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I woke up at 2:00 in the morning to research insulin one last time. I beleived that I had found something. What I found was shocking. Here it is: https://www.novapublishers.com/catalog/product_info.php?products_id=4933

"A transient insulin resistant state occurs during puberty and is part of normal human development. Insulin resistance increases immediately at the beginning of puberty, peaks at mid-puberty, and then declines to nearly prepubertal levels by early adulthood. Girls are more insulin resistant than boys during puberty which is related in part to differences in adiposity between the sexes. Glucose homeostasis is maintained during puberty through compensatory hyperinsulinemia. While resistance to insulin’s effect on glucose metabolism is present, insulin-stimulated protein metabolism is normal. Therefore, a physiologic consequence of insulin resistance during puberty may be augmentation of rapid growth by promotion of protein anabolism.

The causes of physiological insulin resistance during puberty have not been definitively established. Gonadal sex steroids do not appear to play a central role. There is strong evidence, however, that GH/IGF-I activity contributes to pubertal insulin resistance. GH and IGF-I levels increase and then decrease during puberty, following a pattern similar to that of insulin resistance. A significant association between IGF-I levels and pubertal insulin resistance has been demonstrated in many studies. Some studies find that African Americans are more insulin resistant during puberty than their white counterparts, although this was not found to be the case in a study where the black youth were lean and physically active. "

In puberty insulin resistance develops and then it goes away at the end of puberty. Sound familiar? in puberty, if one has acne, acne is beleived to start and then you "grow out" of it.

okay so that sounds strange right? a coincidence? i think not

then i said what does insulin have to do with sebum and acne?

i found this: http://www.ncbi.nlm.nih.gov/pubmed/10428145

Good correlations, although lower, between insulin and T, and BMI, insulin, and T with triglycerides were also found in patients with PCOS. These patients fell into clearly distinct categories: with or without insulin resistance and with or without obesity, but slim women with PCOS had insulin and metabolic variables similar to those without PCOS, and most obese women with PCOS were insulin-resistant and more hyperandrogenic and hypertriglyceridemic.


Insulin, androgens, and BMI are related in women both with PCOS and without PCOS, especially in obese ones. Insulin and metabolic indices are similar in lean women with PCOS and those without PCOS, but obese women with PCOS are more insulin-resistant, hyperandrogenic, and hypertriglyceridemic. Three types of disorders can be distinguished: simple nonhyperandrogenic obesity, typical nonhyperinsulinemic PCOS, and insulin-resistant PCOS.

So inslun is related positively to androgens?

Then i found this: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3051853/

"Typical western diet, comprised of milk and hyperglycaemic foods, may have potentiating effects on serum insulin and insulin-like growth factor-I (IGF-I) levels, thereby promoting the development of acne.17"

then i found this: http://www.ncbi.nlm.nih.gov/pubmed/19709092

"It is the purpose of this viewpoint article to delineate the regulatory network of growth hormone (GH), insulin, and insulin-like growth factor-1 (IGF-1) signalling during puberty, associated hormonal changes in adrenal and gonadal androgen metabolism, and the impact of dietary factors and smoking involved in the pathogenesis of acne. The key regulator IGF-1 rises during puberty by the action of increased GH secretion and correlates well with the clinical course of acne. In acne patients, associations between serum levels of IGF-1, dehydroepiandrosterone sulphate, dihydrotestosterone, acne lesion counts and facial sebum secretion rate have been reported. IGF-1 stimulates 5alpha-reductase, adrenal and gonadal androgen synthesis, androgen receptor signal transduction, sebocyte proliferation and lipogenesis. Milk consumption results in a significant increase in insulin and IGF-1 serum levels comparable with high glycaemic food. Insulin induces hepatic IGF-1 secretion, and both hormones amplify the stimulatory effect of GH on sebocytes and augment mitogenic downstream signalling pathways of insulin receptors, IGF-1 receptor and fibroblast growth factor receptor-2b. Acne is proposed to be an IGF-1-mediated disease, modified by diets and smoking increasing insulin/IGF1-signalling. Metformin treatment, and diets low in milk protein content and glycaemic index reduce increased IGF-1 signalling. Persistent acne in adulthood with high IGF-1 levels may be considered as an indicator for increased risk of cancer, which may require appropriate dietary intervention as well as treatment with insulin-sensitizing agents."

very strange. i'm not sure whether or not its igf-1 or insulin. i beleive it is inslun resistance which is brought on my puberty! but!!!!!!!!

theres a missing link here. something that doesn't make sense! if insulin resistance is a marker of puberty then why doesn't everyone have acne and have it to the same extent. Well the asnwer to this is complicated. One of the factors is diet. People who eat a better less simple sugar diet will not have as much acne. But this isn't true for all. How many people have heard the man say "my friend eats junk all the time and has no acne. WHy me!!" Well i beleive their is a missing link here. Only certain people have some sort of genetical DNA structure that makes insulin resistance trigger acne for them. This is why diabetic people do not neccesarily have acne.

Now Acne is supposed to pass during adulthood but a lot of people here on the board have acne and are passed their mid 25's. This is a serious health risk. It will probably lead to diabetes. Now, why???

Hypothesis: So i beleive that insulin resistance which is a normal part of puberty leads to increased androgens which leads to acne for those who have that genetic disposal. Which, if you are reading this, you have that genetic disposal.

