Afiwe Mimicking Diet Ṣafihan

Loye ProLon Ounjẹ Mimicking Fasting

Fasting is associated with numerous health benefits; from weight loss to longevity. There are many different types of fasting methods, such as intermittent fasting. The fasting mimicking diet allows you to experience the benefits of traditional fasting without depriving your body of food. The main difference of the FMD is that instead of completely eliminating all food for several days or even weeks, you only restrict your calorie intake for five days out of the month. The FMD can be practiced once a month to promote well-being.

Nigba ti ẹnikẹni le tẹle FMD lori ara wọn, ni ProLon Pẹwẹ mimicking onje nfunni ni eto ounjẹ ounjẹ 5-ọjọ ti a ti sọpo ati pe kọọkan fun ọjọ kọọkan ati pe o jẹ awọn ounjẹ ti o nilo fun FMD ni awọn titobi deede ati awọn akojọpọ. Eto ounjẹ naa jẹ apẹrẹ lati jẹun tabi rọrun-si-mura, awọn ounjẹ orisun, pẹlu awọn ifipa, awọn obe, awọn ipanu, awọn afikun, ohun ti o wa ninu iṣan, ati awọn teas. Awọn ọja ti a ṣe agbekalẹ ijinle sayensi ati ipanu nla. Ṣaaju ki o to bẹrẹ ProLon aawẹ mimicking onje, eto ounjẹ ọjọ 5, jọwọ rii daju lati sọrọ si oniṣẹ ilera kan lati wa boya FMD ba tọ fun ọ. Idi ti iwadi iwadi ni isalẹ ni lati ṣe afihan awọn ijẹ-ara molikali ati awọn ohun elo iwadii ti ãwẹ ni FMD.

Ãwẹ: Awọn ilana Iṣelọpọ Molescular ati Awọn Ohun elo Iwosan

Fasting has been practiced for millennia, but only recently studies have shed light on its role in adaptive cellular responses that reduce oxidative damage and inflammation, optimize energy metabolism and bolster cellular protection. In lower eukaryotes, chronic fasting extends longevity in part by reprogramming metabolic and stress resistance pathways. In rodents intermittent or periodic fasting protects against diabetes, cancers, heart disease and neurodegeneration, while in humans it helps reduce obesity, hypertension, asthma and rheumatoid arthritis. Thus, fasting has the potential to delay aging and help prevent and treat diseases while minimizing the side effects caused by chronic dietary interventions.

ifihan

In humans, fasting is achieved by ingesting no or minimal amounts of food and caloric beverages for periods that typically range from 12 hours to three weeks. Many religious groups incorporate periods of fasting into their rituals including Muslims who fast from dawn until dusk during the month of Ramadan, and Christians, Jews, Buddhists and Hindus who traditionally fast on designated days of the week or calendar year. In many clinics, patients are now monitored by physicians while undergoing water only or very low calorie (less than 200 kcal/day) fasting periods lasting from 1 week or longer for weight management, and for disease prevention and treatment. Fasting is distinct from caloric restriction (CR) in which the daily caloric intake is reduced chronically by 20�40%, but meal frequency is maintained. Starvation is instead a chronic nutritional insufficiency that is commonly used as a substitute for the word fasting, particularly in lower eukaryotes, but that is also used to define extreme forms of fasting, which can result in degeneration and death. We now know that fasting results in ketogenesis, promotes potent changes in metabolic pathways and cellular processes such as stress resistance, lipolysis and autophagy, and can have medical applications that in some cases are as effective as those of approved drugs such as the dampening of seizures and seizure-associated brain damage and the amelioration of rheumatoid arthritis (Bruce-Keller et al., 1999; Hartman et al., 2012; Muller et al., 2001). As detailed in the remainder of this article, findings from well-controlled investigations in experimental animals, and emerging findings from human studies, indicate that different forms of fasting may provide effective strategies to reduce weight, delay aging, and optimize health. Here we review the fascinating and potent effects of different forms of fasting including intermittent fasting (IF, including alternate day fasting, or twice weekly fasting, for example) and periodic fasting (PF) lasting several days or longer every 2 or more weeks. We focus on fasting and minimize the discussion of CR, a topic reviewed elsewhere (Fontana et al., 2010; Masoro, 2005).

Awọn ẹkọ lati Awọn Aṣoju Ọdun

The remarkable effects of the typical 20�40% CR on aging and diseases in mice and rats are often viewed as responses evolved in mammals to adapt to periods of limited availability of food (Fontana and Klein, 2007; Fontana et al., 2010; Masoro, 2005; Weindruch and Walford, 1988). However, the cellular and molecular mechanisms responsible for the protective effects of CR have likely evolved billions of years earlier in prokaryotes attempting to survive in an environment largely or completely devoid of energy sources while avoiding age-dependent damage that could compromise fitness. In fact, E. coli switched from a nutrient rich broth to a calorie-free medium survive 4 times longer, an effect reversed by the addition of various nutrients but not acetate, a carbon source associated with starvation conditions (Figure 1A) (Gonidakis et al., 2010). The effect of rich medium but not acetate in reducing longevity raises the possibility that a ketone body-like carbon source such as acetate may be part of an �alternate metabolic program� that evolved billions of years ago in microorganisms and that now allows mammals to survive during periods of food deprivation by obtaining much of the energy by catabolizing fatty acids and ketone bodies including acetoacetate and ?-hydroxybutyrate (Cahill, 2006).

In the yeast S. cerevisiae, switching cells from standard growth medium to water also causes a consistent 2-fold chronological lifespan extension as well as a major increase in the resistance to multiple stresses (Figure 1B) (Longo et al., 1997; Longo et al., 2012). The mechanisms of food deprivation-dependent lifespan extension involve the down-regulation of the amino acid response Tor-S6K (Sch9) pathway as well as of the glucose responsive Ras-adenylate cyclase-PKA pathway resulting in the activation of the serine/threonine kinase Rim15, a key enzyme coordinating the protective responses (Fontana et al., 2010). The inactivation of Tor-S6K, Ras-AC-PKA and activation of Rim15 result in increased transcription of genes including superoxide dismutases and heat shock proteins controlled by stress responsive transcription factors Msn2, Msn4 and Gis1, required for the majority of the protective effects caused by food deprivation (Wei et al., 2008). Notably, when switched to food deprivation conditions, both bacteria and yeast enter a hypometabolic mode that allows them to minimize the use of reserve carbon sources and can also accumulate high levels of the ketone body-like acetic acid, analogously to mammals.

