toxin -- (a poisonous substance produced during the metabolism and growth of certain microorganisms and some higher plant and animal species)

MedicineNet http://www.medterms.com/script/main/art.asp?articlekey=5828

Toxin: One of a number of poisons produced by certain plants, animals, and bacteria.

The term "toxin" is frequently used to refer specifically to a particular protein produced by some higher plants, animals and pathogenic (disease-causing) bacteria. A toxin typically has a high molecular weight (as compared to a simple chemical poison), is antigenic (elicits an antibody response), and is highly poisonous to living creatures.

The word "toxin" comes from the Greek "toxikon" = arrow poison and was introduced to medicine in 1888 by the Berlin physician Ludwig Brieger (1849-1909) as a name for poisons made by infectious agents.

Based on the above, hopefully we can now establish just what is meant by "a very particular kind of highly congesting blood and lymph fluid toxins" that you quoted earlier. Hmm...well at least the ability to understand that "toxins" isn't something that we get just from pollution & chemicals & synthetics, but that animals, and thus human beings, bacteria, other microorganisms & organisms (i.e. parasites) and plants are also capable of producing toxins.

So even if one does have high androgen levels, for example, if the liver is capable of breaking down (inactivating) and then they are eliminated, then theorectically we shouldn't have any problems. http://www.ncbi.nlm.nih.gov/entrez/query.f...126&query_hl=10

For those that don't know, the liver has a ton of enzymes that it produces to either make hormones or break them down. It also has enzymes to break down food particles (or substances on the food), and sometimes these particles have by-products that are toxic, BUT the liver has enzymes to neutralize most/some of these....IF it can produce enough.

Indeed, the liver is an amazing warehouse or factory where upon it it not only creates enzymes, to help metabolize foods, drugs, & detoxify, but also creates growth factors (IGF-1), filters antigens (basis for liver flush), and immune mediators (think inflammatory products) that all play a role in acne development, among other disease. http://biomed.brown.edu/Courses/BI108/BI10...NormalLiver.htm

So, when the above definitions mentioned animals and plants as producing toxins...did food come to mind when you read that? Whatever toxins (excess Growth Hormones, viruses, etc) that animal has, can sometimes be passed on to other animals and humans, i.e. mad cow disease (shudder). Of course, plant foods can also produce their own toxins, which is why some foods or parts of a plant are NEVER eaten (a seed, a root, a leaf etc).

Here's the kicker though, plant foods can be toxic to those that have an inability to metabolize them properly. Yet what makes this so confusing is that what is toxic to one person, may not be toxic to another and vice versa (think genetics x environmental exposures).

Hmm, so what inability could determine this?

A Damaged Liver - a Liver Panel will detect this in cases of cirrohsis, hepatitis, but this is only a handful of enzymes that the liver produces.

A Homornal Disorder - Your liver doesn't have to show "damage" to have a chronic, long term, imbalance. You must check for each enzyme.

A Leaky Gut - More scientific term would be intestinal hyperpermeability or increased permeability to foods, chemicals, or other substances that would normally not be capable of entering the blood stream. http://www.ncbi.nlm.nih.gov/entrez/query.f...0980&query_hl=1

A Food Allergy - A state of hypersensitivity induced by exposure to a particular antigen (allergen) resulting in harmful immunologic reactions on subsequent exposures, the term is usually used to refer to hypersensitivity to an environmental antigen (atopic allergy or contact dermatitis) or to drug allergy.
http://cancerweb.ncl.ac.uk/cgi-bin/omd?query=allergy

A Food Intolerance - see above. Aside from different antigens & enzymes involved, the main difference is that this happens to be a delayed reaction that can take several days, years, or decades before signs, symptoms, or disease occurs (remember this for later).

A Chemical Sensitivity - see above

Unknown Factor(s) - ???

With most of the above, the tricky part is that genetics isn't always solely at play here. Sometimes it's because of a certain combination of events that can cause these problems to occur. High doses of NSAIDS (non-steriodal anti-inflammatories, i.e. Motrin, Asprin) over a long period of time, antibiotics use over a long period of time, coupled with too much of a certain food, and you've created an environment that could lead to intestinal damage, and thus increased intestinal permeability.

Therefore, after you've eaten and digested a particular food in such an environment, while broke down as it may be, it's particles are now small enough to enter into the blood stream, due to increased intestinal permeabilty, and your body will from then on determine that food particle is an invader (antigen) and attack it with antibodies. This pretty much explains Food Allergies, Food Intolerances, and perhaps certain Chemical Sensitivities....and possibly other Inflammatory Diseases (like acne). http://www.mightyzero.com/restoring_gut_permeability


So, hopefully explains why some of you may feel that there's "nothing safe to eat" when you read other members anti-acne diets. Yes there may be foods that we have in common, but due to the above circumstances, that can also vary from person to person and only you can determine what foods affect you in this manner. Afterall, how can I tell you exactly what to avoid, when I wasn't around when you were 14 or 16, consuming who knows how many types of NSAIDs, alcoholic breverages, cigarrettes, nor the amount of stress you were under, the amount of nutrients you consumed (or didn't), and what foods you ate during that time period? Sadly, those are all factors.

Of course, if you know you have one of the above health problems, there are methods and actual lab tests one can take (more on this later) to help you figure this out, and as such, I hope that brings you some comfort. Along with the comfort in that there's no need to be paranoid and there's especially no need to avoid ALL foods that you see us avoiding (do not do this). If you know what you have, you could probably take a pill for it...if that's what you want to do.

Although, I believe the protocol of choice here is that if one finds that the foods they avoid have nothing (directly) to do with the Insulin-Hormone response (see next post), then it's possible that by healing your leaky gut and doing what you can to strengthen your liver (liver aids, liver flush, detoxes, etc) you may be able to eat more or all of those foods once again. Doesn't that sound fantastic?

[kel]

i hate it when my boyf eats crap all the time and his skin glows and is spot free

[igotmyphilosophy]

sweetjade, you are phenomenal. thank you!

[SweetJade1980]

i hate it when my boyf eats crap all the time and his skin glows and is spot free

LOL, just remember that usually no one is perfect. Yet I certainly do hope that in all ways he is still a picture of health.

[SweetJade1980]

sweetjade, you are phenomenal. thank you!

Aww thank you, that's so sweet of you to say. BTW, have you gotten an Endocrinologist appt. yet?

[SweetJade1980]

Diets Role in Hormonal Balance

First of all, when it comes to the role that androgen hormones play, there appears to be 2 Types of Acne Sufferers:

A) Those that have skin that is sensitive to normal amounts of androgens (90% of sufferers)

B) Those that overproduce androgens or have hyperandrogenism (10% of suffers)

While hyperandrogenism seems like the likely place to start, I can't help but think that the 90% of acne sufferers would love to know diets role in their life first. Well, what immediately jumps out at me is the word "sensitive'. Majority of acne suffers are just sensitive to normal amounts of androgens! In other words, the skin of most acne sufferers for some reason is sensitive, hyper-responsive, overreacting, to something that is....Normal???

HOW can that be?

LOL, well I don't know that answer, but the predominant theory is that there is an androgen receptor defect or some other malfunctioning receptor or defect in the skin that is causing this increased sensitivity. Well OK, that makes sense after all, not everyone gets acne, and even those that have hyperandrogenism don't always have acne. So, yea there is a genetic component to this, BUT our diet has the ability to turn on or off certain genes!

