Ukuzila Ukutya Ukutya Ukuchazwa

Ukuqonda ukutya kweProLon Ukuzila ukutya

Ukuzila ukutya kunxulunyaniswa neenzuzo ezininzi zempilo; ukusuka ekulahlekeni kobunzima ukuya kubomi obude. Kukho iintlobo ezininzi zeendlela zokuzila ukutya, ezifana nokuzila ukutya okwethutyana. Ukuzila ukutya okulingisayo kukuvumela ukuba ufumane izibonelelo zokuzila ukutya kwendabuko ngaphandle kokunciphisa umzimba wakho wokutya. Umahluko ophambili we-FMD kukuba endaweni yokuphelisa ngokupheleleyo ukutya kangangeentsuku ezininzi okanye iiveki, unqanda kuphela ukutya kwakho kwekhalori kwiintsuku ezintlanu ngaphandle kwenyanga. I-FMD inokuqhutywa kanye ngenyanga ukukhuthaza impilo-ntle.

Nangona nabani na onokulandela i-FMD ngokwabo, i ProLon Ukuzila ukutya ukutshatya ukutya kunika inkqubo ye-5 yosuku lokutya oluye lwaphawulwa ngabanye kwaye lubhalwe usuku ngalunye kwaye lusebenza ukutya okufunayo kwi-FMD ngobungakanani obuchanekileyo kunye nokudibanisa. Iprogram yokutya iqulethwe ngokulungele ukutya okanye ukulungiselela ukulula, ukutya okusezityalo, kubandakanya imivalo, isobho, ukutya, ukutya, ukuxiliswa kwamanzi kunye ne teas. Iimveliso zenzelwe isayensi kwaye zizonambitha kakhulu. Ngaphambi kokuqala Ukuzila ukutya kweProLon yokulinganisa ukutya, inkqubo yeentsuku ezi-5 zokutya, nceda qiniseka ukuthetha nomsebenzi wezonyango ukuze ubone ukuba i-FMD ilungile kuwe. Injongo yocwaningo olungaphantsi apha kukubonisa iindlela zee molecular kunye nezicelo zekliniki zokuzila ukutya kwi-FMD.

Ukuzila: Iinkqubo zeMolcular and Applications Clinical

Ukuzila ukutya kuye kwenziwa iwaka leminyaka, kodwa kutsha nje izifundo ziye zanika ukukhanya kwindima yayo kwiimpendulo zeselula eziguquguqukayo ezinciphisa umonakalo we-oxidative kunye nokuvutha, ukwandisa amandla e-metabolism kunye nokukhusela ukhuseleko lwamaselula. Kwi-eukaryotes esezantsi, ukuzila ukutya okungapheliyo kwandisa ixesha elide ngokuyinxenye ngokucwangcisa inkqubo yemetabolism kunye neendlela zokumelana noxinzelelo. Kwiimpuku ezinqumayo okanye ngamaxesha athile zikhusela isifo seswekile, umhlaza, isifo sentliziyo kunye ne-neurodegeneration, ngelixa ebantwini kunceda ukunciphisa ukutyeba, uxinzelelo lwegazi, isifuba kunye nesifo samathambo. Ngaloo ndlela, ukuzila ukudla kunako ukulibazisa ukuguga kunye nokunceda ukukhusela nokuphatha izifo ngelixa unciphisa imiphumo emibi ebangelwa ukungenelela kokutya okungapheliyo.

intshayelelo

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).

Izifundo ezivela kwizinto ezilula

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).

Kwigwele S. cerevisiae, ukutshintsha iiseli ukusuka kwinqanaba eliqhelekileyo lokukhula ukuya emanzini nako kubangela ukongezwa kobomi obuphindwe kabini ngokulandelelana kunye nokwanda okukhulu kokumelana noxinzelelo oluninzi (Umfanekiso 2B) (Longo et al., 1; Longo et al., 1997). Iindlela zokwandiswa kokutya okuxhomekeke kubomi bobomi zibandakanya ukulawulwa phantsi kwempendulo ye-amino acid ye-Tor-S2012K (Sch6) indlela kunye ne-glucose ephendulayo ye-Ras-adenylate cyclase-PKA indlela ekhokelela ekusebenzeni kwe-serine/threonine kinase. I-Rim9, i-enzyme ephambili yokulungelelanisa iimpendulo ezikhuselayo (Fontana et al., 15). Ukungasebenzi kwe-Tor-S2010K, i-Ras-AC-PKA kunye nokusebenza kwe-Rim6 kubangela ukunyuswa kokunyuswa kweejeni ezibandakanya i-superoxide dismutases kunye neeprotheni zokutshatyalaliswa kobushushu ezilawulwa yi-stress responsive transcription factor Msn15, Msn2 kunye ne-Gis4, efunekayo kuninzi lweziphumo zokukhusela ezibangelwayo. ngokunqongophala kokutya (Wei et al., 1). Ngokucacileyo, xa utshintshelwa kwiimeko zokunqongophala kokutya, zombini iibhaktheriya kunye negwele zingena kwimodi ye-hypometabolic ebavumela ukuba banciphise ukusetyenziswa kwemithombo yekhabhoni egciniweyo kwaye banokuqokelela amanqanaba aphezulu e-ketone yomzimba njenge-acetic acid, ngokufana nezilwanyana ezincancisayo.