Another major model organism in which fasting extends lifespan is the nematode C. elegans. Food deprivation conditions achieved by feeding worms little or no bacteria, lead to a major increase in lifespan (Figure 1C) (Kaeberlein et al., 2006; Lee et al., 2006), which requires AMPK as well as the stress resistance transcription factor DAF-16, similarly to the role of transcription factors Msn2/4 and Gis1 in yeast and FOXOs in flies and mammals (Greer et al., 2007). Intermittent food deprivation also extends lifespan in C. elegans by a mechanism involving the small GTPase RHEB-1 (Honjoh et al., 2009).

Ni awọn ẹja, ọpọlọpọ awọn ijinlẹ fihan pe aifọkọja ounje nigbagbogbo ko ni ipa lori igbesi aye (Grandison et al, 2009). Sibẹsibẹ, idinku ounje tabi dilution ounje ni a fihan nigbagbogbo lati fa pipaduro pipọ Drosophila (Piper ati Partridge, 2007) ni imọran pe awọn eṣinṣin le ni anfaani lati ipalara ti o jẹun ti o jẹun ṣugbọn o le jẹ ki awọn akoko kukuru kukuru kuru.

Papọ awọn abajade wọnyi fihan pe aiyina ounje le ja si awọn ipa-ipa ti o pọju ni awọn oriṣiriṣi awọn oganisimu, ṣugbọn tun ṣe afihan pe awọn oganisimu oriṣiriṣi yatọ si awọn idahun si awọn ẹwẹ.

Awọn idahun ti o ṣe atunṣe si Nwẹ ni awọn ẹranko

In most mammals, the liver serves as the main reservoir of glucose, which is stored in the form of glycogen. In humans, depending upon their level of physical activity, 12 to 24 hours of fasting typically results in a 20% or greater decrease in serum glucose and depletion of the hepatic glycogen, accompanied by a switch to a metabolic mode in which non-hepatic glucose, fat-derived ketone bodies and free fatty acids are used as energy sources (Figures 2 and 3). Whereas most tissues can utilize fatty acids for energy, during prolonged periods of fasting, the brain relies on the ketone bodies ?-hydroxybutyrate and acetoacetate in addition to glucose for energy consumption (Figure 3B). Ketone bodies are produced in hepatocytes from the acetyl-CoA generated from ? oxidation of fatty acids released into the bloodstream by adipocytes, and also by the conversion of ketogenic amino acids. After hepatic glycogen depletion, ketone bodies, fat-derived glycerol, and amino acids account for the gluconeogenesis-dependent generation of approximately 80 grams/day of glucose, which is mostly utilized by the brain. Depending on body weight and composition, the ketone bodies, free fatty acids and gluconeogenesis allow the majority of human beings to survive 30 or more days in the absence of any food and allow certain species, such as king penguins, to survive for over 5 months without food (Eichhorn et al., 2011) (Figure 3C). In humans, during prolonged fasting, the plasma levels of 3-?-hydroxybutyrate are about 5 times those of free fatty acids and acetoacetic acid (Figure 3A and 3B). The brain and other organs utilize ketone bodies in a process termed ketolysis, in which acetoacetic acid and 3-?- hydroxybutyrate are converted into acetoacetyl-CoA and then acetyl-CoA. These metabolic adaptations to fasting in mammals are reminiscent of those described earlier for E. coli and yeast, in which acetic acid accumulates in response to food deprivation (Gonidakis et al., 2010; Longo et al., 2012). In yeast, glucose, acetic acid and ethanol, but not glycerol which is also generated during fasting from the breakdown of fats, accelerate aging (Fabrizio et al., 2005; Wei et al., 2009). Thus, glycerol functions as a carbon source that does not activate the pro-aging nutrient signaling pathways but can be catabolized by cells. It will be important to understand how the different carbon sources generated during fasting affect cellular protection and aging. and to determine whether glycerol, specific ketone bodies or fatty acids can provide nourishment while reducing cellular aging in mammals, a possibility suggested by beneficial effects of a dietary ketone precursor in a mouse model of Alzheimer�s disease (Kashiwaya et al., 2012). It will also be important to study, in various model organisms and humans, how high intake of specific types of fats (medium- vs.

Ãwẹ ati Brain

In mammals, severe CR/food deprivation results in a decrease in the size of most organs except the brain, and the testicles in male mice (Weindruch and Sohal, 1997). From an evolutionary perspective this implies that maintenance of a high level of cognitive function under conditions of food scarcity is of preeminent importance. Indeed, a highly conserved behavioral trait of all mammals is to be active when hungry and sedentary when satiated. In rodents, alternating days of normal feeding and fasting (IF) can enhance brain function as indicated by improvements in performance on behavioral tests of sensory and motor function (Singh et al., 2012) and learning and memory (Fontan-Lozano et al., 2007). The behavioral responses to IF are associated with increased synaptic plasticity and increased production of new neurons from neural stem cells (Lee et al., 2002).

Particularly interesting with regards to adaptive responses of the brain to limited food availability during human evolution is brain-derived neurotrophic factor (BDNF). The genes encoding BDNF and its receptor TrkB appeared in genomes relatively recently as they are present in vertebrates, but absent from worms, flies and lower species (Chao, 2000). The prominent roles of BDNF in the regulation of energy intake and expenditure in mammals is highlighted by the fact that the receptors for both BDNF and insulin are coupled to the highly conserved PI3 kinase � Akt, and MAP kinase signaling pathways (Figure 4). Studies of rats and mice have shown that running wheel exercise and IF increase BDNF expression in several regions of the brain, and that BDNF in part mediates exercise- and IF-induced enhancement of synaptic plasticity, neurogenesis and neuronal resistance to injury and disease (see sections on fasting and neurodegeneration below). BDNF signaling in the brain may also mediate behavioral and metabolic responses to fasting and exercise including regulation of appetite, activity levels, peripheral glucose metabolism and autonomic control of the cardiovascular and gastrointestinal systems (Mattson, 2012a, b; Rothman et al., 2012).