So, does that mean that changing my diet will fix the defect?

Well, I can't say for certain because the defect(s) haven't been fully discovered yet. Therefore, on a cellular level we can't ethically compare the skin of an acne sufferer before dietary changes and then after to see how much repair was done. However, what we can do is look at testimonials, anecdotal evidence, and journal articles which gives myself, fellow members, and others including doctors, nutritionists, biologists and other scientists a better idea of what's going on. Aside from just looking at before and after pictures or lesions counts, there is also a wide variety of chemical & hormonal changes that occur that can also be compared by analyzing various blood and urine samples (see your Endocrinologist). For example, an acne sufferer that is actually hyperandrogenic, will discover that their excess hormones will be reduced upon following a diet (& exercise) regimen tailored specifically for them.

Now getting back to the whole “sensitive� issue, what do you know about people that are sensitive to things, especially things that are considered normal? Doesn’t that remind you of a(n):

Auto-immune disease - body attacks something of self, something it produces. This would include diseases such as Thyroidititis, Lupus, Rheumatoid Arthritis, etc (btw, those listed have acne as a symptom or involve an androgen disorder).

Allergy - attacks something of non-self, but is usually considered harmless to other people. This is more of an instant or immediate reaction occurring within minutes to 24 hours of exposure.

Food Intolerance - attacks something of non-self, but is usually considered harmless to other people. This is a delayed response where it can take days, months, or even years to develop signs, symptoms, or a disease from usually constant exposure.

Chemical Sensitivity - attacks something of non-self, but is thought to be harmless to most people. This would include things like Sulfites, Food Coloring, MSG, Splenda, etc and can have an immediate or delayed response.

Well, at least that's what comes to mind when I think of sensitivity. Furthermore, after one has been exposed to their stimuli, the body is capable of doing something that would normally take weeks or months to do, in a much shorter period of time. Along with being sensitive, one of the symptoms can be irritation. If something gets irritated enough it can thicken and scale up (hyperkeritinization?) and/or become inflammed. Hmm…isn’t acne an inflammatory skin disease? In fact, some believe that ALL forms of acne are inflammatory…keep this in mind for later. However, regarding hormones, lets start at the beginning.

Now, of course it doesn’t matter WHAT you eat before you hit puberty, chances are you won’t develop acne as a result because you do not have (enough of) the hormones to do so yet! Granted, there are cases where about 20% of infants and toddlers develop a form of acne (acne infantum/infantilis) that usually goes away in a few weeks, or if it is due to a hormonal disorder, it must be corrected for, otherwise acne doesn't occur without good reason. See, acne CAN be a sign of something temporarily or seemingly permanently imbalanced in our system and it’s best if we can all learn to accept that so we can move on to fixing it, right?

So once you hit precocious puberty (< 8 years of age), another sign that you are more at risk for health and hormonal problems, or just puberty, your body enters into “a temporary state of insulin resistance�, except did you know that insulin resistance is also considered a chronic inflammatory disease? Nonetheless, as a result of this increase in insulin, what signs appear during the pubertal teen years? Acne, Weight problems, Diabetes (type I), Depression…OK just as long as you know that these same health problems, among many others, occur in adults later on in life presumably due to the same thing…Insulin Resistance.

Fine. So WHAT is the big deal with Insulin?

Well it is this amazing pro-hormone that can initiate a wide range of metabolic events necessary for proper growth and development. It’s not just about ensuring that our cells get filled with glucose and fats, but it’s presence for some reason also affects our steroid hormone levels. Steriod hormones include aldosterone, cortisol, pregnenolone, progesterones, androgens, and estrogens. Depending on what type of hormonal disorder one may have, most of these play a role in acne development. Due to there being quite a few hormonal disorders that can have acne as a symptom, I’m going to stick to the most popular hormone and focus on androgens role in all of this.

Now, the way insulin affects our androgen levels is by reducing our levels of Sex Hormone Binding Globulin (SHBG). SHBG has a much higher affinity for binding to androgens than it does estrogens. In fact, it is something that increases with our estrogen levels and with lower levels of insulin. So if SHBG is lowered by higher amounts of insulin, then our Free Testosterone (Androgen) will also be higher. I believe we are supposed to have no more than 2% of our androgens in Free Testosterone form. This amount is what will bind to the androgen receptors in various parts of the body to initiate growth. Growth of muscles, of the prostate, and of sebaceous glands, are examples of what this anabolic (building) hormone can do.

So, what happens when we have more than 2% Free Testosterone?

Well, it differs for everyone, but some will have a fantastic libido, or big muscles, others experience androgenic alopecia (male pattern baldness), hirstuism, acne, seborrhea, etc. Doesn’t always sound like a good thing, does it? Well that’s where our diet comes into play.

The foods we eat, our diet, contain macronutrients (water, carbohydrates, protein, fats, vitamins & minerals) and serve as the building blocks for the human body. Did you get that? These macronutrients are the Building Blocks, our FUEL, our brick & mortar and everything in between! They usually work for us, but unfortunately during misguided times (clashes with your genetic makeup) or abuse (over-consumption) they can work against us. This is especially true with all the pesticides, natural & chemical hormone-mimickers, and trans fats in our foods. All of these things and more have the ability to affect certain people more than others, which is why not all have us have the exact same “anti-acne� diet.

Now, these macronutrients have the ability to mess with our hormone levels by for starters increasing our glucose levels, which will increase our insulin levels. As a result of the increase in insulin, there will usually be an increase in IGF-1. Now, IGF-1 is apparently 10x more potent than just insulin and that’s thought to be due to it binding to insulin, in order to reduce it’s presence in the blood stream, but this doesn’t always happen. Indeed, an increase in insulin doesn’t only decrease SHBG, but it also decreases IGFBP-3 (& IGFBP-1), which is known as Insulin-like Growth Factor Binding Protein-3. It’s job…wanna guess? Alright fine, it’s job is to bind to IGF-1. That’s right, but that can’t happen if our body has too much insulin present in the blood stream. So as a result, other growth factors (happen to be inflammatory) will come along and bind to IGF-1 in order to reduce its presence and activity in the body.

Hmm…OK, did anyone catch what just happened?

Insulin lowered our SHBG & our IGFBP-3 the two things we need to safely keep Free Testosterone and IGF-1 in check! Now that these aren’t in check, they are free to do their worst. So not only has our Free Testosterone reached the androgen receptor on the skin cells, but IGF-1 has joined and is quite happily working on enlarging the sebaceous gland, increasing oil production (that’s another theory), initiating other growth-related events, and because it can’t be bound sufficiently, inflammatory products have come along to do so. Funny, kinda sounds like the pathway to possibly developing cystic acne. You know, that sore, swollen, enlarged type…although it could also be a microcomedone, but more about that later.