Now, what backs this hypothesis up? the best way is to look at some of successful acne treatments:

i will start with vitamin A

i found this: http://www.ncbi.nlm.nih.gov/pubmed/10966898

"Statistically significant direct relations were observed between SSPG and mean arterial blood pressure (r = 0.44, P: = 0.008) and plasma lipid hydroperoxide concentrations (r = 0.42, P: = 0.01), whereas significant inverse correlations were found between SSPG and alpha-carotene (r = -0.58, P: = 0.0002), beta-carotene (r = -0.49, P: = 0.004), lutein (r = -0.35, P: = 0.04), alpha-tocopherol (r = -0. 36, P: = 0.04), and delta-tocopherol (r = -0.45, P: = 0.007).


Variations in insulin-mediated glucose disposal in healthy individuals are significantly related to plasma concentrations of lipid hydroperoxides and liposoluble antioxidant vitamins. These findings suggest that total plasma lipid peroxidation is increased in insulin-resistant individuals at an early, preclinical stage, ie, well before the development of glucose intolerance and type 2 diabetes."

sound familiar? vitamin A is lipid soluble and is beta carotene. now maybe we know why accutane works so well????

okay that's only one example. lets go for zinc:

"Regarding obesity and insulin resistance, alterations in zinc concentration and distribution in tissues, as well as improvement in sensitivity to insulin after supplementation with this element, have been detected. Thus, the metabolic role of zinc in the insulin resistance syndrome should be further investigated having in mind that this element may contribute to the control of the usual metabolic alterations present in obese patients."

The studies are there that zinc improves acne by 85%! no one knows why. turns out it improves insulin sensitivity.

how about antibiotics?

here you go: http://www.trialregister.nl/trialreg/admin/rctview.asp?TC=2566

"Accumulating data from both patients and animal models indicates that imbalances in the composition of the gut microbiota are related to obesity and its associated diseases However, the exact role of the microbiota and the mechanism mediating its impact on metabolic functions are poorly understood.

Interestingly, antibiotics have been shown to produce drastic short- and long-term alterations of the human indwelling microbiota. After a 2 wk intervention with norfloxacin in combination with ampicillin the numbers of aerobic and anaerobic gut bacteria in ob/ob mice were maximally suppressed. The ob/ob mice showed a significant improvement in fasting glycemia and oral glucose tolerance by 30%. Concomitant reduction of liver triglycerides, reduction of lipopolysaccharides supported the antidiabetic effects of antibiotic treatment. This study showed that modulation of gut microbiota with antibiotics improved glucose tolerance in mice by altering the expression of hepatic and intestinal genes involved in inflammation and metabolism.

wow! so turns out antibiotics improve insulin resistance. who would have thought? the list goes on with popular suplements for acne such as vitamin c, chromium, magnesium.

how about omega 3's???

here you go: http://www.ncbi.nlm.nih.gov/pubmed/18348080

"Aging diminishes hormone secretion and target cell responsiveness, possibly due to loss of cell membrane fluidity or alteration of membrane phospholipids affecting signal transduction. We investigated whether a high omega-3 polyunsaturated fatty acid diet would improve endocrine function in 6 men and 6 women aged over 60 years. Subjects first ate an isocaloric control diet for 6 weeks, followed by an 8-week experimental diet, which included 720 g of fatty fish weekly plus 15 ml of sardine oil daily. In the last week, we measured RBC membrane fatty acids on each diet, performed pituitary, adrenal, hepatic, and Leydig cell endocrine provocative testing, and assayed selected cytokines. We also assessed insulin sensitivity utilizing octreotide insulin suppression testing and assessed free fatty acid (FFA) responses to isoproteronol. Insulin sensitivity increased significantly after 8 weeks on the omega-3 diet and FFA responses trended lower. Serum C-reactive protein was significantly reduced and a trend towards lower IL-6 was noted. No differences were found in other metabolic parameters, adiponectin levels, or hormone responses. We conclude that, in older people, high omega-3 consumption increases insulin sensitivity, may reduce FFA mobilization by catecholamines, and reduces inflammatory markers, but did not alter endocrine responsiveness after 8 weeks

omega 3's are missing in the american diet according to many. acne is prevalent in america in many populations that it was not! coincidence? you tell me.

how about those omega 6's that are part of the SAD:

"Relationships between polyunsaturated FA type and IR vary according to the presence or absence of MS. N-3 FAs including EPA and DHA are associated with lower HOMA-IR, while the opposite is true for n-6 FAs. Prospective studies are required to address the potential effects of intermediate dose EPA and DHA on glucose handling in MS patients.

the opposite!!! so omega 6's fuel insulin resistance. btw, insulin is a hormone.

in science there are theories and there are hypothesis's. When you can back something you can challenge other previous wrong things.

The hypothesis: acne is caused by insulin resistance that is normal during puberty. The missing link is that genetic code that makes us all here predisposed to acne. This provides hope for the future as humankind can find that genetic peice and take it out. So for most teens they would normally grow out of their acne and you shouldn't be worried. You should be worried on the other hand, if you get poor exercise, are overweight, and you eat a simple sugar diet. sounds like most americans, doesn't it??? well acne is extremely prevalent in well developed societies. coincidence? you tell me.

so what does this all mean for me. it means i'm not sure i can ever forgive god for giving that genetic disposal to acne. It's unfair and it's not right. but boo hoo everyone knows, life is unfair. that's just the way it is.

so this now makes treating acne a lot easier for people who know about this info. turns out a lot of people on the board already do and doctors do as well. its an internal fight. its a fight against genetics. however, it may be a loosing battle for many of us with teenage acne. After all, insulin resistance is a normal part of puberty.

this is all a theory but it the most shocking, rare, and formidable back up that i have ever seen in a theory. It has the biology to back it up, the research, the chemistry, and the evidence of current treatment. This was all written by someone who went to bed at 3 in the morning last night so i do apologize for my typo's.


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