Hunger is an adaptive response to food deprivation that involves sensory, cognitive and neuroendocrine changes which motivate and enable food seeking behaviors. It has been proposed that hunger-related neuronal networks, neuropeptides and hormones play pivotal roles in the beneficial effects of energy restriction on aging and disease susceptibility. As evidence, when mice in which the hypothalamic �hunger peptide� NPY is selectively ablated are maintained on a CR diet, the ability of CR to suppress tumor growth is abolished (Shi et al., 2012). The latter study further showed that the ability of CR to elevate circulating adiponectin levels was also compromised in NPY-deficient mice, suggesting a key role for the central hunger response in peripheral endocrine adaptations to energy restriction. Adiponectin levels increase dramatically in response to fasting; and data suggest roles for adiponectin in the beneficial effects of IF on the cardiovascular system (Wan et al., 2010). The hunger response may also improve immune function during aging as ghrelin-deficient mice exhibit accelerated thymic involution during aging, and treatment of middle age mice with ghrelin increases thymocyte numbers and improves the functional diversity of peripheral T cell subsets (Peng et al., 2012). In addition to its actions on the hypothalamus and peripheral endocrine cells, fasting may increase neuronal network activity in brain regions involved in cognition, resulting in the production of BDNF, enhanced synaptic plasticity and improved stress tolerance (Rothman et al., 2012). Thus, hunger may be a critical factor involved in widespread central and peripheral adaptive responses to the challenge of food deprivation for extended time periods.

Ṣiṣewẹ, Agbo, ati Arun ni Awọn Irọrun Rodent

Awọn ọna Itọsọna Yara ati Agbo

The major differences between IF and PF in mice are the length and the frequency of the fast cycles. IF cycles usually last 24 hours and are one to a few days apart, whereas PF cycles last 2 or more days and are at least 1 week apart, which is necessary for mice to regain their normal weight. One difference in the molecular changes caused by different fasting regimes is the effect on a variety of growth factors and metabolic markers, with IF causing more frequent but less pronounced changes than PF. It will be important to determine how the frequency of specific changes such as the lowering of IGF-1 and glucose affect cellular protection, diseases and longevity. The most extensively investigated IF method in animal studies of aging has been alternate day fasting (food is withdrawn for 24 hours on alternate days, with water provided ad libitum) (Varady and Hellerstein, 2007). The magnitude of the effects of alternate day fasting on longevity in rodents depends upon the species and age at regimen initiation, and can range from a negative effect to as much as an 80% lifespan extension (Arum et al., 2009; Goodrick et al., 1990). IF every other day extended the lifespan of rats more than fasting every 3rd or 4th day (Carlson and Hoelzel, 1946). Fasting for 24 hours twice weekly throughout adult life resulted in a significant increase in lifespan of black-hooded rats (Kendrick, 1973). In rats, the combination of alternate day fasting and treadmill exercise resulted in greater maintenance of muscle mass than did IF or exercise alone (Sakamoto and Grunewald, 1987). Interestingly, when rats were maintained for 10 weeks on a PF diet in which they fasted 3 consecutive days each week, they were less prone to hypoglycemia during 2 hours of strenuous swimming exercise as a result of their accumulation of larger intramuscular stores of glycogen and triglycerides (Favier and Koubi, 1988). Several major physiological responses to fasting are similar to those caused by regular aerobic exercise including increased insulin sensitivity and cellular stress resistance, reduced resting blood pressure and heart rate, and increased heart rate variability as a result of increased parasympathetic tone (Figure 2) (Anson et al., 2003; Mager et al., 2006; Wan et al., 2003). Emerging findings suggest that exercise and IF retard aging and some age-related diseases by shared mechanisms involving improved cellular stress adaptation (Stranahan and Mattson, 2012). However, in two different mouse genetic backgrounds, IF did not extend mean lifespan and even reduced lifespan when initiated at 10 months (Goodrick et al., 1990). When initiated at 1.5 months, IF either increased longevity or had no effect (Figure 1D) (Goodrick et al., 1990). These results in rodents point to conserved effects of fasting on lifespan, but also to the need for a much better understanding of the type of fasting that can maximize its longevity effects and the mechanisms responsible for the detrimental effects that may be counterbalancing its anti-aging effects. For example, one possibility is that fasting may be consistently protective in young and middle aged laboratory rodents that are either gaining or maintaining a body weight, but may be detrimental in older animals that, similarly to humans, begin to lose weight prior to their death. Notably, whereas bacteria, yeast and humans can survive for several weeks or more without nutrients, most strains of mice are unable to survive more than 3 days without food.

Ãwẹ ati Akàn

Fasting can have positive effects in cancer prevention and treatment. In mice, alternate day fasting caused a major reduction in the incidence of lymphomas (Descamps et al., 2005) and fasting for 1 day per week delayed spontaneous tumorigenesis in p53-deficient mice (Berrigan et al., 2002). However, the major decrease in glucose, insulin and IGF-1 caused by fasting, which is accompanied by cell death and/or atrophy in a wide range of tissues and organs including the liver and kidneys, is followed by a period of abnormally high cellular proliferation in these tissues driven in part by the replenishment of growth factors during refeeding. When combined with carcinogens during refeeding, this increased proliferative activity can actually increase carcinogenesis and/or pre-cancerous lesions in tissues including liver and colon (Tessitore et al., 1996). Although these studies underline the need for an in depth understanding of its mechanisms of action, fasting is expected to have cancer preventive effects as indicated by the studies above and by the findings that multiple cycles of periodic fasting can be as effective as toxic chemotherapy in the treatment of some cancers in mice (Lee et al., 2012).