Enye imodeli engundoqo ephilayo apho ukuzila kwandisa ixesha lokuphila yi-nematode C. elegans. Iimeko zokunqongophala kokutya eziphunyeziweyo ngokutya iintshulube zincinci okanye zingabikho iibhaktheriya, zikhokelela ekunyukeni okukhulu kwexesha lokuphila (Umfanekiso 1C) (Kaeberlein et al., 2006; Lee et al., 2006), efuna i-AMPK kunye noxinzelelo lwe-transcription factor I-DAF-16, ngokufanayo nendima yezinto ezikhutshelweyo i-Msn2 / 4 kunye ne-Gis1 kwimvubelo kunye ne-FOXO kwiimpukane kunye nezilwanyana ezincelisayo (Greer et al., 2007). Ukunqongophala kokutya okwethutyana kwandisa ixesha lokuphila kwi-C. elegans ngomatshini obandakanya i-GTPase encinci ye-RHEB-1 (Honjoh et al., 2009).

Ngezimpukane, uphando oluninzi lubonisa ukuba ukungabikho kokutya okuphakathi kokuchaphazelekayo akuchaphazeli ubomi (Grandison et al., 2009). Nangona kunjalo, ukunciphisa ukutya okanye ukuhluthwa kokutya kuye kwabonakaliswa ngokuqhubekayo kwandisa i-Drosophila longevity (i-Piper kunye ne-Partridge, i-2007) ebonisa ukuba iimpukane zinokuzuza kwizithintelo zokutya kodwa zinokuthi zivelele nakwixesha elifutshane leendlala.

Ezi ziphumo zibonisa ukuba ukungabikho kokutya kunokubangela iziphumo ezinobungakanani bexesha elide kwizinto ezahlukeneyo zezinto eziphilayo, kodwa kwakhona ugxininise ukuba izilwanyana ezahlukeneyo zineempendulo ezahlukeneyo zokuzila ukutya.

Izimpendulo ezixhasayo zokuzila ukutya kwizilwanyana

Kwizilwanyana ezininzi ezincancisayo, isibindi sisebenza njengomthombo oyintloko weglucose, egcinwa ngendlela ye-glycogen. Kubantu, ngokuxhomekeke kwinqanaba lomsebenzi wabo womzimba, i-12 kwiiyure ze-24 zokuzila ukutya ngokuqhelekileyo kubangela i-20% okanye ukuncipha okukhulu kwi-serum glucose kunye nokuncipha kwe-hepatic glycogen, ehamba kunye nokutshintshela kwimodi ye-metabolic apho i-glucose engeyiyo ye-hepatic. , imizimba ye-ketone efunyenwe ngamafutha kunye ne-fatty acids yamahhala isetyenziswa njengemithombo yamandla (Amanani 2 kunye ne-3). Ngelixa uninzi lwezicubu zinokusebenzisa i-acids enamafutha kumandla, ngexesha lokuzila ixesha elide, ingqondo ixhomekeke kwimizimba ye-ketone? Imizimba yeKetone iveliswa kwi-hepatocytes evela kwi-acetyl-CoA eyenziwe kwi-? I-oxidation ye-fatty acids ekhutshwe kwigazi nge-adipocytes, kunye nokuguqulwa kwe-ketogenic amino acids. Emva kwe-hepatic glycogen depletion, imizimba ye-ketone, i-glycerol ephuma kumafutha, kunye ne-amino acids i-akhawunti yesizukulwana esixhomekeke kwi-gluconeogenesis malunga ne-80 grams / ngosuku lwe-glucose, esetyenziswa kakhulu yingqondo. Ngokuxhomekeke kubunzima bomzimba kunye nokwakheka, imizimba yeketone, i-acids yasimahla kunye ne-gluconeogenesis ivumela uninzi lwabantu ukuba luphile iintsuku ezingama-30 okanye ngaphezulu ngokungabikho kokutya kunye nokuvumela iintlobo ezithile, ezifana ne-king penguins, ukuba ziphile ngaphezulu kweenyanga ezi-5. ngaphandle kokutya (Eichhorn et al., 2011) (Umfanekiso 3C). Kubantu, ngexesha lokuzila ixesha elide, amanqanaba e-plasma ye-3-?-hydroxybutyrate malunga namaxesha angama-5 e-fatty acids yamahhala kunye ne-acetoacetic acid (Umfanekiso 3A kunye ne-3B). Ingqondo kunye namanye amalungu asebenzisa imizimba ye-ketone kwinkqubo ebizwa ngokuba yi-ketolysis, apho i-acetoacetic acid kunye ne-3-?- i-hydroxybutyrate iguqulwa ibe yi-acetoacetyl-CoA kwaye emva koko i-acetyl-CoA. Olu tshintsho lwemetabolism ekuzileni ukutya kwizilwanyana ezanyisayo zisikhumbuza ezo zichazwe ngaphambili kwi-E. coli kunye nemvubelo, apho i-acetic acid iqokelela ekuphenduleni ukunqongophala kokutya (Gonidakis et al., 2010; Longo et al., 2012). Kwimvubelo, i-glucose, i-acetic acid kunye ne-ethanol, kodwa kungekhona i-glycerol eyenziwa ngexesha lokuzila ukutya ukusuka ekuqhekekeni kwamafutha, ukukhawuleza ukuguga (Fabrizio et al., 2005; Wei et al., 2009). Ngaloo ndlela, i-glycerol isebenza njengomthombo wekhabhoni ongasebenzisi iindlela zokubonisa izondlo ze-pro-aging kodwa zinokuthi zenziwe ngeeseli. Kuya kubaluleka ukuqonda indlela imithombo yekhabhoni eyahlukeneyo eyenziwa ngayo ngexesha lokuzila ukutya ichaphazela ukukhuselwa kwamaselula kunye nokuguga. 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). Kuya kubaluleka kwakhona ukufunda, kwiimodeli ezahlukeneyo zezinto eziphilayo kunye nabantu, ukuba kuphezulu kangakanani ukutya kweentlobo ezithile zamafutha (okuphakathi- vs.

