Darth Nostril wrote:Why have you not been institutionalised yet?
Lol did you read my post while stuffing your face or something? Fasting (starvation on pubmed) is not remotely close to any kind of bunk.
What bandwagon? You mean physical exercise? Eating vegetables and nuts and olive oil?
Fasting is nothing weird and I suspect it will be a core concept in most cancer treatments in the nearby future. Aside from rare cancers that rely on ketone bodies almost every cancer is vulnerable to fasting.
Aging Cell. 2015 Apr 22. doi: 10.1111/acel.12338. [Epub ahead of print]
Interventions to Slow Aging in Humans: Are We Ready?
Longo VD1, Antebi A, Bartke A, Barzilai N, Brown-Borg HM, Caruso C, Curiel TJ, de Cabo R, Franceschi C, Gems D, Ingram DK, Johnson TE, Kennedy BK, Kenyon C, Klein S, Kopchick JJ, Lepperdinger G, Madeo F, Mirisola MG, Mitchell JR, Passarino G, Rudolph KL, Sedivy JM, Shadel GS, Sinclair DA, Spindler SR, Suh Y, Vijg J, Vinciguerra M, Fontana L.
Author information
Abstract
The workshop entitled 'Interventions to Slow Aging in Humans: Are We Ready?' was held in Erice, Italy, on October 8-13, 2013, to bring together leading experts in the biology and genetics of aging and obtain a consensus related to the discovery and development of safe interventions to slow aging and increase healthy lifespan in humans. There was consensus that there is sufficient evidence that aging interventions will delay and prevent disease onset for many chronic conditions of adult and old age. Essential pathways have been identified, and behavioral, dietary, and pharmacologic approaches have emerged. Although many gene targets and drugs were discussed and there was not complete consensus about all interventions, the participants selected a subset of the most promising strategies that could be tested in humans for their effects on healthspan. These were: (i) dietary interventions mimicking chronic dietary restriction (periodic fasting mimicking diets, protein restriction, etc.); (ii) drugs that inhibit the growth hormone/IGF-I axis; (iii) drugs that inhibit the mTOR-S6K pathway; or (iv) drugs that activate AMPK or specific sirtuins. These choices were based in part on consistent evidence for the pro-longevity effects and ability of these interventions to prevent or delay multiple age-related diseases and improve healthspan in simple model organisms and rodents and their potential to be safe and effective in extending human healthspan. The authors of this manuscript were speakers and discussants invited to the workshop. The following summary highlights the major points addressed and the conclusions of the meeting.
http://www.ncbi.nlm.nih.gov/pubmed/25902704
Oncotarget. 2015 May 20;6(14):11820-32.
Fasting potentiates the anticancer activity of tyrosine kinase inhibitors by strengthening MAPK signaling inhibition.
Caffa I1, D'Agostino V2, Damonte P1, Soncini D1, Cea M1, Monacelli F1, Odetti P1,3, Ballestrero A1,3, Provenzani A2, Longo VD4,5, Nencioni A1,3.
Author information
Abstract
Tyrosine kinase inhibitors (TKIs) are now the mainstay of treatment in many types of cancer. However, their benefit is frequently short-lived, mandating the search for safe potentiation strategies. Cycles of fasting enhance the activity of chemo-radiotherapy in preclinical cancer models and dietary approaches based on fasting are currently explored in clinical trials. Whether combining fasting with TKIs is going to be potentially beneficial remains unknown. Here we report that starvation conditions increase the ability of commonly administered TKIs, including erlotinib, gefitinib, lapatinib, crizotinib and regorafenib, to block cancer cell growth, to inhibit the mitogen-activated protein kinase (MAPK) signaling pathway and to strengthen E2F-dependent transcription inhibition. In cancer xenografts models, both TKIs and cycles of fasting slowed tumor growth, but, when combined, these interventions were significantly more effective than either type of treatment alone. In conclusion, cycles of fasting or of specifically designed fasting-mimicking diets should be evaluated in clinical studies as a means to potentiate the activity of TKIs in clinical use.
Cell Stem Cell. 2014 Jun 5;14(6):810-23. doi: 10.1016/j.stem.2014.04.014.
Prolonged fasting reduces IGF-1/PKA to promote hematopoietic-stem-cell-based regeneration and reverse immunosuppression.
Cheng CW1, Adams GB2, Perin L3, Wei M1, Zhou X2, Lam BS2, Da Sacco S3, Mirisola M4, Quinn DI5, Dorff TB5, Kopchick JJ6, Longo VD7.
Author information
Abstract
Immune system defects are at the center of aging and a range of diseases. Here, we show that prolonged fasting reduces circulating IGF-1 levels and PKA activity in various cell populations, leading to signal transduction changes in long-term hematopoietic stem cells (LT-HSCs) and niche cells that promote stress resistance, self-renewal, and lineage-balanced regeneration. Multiple cycles of fasting abated the immunosuppression and mortality caused by chemotherapy and reversed age-dependent myeloid-bias in mice, in agreement with preliminary data on the protection of lymphocytes from chemotoxicity in fasting patients. The proregenerative effects of fasting on stem cells were recapitulated by deficiencies in either IGF-1 or PKA and blunted by exogenous IGF-1. These findings link the reduced levels of IGF-1 caused by fasting to PKA signaling and establish their crucial role in regulating hematopoietic stem cell protection, self-renewal, and regeneration.
http://www.ncbi.nlm.nih.gov/pubmed/24905167
Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients
C Lee1 and V D Longo1
1Andrus Gerontology Center, Department of Biological Sciences and Norris Cancer Center, University of Southern California, Los Angeles, CA, USA
Correspondence: Professor VD Longo, Andrus Gerontology Center, Department of Biological Sciences and Norris Cancer Center, University of Southern California, 3715 McClintock Avenue, Los Angeles, CA 90089-0191, USA. E-mail:
vlongo@usc.edu
Received 6 December 2010; Revised 11 February 2011; Accepted 11 February 2011; Published online 25 April 2011.
