The purpose of this paper is to highlight the endocrine signaling of Western diet, a fundamental environmental factor involved in the pathogenesis of epidemic acne. Western nutrition is characterized by high calorie uptake, high glycemic load, high fat and meat intake, as well as increased consumption of insulin- and IGF-1-level elevating dairy proteins. Metabolic signals of Western diet are sensed by the nutrient-sensitive kinase, mammalian target of rapamycin complex 1 (mTORC1), which integrates signals of cellular energy, growth factors (insulin, IGF-1) and protein-derived signals, predominantly leucine, provided in high amounts by milk proteins and meat. mTORC1 activates SREBP, the master transcription factor of lipogenesis. Leucine stimulates mTORC1-SREBP signaling and leucine is directly converted by sebocytes into fatty acids and sterols for sebaceous lipid synthesis. Over-activated mTORC1 increases androgen hormone secretion and most likely amplifies androgen-driven mTORC1 signaling of sebaceous follicles. Testosterone directly activates mTORC1. Future research should investigate the effects of isotretinoin on sebocyte mTORC1 activity. It is conceivable that isotretinoin may downregulate mTORC1 in sebocytes by upregulation of nuclear levels of FoxO1. The role of Western diet in acne can only be fully appreciated when all stimulatory inputs for maximal mTORC1 activation, i.e., glucose, insulin, IGF-1 and leucine, are adequately considered. Epidemic acne has to be recognized as an mTORC1-driven disease of civilization like obesity, type 2 diabetes, cancer and neurodegenerative diseases. These new insights into Western diet-mediated mTORC1-hyperactivity provide a rational basis for dietary intervention in acne by attenuating mTORC1 signaling by reducing (1) total energy intake, (2) hyperglycemic carbohydrates, (3) insulinotropic dairy proteins and (4) leucine-rich meat and dairy proteins. The necessary dietary changes are opposed to the evolution of industrialized food and fast food distribution of Westernized countries. An attenuation of mTORC1 signaling is only possible by increasing the consumption of vegetables and fruit, the major components of vegan or Paleolithic diets. The dermatologist bears a tremendous responsibility for his young acne patients who should be advised to modify their dietary habits in order to reduce activating stimuli of mTORC1, not only to improve acne but to prevent the harmful and expensive march to other mTORC1-related chronic diseases later in life.
http://www.landesbio.../article/19828/
Natural mTORC1 inhibitors areEGCG, Resveratrol, Curcumin
"high calorie uptake, high glycemic load, high fat and meat intake"
I do all this and have no reaction (knock on wood) to eating and acne. Intake of calories up to 5-6k daily, eating high glycemic foods, meats and foods high in fat.
So.. this is a cause for some people. Others no. Good information though.
"high calorie uptake, high glycemic load, high fat and meat intake"
I do all this and have no reaction (knock on wood) to eating and acne. Intake of calories up to 5-6k daily, eating high glycemic foods, meats and foods high in fat.
So.. this is a cause for some people. Others no. Good information though.
Yes, just like not everyone gets cancer or diabetes [but many people do].
Acne is more or less a genetic condition and your diet is not the only [albeit very important] factor that determines if one will have acne or not. You also have to consider growth factors [particularly IGF-1]. People with low basal IGF-1 [like people with laron syndrome or "dwarfism"] rarely get acne, diabetes or cancer. People with high serum IGF-1 [people with acromegaly] often get acne, diabetes and cancer. If someone have susceptible genetic makeup then he will easily induce or aggravate acne with the regular consumption of dairy, processed grains or simple carbohydrates. Almost 50% of adults have acne to some degree and considering that human genome didn't changed [unlike our diet] since at least 10,000 years, then we can't blame it solely on the genes. Acne is most likely a combination of susceptible genes and western diet [with western diet playing the key role].
Well, again much more complicated then your very nice explanation which i very much like btw.
"genetic condition"
My parents never had acne; their parents are the same. Granted we eat differently in this era, but like i said food isn't the smoking gun.
I am almost 6ft tall or over I haven't checked. My dad's side is very tall, my mothers their more medium set and not over weight. Very slender like me. My dad's side has more of the weight issues surprisingly. But im guessing that is only because now its starting to show it self as my grandparents and their sons start to age into their 50's.
Though acromegaly is probably considered for people over 6'5" im guessing
It sucks because even genetics are not a pin point answer, though a very good insight.
Full article can be found here: HERE
I've seen and know PLENTY of people who do not eat anything entailing "high calorie uptake, high glycemic load, high fat intake, high meat intake, lots of insulin, etc." but still have acne. I know plenty of actual Asians (non-westerners... I think it's B.S. that the diet is called a "western diet" - ppl all over the world can eat in that manner) who have acne but don't eat anything like what the "Western Diet" describes.
Diet certainly affects acne, but so do many, many other factors. VanceAstro, do you have experience with reducing mTORC1 and noting the results of doing so or did you just find and post this paper abstract?
VanceAstro, do you have experience with reducing mTORC1 and noting the results of doing so or did you just find and post this paper abstract?
Mtorc1 & acne connection is still just a working hypothesis (I am not aware of any clinical trials that would either confirm or reject it empirically). I also don't think it's possible to significantly downregulate mTORC1 with OTC supplements, although highly bioavailable nano-curcumin is probably worth a try (to my knowledge there is only one such product on the market right now). Unfortunately, the most potent curcumin, resveratrol and EGCG derivatives are still under investigation in clinical trials (but it has been shown - in vivo - that they inhibit the AKT-mTOR pathway).