Ukuzila nokuBongo

Kwizilwanyana ezincancisayo, i-CR enzima / ukunqongophala kokutya kubangela ukuhla kwenani lamalungu amaninzi ngaphandle kwengqondo, kunye namasende kwiigundane zamadoda (Weindruch noSohal, 1997). Ukusuka kwimbono yendaleko oku kuthetha ukuba ukugcinwa kwenqanaba eliphezulu lomsebenzi wokuqonda phantsi kweemeko zokunqongophala kokutya kubaluleke kakhulu. Ngokwenene, uphawu lokuziphatha olulondolozwe kakhulu kuzo zonke izilwanyana ezanyisayo kukusebenza xa zilambile kwaye zihleli xa zihluthi. Kwiigundane, ukutshintshwa kweentsuku zokutya okuqhelekileyo kunye nokuzila ukudla (IF) kunokuphucula ukusebenza kwengqondo njengoko kuboniswe ngokuphuculwa kwentsebenzo kwiimvavanyo zokuziphatha ze-sensor kunye nokusebenza kwemoto (Singh et al., 2012) kunye nokufunda kunye nememori (Fontan-Lozano et al. , 2007). Iimpendulo zokuziphatha kwi-IF zihambelana nokunyuka kweplastiki ye-synaptic kunye nokwanda kwemveliso ye-neurons entsha kwiiseli ze-neural stem (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.

Ukuzila, Ukuguga, kunye Nezifo Kwiimodeli Zobunzima

Iinkqubo ezahlukeneyo zokuzila nokuguga

Umahluko omkhulu phakathi kwe-IF kunye ne-PF kwiigundane ubude kunye nokuphindaphinda komjikelezo okhawulezayo. UKUBA imijikelezo ihlala ihlala kwiiyure ze-24 kwaye inye ukuya kwiintsuku ezimbalwa ngaphandle, kanti imijikelezo ye-PF igcina i-2 okanye ngaphezulu kweentsuku kwaye ubuncinane i-1 iveki ngaphandle, okuyimfuneko ukuba iigundane zibuyisele ubunzima bazo obuqhelekileyo. Umehluko omnye kwiinguqu ze-molekyuli ezibangelwa yimithetho eyahlukeneyo yokuzila ukutya yimpembelelo kwizinto ezahlukeneyo zokukhula kunye namanqaku okumakisha, kunye ne-IF ebangela utshintsho oluqhelekileyo kodwa oluncinci kune-PF. Kuya kubaluleka ukumisela ukuba ukuphindaphinda kweenguqu ezithile ezifana nokuthotywa kwe-IGF-1 kunye ne-glucose kuchaphazela njani ukukhuselwa kwamaselula, izifo kunye nokuphila ixesha elide. Indlela ye-IF ephandwe kakhulu kwizifundo zezilwanyana zokuguga iye yaba yinye ukuzila ukutya (ukutya kuhoxiswa kwiiyure ze-24 ngeentsuku ezitshintshileyo, ngamanzi anikezelweyo ad libitum) (Varady noHellerstein, 2007). Ubungakanani beziphumo zolunye usuku lokuzila ukutya kubomi obude kwiimpuku buxhomekeke kuhlobo kunye nobudala ekuqalweni kwerejimeni, kwaye inokusukela kwisiphumo esibi ukuya kuthi ga kwi-80% yokwandiswa kwexesha lokuphila (Arum et al., 2009; Goodrick et al. ., 1990). UKUBA yonke enye imini yandisa ubomi beegundane ngaphezu kokuzila ukutya rhoqo nge-3rd okanye i-4th ngosuku (Carlson noHoelzel, 1946). Ukuzila ukutya kwiiyure ze-24 kabini ngeveki kubo bonke ubomi babantu abadala kubangele ukwanda okuphawulekayo kubomi beegundane ezimnyama (Kendrick, 1973). Kwiigundane, ukudityaniswa kolunye usuku lokuzila ukutya kunye nokuzivocavoca kwe-treadmill kubangele ukugcinwa okukhulu kwe-muscle mass kunokuba IF okanye ukuzivocavoca yedwa (Sakamoto kunye noGrunewald, 1987). Okubangel 'umdla kukuba, xa iigundane zigcinwe kwiiveki ze-10 kwisidlo se-PF apho zazizila khona iintsuku ze-3 ezilandelelanayo ngeveki nganye, zazingaphantsi kwe-hypoglycemia ngexesha leeyure ze-2 zomthambo onzima wokuqubha ngenxa yokuqokelela kweevenkile ezinkulu ze-intramuscular ze-glycogen kunye ne-triglycerides. (Favier noKoubi, 1988). Iimpendulo ezininzi ze-physiological ekuzileni zifana nezo zibangelwa ukuzivocavoca rhoqo kwe-aerobic kuquka ukunyuka kwe-insulin ukuzwela kunye nokunyanzeliswa koxinzelelo lweselula, ukunciphisa uxinzelelo lwegazi kunye nesantya senhliziyo, kunye nokwandiswa kwesantya senhliziyo ngenxa yokwanda kwethoni ye-parasympathetic (Umfanekiso 2) (Anson) et al., 2003; Mager et al., 2006; Wan et al., 2003). Iziphumo ezivelayo zibonisa ukuba umthambo kunye ne-IF ibuyisela ukuguga kunye nezinye izifo ezinxulumene neminyaka ngeendlela ekwabelwana ngazo ezibandakanya ukulungiswa koxinzelelo lweselula (uStranahan noMattson, 2012). Nangona kunjalo, kwimvelaphi emibini eyahlukeneyo yemfuza yemouse, i-IF ayizange yandise ubude bokuphila kunye nokunciphisa ixesha lokuphila xa iqaliswe kwiinyanga ze-10 (Goodrick et al., 1990). Xa iqaliswe kwiinyanga ze-1.5, UKUBA inyuse ixesha elide okanye ayinayo impembelelo (Umfanekiso we-1D) (uGoodrick et al., 1990). Ezi ziphumo kwiimpuku zikhomba kwimiphumo egciniweyo yokuzila ukutya kwixesha lokuphila, kodwa kunye nesidingo sokuqonda ngcono kakhulu uhlobo lokuzila ukutya okunokwandisa imiphumo yayo yokuphila ixesha elide kunye neendlela ezijongene nemiphumo emibi enokuthi iphikisana nokuchasana nokuguga. iziphumo. Umzekelo, enye into enokwenzeka kukuba ukuzila ukutya kunokukhusela rhoqo kwiimpuku zaselabhoratri ezincinci neziphakathi ezifumana okanye zigcina ubunzima bomzimba, kodwa kunokuba yingozi kwizilwanyana ezindala ezithi, ngokufanayo nabantu, ziqale ukunciphisa umzimba ngaphambi kokuba zife. . Ngokucacileyo, ngelixa iibhaktheriya, igwele kunye nabantu banokuphila iiveki ezininzi okanye ngaphezulu ngaphandle kwezondlo, uninzi lweentlobo zeempuku azikwazi ukuphila ngaphezulu kweentsuku ezi-3 ngaphandle kokutya.