In the treatment of cancer, fasting has been shown to have more consistent and positive effects. PF for 2�3 days was shown to protect mice from a variety of chemotherapy drugs, an effect called differential stress resistance (DSR) to reflect the inability of cancer cells to become protected based on the role of oncogenes in negatively regulating stress resistance, thus rendering cancer cells, by definition, unable to become protected in response to fasting conditions (Figure 5) (Raffaghello et al., 2008). PF also causes a major sensitization of various cancer cells to chemo-treatment, since it fosters an extreme environment in combination with the stress conditions caused by chemotherapy. In contrast to the protected state entered by normal cells during fasting, cancer cells are unable to adapt, a phenomenon called differential stress sensitization (DSS), based on the notion that most mutations are deleterious and that the many mutations accumulated in cancer cells promote growth under standard conditions but render them much less effective in adapting to extreme environments (Lee et al., 2012). In mouse models of metastatic tumors, combinations of fasting and chemotherapy that cause DSR and DSS, result in 20 to 60% cancer-free survival compared to the same levels of chemotherapy or fasting alone, which are not sufficient to cause any cancer-free survival (Lee et al., 2012; Shi et al., 2012). Thus, the idea that cancer could be treated with weeks of fasting alone, made popular decades ago, may be only partially true, at least for some type of cancers, but is expected to be ineffective for other types of cancers. The efficacy of long-term fasting alone (2 weeks or longer) in cancer treatment will need to be tested in carefully designed clinical trials in which side effects including malnourishment and possibly a weakened immune system and increased susceptibility to certain infections are carefully monitored. By contrast, animal data from multiple laboratories indicate that the combination of fasting cycles with chemotherapy is highly and consistently effective in enhancing chemotherapeutic index and has high translation potential. A number of ongoing trials should soon begin to determine the efficacy of fasting in enhancing cancer treatment in the clinic.

Iwẹ ati Neurodegeneration

Ti a fiwera si awọn idari ti ajẹsara libitum, awọn eku ati awọn eku ti o tọju lori IF ba jẹun ti o ṣe afihan aiṣedede iṣan ati ibajẹ, ati awọn aami aisan ti o dinku ni awọn awoṣe ti aisan Alzheimer s (AD), Arun Parkinson s (PD) ati arun Huntington (HD) Awọn awoṣe wọnyi pẹlu awọn eku transgenic ti n ṣalaye awọn Jiini ẹda eniyan ti o fa jogun pupọ (amyloid precursor protein and presenilin-1) ati iyawere iwaju iwaju iwaju (Tau) (Halagappa et al., 2007), PD (? -Synuclein) (Griffioen et al. , 2012) ati HD (huntingtin) (Duan et al., 2003), ati awọn awoṣe ti o da lori neurotoxin to ṣe pataki si AD, PD ati HD (Bruce-Keller et al., 1999; Duan ati Mattson, 1999). Awọn ẹranko lori ounjẹ IF tun dara ju awọn iṣakoso ifunni libitum lọ lẹhin ipalara nla pẹlu awọn ijakalẹ apọju nla, ikọlu, ati ọpọlọ ọgbẹ ati awọn ọgbẹ ẹhin (Arumugam et al., 2010; Bruce-Keller et al., 1999; Plunet et al., 2008).

Several interrelated cellular mechanisms contribute to the beneficial effects of IF on the nervous system including reduced accumulation of oxidatively damaged molecules, improved cellular bioenergetics, enhanced neurotrophic factor signaling, and reduced inflammation (Mattson, 2012a). The latter neuroprotective mechanisms are supported by studies showing that IF diets boost levels of antioxidant defenses, neurotrophic factors (BDNF and FGF2) and protein chaperones (HSP-70 and GRP-78), and reduce levels of pro- inflammatory cytokines (TNF?, IL-1? and IL-6) (Figure 4) (Arumugam et al., 2010). IF may also promote restoration of damaged nerve cell circuits by stimulating synapse formation and the production of new neurons from neural stem cells (neurogenesis) (Lee et al., 2002). Interestingly, while beneficial in models of most neurodegenerative conditions, there is evidence that fasting can hasten neurodegeneration in some models of inherited amyotrophic lateral sclerosis, perhaps because the motor neurons affected in those models are unable to respond adaptively to the moderate stress imposed by fasting (Mattson et al., 2007; Pedersen and Mattson, 1999).

Ãwẹ ati Ọdun Ibaramu Aisan

Metabolic syndrome (MS), defined as abdominal adiposity, combined with insulin resistance, elevated triglycerides and/or hypertension, greatly increases the risk of cardiovascular disease, diabetes, stroke and AD. Rats and mice maintained under the usual ad libitum feeding condition develop an MS-like phenotype as they age. MS can also be induced in younger animals by feeding them a diet high in fat and simple sugars (Martin et al., 2010). IF can prevent and reverse all aspects of the MS in rodents: abdominal fat, inflammation and blood pressure are reduced, insulin sensitivity is increased, and the functional capacities of the nervous, neuromuscular and cardiovascular systems are improved (Castello et al., 2010; Wan et al., 2003). Hyperglycemia is ameliorated by IF in rodent models of diabetes (Pedersen et al., 1999) and the heart is protected against ischemic injury in myocardial infarction models (Ahmet et al., 2005). A protective effect of fasting against ischemic renal and liver injury occurs rapidly, with 1 � 3 days of fasting improving functional outcome and reducing tissue injury and mortality (Mitchell et al., 2010). Six days on a diet missing just a single essential amino acid such as tryptophan can also elicit changes in metabolism and stress resistance, similar to those caused by fasting, which are dependent on the amino acid sensing kinase Gcn2 (Peng et al., 2012).

Multiple hormonal changes that typify MS in humans a re observed in rodents maintained on high fat and sugar diets including elevated levels of insulin and leptin and reduced levels of adiponectin and ghrelin. Elevated leptin levels are typically reflective of a pro- inflammatory state, whereas adiponectin and ghrelin can suppress inflammation and increase insulin sensitivity (Baatar et al., 2011; Yamauchi et al., 2001). Local inflammation in hypothalamic nuclei that control energy intake and expenditure may contribute to a sustained positive energy balance in MS (Milanski et al., 2012). Fasting results in a lowering of insulin and leptin levels and an elevation of adiponectin and ghrelin levels. By increasing insulin and leptin sensitivity, suppressing inflammation and stimulating autophagy, fasting reverses all the major abnormalities of the MS in rodents (Singh et al., 2009; Wan et al., 2010). Finally, in addition to its many effects on cells throughout the body and brain, IF may elicit changes in the gut microbiota that protect against MS (Tremaroli and Backhed, 2012). Naturally, the challenge of applying fasting-based interventions to treat MS in humans is a major one, as some obese individuals may have difficulties in following IF for long periods.