Furthermore, noticed when I mentioned fats earlier? Well, the most amazing thing about the whole diet-acne connection is that without fat, theorectically we couldn't have acne. See, sex steriod hormones such as Testosterone are derived from cholesterol and cholesterol is made from lipids. Not to mention, a certain amount of inflammatory products also rely on lipids or fatty acids for their production such as arachidonic acid, which increases PGE2 (hormone regulating & inflammatory prostaglandin). I suppose that's why in 1977 a medical doctor published Acne Can Be Cured (I've got a copy) and I believe one of our members, Doberwoman (a scientist), says when she follows his diet perfectly, she's clear. http://www.amazon.com/exec/obidos/tg/detai...=books&n=507846

So, that is the short end of how our diet affects the amount of not just insulin, but hormones, chemicals, growth factors, and inflammatory products that are also associated with acne development. So for those that are just “sensitive,� when you change your diet you’re doing so not so much to balance your androgen levels, but in hopes of lowering your IGF-1 (skin cell proliferator), your PGE2 (inflammatory prostaglandin), TNFa (immune mediator, pro-inflammatory) etc (semi-long list).



(to be continued)

[SweetJade1980]

Ok, so want examples now?

While I’m a fan of recent studies, below I’ve also posted some older ones because I want you to see the progression of technology and discovery and of course because I want you to know how long they’ve been aware of these various connections:

Acne – Hormone Connection
http://www.ncbi.nlm.nih.gov/entrez/query.f...206&query_hl=41 (1965 – males) – NO abstract available

http://www.ncbi.nlm.nih.gov/entrez/query.f...164&query_hl=41 (1975 – females)

http://www.ncbi.nlm.nih.gov/entrez/query.f...451&query_hl=51 (1992 – female)

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. ddeplews@peds.bsd.uchicago.edu

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.
http://www.ncbi.nlm.nih.gov/entrez/query.f...157&query_hl=54

(2000) FREE Full Text

http://www.ncbi.nlm.nih.gov/entrez/query.f...41&query_hl=157 (2003)

http://www.ncbi.nlm.nih.gov/entrez/query.f...747&query_hl=62 (2004) Free Full Text



Acne – Insulin/IGF-1 Connection

Br J Dermatol. 1988 May;118(5):613-9. Related Articles, Links 


Acanthosis nigricans, insulin resistance and cutaneous virilism.

Barth JH, Ng LL, Wojnarowska F, Dawber RP.

Department of Dermatology, Slade Hospital, Oxford, U.K.

Thirteen patients with the syndrome of acanthosis nigricans and insulin resistance are described. They all had a combination of dermatoses related to hyperandrogenism (cutaneous virilism): hirsuties (II), acne vulgaris (6), hidradenitis suppurativa (5) and androgenic alopecia (4). In addition, 9 out of 13 had keratosis pilaris. The patients had raised fasting plasma insulin levels compared with matched normal controls (P less than 0.01) and increased insulin resistance (P less than 0.02). Insulin resistance correlated with total serum testosterone (rs = 0.65; P less than 0.02).
http://www.ncbi.nlm.nih.gov/entrez/query.f...47&query_hl=188

(1988)

http://www.ncbi.nlm.nih.gov/entrez/query.f...072&query_hl=47 (1998)

http://www.ncbi.nlm.nih.gov/entrez/query.f...68&query_hl=188 (1999 - females)

http://www.ncbi.nlm.nih.gov/entrez/query.f...448&query_hl=62 (2003 – females)

http://www.ncbi.nlm.nih.gov/entrez/query.f...33&query_hl=100 (2003)

CONCLUSIONS: Increased IGF-1 levels in addition to androgens may influence acne in adult men and women. While IGF-1 appears to have a stronger effect on acne in women, androgens may play a greater role in acne for men. However, in both men and women these hormones are interrelated, possibly owing to reciprocal effects on hormone production.
http://www.ncbi.nlm.nih.gov/entrez/query.f...674&query_hl=51

(2005) Free Full Text



Insulin/IGF-1 – Hormone Connection
http://www.ncbi.nlm.nih.gov/entrez/query.f...454&query_hl=27 (1980 – males)

http://www.ncbi.nlm.nih.gov/entrez/query.f...174&query_hl=27 (1980 – females)

http://www.ncbi.nlm.nih.gov/entrez/query.f...97&query_hl=177 (1985)

http://www.ncbi.nlm.nih.gov/entrez/query.f...56&query_hl=177 (1989)

http://www.ncbi.nlm.nih.gov/entrez/query.f...46&query_hl=177 (1992)

http://www.ncbi.nlm.nih.gov/entrez/query.f...88&query_hl=160 (2003)

http://www.ncbi.nlm.nih.gov/entrez/query.f...34&query_hl=177 (2003 – females)

Diabetes. 2004 Sep;53(9):2353-8. Related Articles, Links 

 
Glucose intolerance in a large cohort of mediterranean women with polycystic ovary syndrome: phenotype and associated factors.

Gambineri A, Pelusi C, Manicardi E, Vicennati V, Cacciari M, Morselli-Labate AM, Pagotto U, Pasquali R.

U.O. di Endocrinologia, Dipartimento di Medicina Interna e Gastroenterologia, Policlinico Sant' Orsola-Malpighi, via Massarenti 9, 40138 Bologna, Italy.

The aim of this study was to investigate the phenotypic parameters and associated factors characterizing the development of glucose intolerance in polycystic ovary syndrome (PCOS). Among the 121 PCOS female subjects from the Mediterranean region, 15.7 and 2.5% displayed impaired glucose tolerance and type 2 diabetes, respectively. These subjects were included in a single group of overweight or obese subjects presenting with glucose intolerance (GI) states. PCOS women with normal glucose tolerance (81.8%) were subdivided into two groups: those who were overweight or obese and those of normal weight. Metabolic and hormonal characteristics of the GI group included significantly higher fasting and glucose-stimulated insulin levels, more severe insulin resistance, hyperandrogenemia, and significantly higher cortisol and androstenedione responses to 1-24 ACTH stimulation. One important finding was that lower birth weight and earlier age of menarche were associated with GI in PCOS women. Frequency of hirsutism, oligomenorrhea, acne, and acanthosis nigricans did not characterize women with GI. Our findings indicate that PCOS patients with GI represent a subgroup with specific clinical and hormonal characteristics. Our observations may have an important impact in preventative and therapeutic strategies.

http://www.ncbi.nlm.nih.gov/entrez/query.f...45&query_hl=157

(2004 - females) Free Full Text

http://www.ncbi.nlm.nih.gov/entrez/query.f...17&query_hl=167 (2004 - males) Free Full Text

http://www.ncbi.nlm.nih.gov/entrez/query.f...28&query_hl=173 (2004 – male) Free Full Text

http://www.ncbi.nlm.nih.gov/entrez/query.f...68&query_hl=157 (2005 – females)

http://www.ncbi.nlm.nih.gov/entrez/query.f...41&query_hl=157 (2005 – females)



Diet/Food – Insulin/IGF-1 Connection
http://www.ncbi.nlm.nih.gov/entrez/query.f...65&query_hl=146 (1996 – females)

http://www.ncbi.nlm.nih.gov/entrez/query.f...29&query_hl=138 (2000) Free Full Text

http://www.ncbi.nlm.nih.gov/entrez/query.f...59&query_hl=127 (2002 - males) Free Full Text

CONCLUSIONS: High intake of milk and not meat, increased concentrations of s-IGF-I and s-IGF-I/s-IGFBP-3 significantly. Compounds in milk and not a high PI as such seem to stimulate IGF-I. This might explain the positive effect of milk intake on growth seen in some studies.
http://www.ncbi.nlm.nih.gov/entrez/query.f...33&query_hl=138

(2004 – males)

http://www.ncbi.nlm.nih.gov/entrez/query.f...80&query_hl=167 (2004)

http://www.ncbi.nlm.nih.gov/entrez/query.f...20&query_hl=177 (2004) Free Full Text



Diet/Food – Hormone Connection

J

Clin Endocrinol Metab. 1987 May;64(5):1083-5. Related Articles, Links 


Dietary lipids: an additional regulator of plasma levels of sex hormone binding globulin.