Ukuzila ukutya kunye neCarcer

Ukuzila ukutya kunokuba nemiphumo emihle ekuthinteleni umhlaza kunye nonyango. Kwiimpuku, ukuzila ukutya okulolunye usuku kubangele ukuncipha okukhulu kwezehlo ze-lymphomas (i-Descamps et al., 2005) kunye nokuzila ukutya kosuku lwe-1 ngeveki kulibaziseke kwi-tumorigenesis ezenzekelayo kwiimpuku ezisweleyo ze-p53 (Berrigan et al., 2002). Nangona kunjalo, ukuncipha okukhulu kwe-glucose, i-insulin kunye ne-IGF-1 ebangelwa ukuzila ukudla, ehamba kunye nokufa kweeseli kunye / okanye i-atrophy kuluhlu olubanzi lwezicubu kunye nezitho ezibandakanya isibindi kunye nezintso, zilandelwa lixesha leeselula eziphezulu ngokungaqhelekanga. ukwanda kwezi zicubu eziqhutywe ngokuyinxenye ngokuzaliswa kwezinto zokukhula ngexesha lokuncelisa. Xa kudibaniswa ne-carcinogens ngexesha lokutya, lo msebenzi wokwandisa ukunyusa unokunyusa i-carcinogenesis kunye / okanye izilonda zangaphambili zomhlaza kwizicubu ezibandakanya isibindi kunye nekholoni (Tessitore et al., 1996). Nangona ezi zifundo zigxininisa imfuneko yokuqonda nzulu iindlela zayo zokwenza, ukuzila ukutya kulindeleke ukuba kube neziphumo zokuthintela umhlaza njengoko kubonisiwe luphononongo olungasentla kunye neziphumo zokuthi imijikelo emininzi yokuzila ixesha inokusebenza njenge-chemotherapy enetyhefu kwi-chemotherapy. unyango lwezinye iicancer kwiimpuku (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.

Ukuzila ukutya kunye ne-neurodegeneneration

Xa kuthelekiswa nolawulo lwe-libitum-fed, iigundane kunye neempuku ezigcinwe kwindawo yokutya ye-IF zibonisa ukungasebenzi kakuhle kwe-neuronal kunye nokudodobala, kunye neempawu zeklinikhi ezimbalwa kwiimodeli zesifo i-Alzheimer's (AD), isifo sika-Parkinson's (PD) kunye nesifo sikaHuntington (HD). Ezi modeli zibandakanya iimpuku ze-transgenic ezibonisa uguquko lomntu oguqula i-AD (i-amyloid precursor protein kunye ne-presenilin-1) kunye ne-frontotemporal lobe dementia (Tau) (Halagappa et al., 2007), PD (? -Synuclein) (Griffioen et al. , 2012) kunye ne-HD (Huntingtin) (UDuan et al., 2003), kunye neemodeli ezisekwe kwi-neurotoxin ezifanelekileyo kwi-AD, PD kunye ne-HD (UBruce-Keller et al., 1999; UDuan noMattson, 1999). Izilwanyana ezikukutya kwe-IF nazo zihamba ngcono kune-ad libitum-fed controls emva kokonzakala okuqatha kubandakanya ukuxhuzula okukhulu, ukubetha, kunye nengqondo eyenzakalisayo kunye nokwenzakala kwethambo lomqolo (Arumugam et al., 2010; UBruce-Keller et al., 1999; IPlunet et al., 2008).

Iindlela ezininzi ezihambelanayo zeselula zifaka isandla kwimiphumo enenzuzo ye-IF kwinkqubo ye-nervous system kuquka ukunciphisa ukuqokelelwa kweeamolekyu ezonakaliswe nge-oxidative, ukuphuculwa kwe-bioenergetics yeselula, ukubonakalisa i-neurotrophic factor signaling, kunye nokunciphisa ukuvuvukala (Mattson, 2012a). Iindlela zokugqibela ze-neuroprotective zixhaswa zizifundo ezibonisa ukuba ukutya kwe-IF kwandisa amanqanaba okukhusela i-antioxidant, i-neurotrophic factor (BDNF kunye ne-FGF2) kunye ne-protein chaperones (HSP-70 kunye ne-GRP-78), kunye nokunciphisa amanqanaba e-pro- inflammatory cytokines (TNF?, I-IL-1 kunye ne-IL-6) (Umfanekiso 4) (Arumugam et al., 2010). I-IF ingaphinda ikhuthaze ukubuyiselwa kweesekethe zeeseli ze-nerve eyonakalisiweyo ngokuvuselela ukubunjwa kwe-synapse kunye nokuveliswa kwe-neurons entsha kwiiseli ze-neural stem (neurogenesis) (Lee et al., 2002). Okubangela umdla kukuba, ngelixa kuluncedo kwiimodeli zeemeko ezininzi ze-neurodeergenerative, kukho ubungqina bokuba ukuzila ukutya kunokukhawulezisa i-neurodegeneration kwezinye iimodeli ze-amyotrophic lateral sclerosis, mhlawumbi ngenxa yokuba i-motor neurons echaphazelekayo kwezo modeli azikwazi ukuphendula ngokufanelekileyo kuxinzelelo oluphakathi olubekwe ngokuzila ukutya. Mattson et al., 2007; Pedersen and Mattson, 1999).