The ProLon� fasting mimicking diet is a 5-day meal program consisting of scientifically developed and clinically tested, natural ingredients which “trick” the human body into a fasting mode. The FMD is low in carbohydrates as well as proteins and it’s high in fats. The ProLon� fasting mimicking diet promotes a variety of healthy benefits, including weight loss and decreased abdominal fat, all while preserving lead body mass, improved energy levels, softer and healthier looking skin, as well as overall health and wellness. The FMD can promote longevity.

Ãwẹ, Agbo, ati Arun ninu Awọn eniyan

Iwẹ ati Awọn Okunfa idiju ni Aging

Clinical and epidemiological data are consistent wit h an ability of fasting to retard the aging process and associated diseases. Major factors implicated in aging whose generation are accelerated by gluttonous lifestyles and slowed by energy restriction in humans include: 1) oxidative damage to proteins, DNA and lipids; 2) inflammation; 3) accumulation of dysfunctional proteins and organelles; and 4) elevated glucose, insulin and IGF-I, although IGF-1decreases with aging and its severe deficiency can be associated with certain pathologies (Bishop et al., 2010; Fontana and Klein, 2007). Serum markers of oxidative damage and inflammation as well as clinical symptoms are reduced over a period of 2�4 weeks in asthma patients maintained on an alternate day fasting diet (Johnson et al., 2007). Similarly, when on a 2 days/week fasting diet overweight women at risk for breast cancer exhibited reduced oxidative stress and inflammation (Harvie et al., 2011) and elderly men exhibited reductions in body weight and body fat, and improved mood (Teng et al., 2011). Additional effects of fasting in human cells that can be considered as potentially �anti-aging� are inhibition the mTOR pathway, stimulation of autophagy and ketogenesis (Harvie et al., 2011; Sengupta et al., 2010).

Among the major effects of fasting relevant to aging and diseases are changes in the levels of IGF-1, IGFBP1, glucose, and insulin. Fasting for 3 or more days causes a 30% or more decrease in circulating insulin and glucose, as well as rapid decline in the levels of insulin- like growth factor 1 (IGF-1), the major growth factor in mammals, which together with insulin is associated with accelerated aging and cancer (Fontana et al., 2010). In humans, five days of fasting causes an over 60% decrease in IGF-1and a 5-fold or higher increase in one of the principal IGF-1-inhibiting proteins: IGFBP1 (Thissen et al., 1994a). This effect of fasting on IGF-1is mostly due to protein restriction, and particularly to the restriction of essential amino acids, but is also supported by calorie restriction since the decrease in insulin levels during fasting promotes reduction in IGF-1(Thissen et al., 1994a). Notably, in humans, chronic calorie restriction does not lead to a decrease in IGF-1unless combined with protein restriction (Fontana et al., 2008).

IF can be achieved in with a minimal decrease in overall calorie intake if the refeeding period in which subjects overeat is considered. Thus, fasting cycles provide a much more feasible strategy to achieve the beneficial effects of CR, and possibly stronger effects, without the burden of chronic underfeeding and some of the potentially adverse effects associated with weight loss or very low BMIs. In fact, subjects who are moderately overweight (BMI of 25�30) in later life can have reduced overall mortality risk compared to subjects of normal weight (Flegal et al., 2013). Although these results may be affected by the presence of many existing or developing pathologies in the low weight control group, they underline the necessity to differentiate between young individuals and elderly individuals who may use CR or fasting to reduce weight or delay aging. Although extreme dietary interventions during old age may continue to protect from age-related diseases, they could have detrimental effects on the immune system and the ability to respond to certain infectious diseases, wounds and other challenges (Kristan, 2008; Reed et al., 1996). However, IF or PF designed to avoid weight loss and maximize nourishment have the potential to have beneficial effects on infectious diseases, wounds and other insults even in the very old. Nourishment of subjects can be achieved by complementing IF or PF with micro- and macro Studies to test the effect of IF or PF regimens on markers of aging, cancer, cognition and obesity are in progress (V. Longo and M. Mattson).

Ãwẹ ati Akàn

Ãwẹ ni o ni agbara fun awọn ohun elo ni idena ati iṣeduro akàn. Biotilẹjẹpe ko si data eniyan ni o wa lori ipa ti IF tabi PF ni idena akàn, ipa wọn lori dinku IGF-1, insulin ati glucose ipele, ati jijẹ IGFBP1 ati awọn ipele ara ketone le ṣe aabo ayika ti o dinku ibajẹ DNA ati carcinogenesis, lakoko ti o ti ni akoko kanna ṣiṣẹda awọn ipo idaniloju fun tumo ati awọn ẹyin ti o ti le tete-cancerous (Ẹka 5). Ni otitọ, IGF-1 ti o kaakiri ni nkan ṣe pẹlu ewu ti o pọju lati ṣe idagbasoke awọn aarun kan (Chan et al., 2000; Giovannucci et al., 2000) ati awọn eniyan pẹlu IGF-1deficiency ti o lagbara nipasẹ ailewu idaabobo idaamu ti idagba, Guevara-Aguirre et al., 2011; Shevah ati Laron, 2007, Steuerman et al., 2011). Pẹlupẹlu, omi ara lati awọn ipilẹ IGF-1deficient wọnyi ni idaabobo awọn ẹda epithelial eniyan lati awọn idibajẹ DNA ti o ni idamu-agbara. Pẹlupẹlu, ni kete ti DNA wọn ti bajẹ, awọn sẹẹli ni o le ṣe diẹ ninu ẹjẹ iku (Guevara-Aguirre et al., 2011). Bayi, igbadun le dabobo lati akàn nipasẹ didawọn ibajẹ cellular ati DNA ṣugbọn tun nipasẹ gbigbọn iku awọn ẹyin ti o ti tete ṣaju.

Ninu iwadi akọkọ ti awọn ohun elo 10 pẹlu ọpọlọpọ awọn aiṣedede, idapọ ti chemotherapy pẹlu ãwẹ jẹ ki o dinku ni ibiti o ti jẹ ki awọn ayẹwo ti o jẹ deede ti o niiṣe nipasẹ chemotherapy ti a bawe si awọn ipele kanna ti o gba chemotherapy lakoko ti o jẹun deede (Safdie ati al., 2009). Ipa ti awẹ lori kemikali ti o ni iṣiro ati ilọsiwaju akàn ni a ti ni idanwo ni awọn idanwo ile-iwadii ni Europe ati US (0S-08-9, 0S-10-3).

