O le faʻataʻitaʻiina o taumafa faʻamatalaga

by Dr Alex Jimenez | Paʻu, Anapogi, Faafomai e faaaogaina i, Soifua Maloloina, Faafomai Holistic, Soifua Maloloina Faʻatinoina, Faafomai Integrative, Soifua Maloloina, taumafa, ProLon, faaopoopo, Lelei

Understanding the ProLon� Fasting Mimicking Diet

O le anapogi e fesootaʻi ma le tele o aogā tau soifua maloloina; mai le mamafa o le gau i le umi. E tele ituaiga eseese o metotia anapogi, e pei o le anapogi faʻafefe. O le anapogi e faʻatatau ai mea taumafa e mafai ai e oe ona e maua le aoga o le masani masani e aunoa ma le faʻaaogaina o lau tino. O le eseesega autu o le FMD o le nai lo le faʻaaogaina atoatoa o mea taumafa mo le tele o aso poʻo ni vaiaso foʻi, e na o le faʻagataina o lau kalori mo le lima aso mai le masina. O le FMD e mafai ona faʻataʻitaʻi tasi i le masina e faʻaleleia le soifua manuia.

E ui e mafai e se tasi ona mulimuli i le FMD ia latou lava, le ProLon O le anapogi anapogi o meaʻai e ofoina atu ai le polokalama o le taumafataga o le 5-aso ua uma ona siakiina ma faailogaina mo aso taitasi ma e teu meaʻai e te manaʻomia mo le FMD i fuainumera maʻoti ma faʻapotopotoga. O le taumafataga o le taumafataga o le saunia lea e faʻatau ma faigofie-i-sauniuni, meaʻai faʻatoʻaga, e aofia ai faʻamau, sou, snack, supplements, mea inu inu, ma teas. O oloa o loʻo faʻatulagaina faasaienisi ma le tofo tele. A o lei amataina le ProLon` anapogi mimicking meaai, 5-aso taumafataga polokalama, faamolemole ia mautinoa e te talanoa i se fomai tausi soifua maloloina e saili ai pe saʻo le FMD mo oe. O le faʻamoemoega o le suʻesuʻega suʻesuʻeina i lalo o le faʻaalia lea o mea faʻavae mole mole ma faʻamatalaga o le anapogi i le FMD.

Anapogi: Faʻamatalaga Faʻamataʻu ma Talosaga Fomaʻi

O le anapogi ua faia mo le tele o tausaga, ae na o le leʻi leva o suʻesuʻega ua faʻamalamalamaina ai lana matafaioi i tali fetaui lelei o le telefoni e faʻaitiitia ai le faʻamaʻiina o le oxidative ma le mumū, faʻamalosia ai le malosi o le gaosiga ma le faʻamalosia le puipuia o le cellular. I lalo o le eukaryotes, o le anapogi masani e faʻateleina le ola umi i se vaega e ala i le faʻasologaina o auala faʻafesoʻotaʻi ma faʻafitauli faʻafefe. I totonu togitogi Ole taimi ole taimi ole anapogi e puipuia ai mai le maʻisuka, maʻi, fatu fatu ma le neurodegeneration, aʻo iai i tagata e fesoasoani e faʻaitiitia le meaʻai, toto maualuga, foma ma fomaʻi faʻamaʻi. O le mea lea, o le anapogi e mafai ona faʻatuai le matua ma fesoasoani e puipuia ma togafitiga faʻamaʻi ao faʻaitiitia le aʻafiaga o aʻafiaga e mafua mai i taimi masani o taumafa.

faʻatomuaga

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 suʻesuʻega, faailoa mai o ituaiga eseese o le anapogi e mafai ona maua ai ni auala lelei e faʻaitiitia ai le mamafa, faʻatuai le matua, ma sili atu le soifua maloloina. O iinei tatou te iloiloina ai le matagofie ma le malosi o aʻafiaga eseese o le anapogi e aofia ai le anapogi faʻatasi (IF, e aofia ai le aso anapogi anapogi, poʻo le faalua vaiaso anapogi, mo se faataitaiga) ma le anapogi faʻavaitaimi (PF) tumau mo ni nai aso pe sili atu i 2 uma pe sili atu vaiaso. Matou te taulai atu i le anapogi ma faaitiitia le talanoaga a le CR, o se autu ua toe faamanatu i isi mea (Fontana et al., 2010; Masoro, 2005).