Ukuzila ukutya kunye ne-Metabolic Syndrome

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).

Utshintsho lweehomoni ezininzi ezifanekisela i-MS ebantwini ukujongwa kwakhona kwiimpuku ezigcinwe kumafutha aphezulu kunye nokutya kweswekile kubandakanya amanqanaba aphezulu e-insulin kunye ne-leptin kunye namanqanaba ancitshisiweyo e-adiponectin kunye ne-ghrelin. Amanqanaba e-leptin aphakanyisiweyo ahlala ebonakalisa imeko yokuvuvukala, ngelixa i-adiponectin kunye ne-ghrelin zinokucinezela ukuvuvukala kunye nokwandisa uvakalelo lwe-insulin (Baatar et al., 2011; Yamauchi et al., 2001). Ukuvuvukala kwendawo kwi-nuclei ye-hypothalamic elawula ukuthathwa kwamandla kunye nenkcitho kunokufaka isandla kwi-balance balance energy kwi-MS (Milanski et al., 2012). Ukuzila ukutya kubangela ukuthotywa kwe-insulin kunye namanqanaba e-leptin kunye nokuphakama kwe-adiponectin kunye namanqanaba e-ghrelin. Ngokunyusa i-insulin kunye novelwano lwe-leptin, ukucinezela ukudumba kunye nokuvuselela i-autophagy, ukuzila ukutya kubuyisela umva zonke izinto ezingaqhelekanga ze-MS kwiimpuku (Singh et al., 2009; Wan et al., 2010). Ekugqibeleni, ukongeza kwiimpembelelo zayo ezininzi kwiiseli kuwo wonke umzimba kunye nengqondo, i-IF inokubangela utshintsho kwi-gut microbiota ekhusela i-MS (i-Tremaroli kunye ne-Backhed, i-2012). Ngokwendalo, umngeni wokusebenzisa ungenelelo olusekwe ekuzileni ukutya ukunyanga i-MS ebantwini ngowona mkhulu, njengoko abanye abantu abatyebe kakhulu banokuba nobunzima ekulandeleni i-IF ixesha elide.

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.

Ukuzila, ukuguga, kunye nezifo kubantu

Ukuzila ukutya kunye neengxaki ezichaphazelekayo ekuguga

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).

Phakathi kweempembelelo ezinkulu zokuzila ukutya okuhambelana nokuguga kunye nezifo zitshintsho kumanqanaba e-IGF-1, IGFBP1, i-glucose, kunye ne-insulin. Ukuzila ukutya kwe-3 okanye ngaphezulu kweentsuku kubangela i-30% okanye ukuncipha okungaphezulu kwi-insulin ejikelezayo kunye ne-glucose, kunye nokuhla ngokukhawuleza kumanqanaba e-insulin-efana nokukhula kwe-1 (IGF-1), eyona nto ibalulekileyo yokukhula kwezilwanyana ezincelisayo, ezithi kunye i-insulin inxulumene nokuguga okukhawulezayo kunye nomhlaza (Fontana et al., 2010). Kubantu, iintsuku ezintlanu zokuzila ukutya kubangela ukwehla kwe-60% kwi-IGF-1 kunye ne-5-fold okanye ukunyuka okuphezulu kwenye yeeprotheyini eziphambili ze-IGF-1-inhibiting: IGFBP1 (Thissen et al., 1994a). Lo mphumo wokuzila ukutya kwi-IGF-1 ubukhulu becala ubangelwa kukuthintelwa kweeprotheyini, kwaye ngakumbi kuthintelo lwee-amino acids ezibalulekileyo, kodwa ikwaxhaswa sisithintelo sekhalori kuba ukuhla kwamanqanaba e-insulin ngexesha lokuzila ukutya kukhuthaza ukunciphisa i-IGF-1 (Thissen et al. , 1994a). Ngokucacileyo, kubantu, ukukhawulwa kwekhalori engapheliyo akukhokelela ekunciphiseni kwe-IGF-1 ngaphandle kokuba kudityaniswe nokuthintelwa kweprotheyini (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).