Iwẹ ati Neurodegeneration

Imọ wa ti o wa lọwọlọwọ lori ikolu ti IF lori eto aifọkanbalẹ ati awọn iṣẹ inu-inu jẹ eyiti a kọ lati inu imọ-ẹrọ eranko (wo loke). Awọn ilọmọ-ṣiṣe ti ihamọ lati pinnu idibajẹ ti iwẹwẹ lori iṣẹ iṣọn ati awọn ilana aisan ailera ti ko ni ọkan.

Lẹhin oṣu 3 4, CR ṣe ilọsiwaju iṣẹ iṣaro (iranti ọrọ) ninu awọn obinrin apọju (Kretsch et al., 1997) ati ninu awọn akọle arugbo (Witte et al., 2009). Bakan naa, nigbati awọn akẹkọ ti o ni aipe aitọ ọlọgbọn ti wa ni itọju fun oṣu 1 lori ounjẹ glycemic kekere, wọn ṣe afihan iranti iwoye ti o pẹ, awọn alakọja omi ara ọpọlọ ti A? iṣelọpọ ati ọpọlọ bioenergetics (Bayer-Carter et al., 2011). Awọn ẹkọ eyiti iṣẹ iṣọn-ọpọlọ, awọn iwọn ọpọlọ ọpọlọ agbegbe, iṣẹ nẹtiwọọki ti nkankikan, ati awọn itupalẹ biokemika ti iṣan cerebrospinal ni a wọn ninu awọn akọle eniyan ṣaaju ati lakoko akoko ti o gbooro sii ti IF yẹ ki o ṣalaye ipa ti IF lori ilana ọpọlọ ati iṣẹ eniyan.

Asẹ, Imunimu ati Haipatensonu

Ninu awọn eniyan, ọkan ninu awọn ifihan ti o dara julọ ti awọn ipa anfani ti igba pipẹ ti o pẹ to ọsẹ mẹta si mẹta ni itọju ti arthritis rheumatoid (RA). Ni adehun pẹlu awọn abajade ninu awọn eku, iyemeji diẹ wa pe lakoko asiko aawẹ mejeeji igbona ati irora dinku ni awọn alaisan RA (Muller et al., 3). Sibẹsibẹ, lẹhin ti a tun bẹrẹ ounjẹ deede, igbona pada ayafi ti akoko aawẹ ba tẹle pẹlu ounjẹ ajewebe (Kjeldsen-Kragh et al., 2001), itọju idapọ kan ti o ni awọn anfani anfani ti o pẹ fun ọdun meji tabi ju bẹẹ lọ (Kjeldsen-Kragh et al., 1991). Wiwulo ti ọna yii ni atilẹyin nipasẹ awọn ẹkọ iṣakoso mẹrin ti o yatọ, pẹlu awọn idanwo alailẹgbẹ meji (Muller et al., 1994). Nitorinaa, aawẹ ni idapo pẹlu ounjẹ ounjẹ ajewebe ati ṣeeṣe pẹlu awọn ounjẹ ti a tunṣe miiran pese awọn ipa anfani ni itọju RA. Ọjọ miiran TI tun tun ṣe iyọrisi awọn iyọkuro pataki ninu omi ara TNF? ati ceramides ninu awọn alaisan ikọ-fèé lakoko akoko oṣu meji kan (Johnson et al., 2001). Iwadii ti o kẹhin fihan siwaju pe awọn ami ami ti aapọn ifasita nigbagbogbo ni nkan ṣe pẹlu iredodo (amuaradagba ati ifoyina ọra) ni dinku dinku ni idahun si IF. Nitorinaa, fun ọpọlọpọ awọn alaisan ti o ni anfani ati imurasilẹ lati farada aawẹ igba pipẹ ati lati yi ijẹẹmu wọn pada titilai, awọn iyipo awẹ yoo ni agbara lati kii ṣe alekun nikan ṣugbọn tun rọpo awọn itọju iṣoogun to wa tẹlẹ.

Water only and other forms of long-term fasting have also been documented to have potent effects on hypertension. An average of 13 days of water only fasting resulted in the achievement of a systolic blood pressure (BP) below 120 in 82% of subjects with borderline hypertension with a mean 20 mm Hg reduction in BP (Goldhamer et al., 2002). BP remained significantly lower compared to baseline even after subjects resumed the normal diet for an average of 6 days (Goldhamer et al., 2002). A small pilot study of patients with hypertension (140 mm and above systolic BP) also showed that 10�11 days of fasting caused a 37�60 mm decrease in systolic BP (Goldhamer et al., 2001). These preliminary studies are promising but underscore the need for larger controlled and randomized clinical studies that focus on periodic fasting strategies that are feasible for a larger portion of the population.

For both hypertension and RA it will be important to develop PF mimicking diets that are as effective as the fasting regimens described above but that are also tolerable by the great majority of patients.

Ãwẹ ati Ọdun Ibaramu Aisan

Periodic fasting can reverse multiple features of the metabolic syndrome in humans: it enhances insulin sensitivity, stimulates lipolysis and reduces blood pressure. Body fat and blood pressure were reduced and glucose metabolism improved in obese subjects in response to an alternate day modified fast (Klempel et al., 2013; Varady et al., 2009). Overweight subjects maintained for 6 months on a twice weekly IF diet in which they consumed only 500�600 calories on the fasting days, lost abdominal fat, displayed improved insulin sensitivity and reduced blood pressure (Harvie et al., 2011). Three weeks of alternate day fasting resulted in reductions in body fat and insulin levels in normal weight men and women (Heilbronn et al., 2005) and Ramadan fasting (2 meals/day separated by approximately 12 hours) in subjects with MS resulted in decreased daily energy intake, decreased plasma glucose levels and increased insulin sensitivity (Shariatpanahi et al., 2008). Subjects undergoing coronary angiography who reported that they fasted regularly exhibited a lower prevalence of diabetes compared to non-fasters (Horne et al., 2012). Anti- metabolic syndrome effects of IF were also observed in healthy young men (BMI of 25) after 15 days of alternate day fasting: their whole-body glucose uptake rates increased significantly, levels of plasma ketone bodies and adiponectin were elevated, all of which occurred without a significant decrease in body weight (Halberg et al., 2005). The latter findings are similar to data from animal studies showing that IF can improve glucose metabolism even with little or no weight change (Anson et al., 2003). It will be important to determine if longer fasting periods which promote a robust switch to a fat breakdown and ketone body-based metabolism, can cause longer lasting and more potent effects.