Lesona mai le Faigofie Ofaiga

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 meaʻai suamalie 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).

I le fefete S. cerevisiae, o le fesuiaiga o siama mai le tuputupu aʻe o le tuputupu ae i le vai e mafua ai foi le faʻaauau pea o le 2 ma le maualuga tele o le tetee atu i le tele o faʻafitauli (Ata 1B) (Longo et al., 1997; Longo et al., 2012). O le faʻaaogaina o mea taumafa-faʻalagolago i le faʻaleleia o meaʻai e aofia ai le faʻavaeina o le amino acid feedback Tor-S6K (Sch9) faʻapea foi ma le glucose tali Alafua-adenylate cyclase-PKA e mafua ai le faʻafouina o le serine / threonine kinase Rim15, o se enzyme autu e faʻapipiʻi ai tali puipui (Fontana et al., 2010). O le le faʻamalosia o le Tor-S6K, Ras-AC-PKA ma le faʻafouina o le Rim15 ua mafua ai le faateleina o le transcription o genes e aofia ai le superoxide dismutases ma le vevela proteins e pulea e popolega tali Faʻaliliuga o Faʻamatalaga Msn2, Msn4 ma Gis1, e manaʻomia mo le tele o aʻafiaga e mafua mai i meaʻai (Wei et al., 2008). E le gata i lea, pe a suia i tulaga o meaʻai, e mafai e le siama ma le fefete ona ulufale atu i se tulaga o le hypometabolic e mafai ai ona faʻaitiitia le faʻaaogaina o punaoa o loʻo maua ai le gaʻo ma e mafai foi ona faʻaopoopo maualuga maualuga o le ketone body-like acetic acid, e tutusa lelei ma mamame.

O le isi tino tele o le meaola lea o le anapogi e faʻalautele ai le ola o le nematode C. elegans. O meaʻai e le maua i le fafagaina o anufe itiiti pe leai foi siama, e taʻitaʻia ai le maualuga o le vavalalata (Ata 1C) (Kaeberlein et al., 2006; Lee et al., 2006), lea e manaʻomia ai le AMPK ma le numera o le transcription DAF-16, e tutusa lelei ma le taua o le tusiga o le Msn2 / 4 ma le Gis1 i le fefete ma FOXO i lago ma mammals (Greer et al., 2007). O le faʻalauteleina o mea taumafa faʻaleagaina e faʻalauteleina ai le ola i C. elegans e ala i se masini e aofia ai le small GTPase RHEB-1 (Honjoh et al., 2009).

I lago, o le tele o suʻesuʻega o loʻo faailoa mai ai o le faʻatafunaina o mea taumafa e le afaina ai le ola vavalalata (Grandison et al., 2009). Ae peitaʻi, o le faʻaitiitia o taumafa poʻo le taumafa o taumafa na faʻaalia i taimi uma e faʻalautele le umi o le Drosophila (Piper ma Partridge, 2007) e fai mai o lago e mafai ona manuia mai le faʻasaina o mea taumafa ae atonu e nofouta i vaitau pupuu.

Faʻatasi ai, o nei faʻamatalaga e iloa ai o le fafagaina o taumafa e mafai ona oʻo i aafiaga o le ola umi i le tele o ituaiga meaola, ae ia faʻamaonia foi o mea eseese faʻalapotopotoga e eseese tali i anapogi.

