Eating less good for acne?
Posted 18 December 2004 - 05:02 AM
Is this legit?
Posted 18 December 2004 - 05:57 AM
Posted 18 December 2004 - 12:25 PM
Posted 19 December 2004 - 12:20 AM
but if you overeat, you do stress your body. your body can only produce so many bile acids etc, and digestive enzymes to break down the food.
so eating smalller, more frequent portions is a good thing.
Posted 19 December 2004 - 12:27 AM
at least it works for me..
Posted 19 December 2004 - 07:22 AM
Posted 19 December 2004 - 08:01 AM
Posted 19 December 2004 - 11:16 AM
Interestingly enough, when those of us on here change our diets, they aren't as high calorie as they were before. I'm not certain if it's a combination of both high calorie, high carbs/gluten & LOW fiber, or if it's just high calories, but those foods that are generally considered "unhealthy, bad, aggrivating" for us, tend to fall on the high calorie list anyway.
Now, that doesn't mean you have to skip meals. You can eat 2 - 6 meals a day if you like, it all depends on what foods you are eating (& how active you are). Just to get a visual idea, there's a book out there called "Picture Perfect Weightloss" not that that's your goal, but it shows you how you can eat MORE food that's lower in calories compared to what you would normally eat. In general, "healthy" foods, fruits, veggies (except avacados) are lower in calories (higher in soluble fiber) and these tend to be what the "average american" doesn't eat enough of.
These are just abstracts as most of you may not be able to access the full texts, so why post them. Of course if it's a really good study, I try to find a link for guys ;-)
[The significance of lifestyle as a risk factor for the metabolic syndrome]
[Article in Japanese]
Tsujii S, Kuzuya H.
Tenri Yorozu-sodansho Hospital Diabetes Center.
The metabolic syndrome is featured by obesity, dyslipidemia and insulin resistance, additionally associated with inflammatory and fibrinolytic dysfunctions, all of which are risk factors of cardiovascular diseases and type 2 diabetes. The lifestyle factors that could cause and aggravate the metabolic syndrome are physical inactivity, calorie-dense diet, habitual alcohol drinking and smoking, and psychosocial stress. Energy excess along with a lot of saturated fat, i.e. more fast food and sugar-containing drinks, and sedentary lifestyle like television viewing are contributing to the epidemic of obesity. The significance of lifestyle from birth to adulthood will be reviewed in the context of the metabolic syndrome, as well as the background and environment in which the convenient lifestyle spread far and wide among us.Ă‚Â http://www.ncbi.nlm....t_uids=15206140
Insulin Resistance Syndrome, Syndrome X, & Metabolic Syndrome seem to all be the same thing. I'm guessing that the new name for this is now "Metabolic Syndrome" as that would then include insulin resistance.
[Insulin resistance and adipose tissue gene expression in humans]
[Article in French]
Service de biochimie et hormonologie, Hopital Tenon, 4, rue de la Chine, 75970 Paris. firstname.lastname@example.org
Obesity is a risk factor for type 2 diabetes and cardiovascular diseases. The hypothesis that cytokines could play a role in the pathophysiology of obesity and insulin resistance is suggested in the last few years. We showed a positive correlation between circulating interleukin (IL-6) levels and obesity and insulin resistance suggesting that IL-6 could be involved in insulin resistance in humans. We showed a decrease of both circulating and adipose tissue IL-6 levels in non-diabetic obese subjects after a very low calorie diet program inducing weight loss. This suggests that adipose tissue could be involved in the regulation of circulating IL-6 levels in these subjects. Adipose tissue is also involved in lipodystrophies particularly in HIV patients on antiviral therapy. We showed an alteration of the SREBP-1 transcription step in subcutaneous abdominal adipose tissue from HIV patients. We found an inverse correlation between circulating adiponectin levels and both insulin resistance and cardiovascular risk factors such as CRP levels and apolipoprotein B/A1 ratio. These findings suggest that adipose tissue is involved in insulin resistance in humans particularly via adipocytokine secretion. Copyright John Libbey Eurotext 20003.Ă‚Â http://www.ncbi.nlm....t_uids=15047487
Now this one is more relevant for another topic about inflammation & acne on this forum, but I posted it to show you that Insulin Resistance (IR) goes in hand with production of Inflammatory Products (as well as increased androgens) & by following a lower calorie diet, both IR & IL-6 (pro-inflammatory cytokine) are reduced! There's plenty of other studies involving IR & inflammation, but this one mentions about how calories can influence it (wish they would specifically tell what type of foods they ate).