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Abstract
The dietary recommendation for cancer patients receiving chemotherapy, as described by the American Cancer Society, is to increase calorie and protein intake. Yet, in simple organisms, mice, and humans, fasting—no calorie intake—induces a wide range of changes associated with cellular protection, which would be difficult to achieve even with a cocktail of potent drugs. In mammals, the protective effect of fasting is mediated, in part, by an over 50% reduction in glucose and insulin-like growth factor 1 (IGF-I) levels. Because proto-oncogenes function as key negative regulators of the protective changes induced by fasting, cells expressing oncogenes, and therefore the great majority of cancer cells, should not respond to the protective signals generated by fasting, promoting the differential protection (differential stress resistance) of normal and cancer cells. Preliminary reports indicate that fasting for up to 5 days followed by a normal diet, may also protect patients against chemotherapy without causing chronic weight loss. By contrast, the long-term 20 to 40% restriction in calorie intake (dietary restriction, DR), whose effects on cancer progression have been studied extensively for decades, requires weeks–months to be effective, causes much more modest changes in glucose and/or IGF-I levels, and promotes chronic weight loss in both rodents and humans. In this study, we review the basic as well as clinical studies on fasting, cellular protection and chemotherapy resistance, and compare them to those on DR and cancer treatment. Although additional pre-clinical and clinical studies are necessary, fasting has the potential to be translated into effective clinical interventions for the protection of patients and the improvement of therapeutic index.
Conclusions and Recommendations
Based on the existing evidence from animal and human studies described, we conclude that there is great potential for lifestyles that incorporate IF or PF during adult life to promote optimal health and reduce the risk of many chronic diseases, particularly for those who are overweight and sedentary. Animal studies have documented robust and replicable effects of fasting on health indicators including greater insulin sensitivity and reduced levels of blood pressure, body fat, IGF-I, insulin, glucose, atherogenic lipids, and inflammation. Fasting regimens can ameliorate disease processes and improve functional outcome in animal models of disorders that include cancer, myocardial infarction, diabetes, stroke, AD, and PD. One general mechanism of action of fasting is that it triggers adaptive cellular stress responses, which result in an enhanced ability to cope with more severe stress and counteract disease processes. In addition, by protecting cells from DNA damage, suppressing cell growth, and enhancing apoptosis of damaged cells, fasting could retard and/or prevent the formation and growth of cancers.
However, studies of fasting regimens have not been performed in children, the very old, and underweight individuals, and it is possible that IF and PF would be harmful to these populations. Fasting periods lasting longer than 24 hr, and particularly those lasting 3 or more days, should be done under the supervision of a physician and preferably in a clinic. IF- and PF-based approaches toward combating the current epidemics of overweight, diabetes, and related diseases should be pursued in human research studies and medical treatment plans. Several variations of potential “fasting prescriptions” that have been adopted for overweight subjects revolve around the common theme of abstaining from food and caloric beverages for at least 12–24 hr on 1 or more days each week or month, depending on the length, combined with regular exercise. For those who are overweight, physicians could ask their patients to choose a fasting-based intervention that they believe they could comply with based upon their daily and weekly schedules. Examples include the “5:2” IF diet (Harvie et al., 2011), the alternate day modified fasting diet (Johnson et al., 2007 and Varady et al., 2009), a 4–5 day fast (Lee et al., 2012 and Safdie et al., 2009), or low-calorie-but high-nourishment fasting-mimicking diets once every 1–3 months followed by the skipping of one major meal every day if needed (V.D.L., unpublished data). One of the concerns with unbalanced alternating diets, such as those in which low calorie intake is only observed for 2 days a week, are the potential effects on circadian rhythm and the endocrine and gastrointestinal systems, which are known to be influenced by eating habits. During the first 4–6 weeks of implementation of the fasting regimen, a physician or registered dietitian should be in regular contact with the patient to monitor their progress and to provide advice and supervision.
Fasting regimens could also be tailored for specific diseases as stand-alone or adjunct therapies. Results of initial trials of IF (fasting 2 days per week or every other day) in human subjects suggest that there is a critical transition period of 3–6 weeks during which time the brain and body adapt to the new eating pattern and mood is enhanced (Harvie et al., 2011 and Johnson et al., 2007). Though speculative, it is likely that during the latter transition period brain neurochemistry changes so that the “addiction” to regular consumption of food throughout the day is overcome. Notably, the various fasting approaches are likely to have limited efficacy, particularly on aging and conditions other than obesity, unless combined with high-nourishment diets such as the moderate calorie intake and mostly plant-based Mediterranean or Okinawa low-protein diets (0.8 g protein/kg of body weight), consistently associated with health and longevity.
In the future, it will be important to combine epidemiological data, studies of long-lived populations and their diets, and results from model organisms connecting specific dietary components to proaging and prodisease factors, with data from clinical studies, to design large clinical studies that integrate fasting with diets recognized as protective and enjoyable. A better understanding of the molecular mechanisms by which fasting affects various cell types and organ systems should also lead to the development of novel, FDA-approved prophylactic and preventive and therapeutic interventions for a wide range of disorders.
http://www.sciencedirect.com/science/ar ... 3113005032
OK by the way I do take two supplements right now, MitoQ and C60oliveoil on alternating days (10mg of MitoQ, and 5ml of C60oil, sometimes I skip a few days).
They might be really good, might be bad somehow, I know it's a kind of bet. Time will tell, if I get fucked up by them I will necro my C60 thread.