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Showing results for tags 'caloric restriction'.
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The email list system is broken. Posts cannot be searched. Many of the posts do not make it to the messages I receive individually and via the daily mailings. Therefore, I am sending this message, comprised of citations papers that seem to be appropriate to the room of the Forum. I will try to also provide full-text links and a very brief excerpt or within brackets my synopsis of the paper. I apologize for the fact some papers discuss results of studies on the overweight or obese, but feel that some benefits seen in such subjects bears on a continuum of benefits accrued by CR and provide incentive to folks who are overweight or obese. Below are today's papers. Altered consolidation of extinction-like inhibitory learning in genotype-specific dysfunctional coping fostered by chronic stress in mice. Campus P, Maiolati M, Orsini C, Cabib S. Behav Brain Res. 2016 Aug 6. pii: S0166-4328(16)30505-8. doi: 10.1016/j.bbr.2016.08.014. [Epub ahead of print] PMID: 27506654 http://linkinghub.elsevier.com.sci-hub.cc/retrieve/pii/S0166432816305058 These findings support the conclusion that an experience of reduced food availability strain-specifically affects persistence of newly acquired passive coping strategies by altering consolidation of extinction-like inhibitory learning. The interaction of fasting, caloric restriction, and diet-induced obesity with 17β-estradiol on the expression of KNDy neuropeptides and their receptors in the female mouse. Yang JA, Yasrebi A, Snyder M, Roepke TA. Mol Cell Endocrinol. 2016 Aug 6. pii: S0303-7207(16)30298-2. doi: 10.1016/j.mce.2016.08.008. [Epub ahead of print] PMID: 27507595 http://linkinghub.elsevier.com.sci-hub.cc/retrieve/pii/S0303720716302982 [This paper suggests that steroidal environment and energy state negatively regulate KNDy (Kisspeptin/Neurokinin B/Dynorphin) gene which plays an important role in the https://en.wikipedia.org/wiki/Hypothalamic%E2%80%93pituitary%E2%80%93gonadal_axis] Effects of dietary supplementation with EPA and/or α-lipoic acid on adipose tissue transcriptomic profile of healthy overweight/obese women following a hypocaloric diet. Huerta AE, Prieto-Hontoria PL, Fernández-Galilea M, Escoté X, Martínez JA, Moreno-Aliaga MJ. Biofactors. 2016 Aug 10. doi: 10.1002/biof.1317. [Epub ahead of print] PMID: 27507611 http://sci-hub.cc/doi/10.1002/biof.1317 α-lipoic acid, especially in combination with EPA, upregulated the expression of genes associated with lipid catabolism while downregulated genes involved in lipids storage. Association of the TNF-alpha -308 G/A polymorphisms with metabolic responses secondary to a high protein/low carbohydrate versus a standard hypocaloric diet. De Luis DA, Aller R, Izaola O, Romero E. Nutr Hosp. 2016 Jun 30;33(3):267. doi: 10.20960/nh.267. Spanish. PMID: 27513494 [i have no access to this paper's full texts.] Carriers of -308 GG promoter variant of TNF-alpha gene have a better metabolic response than -308 GA obese with a high protein hypocaloric diet.
Hi ? I'm new here. I'm a 20 years old girl from Italy (forgive my eventual english mistakes, please), psychology undergraduate. I'm interested in CR for its immediate health benefits and the promise of aging well more than for increasing lifespan (and since my budget is not infinite I like the fact that buying less food would allow me to invest on quality). I would like to understand if and how it could be compatible with an optimal reproductive health, since I'm young and the goal here is to feel better, not worse, and since from what I understand women's hormones balance is more vulnerable to caloric restriction and fat loss. I'm on the high end of the healthy range of BMI (24.1) but I have a high waist to hip ratio for my age (0.78) that I would like to reduce so I'm pretty sure I could benefit from a patient, balanced, weight loss diet, but the question is: as a young woman how far should I go for optimal health (immediate physical health + hormonal balance, meaning reproductive and mental health + aging well)? Should I do a common diet limited in time and then raise my calories for hormonal balance hoping to mantain eating clean as much as my budget allows or prefer a slight chronic caloric restriction that would allow me to buy and eat only high quality food (with the exception of social occasions)?
Every-other-day feeding extends lifespan but fails to delay many symptoms of aging in mice. Xie K, Neff F, Markert A, Rozman J, Aguilar-Pimentel JA, Amarie OV, Becker L, Brommage R, Garrett L, Henzel KS, Hölter SM, Janik D, Lehmann I, Moreth K, Pearson BL, Racz I, Rathkolb B, Ryan DP, Schröder S, Treise I, Bekeredjian R, Busch DH, Graw J, Ehninger G, Klingenspor M, Klopstock T, Ollert M, Sandholzer M, Schmidt-Weber C, Weiergräber M, Wolf E, Wurst W, Zimmer A, Gailus-Durner V, Fuchs H, Hrabě de Angelis M, Ehninger D. Nat Commun. 2017 Jul 24;8(1):155. doi: 10.1038/s41467-017-00178-3. PMID: 28761067 https://www.nature.com/articles/s41467-017-00178-3 https://www.nature.com/articles/s41467-017-00178-3.pdf http://www.nature.com.sci-hub.cc/articles/s41467-017-00178-3 Abstract Dietary restriction regimes extend lifespan in various animal models. Here we show that longevity in male C57BL/6J mice subjected to every-other-day feeding is associated with a delayed onset of neoplastic disease that naturally limits lifespan in these animals. We compare more than 200 phenotypes in over 20 tissues in aged animals fed with a lifelong every-other-day feeding or ad libitum access to food diet to determine whether molecular, cellular, physiological and histopathological aging features develop more slowly in every-other-day feeding mice than in controls. We also analyze the effects of every-other-day feeding on young mice on shorter-term every-other-day feeding or ad libitum to account for possible aging-independent restriction effects. Our large-scale analysis reveals overall only limited evidence for a retardation of the aging rate in every-other-day feeding mice. The data indicate that every-other-day feeding-induced longevity is sufficiently explained by delays in life-limiting neoplastic disorders and is not associated with a more general slowing of the aging process in mice. Dietary restriction can extend the life of various model organisms. Here, Xie et al. show that intermittent periods of fasting achieved through every-other-day feeding protect mice against neoplastic disease but do not broadly delay organismal aging in animals.
Hi, everyone, reading some recent books and papers I've gathered some clues that not caloric restriction in general but the blood sugar control/insulin control might be the major cornerstone for longevity - so I wonder if low-carb, low-glycemic (but fructose-limited) oder even low-carb high-fat (good fats like Omega-3 rich plant oils) diets could give the same fine results like caloric restriction. Is there any recent reseach available focussing this issue? Any ideas/hints or publications are much appreciated! Thanks! Max