Reed MJ, Cheng RW, Simmonds M, Richmond W, James VH.

The effect of dietary lipid consumption on plasma levels of sex-hormone binding globulin (SHBG), free testosterone and cholesterol was studied in 6 normal men. After consuming a diet with a high fat content (greater than 100 g fat/day) for two weeks, the mean plasma cholesterol level increased (p less than 0.02) while the mean SHBG level decreased (p less than 0.02). Changing the diet from one with a high fat to low fat content (less than 20 g fat/day) for a further two week period resulted in a significant reduction in mean plasma cholesterol level (p less than 0.001) while the mean SHBG level increased (p less than 0.01). The increase in plasma SHBG was associated with a significant decrease in the free testosterone fraction and free testosterone concentration. No significant changes were detected in plasma samples obtained from the same men during a control period. The results from this study demonstrate that dietary lipid intake is an additional factor involved in the regulation of plasma levels of SHBG.
http://www.ncbi.nlm.nih.gov/entrez/query.f...725&query_hl=11

(1987 – males)

Beneficial effects of diet were not significantly different in the patients who were given metformin instead of placebo. These results confirm that weight loss induced by a low calorie diet is effective in improving hyperinsulinemia and hyperandrogenism in obese and hirsute women. With our study design, metformin administration had no additional benefit over the effect of diet.
http://www.ncbi.nlm.nih.gov/entrez/query.f...55&query_hl=127

(1995 – females)


http://www.ncbi.nlm.nih.gov/entrez/query.f...24&query_hl=114 (1998 - male)

http://www.ncbi.nlm.nih.gov/entrez/query.f...41&query_hl=114 (1998) Free Full Text

http://www.ncbi.nlm.nih.gov/entrez/query.f...10&query_hl=114 (2001 – male)

http://www.ncbi.nlm.nih.gov/entrez/query.f...18&query_hl=127 (2003 – female) Free Full Text

http://www.ncbi.nlm.nih.gov/entrez/query.f...46&query_hl=177 (2003)

http://www.ncbi.nlm.nih.gov/entrez/query.f...82&query_hl=167 (2005 – males)


Diet/Food Macronutrients – Acne Connection
http://www.ncbi.nlm.nih.gov/entrez/query.f...252&query_hl=70 (1975) NO Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.f...553&query_hl=92 (1976)

http://www.ncbi.nlm.nih.gov/entrez/query.f...350&query_hl=70 (1978)

http://www.ncbi.nlm.nih.gov/entrez/query.f...616&query_hl=90 (1985)
http://www.ncbi.nlm.nih.gov/entrez/query.f...543&query_hl=89 (1991)

http://www.ncbi.nlm.nih.gov/entrez/query.f...437&query_hl=92 (2001)

http://www.ncbi.nlm.nih.gov/entrez/query.f...46&query_hl=100 (2002)

http://www.ncbi.nlm.nih.gov/entrez/query.f...56&query_hl=153 (2004) Abstract

Update to study: Minnymouse posted this email from Dr. Mann in March 2005.

We are nearing completion of our study and will publish this year.
Slow process because we not only need to show an improvement in visual
acne condition but blood chemistry changes that can be used to develop
an hypothesis as to what aspects of metabolism are being altered by diet to effect an acne change. This blood analytical work is happening now
and we are seeing complex metabolic changes that relate to various skin
cell abnormalities and acne. The dermatology side did show improvement
on our diet but I need to qualify this a little. Young boys do not
stick well on diets when they are free living and exposed to abundance
of processed foods. The boys on low glycaemic load diets did gradually
improve (4-8 weeks) if they kept to the diet which included:

Low starch and sugar intake, ie eliminate all high GI foods, which
eliminated most bread, potatoes, most rice, baked goods made from any
flour ie any refined carb product, some fruits also can have high carb
eg bananas so go easy on these, sweetened products with much added sugar,
glucose or corn syrup are very bad even fruit juices with added carb
sweeteners should be avoided.

Our diets were rich in meat, fish, vegetables, salads, most fruits,
nuts and very low in grain and sweetened foods. The unfortunate part
is that it takes several weeks to clear up the acne but only a day or
two to reactivate if a high GI carb food is consumed, this we cannot
alter, its just the way the metabolic process works, so the person must
be careful.

Finally we are not all genetically the same and your sons acne may not
respond to the same extent as others and there seem to be some rare
cases where the person has an intolerance to a particular food or food
group that stimulates acne for them individually, dairy is an example
for some people, so if the above does not work try food eliminations
over several weeks and try and identify any food group that he may be
reacting to. http://www.acne.org/messageboard/index.php...39&#entry522039

http://www.ncbi.nlm.nih.gov/entrez/query.f...64&query_hl=155 (2005)


Yes, I know perhaps some of you will accuse me of bombarding and trying to overwhelm and confuse you with all of these abstracts, but that is why I predominantly posted links instead. You can pick and choose from them as you like, but most of them vary in some form or another. Of course, if you chose not to read them or the full studies (the coveted scientific evidence you long for) and you chose not to believe what I say, nor what others say, then that decision is what you will have to live. Unfortunately, I’ve had to learn that no matter what some of us do, there are people that won’t listen and won’t believe the truth no matter what.

Now, for those of you that did manage to sift through some of the links and you’ve got more questions, please ask them, but hopefully some of the answers will be found in later posts. I honestly hope that this will help you better understand the diet-acne connection. I know it doesn’t fit with what most doctors and dermatologists are telling you, but you have to remember, that some are General doctors, focusing on basic & multiple aspects of health, and others are Specilazed, focusing on 1 - 3 aspects. That means that some aren't paying enough attention and others aren't paying ANY attention to certain things. Besides with all of their patients, most doctors aren’t always able to be research oriented, but when looking for answers, we should still look toward scientific research and, more importantly, those that are peer-reviewed clinically controlled double-blinded studies, right? Well, most of the studies I posted fall into that category and I couldn’t say what I say or feel what I feel without knowing that there’s research to back me up.

Furthermore, I don’t know if any of you caught it, but I did post studies that seemed to almost conflict with our usual theory that these diets are anti-androgenic. Why? Well for those that are concerned it may affect your masculinity, it doesn’t quite work that way. There have been times when I found articles that said the opposite and, after looking at additional articles along with factoring in one’s age, gender etc., I learned that these diets can also be anti-estrogenic!

What, HOW can that be?

Yeah, that’s when I realized that ultimately these diets goal is to bring about hormonal balance and depending on what gender you are and/or your imbalance, the diet will work to correct for it. LOL, well no wonder, after all the same basic aspect of these diets happen also to fall under anti-proliferative (anti-cancer), anti-hyperkertinization, and anti-inflammatory all of which happen to contribute to the development of acne, right?


OK, OK so what foods can affect hormonal balance for those that have a sensitivity to normal amounts or for those that have a hormonal disorder?

Alcohol - with Gluten, all grain based, or high carbohydrate versions

“Too Much� Food – Too many calories or certain macronutrients.