Awọn ipinnu ati awọn iṣeduro

Da lori awọn ẹri ti o wa tẹlẹ lati awọn ohun elo ẹranko ati awọn eniyan ti a ṣàpèjúwe, a pinnu pe o pọju agbara fun awọn igbesi aye ti o npo igbaduro akoko ni igbesi aye agbalagba lati ṣe igbelaruge ilera ti o dara julọ ati dinku ewu ti ọpọlọpọ awọn arun alaisan, paapa fun awọn ti o ni iwọn apọju ati sedentary. Awọn ijinlẹ ti eranko ti ṣafihan awọn ohun elo ti o lagbara ati awọn ohun elo ti o ṣe pataki lori awọn ifihan ilera gẹgẹbi ifarahan isanini ti o tobi, ati awọn ipele ti o dinku ti titẹ ẹjẹ, ara ti, IGF-I, insulin, glucose, lipids atherogenic and inflammation. Awọn atunṣe igbaradi le ṣe atunṣe awọn ilana aisan ati mu abajade iṣẹ ṣiṣẹ ni awọn awoṣe ti awọn ẹranko ti o ni iṣiro-ọgbẹ-ẹjẹ, iṣiro, igun-ọwọ, AD ati PD. Ilana ọkan gbogboogbo ti ãwẹ jẹ pe o nfa awọn ibaraẹnisọrọ cellular stress responses, eyi ti o mu ni agbara ti o ni ilọsiwaju lati dojuko pẹlu wahala ti o nira pupọ ati lati koju awọn ilana aisan. Ni afikun, nipa idaabobo awọn ẹyin lati ipalara DNA, idinku idagbasoke ẹyin alagbeka ati igbelaruge apoptosis ti awọn ẹyin ti o ti bajẹ, ipamọwẹ le ṣagbe ati / tabi dena iṣeduro ati idagbasoke awọn aarun.

Bibẹẹkọ, awọn iwadii ti awọn ilana aawẹ ko ti ṣe ni awọn ọmọde, awọn ti o ti dagba pupọ ati ti iwọn apọju, ati pe o ṣee ṣe pe IF ati PF yoo jẹ ipalara si awọn eniyan wọnyi. Awọn akoko aawẹ ti o gun ju wakati 24 lọ ati ni pataki awọn ti o wa fun ọjọ mẹta 3 tabi diẹ sii yẹ ki o ṣee ṣe labẹ abojuto dokita kan ati ni pataki ni ile-iwosan kan. IF- ati awọn ọna ti o da lori PF si jijakadi awọn ajakale-arun lọwọlọwọ ti iwọn apọju, àtọgbẹ ati awọn aisan ti o jọmọ yẹ ki o lepa ninu awọn iwadii iwadii eniyan ati awọn ero itọju iṣoogun. Ọpọlọpọ awọn iyatọ ti agbara awọn ilana gbigba gbigba gbigba ti a ti gba fun awọn akọle apọju wa ni ayika akori ti o wọpọ ti yiyọ kuro ninu ounjẹ ati awọn ohun mimu kalori fun o kere ju wakati 12 24 ni ọjọ kan tabi diẹ sii ni ọsẹ kọọkan tabi oṣu, da lori gigun, ni idapo pẹlu idaraya deede. Fun awọn ti o ni iwuwo apọju, awọn oṣoogun le beere lọwọ awọn alaisan wọn lati yan idawọle ti o da lori awẹ ti wọn gbagbọ pe wọn le ni ibamu pẹlu awọn iṣeto ojoojumọ ati ti ojoojumọ. Awọn apẹẹrẹ pẹlu 5: 2 IF ijẹẹmu (Harvie et al., 2011), ọjọ miiran ti a ṣe atunṣe ounjẹ awẹwẹ (Johnson et al., 2007; Varady et al., 2009), iyara 4 5 kan tabi kalori kekere ṣugbọn awọn ounjẹ ti o jẹ awẹ ti o ngbawe awẹwẹ ni ẹẹkan ni gbogbo oṣu 1 3 ti o tẹle pẹlu yiyọ ti ounjẹ pataki kan ni gbogbo ọjọ ti o ba nilo (V. Longo, iwadii iwadii ni ilọsiwaju). Ọkan ninu awọn ifiyesi pẹlu awọn ounjẹ oniduro aiṣedeede gẹgẹbi awọn eyiti eyiti gbigbe kalori kekere jẹ eyiti a ṣe akiyesi nikan fun awọn ọjọ 2 ni ọsẹ kan ni awọn ipa ti o le ṣe lori rirọ circadian ati endocrine ati awọn ọna inu ikun, eyiti a mọ pe o ni ipa nipasẹ awọn iwa jijẹ. Lakoko awọn ọsẹ 4 6 akọkọ ti imuse ti ilana aawẹ, oniwosan tabi onjẹ ounjẹ ti a forukọsilẹ yẹ ki o wa ni ibasọrọ deede pẹlu alaisan lati ṣe atẹle ilọsiwaju wọn ati lati pese imọran ati abojuto.