Ukuzila ukutya kunye neCarcer

Ukuzila ukutya kunakho ukufaka izicelo ekukhuselweni komhlaza kunye nonyango. Nangona akukho datha yoluntu ekhoyo kwi-IF okanye iPP ekukhuselweni komhlaza, isiphumo sayo ekunciphiseni i-IGF-1, i-insulin kunye ne-glucose, kunye nokwanda kwamazinga omzimba we-IGFBP1 kunye ne-ketone kungavelisa indawo yokukhusela eyenza umonakalo we-DNA kunye ne-carcinogenesis, ngexesha elifanayo ukudala iimeko ezichasayo zesifo kunye neeseli zangaphambi komhlaza (Umfanekiso 5). Enyanisweni, ukuphakanyiswa kwe-IGF-1 ephakamileyo kuhambelana nomngcipheko okhulayo wokuphuhlisa umdlavuza othile (Chan et al., 2000; Giovannucci et al., 2000) kunye nabantu abane-IGF-1 ekwenzeni ubuchule obukhulu obubangelwa ukulahleka kwe-hormone ye-receptor, Guevara-Aguirre et al., 2011; uShava noLaron, 2007; Steuerman et al., 2011). Ukongezelela, i-serum evela kulezi zihloko ze-IGF-1de ezizikhuselekileyo ezikhuselekileyo ziseli ze-epithelial ezivela kumonakalo we-DNA obangela uxinzelelo. Ukongezelela, xa iDNA yabo yonakaliswe, iiseli zazingenakwenzeka ukuba zifakwe kwiiselfini zokufa (uGuevara-Aguirre et al., 2011). Ngako oko, ukuzila ukutya kunokukhusela kumhlaza ngokunciphisa umonakalo we-cellular kunye ne-DNA kodwa kwakhona ngokuphucula ukufa kweeseli zangaphambi komhlaza.

Kwisifundo sokuqala kwezifundo ze-10 ezineentlobo ezininzi zeentlondi, ukuhlanganiswa kwe-chemotherapy nokuzila ukutya kwaphumela ekunciphiseni kwimiba echaphazelekayo echaphazelekayo ebangelwa yi-chemotherapy xa kuthelekiswa nezifundo ezifanayo zifumana i-chemotherapy ngexesha lokutya okuqhelekileyo (Safdie kunye al., 2009). Impembelelo yokuzila ukutya kwe-chemotherapy kunye nokunyuswa komhlaza ngoku ivavanywa kwizilingo ze-klinikhi kwi-Yurophu nase-US (0S-08-9, 0S-10-3).

Ukuzila ukutya kunye ne-neurodegeneneration

Ukuqonda kwethu kwangoku kwimpembelelo ye-IF kwiinkqubo zeentlanzi kunye nemisebenzi yengqiqo ixhomekeke kakhulu kwizifundo zezilwanyana (jonga ngasentla). Uphando lweeNkcazo ukufumana ingqwalasela yokuzila kwi-brain function kunye neenkqubo ze-neurodegeneneral disease.

Emva kwenyanga yesi-3 4, i-CR iphucule ukusebenza kwengqondo (inkumbulo yomlomo) kubafazi abagqithisileyo (UKretsch et al., 1997) nakwizifundo zabantu abadala (Witte et al., 2009). Kwangokunjalo, xa izifundo ezinokuphazamiseka kwengqondo okucothayo zigcinwa kwinyanga e-1 kwisidlo esisezantsi se-glycemic, zibonise imemori ebonakalayo yokulibaziseka, i-cerebrospinal fluid biomarkers ye-A? imetabolism kunye nengqondo ye-bioenergetics (Bayer-Carter et al., 2011). Izifundo apho umsebenzi wokuqonda, ubungakanani bengqondo yengingqi, imisebenzi yenethiwekhi ye-neural, kunye nohlalutyo lwe-biochemical ye-cerebrospinal fluid ilinganiswa kwizifundo zabantu ngaphambi nangexesha elandisiweyo le-IF kufuneka icacise ifuthe le-IF kulwakhiwo lobuchopho bomntu kunye nokusebenza.

Ukuzila ukutya, ukuvutha nokunyuka kwengqondo

Emntwini, omnye weyona miboniso mihle yeziphumo zokuzila ukutya ixesha elide ukuya kwiiveki ezi-3 kunyango lwe-rheumatoid arthritis (RA). Ngokuvumelana neziphumo kwiirandi, akukho mathandabuzo okuba ngexesha lokuzila zombini ukudumba kunye nentlungu ziyancitshiswa kwizigulana zeRA (Muller et al., 2001). Nangona kunjalo, emva kokuba ukutya kwesiqhelo kuqale kwakhona, ukudumba kuyabuya ngaphandle kokuba ixesha lokuzila lilandelwa kukutya kwemifuno (Kjeldsen-Kragh et al., 1991), unyango oludibeneyo oluneziphumo eziluncedo ezihlala iminyaka emibini okanye nangaphezulu (Kjeldsen-Kragh et al., 1994). Ukunyaniseka kwale ndlela kuxhaswa zizifundo ezine ezilawulwa ngokwahlukeneyo, kubandakanya izilingo ezimbini ezingahleliwe (UMuller et al., 2001). Ke ngoko, ukuzila ukutya kudityaniswe nokutya kwemifuno kwaye kunokwenzeka kunye nezinye izidlo eziguqulweyo kunika iziphumo eziluncedo kunyango lwe-RA. Olunye usuku IF ukuba lukhokelele ekunciphiseni okubonakalayo kwi-serum TNF? kunye neekeramide kwizigulana zesifuba ngexesha leenyanga ezi-2 (Johnson et al., 2007). Olu phononongo lwamva luqhubeke lubonakalise ukuba amanqaku oxinzelelo lwe-oxidative ahlala enxulunyaniswa nokudumba (iprotein kunye neepid oxidation) zincitshiswe kakhulu ekuphenduleni i-IF. Ke ngoko, kwizigulana ezininzi ezinakho kwaye zikulungele ukunyamezela ukuzila ukutya ixesha elide kunye nokutshintsha ngokusisigxina ukutya kwabo, imijikelezo yokuzila ukutya ayinakuba nakho ukonyusa kuphela kodwa iphinde ithathe indawo yonyango esele lukhona.

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.

Kuzo zombini i-hypertension kunye ne-RA kuya kubaluleka ukuphuhlisa i-PF yokulinganisa ukutya okusebenzayo njengerejimeni yokuzila ukutya echazwe ngasentla kodwa ekwazi ukunyamezela uninzi lwezigulane.