Altered Food – Trans Fats, Genetically Modified Foods (GMO), Fermented foods

(Factory) Farmed Animals – mercury, growth hormones, antibiotics

Inorganic plant foods – pesticides, herbicides, etc

Goitrogenic foods – Special category for those susceptible to Hypothyroidism and well, sometimes too much soy products can induce this in those that weren’t susceptible.

Chemicals (added to foods) – Caffiene, MSG, Sulfates, Nitrates, Food Colorings (not all but some), Splenda/Sucralose

Inflammatory Foods – Allergenic, Intolerant, or some other food unique to the individual

Mishandled Foods - not refrigerated properly or cooked properly can increase exposure to bacteria and possibly parasites.

(Smoking - Nicotine increases inflammation among other problems)

(Lack of Exercise – slows metabolism, increases disease)

(Lack of Sleep – disrupts circadian rhythm)


Hmm...does that mean I have to avoid ALL of these things?

Of course not. While in an ideal world it would be great if we can live that pure organic holistic lifestyle, not everyone is capable of doing so and not everyone has to. With the exception to the way foods are being processed these days, there is NO such thing as purely bad, evil, or wrong foods. If there were, these would be deemed poisonous and NONE of us would be eating them! However there are foods that are more favorable and less favorable in preventing acne and disease, but sometimes this depends on the consumer. In other words, you only have to avoid the foods or chemicals, etc that cause you problems. Once again, if you know your health or hormonal problem, you’ll have a better idea of where to start, but if you don’t, your task is much greater…Yet if you find that your current methods are not effective enough, maybe you’ll want to give this a (2nd) chance.

You know earlier I had been watching Beyond Borders and I must admit, there were parts where I was crying. I just couldn’t understand why people don’t love each other enough, to do what’s right! I thought about how food can a make a world of difference to someone that’s starving and yet here I am talking about how food can contribute to acne. How laughable is that? Then I remembered, food can’t do everything, but for what it CAN do, why aren’t we using it for such? WHY aren’t we doing everything in our power to help ourselves? In countries where food is abundant, we don’t just use it to save our lives, but as unintentional as it may be, to also do us harm. In first world countries where we have the technology to surpass some third world diseases, HOW can we let something that is deemed “preventable� continue to hurt us? Whether it is 2 years, 10 years or 30 years before we feel the waning health effects, there was a point in all of our lives, probably several, where we could have made a different decision that would have prevented what is or what may become...but most people choose not to do anything at all. So when others, including myself, talk about this, it is not to induce fear, guilt or paranoia, but to further educate and empower you so that you are more equipped to help yourselves and, if no one else, those that you love and care for.

[kel]

my dermatlogist actually told me that she feels there is a very stroong link between high gi foods and acne,as people in certain parts of the world who dont have acne,dont have the high gi diet that people in the western world tend to have.

i have followed a diet ,as a vegan for two years i remember my skin was good, but now its shit again,as i began eating milk ext,however i had finished a course of tane the year prior,so not sure if that was the reason i was clear or not

[bexi]

You know earlier I had been watching Beyond Borders and I must admit, there were parts where I was crying.  I just couldn’t understand why people don’t love each other enough, to do what’s right! I thought about how food can a make a world of difference to someone that’s starving and yet here I am talking about how food can contribute to acne.  How laughable is that?  Then I remembered, food can’t do everything, but for what it CAN do, why aren’t we using it for such?  WHY aren’t we doing everything in our power to help ourselves?  In countries where food is abundant, we don’t just use it to save our lives, but as unintentional as it may be, to also do us harm.  In first world countries where we have the technology to surpass some third world diseases, HOW can we let something that is deemed “preventableâ€? continue to hurt us? Whether it is 2 years, 10 years or 30 years before we feel the waning health effects, there was a point in all of our lives, probably several, where we could have made a different decision that would have prevented what is or what may become...but most people choose not to do anything at all. So when others, including myself, talk about this, it is not to induce fear, guilt or paranoia, but to further educate and empower you so that you are more equipped to help yourselves and, if no one else, those that you love and care for.

I reckon most people would rather change their religeon than their diet! You are so right about the way we use food in privelidged societies to harm ourselves and not heal - it comes from our attitude to life in general, I think, and the way we take so much for granted because we have been lucky enough to live in a world where food is'nt something we need so much as something we enjoy, often to excess - the tragedy of living in a throw away society where absolutely everything is wasted, and on more than one level. Mental desenisization on a mass scale....The key is education and a healthy dose of suspicion of all those too good to be true TV ads and the bastards out there who try to make money out of putting crap in our food, on our crops, in our animals and our whole environment generally.

I look forward to your next installment - really interesting and well explained stuff SJ, thanks for sharing your knowledge and making the path to understanding so much clearer....

[SweetJade1980]

THE ROLE OF DIET IN SEBUM PRODUCTION

Alright there are many theories regarding increased sebum production such as, overwashing, excess heat (external or internal), but along with that there still seems to be one that can’t be entirely written off…the role of androgens. http://www.ncbi.nlm.nih.gov/entrez/query.f...7868&query_hl=5

The thing is, we have long thought that DHT or Dihydrotestosterone (super testosterone) was the culprit for sebum production and as such we have all waited for that magic pill, in this case a 5-alpha reductase inhibitor, that would inhibit the enzyme necessary (thought to be Type I 5alpha reductase isozyme) for the conversion of testosterone into DHT. Problem is, 5apha inhibitors for either isozyme 1 or 2 or both….have been:


* Breaking people out that NEVER had acne

* Increasing acne in certain acne sufferers (i.e. males)

* Have yielded no results (i.e. females)


To further support this, here’s the study that seems to currently squash our hopes:

J Am Acad Dermatol. 2004 Mar;50(3):443-7. Related Articles, Links
  
A systemic type I 5 alpha-reductase inhibitor is ineffective in the treatment of acne vulgaris.

Leyden J, Bergfeld W, Drake L, Dunlap F, Goldman MP, Gottlieb AB, Heffernan MP, Hickman JG, Hordinsky M, Jarrett M, Kang S, Lucky A, Peck G, Phillips T, Rapaport M, Roberts J, Savin R, Sawaya ME, Shalita A, Shavin J, Shaw JC, Stein L, Stewart D, Strauss J, Swinehart J, Swinyer L, Thiboutot D, Washenik K, Weinstein G, Whiting D, Pappas F, Sanchez M, Terranella L, Waldstreicher J.

University of Pennsylvania Hospital, 36th and Spruce Streets, Philadelphia, PA 19104, USA.

Excessive sebum production is a central aspect of the pathophysiology of acne vulgaris. Sebaceous gland function is under androgen control and it is hypothesized that dihydrotestosterone is formed by the action of 5 alpha-reductase. Type I is the controlling isoenzyme. This study describes a 3-month, multicenter, randomized, placebo-controlled clinical trial with a potent, selective inhibitor of type I 5 alpha-reductase used alone and in combination with systemic minocycline. Inhibition of type I 5 alpha-reductase was not associated with clinical improvement of acne when used alone and did not enhance the clinical benefit of systemic minocycline. These results indicate the need for further work at the molecular level to better understand the action of androgens on sebaceous gland function.
http://www.ncbi.nlm.nih.gov/entrez/query.f...688&query_hl=16

Therefore, it’s possible that DHT is NOT the contributor here but is just a measure of androgen receptor activity found to be increased in sebum. Granted I’m known for saying that not all studies are perfect, that the experimental designs are flawed or that they didn’t have the technology & knowledge at the time, and so it is still quite possible that DHT also plays a role in sebum production, yet…it still doesn’t discount diets role in affecting other factors in sebum production as well as DHT. After all, through diet (and exercise) if you reduce testosterone production or free testosterone availability then indirectly you’ve reduced the amount of testosterone that can be converted into DHT. Thus, perhaps the goal here isn’t to directly prevent DHT formation, but possibly to reduce or prevent androgen from binding to the androgen receptor.