Awọn ilana aawẹ tun le ṣe apẹrẹ fun awọn aisan kan pato bi iduro-nikan tabi awọn itọju arannilọwọ. Awọn abajade ti awọn idanwo akọkọ ti IF (aawẹ ọjọ meji 2 fun ọsẹ kan tabi gbogbo ọjọ miiran) ninu awọn akọle eniyan daba pe akoko iyipada pataki ti awọn ọsẹ 3 6 lakoko eyiti akoko ọpọlọ ati ara ṣe baamu si ilana jijẹ tuntun ati iṣesi ti ni ilọsiwaju (Harvie et al., 2011; Johnson et al., 2007). Botilẹjẹpe o sọ asọtẹlẹ, o ṣee ṣe pe lakoko akoko iyipada igbeyin ọpọlọ iṣọn-ara iṣan ọpọlọ yipada ki “adarẹ” si lilo deede ti ounjẹ jakejado ọjọ naa bori. Ni pataki, ọpọlọpọ awọn isunmọ awẹ ni o le ni ipa to lopin ni pataki lori ogbó ati awọn ipo miiran ju isanraju ayafi ti o ba ni idapo pẹlu awọn ounjẹ bii gbigbe kalori alabọde ati pupọ julọ orisun Mẹditarenia tabi awọn ounjẹ amuaradagba kekere Okinawa (0.8 g protein / Kg of weight body) ), nigbagbogbo ni nkan ṣe pẹlu ilera ati gigun gigun.

Ni ojo iwaju, yoo ṣe pataki lati darapọ awọn data apaniyan, awọn iwadi ti awọn eniyan ti o pẹ ati awọn ounjẹ wọn, awọn esi lati awọn oganisimu ti o niiṣe pẹlu awọn ohun elo ti o niijẹ pẹlu awọn ohun elo ti o jẹun fun awọn ohun ti o dagba ati awọn aṣiṣe-arun, pẹlu awọn data lati awọn iwadi lori awọn igbarawẹ ti o jẹun ni awọn eniyan , lati ṣe akẹkọ awọn isẹ-iwosan ti o pọju ti awọn ounjẹ ti a mọ bi aabo ati igbadun. Imọye ti o dara julọ nipa awọn iṣelọpọ ti iṣelọpọ nipasẹ eyiti azu yoo ni ipa lori awọn oriṣiriṣi sẹẹli ati awọn eto eto ara eniyan yẹ ki o ja si idagbasoke ti iwe-ara itọju prophylactic ati awọn itọju ilera fun ọpọlọpọ awọn ailera.

Mu Ifiranṣẹ Ile

Awọn ounjẹ igbadun mimu n pese awọn anfani kanna ti iwẹwu ibile pẹlu ihamọ gbigbemi kalori rẹ fun ọjọ marun kuro ninu oṣu dipo ti pa gbogbo ounjẹ kuro ni ọpọlọpọ ọjọ tabi awọn ọsẹ. Awọn ProLon Nmu igbadun mimu ounjẹ n pese eto ounjẹ ounjẹ 5 ọjọ ti a ti sọ papọ ati pe ọkan ni awọn titobi deede ati awọn akojọpọ fun ọjọ kọọkan. Biotilẹjẹpe iwadi iwadi ti o wa loke ti ṣe afihan awọn anfani ilera ti ãwẹ, jọwọ rii daju pe sọrọ si ọjọgbọn ọjọgbọn ṣaaju ki o to bẹrẹ ProLon aawẹ mimicking onje, eto ounjẹ ọjọ 5 lati wa boya FMD, tabi eyikeyi ounjẹ miiran, dara fun ọ.

Iwe atẹjade, atunṣe ti a ṣatunkọ ipari ti iwadi iwadi ti a darukọ loke wa ni o wa ni NIK Public Access Author Iwe afọwọkọ lori PMC Kínní 4, 2015. Awọn alaye ti wa alaye wa ni opin si chiropractic, awọn oran-aisan ati awọn egbogi iṣẹ. Lati ṣe alaye siwaju sii lori ọrọ naa, jọwọ ni irọrun lati beere fun Dr. Alex Jimenez tabi kan si wa ni 915-850-0900 .

Ti a da nipasẹ Dr. Alex Jimenez

Ti firanṣẹ lati: Nih.gov

Ifọrọwerọ Koko-ọrọ Afikun: Irora Pada Laini

Ideri afẹyinti jẹ ọkan ninu awọn okunfa ti o wọpọ julọ ailera ati awọn ọjọ ti o padanu ni iṣẹ agbaye. Awọn irora irora pada si idi keji ti o wọpọ julọ fun awọn ijabọ ọfiisi dokita, ti o pọju nipasẹ awọn àkóràn atẹgun ti oke-atẹgun. Oṣuwọn 80 ninu ogorun olugbe yoo ni iriri iriri irora ni o kere ju lẹẹkan ni gbogbo aye wọn. Ẹhin rẹ jẹ ẹya ti o dapọ ti awọn egungun, awọn isẹpo, awọn ligaments, ati awọn iṣan, laarin awọn ohun elo mimu miiran. Awọn ipalara ati / tabi awọn ipo ti a ṣe ipalara, bii Awọn ẹkunrẹrẹ ti a fi sinu rẹ, le šẹlẹ si awọn aami aiṣan ti ibanujẹ pada. Awọn ipalara fun idaraya tabi awọn ijamba ijamba mọkọ jẹ igbagbogbo ti ibanujẹ irora, sibẹsibẹ, nigbakanna awọn iṣoro ti o rọrun julọ le ni awọn esi ibanuje. O ṣeun, awọn itọju abojuto miiran, gẹgẹbi abojuto ti chiropractic, le ṣe iranlọwọ fun irora irora nipase lilo awọn atunṣe ọpa ẹhin ati awọn ifọwọyi ni ọwọ, ṣiṣe ni afikun imudara irora.

XYMOGEN s Awọn agbekalẹ Ọjọgbọn Alailowaya wa nipasẹ awọn oniṣẹ ilera ilera ti a yan. Awọn titaja ayelujara ati fifunṣowo awọn agbekalẹ XYMOGEN ti wa ni idinamọ patapata.

Ni idunnu, Dokita Alexander Jimenez mu awọn agbekalẹ XYMOGEN wa nikan si awọn alaisan labe itọju wa.

Jọwọ pe ọfiisi wa ki o le fun wa ni imọran dokita fun wiwọle si lẹsẹkẹsẹ.

Ti o ba jẹ alaisan kan Ile-iwosan Ipalara & Ile-iwosan Chiropractic, o le beere nipa XYMOGEN nipa pipe 915-850-0900.

Fun igbadun rẹ ati atunyẹwo ti XYMOGEN Awọn ọja jọwọ ṣe atunwo ọna asopọ atẹle. *XYMOGEN-Catalogue-download

* Gbogbo awọn ilana XYMOGEN ti o wa loke wa ni agbara.

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