Difference in body weight between American and Italian women with polycystic ovary syndrome: influence of the diet.
Carmina E, Legro RS, Stamets K, Lowell J, Lobo RA.
Department of Clinical Medicine, University of Palermo, Italy.
BACKGROUND: The study aim was to determine differences in body mass in two populations of women (USA and Italy) with polycystic ovary syndrome (PCOS), and to assess the effect of diet on body mass and cardiovascular risk factors. METHODS: Pools of women with PCOS from the USA (n = 343) and Italy (n = 301), seen between 1993 and 2001, were available for assessment. From these populations, 20 women who were seen consecutively in 2001 at each site had detailed analyses of diet and cardiovascular risk factors. RESULTS: In the entire group, American women had a significantly higher body mass compared with Italian women (P < 0.01). Also, the 20 women consecutively evaluated in the USA had a significantly higher mean (+/- SD) body mass index (40.3 +/- 1.0 kg/m(2)) than in Italy (29.7 +/- 1.0 kg/m(2)). US women had worse insulin resistance, lower levels of high-density lipoprotein-cholesterol (HDL-C) (P < 0.01) and higher levels of triglycerides (P < 0.01). Dietary analysis in the two groups indicated that the total daily calorific intake was similar (USA 2277 +/- 109; Italy 2325 +/- 68 Kcal), with no appreciable differences in dietary content of protein, carbohydrate and fat. However, the dietary saturated fat content was significantly higher in US women (31.9 +/- 3 versus 18.2 +/- 2 g/day, P < 0.01). Saturated fat intake correlated negatively with HDL-C (P < 0.01). CONCLUSIONS: Among women with PCOS, body mass was significantly higher in US women compared with Italian women. However, total calorie intake and dietary constituents were similar, except for a higher saturated fat in US women. It is hypothesized that diet alone does not explain differences in body mass; genetic and lifestyle factors likely contribute. An increased saturated fat intake may worsen the cardiovascular risk profile.
So this study brings additional possibilities, one of which is the question as to whether it's a high calorie diet in general or if it's just the consumption of certain foods that tend to be HIGER in calories over other foods. In general those foods will be animal products like dairy & oils (due to saturated fat) & refined carbohydrates (fast food, sugar, etc). I eat all the animal products that I care for (most tend to be lean meat though), occassionally I eat fried foods (in olive oil), but I do avoid Trans fats (synthetically induced saturated fats). In case anyone is wondering this study is relevant, PCOS is associated with Insulin Resistance (IR may cause this) as well having acne as one of it's possible symptoms. This is a big one for females, but males can also have a form of PCOS.
Effects of diet and metformin administration on sex hormone-binding globulin, androgens, and insulin in hirsute and obese women.
Crave JC, Fimbel S, Lejeune H, Cugnardey N, Dechaud H, Pugeat M.
Hospices Civils de Lyon, Laboratoire de la Clinique Endocrinologique, Hopital de l'Antiquaille, France.