OK…WHY?

Well, it’s been shown over and over again that various types of anti-androgens (Accutane, RetinA, Spironolactone, Birth Control, Avandia) work, yet currently 5-alphas inhibitors don’t have anything close to the same track record. Perhaps that’s because before or once androgen binds to the androgen receptor a host of processes occur, and while DHT production is one of them, preceding or along with that comes a rise in IGF-1, plus immune mediators that also contribute to the development acne. So what if it’s the IGF-1, PPARs, Iimmune Meadiators, etc that’s the problem?

Ready to find out?

Now, excess sebum has long been thought to be the reason for acne as well, right? OK, what about those people with:

Dry Skin

Oily Skin

That DO NOT have acne???

Hmm... perhaps excess sebum isn’t the main factor, but rather yet another measure of androgen receptor activity.

Notice, the studies on 5-alpha reductase inhibitors mentioned that there WAS a decrease in DHT and an INCREASE in Testosterone found in sebum. Now logically if you prevent DHT formation, you will have an increase in (Free) Testosterone because it’s not being converted. However, what about the other products that are found in sebum? What about those other INCREASED products that are found in sebum that studies have shown more directly participate in the production of acne? As such, the studies do not discount that sebum has a role, but what if that role is merely to act as a transporter for a variety of other factors that play a much larger role in acne production???

Hmm…if this is the case, then it DOES NOT matter how MUCH sebum you produce, what matters is WHAT your sebum contains.

Make sense???

Clin Dermatol. 2004 Sep-Oct;22(5):360-6. Related Articles, Links
  
Acne and sebaceous gland function.

Zouboulis CC.

Department of Dermatology, Charite University Medicine Berlin, Campus Benjamin Franklin, Fabeckstrasse 60-62, 14195 Berlin, Germany. christos.zouboulis@charite.de

The embryologic development of the human sebaceous gland is closely related to the differentiation of the hair follicle and the epidermis. The number of sebaceous glands remains approximately the same throughout life, whereas their size tends to increase with age. The development and function of the sebaceous gland in the fetal and neonatal periods appear to be regulated by maternal androgens and by endogenous steroid synthesis, as well as by other morphogens. The most apparent function of the glands is to excrete sebum. A strong increase in sebum excretion occurs a few hours after birth; this peaks during the first week and slowly subsides thereafter. A new rise takes place at about age 9 years with adrenarche and continues up to age 17 years, when the adult level is reached.

The sebaceous gland is an important formation site of active androgens. Androgens are well known for their effects on sebum excretion, whereas terminal sebocyte differentiation is assisted by peroxisome proliferator-activated receptor ligands. Estrogens, glucocorticoids, and prolactin also influence sebaceous gland function. In addition, stress-sensing cutaneous signals lead to the production and release of corticotrophin-releasing hormone from dermal nerves and sebocytes with subsequent dose-dependent regulation of sebaceous nonpolar lipids. Among other lipid fractions, sebaceous glands have been shown to synthesize considerable amounts of free fatty acids without exogenous influence. Sebaceous lipids are responsible for the three-dimensional skin surface lipid organization. Contributing to the integrity of the skin barrier. They also exhibit strong innate antimicrobial activity, transport antioxidants to the skin surface, and express proinflammatory and anti-inflammatory properties.

Acne in childhood has been suggested to be strongly associated with the development of severe acne during adolescence. Increased sebum excretion is a major factor in the pathophysiology of acne vulgaris. Other sebaceous gland functions are also associated with the development of acne, including sebaceous proinflammatory lipids; different cytokines produced locally; periglandular peptides and neuropeptides, such as corticotrophin-releasing hormone, which is produced by sebocytes; and substance P, which is expressed in the nerve endings at the vicinity of healthy-looking glands of acne patients.

Current data indicate that acne vulgaris may be a primary inflammatory disease. Future drugs developed to treat acne not only should reduce sebum production and Propionibacterium acnes populations, but also should be targeted to reduce proinflammatory lipids in sebum, down-regulate proinflammatory signals in the pilosebaceous unit, and inhibit leukotriene B(4)-induced accumulation of inflammatory cells. They should also influence peroxisome proliferator-activated receptor regulation. Isotretinoin is still the most active available drug for the treatment of severe acne.
http://www.ncbi.nlm.nih.gov/entrez/query.f...719&query_hl=23

Thus sebum contains: hormones, red blood cells, white blood cells, lipids, pro-inflammatory free fatty acids (arachidonic acid), pro-inflammatory cytokines (IL-1, IL-6, IL-8, IL-12), leukotriene-beta, among other things depending on the nature of the your acneic condition (i.e. different types of microbes) that determines the type of acneform you have or will develop.

Furthermore, the above abstract mentioned that Isotretinoin, Accutane, as still being the most active drug for the treatment of severe acne. Yet, did you know that Accutane affects the sebaceous glands not just because of its anti-androgen and 5-alpha reductase abilities, but because of it’s anti-proliferative abilities as well (among other mysteries)???

J Invest Dermatol. 2000 Feb;114(2):349-53. Related Articles, Links
  
The role of specific retinoid receptors in sebocyte growth and differentiation in culture.

Kim MJ, Ciletti N, Michel S, Reichert U, Rosenfield RL.

Departments of Pediatrics and Medicine, Pritzker School of Medicine, The University of Chicago, Chicago, Illinois, USA.

Retinoic acid derivatives (retinoids) exert their pleiotropic effects on cell development through specific nuclear receptors, the retinoic acid receptors and retinoid X receptors. Despite recent progress in understanding the cellular and molecular mechanisms of retinoid activity, it is unknown which of the retinoid receptor pathways are involved in the specific processes of sebocyte growth and development. In this study, we investigated the roles of specific retinoid receptors in sebocyte growth and differentiation, by testing the effects of selective retinoic acid receptor and retinoid X receptor ligands………………  Our data suggest that retinoic acid receptors and retinoid X receptors differ in their roles in sebocyte growth and differentiation:

(i) retinoic acid receptors, especially the beta and/or gamma subtypes, mediate both the antiproliferative and antidifferentiative effects of retinoids;

(ii) retinoid X receptors mediate prominent differentiative and weak proliferative effects;

(iii) the antiproliferative and antidifferentiative effects of all-trans retinoic acid are probably mediated by retinoic acid receptors, whereas its differentiative effect at high dose may be mediated by retinoid X receptors via all-trans retinoic acid metabolism to 9-cis retinoic acid, the natural ligand of retinoid X receptors.
http://www.ncbi.nlm.nih.gov/entrez/query.f...997&query_hl=28

Now, retiniods have this ability to regulate Insulin-like Growth Factor Binding Proteins and Accutane happens to increase IGFBP-3. If you were able to understand hormones role in acne based on my previous post, then you should know that IGFBP-3 binds to IGF-1, a cell proliferator, to lower it. Furthermore, you should have also learned that decreasing your insulin & free fatty acid levels through diet (supplements, or medications), can affect not only your SHBG levels (responsible for binding Free Testosterone) but also affect levels of IGFBP-3. Thus this is one way that diet can affect sebum production via regulating IGFBP-3.