Ukuzila ukutya kunye ne-Metabolic Syndrome

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.

Izigqibo kunye neNcomelo

Ngokusekelwe kubungqina obukhoyo bezilwanyana kunye nezifundo zabantu ezichazwe, siphetha ukuba kukho amathuba amakhulu okuphila okubandakanya ukuzila ngokukhawuleza ngexesha lokuphila komntu omdala ukukhuthaza impilo efanelekileyo kunye nokunciphisa umngcipheko wezifo ezingapheliyo, ngokukodwa kulabo abanomzimba ogqithiseleyo kunye nabahlali. Izifundo zezilwanyana ziye zabonisa iziphumo ezinamandla neziguqukayo zokuzila ukutya kwiinkalo zezempilo kuquka ukukhathazeka okukhulu kwe-insulin, kunye nokunciphisa amanqanaba egazi, i-fat fat, i-IGF-I, i-insulin, i-glucose, i-lipids ye-atherogenic kunye nokuvuvukala. Ukuzila ukutya kuya kuphucula iinkqubo zezifo kwaye kuphuculwe umphumo wokusebenza kwimimiselo yezilwanyana eziphazamisayo ezibandakanya i-myocardial infarction, isifo sikashukela, i-stroke, i-AD kunye ne-PD. Enye indlela esetyenziswayo yokuzila ukutya kukuba kubangela izimpendulo zokuxinwa kwamaseli eziguquguqukayo, okubangela ukuba kube namandla okunyamezela uxinzelelo olunzulu kunye neenkqubo zokulwa nezifo. Ukongezelela, ngokukhusela iiseli ezivela kumonakalo we-DNA, ukunqanda ukukhula kweseli kunye nokuphucula i-apoptosis yeeseli ezilimele, ukuzila ukutya kunokukhawuleza kunye / okanye ukukhusela ukubunjwa nokukhula kweekomhlaza.

Nangona kunjalo, uphononongo lweerejimeni zokuzila azange lwenziwe ebantwaneni, abantu abadala kakhulu nabangaphantsi kobunzima, kwaye kunokwenzeka ukuba i-IF kunye ne-PF zinokuba yingozi kwaba bantu. Ixesha lokuzila ukutya elihlala ixesha elide kuneeyure ezingama-24 kwaye ngakumbi ezo zihlala iintsuku ezi-3 okanye nangaphezulu kufuneka zenziwe phantsi kweliso likagqirha kwaye ngokukhethekileyo kwiklinikhi. Iindlela ze-IF- kunye ne-PF esekwe ekulweni nezifo zangoku zokutyeba kakhulu, isifo seswekile kunye nezifo ezinxulumene noko kufuneka zilandelwe kwizifundo zophando lomntu kunye nezicwangciso zonyango. Umahluko okhoyo kwimigqaliselo yokuzila ukutya eyamkelweyo kwizifundo ezityebe kakhulu ijikeleza kumxholo oqhelekileyo wokungatyi ukutya kunye neziselo ezinekhalori ubuncinci iiyure eziyi-12 - 24 ngosuku olunye okanye nangaphezulu evekini okanye ngenyanga, kuxhomekeke kubude, kudityanisiwe ngokwenza umthambo rhoqo. Kulabo batyebileyo, oogqirha banokucela abaguli babo ukuba bakhethe ungenelelo olusekwe ekukhuleni abakholelwa ukuba banokuthobela ngokusekwe kwiishedyuli zabo zemihla ngemihla nezeveki. Imizekelo ibandakanya i- 5: 2 IF ukutya (uHarvie et al., 2011), olunye usuku olulungisiweyo lokutya ukutya (Johnson et al., 2007; Varady et al., 2009), usuku lwe-4 5 ngokukhawuleza okanye ikhalori ephantsi kodwa ukutya okuphezulu ukuzila ukutya okulinganisa ukutya kanye kwiinyanga ezi-1 3 kulandelwa kukutsiba kwesona sidlo sikhulu mihla le xa kufuneka (V. Longo, uvavanyo lwezonyango luyaqhubeka). Enye yezinto ezixhalabisayo ngokutya okungalinganiyo okunje ngezi apho ukutya kweekhalori ezisezantsi kujongwa kuphela iintsuku ezi-2 ngeveki ziziphumo ezinokubakho kwisingqisho se-circadian kunye ne-endocrine kunye neenkqubo zesisu, ezaziwayo ukuba ziphenjelelwa yimikhwa yokutya. Ngexesha lokuqala le-4 ukuya kwi-6 iiveki zokuphunyezwa kwerejimeni yokuzila, ugqirha okanye umtyi obhalisiweyo kufuneka abe nonxibelelwano rhoqo nesigulana ukujonga inkqubela phambili kunye nokubonelela ngengcebiso kunye nokujonga.

Iirejimeni zokuzila nazo zinokulungelelaniswa nezifo ezithile njengokuma wedwa okanye unyango olwenziweyo. Iziphumo zovavanyo lokuqala lwe-IF (ukuzila ukutya iintsuku ezi-2 ngeveki okanye ngalo lonke usuku) kwizifundo zabantu zibonisa ukuba kukho ixesha elibalulekileyo lenguqu kwiiveki ezi-3 ukuya kwezi-6 ngelo xesha ingqondo nomzimba ziqhelana nendlela entsha yokutya kunye nomoya ophuculweyo. (UHarvie et al., 2011; uJohnson et al., 2007). Nangona uqikelelo, kusenokwenzeka ukuba ngeli xesha lokugqibela lokutshintsha kwengqondo kwi-neurochemistry ukuze i-'addiction 'yokutya rhoqo ukutya kuyo yonke imini yoyiswe. Ngokukodwa, iindlela ezahlukeneyo zokuzila ukutya zinokubanomda wokusebenza ngakumbi ekugugeni nakwimeko ngaphandle kokutyeba ngaphandle kokuba kudityaniswe nokutya okunje ngokutya okuphakathi kwekhalori kunye nokutya okusekwe kwizityalo eziseMeditera okanye zaseOkinawa ukutya okuneprotein ephantsi (0.8 g protein / Kg yomzimba ubunzima ), ihlala inxulunyaniswa nempilo kunye nokuphila ixesha elide.