Evidence suggests that hyperinsulinemic insulin resistance may increase serum levels of ovarian androgens and reduce sex hormone-binding globulin (SHBG) levels in humans. The present study was conducted to assess the effect of administration of the biguanide metformin, a drug commonly used in the treatment of diabetes mellitus, on androgen and insulin levels in 24 hirsute patients. The patients selected for the study were obese, with a body mass index higher than 25 kg/m2 and high fasting insulin (> 90 pmol/L) and low SHBG levels (< 30 nmol/L). All patients were given a low calorie diet (1500 Cal/day) and randomized for either metformin administration at a dose of 850 mg or a placebo, twice daily for 4 months, in a double blind study. In the placebo group, diet resulted in a significant decrease in body mass index (30.8 +/- 1.0 vs. 32.7 +/- 1.5 kg/m2; P < 0.0001), fasting insulin (127 +/- 11 vs. 156 +/- 14 pmol/L; P < 0.01), non-SHBG-bound testosterone [Free Testosterone](0.19 +/- 0.02 vs. 0.28 +/- 0.03 nmol/L; P < 0.02), androstenedione (5.8 +/- 0.5 vs. 9.0 +/- 1.1 nmol/L; P < 0.03), and 3 alpha-diolglucuronide [3-alpha diol G](8.6 +/- 1.1 vs. 11.7 +/- 1.9; P < 0.005) plasma concentrations and a significant increase in the glucose/insulin ratio (0.047 +/- 0.005 vs. 0.035 +/- 0.003; P < 0.001) and plasma concentrations of SHBG (26.0 +/- 3.3 vs. 19.1 +/- 1.9 nmol/L; P < 0.001) and dehydroepiandrosterone sulfate [DHEA-S](8.7 +/- 1.5 vs. 8.4 +/- 1.3; P < 0.05). 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....st_uids=7608255
In case you are wondering, this is what I was diagnosed as 3.5 years ago. I'm actually atypical for both PCOS & IR as I don't carry any of the "classic signs" (ex: you do NOT have to be obese or overweight), yet I do still carry traits for both of these and as such there's actually a PCOS variant known as HAIR-AN Syndrome (Hyperandrogenism, Insulin Resistance, Acanthosis Negricans), that would explain my symptoms the best. Now those words in bold are basically what you want to look for in an ANY acne treatment if your goal is to reduce/inhibit androgens. DHEA-S is a bound form of adrenal androgen DHEA (making it less potent), 3-alpha diol G is the product of DHT (Accutane inhibits this also), Androstendione, and Free Testosterone (convertes to DHT) are all androgens.
That study above describes exactly what happened to me when I stopped my medication and Teplo discovered he could do the same. I was taking Avandia (metaformin made me sick) and 150mg of Spironolcatone, but was only a max of 85% clear (for 3 months of the year). Yet when I initially changed my diet, I went up to a CONSTANT 95% clear! Over time, I permanently dropped avandia (after 3 months into my diet) and even dropped the spiro for 6 months (started back on at 100mg for hirsutism treatment) to make sure that it wasn't my medication. Now, 2.5 years later, I'm 99%+ clear and this includes my face, back, chest, neck, ears (I can breakout in lots of...places), I've got the smallest pores since I hit puberty, have a lot less oil & dandruff, a bit less body hair, and I no longer suffer from horrible menstrual cramps! Trust me, I have not grown out of it, I can still breakout if I eat the "wrong" foods for me, but I usually don't intentionlay do this as most of the time I'll end up with very stubborn cystic acne as a result =/
So that's sorta my success story and why this is one of several theories regarding acne production that I strongly believe in. I do apologize if some of the words are "too big" but initially I had to read and read and read to get some of this myself and even when someone brings something "new" to the board that I haven't heard of, I've gotta research it a bit (which I love doing anyway). So if you REALLY want something, you'll put the time, energy, effort into researching, understanding and, in this case, perhaps even experimenting with your diet to see how relevant this is for you.
Best of luck!
P.S. Notice how, well I've noticed that more of the signifcant research relating to insulin resistance and it's role involving acne inducing hormones and associated dietary factors seem to come from other countries, rather than the MAIN country (U.S.) that the problem occurs in....odd.