J Endocrinol. 2002 Oct;175(1):33-40. Related Articles, Links
  
Nuclear effects: unexpected intracellular actions of insulin-like growth factor binding protein-3.

Lee KW, Cohen P.

Division of Pediatric Endocrinology, Mattel Children's Hospital at UCLA, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, MDCC 22-315, Los Angeles, California 90095-1752, USA.

Insulin-like growth factor (IGF) binding protein (IGFBP)-3 has been shown to be a growth inhibitory, apoptosis-inducing molecule by virtue of its ability to bind IGFs, in addition to previously demonstrated IGF-independent effects. The recent discovery of the interaction between nuclear IGFBP-3 and 9-cis retinoic acid receptor-alpha (retinoid X receptor alpha RXRalpha), a nuclear receptor, and its involvement in the regulation of transcriptional signaling and apoptosis represents an important paradigm shift in the understanding of IGFBP function. RXRalpha is required for the apoptosis-inducing effects of IGFBP-3. IGFBP-3 and RXR ligands are additive in inducing apoptosis in cancer cells. IGFBP-3 has direct effects on gene transcription, as RXR response element reporter signaling was enhanced and the all-trans retinoic acid receptor response element reporter signaling was inhibited. Accumulating evidence further confirms IGF-independent functions of this multifunction binding protein. Other binding proteins, in addition to other members of the IGF axis, have now been described in the nucleus and are postulated to have effects on transcriptional events. Investigation into these new interactions will expose new protein partners in the interface between the nuclear receptor and growth factor pathways and reveal new targets to be exploited in the treatment of cancer and other diseases.
http://www.ncbi.nlm.nih.gov/entrez/query.f...9488&query_hl=3

Hmm… did you notice that this didn’t talk about accutane, 13-cis retinoic acid/Isotretinoin, specifically but mentioned All Trans Retinoic Acid (Retinoic Acid) and 9-cis retinoic acid as being major factors instead? This is because while accutane does increase IGBP-3, it also converts into all trans retinoic acid in order to quite possibly exert further affects on the sebaceous glands.

J Invest Dermatol. 2000 Aug;115(2):321-7. Related Articles, Links
  
13-cis retinoic acid exerts its specific activity on human sebocytes through selective intracellular isomerization to all-trans retinoic acid and binding to retinoid acid receptors.

Tsukada M, Schroder M, Roos TC, Chandraratna RA, Reichert U, Merk HF, Orfanos CE, Zouboulis CC.

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

Despite its potent biologic effect on human sebocytes, 13-cis retinoic acid exhibits low binding affinity for cellular retinoic acid binding proteins and nuclear retinoid receptors. Hence, 13-cis retinoic acid may represent a pro-drug possibly acting through all-trans isomerization. In this study, marked isomerization of 13-cis retinoic acid has been confirmed in cultured SZ95 sebocytes showing 2- to 15-fold higher levels of all-trans retinoic acid at 12-72 h, as measured by high performance liquid chromatography. In contrast, only low amounts of all-trans retinoic acid were converted intracellularly to its 13-cis isoform. 9-cis retinoic acid was not detected after either 13-cis retinoic acid or all-trans retinoic acid treatment. The rapid isomerization of 13-cis retinoic acid to high levels of all-trans retinoic acid was a sebocyte-specific event, as no significant isomerization of 13-cis retinoic acid to all-trans retinoic acid occurred in HaCaT keratinocytes. De novo mRNA expression of cytochrome P450 1A1, a major xenobiotic metabolizing enzyme, in SZ95 sebocytes was induced by all-trans retinoic acid, but not by 13-cis retinoic acid. In addition, mRNA levels of cellular retinoic acid-binding protein II, which is supposed to regulate the concentration of intracellular all-trans retinoic acid, rapidly increased under all-trans retinoic acid treatment (30 min-6 h), whereas the 13-cis retinoic acid effect was markedly weaker and delayed. Both 13-cis retinoic acid and all-trans retinoic acid suppressed mRNA expression of cytochrome P450 1A2. In parallel experiments, 13-cis retinoic acid significantly reduced SZ95 sebocyte proliferation at 10-7 M, show- ing 30-40% inhibition after 9 d. All-trans retinoic acid and 9-cis retinoic acid exhibited similar anti-proliferative effects. AGN 193109, a pan-antagonist of the retinoic acid receptors, antagonized the anti-proliferative activity of all retinoic acid isomers tested in a concentration-dependent manner with complete abolishment at ratios of 1:10 13-cis retinoic acid and 1:1 all-trans retinoic acid. Coincubation of SZ95 sebocytes with 13-cis retinoic acid and AGN 193109 did not alter the intracellular concentration of 13-cis retinoic acid and its isomerization profile. In contrast, the retinoid X receptor antagonist CD 3507 did not affect the inhibition of SZ95 sebocyte proliferation induced by retinoic acids. Our findings indicate:

(i) a selective 13-cis retinoic acid isomerization to all-trans retinoic acid in the intracellular compartment of SZ95 sebocytes;

(ii) a reduced all-trans retinoic acid inactivation process after 13-cis retinoic acid treatment as compared with treatment with all-trans retinoic acid; and

(iii) a retinoic acid receptor-mediated inhibition of SZ95 sebocyte proliferation.

These data explain the sebocyte-specific activity of 13-cis retinoic acid and support a pro-drug/drug relation between 13-cis retinoic acid and all-trans retinoic acid. http://www.ncbi.nlm.nih.gov/entrez/query.f...254&query_hl=89

Furthermore, Retinoid X Receptors, or RXR-alphas, also bind to Peroxisome Proliferator-Activating Receptors (PPARs) to regulate keritinization, inflammation, and sebum production as well.

It has been difficult to induce the expected sebocyte differentiation in vitro with dihydrotestosterone (DHT). We reasoned that our culture system lacks differentiating factors, and peroxisome proliferator-activated receptors (PPARs) were the prime candidates.... http://www.ncbi.nlm.nih.gov/entrez/query.f...23&query_hl=109

We detected RNA expression of PPARalpha, PPARbeta, PPARgamma, retinoid X receptor alpha, liver X receptor alpha (LXRalpha) and pregnane X receptor but not FXR in freshly isolated and 7-day maintained sebaceous glands. PPARalpha, PPARbeta, PPARgamma and LXRalpha protein were detected in nuclear extracts of sebaceous glands. CONCLUSIONS: We conclude that activation of nuclear hormone receptors, in particular activation of PPARalpha and PPARgamma, can regulate lipogenesis in human sebaceous glands. As suppression of sebum secretion is associated with reduced acne activity, the nuclear hormone receptors involved may open new avenues in the development of novel acne treatments. http://www.ncbi.nlm.nih.gov/entrez/query.f...415&query_hl=23

Br J Dermatol. 2003 Aug;149(2):229-36. Related Articles, Links 

 
Peroxisome proliferator-activated receptors in cutaneous biology.