Kwixesha elizayo, kuya kuba kubalulekile ukudibanisa idatha ye-epidemiological, iziphumo zabantu abahlala ixesha elide kunye nezidlo zabo, iziphumo ezivela kwiimpawu zendalo ezidibanisa izixhobo ezithile zokutya kunye nezinto ezinokuguga, kunye nedatha kwizifundo zokuzila ukutya kwabantu , ukuyila iinjongo ezinkulu zekliniki ezidibanisa ukutya ngokutya okunokuthi zikhusele kwaye zizonandipha. Ukuqonda okungcono kweendlela ze-molecular ngokuzila ukutya kuthintela iintlobo ezahlukeneyo zeeseli kunye neenkqubo zesebe kufuneka zikhokele ekuphuhlisweni kwenkqubo yokuvelisa i-prophylactic kunye neendlela zokwelapha ezahlukeneyo.

Thatha Umyalezo Wasekhaya

Ukutya okuxelisa ukutya kukunikezela okufanayo kokutya ngokuqhelekileyo ngokunciphisa ikhalori yakho iintsuku ezintlanu ngaphandle kwenyanga kunokuphelisa ngokupheleleyo ukutya konke iintsuku okanye iiveki. I ProLon Ukuzila ukutya ukuxelisa ukutya kunika inkqubo ye-5 yosuku lokutya oluye lwaphawulwa ngabanye kwaye lubhalwe ngobungakanani obuchanekileyo kunye nokudibanisa kwimihla ngemihla. Nangona uphando olusentla luye lwabonisa izibonelelo zezempilo zokuzila ukudla, nceda qiniseka ukuthetha nochwepheshe bezempilo ngaphambi kokuba uqale Ukuzila ukutya kweProLon yokulinganisa ukutya, inkqubo yeentsuku ezi-5 zokutya ukufumanisa ukuba i-FMD, okanye nayiphi na enye yokutya, ilungile.

Ifomu elipapashwe, lokugqibela lokufunda uphando olukhankanywe ngasentla lenziwe kufumaneka kulo I-NIH yoLuntu yokuFinyelela uMbhalo wesandla kwi-PMC ngoFebhuwari 4, 2015. Ubungakanani beenkcukacha zethu zikhawulelwe kwi-chiropractic, imiba yempilo yomgudu, kunye nezihloko zonyango ezisebenzayo. Ukuqhubela phambili ukuxoxa ngale ndaba, nceda ukhululeke ukubuza uDkt Alex Jimenez okanye uqhagamshelane nathi 915-850-0900 .

Ikhutshwe nguDkt. Alex Jimenez

U khankanywe kwi: Nih.gov

Ingxoxo eyongezelelweyo yesihloko: Ubuhlungu obuBuya buhlungu

Umqolo obuhlungu enye yezona zizathu ezibangeleko zokukhubazeka kunye neentsuku eziphosakeleyo emsebenzini jikelele. Iintlungu ezibuhlungu emva kwesizathu sesibini esivakalayo sokutyelela iofisi yee-dokotela, zibalwa kuphela ngezifo eziphezulu zokuphefumula. Phantse i-80 ipesenti yoluntu iya kubakho ubuhlungu ubuncinane kanye kanye ebomini babo. Umgudu wakho uyisakhiwo esiyinkimbinkimbi esakhiwa ngamathambo, amajoyina, iigaments, kunye nezihlunu, phakathi kwezinye iifomthi ezithambileyo. Ukulimala kunye / okanye imeko ekhutshweyo, njengaye disni, ekugqibeleni unokukhokelela kwiimpawu zentlungu. Ukulimala kwezemidlalo okanye ukulimala kwengozi yeemoto ngokuqhelekileyo kubangelwa yintlungu yokubuhlungu, kodwa ngamanye amaxesha ukuhamba kwezinto ezilula kunokuba neziphumo ezibuhlungu. Ngethamsanqa, ezinye iindlela zokhathalela unyango, ezifana nokunyamekelwa kwe-chiropractic, kunokunceda ukubuyisela intlungu emva kokusetyenziswa kwemilenze kunye nokunyanzeliswa kwemigaqo, ekugqibeleni ukuphucula intlungu.

XYMOGEN's Iifomula zeeNgqungquthela zodwa zifumaneka ngokukhetha abaqeqeshi bezempilo abanemvume. Intengiso ye-intanethi kunye nokuhlaziywa kwamafomula e-XYMOGEN ayinqatshelwe.

Iqhayiya, UDkt. Alexander Jimenez yenza i-XYMOGEN ifomula ifumaneka kuphela kwizigulane ezingaphantsi kwethu.

Nceda ufonele iofisi yethu ukuze sikwazi ukudlulisela udokotela ngokubonisana nokufikelela ngokukhawuleza.

Ukuba uyigulane Iiklinikhi zoNyango kunye neKliniki yeChiropractic, unokubuza malunga ne-XYMOGEN ngokubiza 915-850-0900.

Ukuze ube lula kwaye uhlaziywe XYMOGEN mveliso nceda uhlolisise le nxu lumene. *I-XYMOGEN-Inkcazo-umxokozelo

* Zonke iipolisi ze-XYMOGEN ezingentla zihlala zisebenza ngokuthe ngqo.

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