Kuenzli S, Saurat JH.

Department of Dermatology, University Hospital, Geneva, Switzerland. stephanie.kuenzli@medecine.unige.ch

Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that regulate the expression of target genes involved in many cellular functions including cell proliferation, differentiation and immune/inflammation response. The PPAR subfamily consists of three isotypes: PPAR alpha, PPAR beta/delta and PPAR gamma, which have all been identified in keratinocytes. PPAR beta/delta is the predominant subtype in human keratinocytes, whereas PPAR alpha and PPAR gamma are expressed at much lower levels and increase significantly upon keratinocyte differentiation. PPAR beta/delta is not linked to differentiation, but is significantly upregulated upon various conditions that result in keratinocyte proliferation, and during skin wound healing. In vitro and in vivo evidence suggests that PPARs appear to play an important role in skin barrier permeability, inhibiting epidermal cell growth, promoting epidermal terminal differentiation and regulating skin inflammatory response by diverse mechanisms. These proprieties are pointing in the direction of PPARs being key regulators of skin conditions characterized by hyperproliferation, inflammatory infiltrates and aberrant differentiation such as psoriasis, but may also have clinical implications in inflammatory skin disease (e.g. atopic dermatitis), proliferative skin disease, wound healing, acne and protease inhibitor associated lipodystrophia. http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12932225

Of course, diet affects the activation or upregulation of PPARs. Too many calories, fat or refined carbohydrates in the diet and you’ll upregulate PPAR-beta/delta which is largely responsible for keritinization and a high amount of sebum production. Whereas, you move to a high fiber and low fat diet and you’ll upregulate PPAR-alpha and PPAR gammas, which are responsible for a reduction in sebum output, improving insulin resistance, and decreasing inflammation. Now you can also do this through supplementation if you like, but this thread is more specifically about dietary measures. http://www.acne.org/messageboard/index.php...st=80&p=667715& (page 5)


http://www.ncbi.nlm.nih.gov/entrez/query.f...93&query_hl=127


http://care.diabetesjournals.org/cgi/content/full/27/9/2251

EMBO Rep. 2004 Feb;5(2):142-7. Related Articles, Links
  
Peroxisome proliferator-activated receptor-gamma: too much of a good thing causes harm.

Cock TA, Houten SM, Auwerx J.

Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS/INSERM/Universite Louis Pasteur, 67404 Illkirch, France.


The nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARgamma) helps to translate 'what you eat' into 'what you are' because it allows dietary fatty acids (PPARgamma ligands) to modulate gene transcription. Treatments for diabetes include PPARgamma activators, as they sensitize the body to insulin. Our understanding of PPARgamma function has recently been enhanced by a flurry of human and mouse genetic studies, and the characterization of new PPARgamma ligands. This insight has led us to propose that modulating PPARgamma activity, rather than activating it, might be the most effective strategy for treating metabolic disorders, as this will improve glucose homeostasis while preventing adipogenesis.
http://www.ncbi.nlm.nih.gov/entrez/query.f...07&query_hl=143  (free full text)

Of course some of you may have appreciated those abstracts and some of you probably didn’t. For those that would prefer a summary, I basically was trying to show you how diet affects sebum production via, at least two of the routes that Accutane does. Now we already know that SHBG binds Free Testosterone, but if this is left unbound (thanks to possibly our diets), then it's free to bind to the androgen receptor and continue along the path to acne production.

From a prior abstract in the hormone-diet post, it was indicated that we need both Androgens and IGF-1 to initiate acne development. Since retinoids, and thus accutane, increase IGFBP-3 which not only binds IGF-1, but also binds to the RXR-alpha receptors that are involved in sebum production, increasing this binding protein seems beneficial. Thankfully, we can naturally increase IGFBP-3 by reducing the amount of high calorie foods, insulinotropic (insulin stimulating) foods, animal saturated fats, and eliminating trans fats in the diet.

Furthermore, since those same foods can also activate PPAR beta/delta which further increases sebum production, inflammation, and hyperkeritinization, the goal is to alter your diet to reduce their expression while increasing the expression of PPAR alpha and PPAR gammas…those that reduce insulin resistance, inflammation, and sebum production. Yes while, you can do this through medication (see the supplement link above), they have side effects and can also lead to over-expression of PPAR-gammas, which can lead to further complications. Therefore, to reduce complications and other side effects, or just to save money, more of you may want to consider diets role in acne produciton if your current regiment is working effectively enough for ya!

So, hopefully this helped show you diets role in a few aspects of sebum production. I’m sure there are a few more but, I must admit that my brain has had more than enough of the diet-sebum role in acne production.., would anyone care to take over???

Bye for now

[nick_04]

I still don't have a clue what the connection is, and i doubt i ever will!

[kel]

this is alot of info to read,it seems to just confuse me.
im soon to start my nutrition course so im sure i will no more then,i was a vegan and that helpt my skin? any thoughts on that anyone?

i feel its the dairy connection mainly?

[SweetJade1980]

I still don't have a clue what the connection is, and i doubt i ever will!

LOL, sorry. What exactly is your concern with the connection? Is it the hormones the sebum or some other aspect of acne you've always heard contributed and you don't understand where diet plays a role?

Unfortunately if the above abstracts confused you than I do apologize. They are there so that you can see how my mind works, lend some credibility to what myself and other members are saying, but more so for that that are doubtful, critical, or more scientific or research minded.

Of course, I welcome anyone to decipher what I said in order to make it easier for you and others to understand. I can come at it only so many different ways and reach so many people, but when someone else is capable of coming at it from a few more ways, even more people can be reached!

[kel]

i wana just make sure im doing all the things i can do diet wise i guess,i just wondered what your opinion was on veganism and my thoughts on how my acne was alot better i believe on a veagn diet,why is this so,in your opinion?

[SweetJade1980]

this is alot of info to read,it seems to just confuse me.
im soon to start my nutrition course so im sure i will no more then,i was a vegan and that helpt my skin? any thoughts on that anyone?

i feel its the dairy connection mainly?

LOL, yeah it wasn't as easy for me to put the sebum part together because half of it most of you have never heard of it! Honestly all you can do is reread it, read the links and do your own reserch. I promise you most of what I know I know because I did the exact same thing whenever someone presented something to me. It's not something I learned in biology books, but yes that does help to some extent, most of this I learned by researching, writing it down, writing down definitions and then putting the connections together on paper.


I opted not to mention many specific foods because some of this has to do with the immune response which has nothing to do with some the sugar-acne connection and I couldn't begin to say what food specifically affects someone. However dairy would be one of them for some people for various reasons:

Raisies IGF-1 (casien, & whey) which has an anabolic or building affect and the ability to increase androgens and inflammtory products on it's route to acne production via stimulating the growth of sebeceous glands and sebum prodution (remember IGFPB-3 binds this and can inhibit it's ability to do those things). - This was mentioned in the Hormone-Diet post as well as in the Sebum-Diet post.

Lactose Intolerances - if you are intolerant to something that means you may be lacking an enzyme. Signs include bloating, gas, but also inflammation (acne is an inflammatory disease)

Casien Allergy/Intolerance - ditto

Yup, I'm also studying nutriton now too and have a few classes lined up this fall. I'm really excited about taking the Nutrition & Disease course but unfortunately it was cancelled last year and since only 4 people have registered I fear it will be cancelled again =(