Tali Tali i le Anapogi i Mammals

I le tele o mammals, o le ate o loʻo avea ma vaituloto autu o le kulukose, lea e teuina i foliga o glycogen. I totonu o tagata, e fuafua i luga o le maualuga o le tino, o 12 i 24 itula o le anapogi e masani lava ona maua i le 20% poʻo le faʻaitiitia o le kulūkose ma le faʻaitiitia o le glycogen hepatic, faʻatasi ai ma se ki i se metabolic faiga lea e le o le kosiki, kulukose, tino gaʻo gaʻo ma O fua gaʻo gaʻo e faʻaaogaina ole malosiaga (Faʻatusa 2 ma le 3). Ae o le tele o aano o le tino e mafai ona faʻaaogaina gaʻo gaʻo mo le malosi, i taimi uumi o le anapogi, e faʻamoemoe le faiʻai i tino o le ketone? -Hydroxybutyrate ma le acetoacetate e faʻaopoopo i le suka mo le faʻaaogaina o le malosi (Ata 3B). O tino o le ketone e gaosia i hepatocytes mai le acetyl-CoA na fausia mai? oxidation o gaʻo gaʻoa faʻasaʻolotoina i totonu o le toto ala adipocytes, faʻapea foi ma le liua o ketogenic amino acids. I le maeʻa ai o le hepatic glycogen depletion, ketone tino, gaʻo gaosia glycerol, ma amino acids faʻamatalaga mo le gluconeogenesis-faʻalagolago tupulaga o tusa ma le 80 kalama / aso o kulukose, lea e tele lava faʻaaoga e le faiʻai. Faʻalagolago i le mamafa o le tino ma le tuʻufaʻatasia, o le ketone tino, maua fua gaʻo ma gluconeogenesis faʻatagaina le tele o tagata soifua ola 30 pe sili atu aso i le leai o ni meaai ma faʻatagaina nisi ituaiga, pei o king penguins, e ola mo le sili atu 5 masina aunoa ma meaai (Eichhorn et al., 2011) (Ata 3C). I tagata, i le taimi o le anapogi umi, o le maualuga o le plasma o le 3 -? - hydroxybutyrate e tusa ma le 5 taimi i latou o saoloto gaʻo gaʻo ma acetoacetic acid (Ata 3A ma le 3B). O le faiʻai ma isi totoga faʻaaogaina tino ketone i se gaioiga faʻaigoaina ketolysis, o fea acetoacetic acid ma 3 -? - Hydroxybutyrate ua liua i acetoacetyl-CoA ma acetyl-CoA. O nei metabolic adaptations i le anapogi i mammals o loʻo manatuaina ai na faʻamatalaina muamua mo E. coli ma le fefete, lea e faʻaputuputu ai le acetic acid i le tali atu i le le lava o meaʻai (Gonidakis et al., 2010; Longo et al., 2012). I le fefete, glucose, acetic acid ma 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. long- chain fatty acids, etc.) in substitution of carbohydrates and proteins influences gluconeogenesis and glucose levels as well as aging and diseases.

Anapogi ma le Brain

I pepe, o le CR / food deficit ogaoga e mafua ai ona paʻu i le tele o le tele o okeni sei vagana ai le faiʻai, ma suʻesuʻega i tamaʻi tama (Weindruch and Sohal, 1997). Mai i se evolusione vaaiga o lona uiga o le tausiga o se maualuga maualuga o faapitoa o le mafaufau galuega i lalo o tulaga o taumafa o le utiuti o le taugata e sili ona taua. O le mea moni, o se amioga e matua faʻasaoina lelei o mamame uma o le a gaioiga pe a fiaʻai ma nofo mamao pe a faʻamafanafana. O meaʻai o loʻo masani ai le fafaga ma le anapogi (IF) e mafai ona faʻaleleia ai le galue o le faiʻai e pei ona faʻaalia i le faʻaleleia atili o le faatinoga o suʻesuʻega o amioga ma mea faigaluega (Singh et al., 2012) ma le aʻoaʻoina ma manatua (Fontan-Lozano et al. , 2007). O tali amio ile IF e fesoʻotaʻi ma le faʻateleina o mea faʻatekonolosi faʻapitoa ma faʻalauteleina le gaosiga o ni neu fou mai i vavalaʻau vavaoʻai (Lee et al., 2002).

Ae maise lava le fiafia e tusa ai ma tali talafeagai a le faiʻai e faatapulaa ai le maua o meaʻai i le taimi o le tupuga o tagata faiʻai-maua mai Neurotrophic factor (BDNF). O genes o loʻo faʻapipiʻi ai le BDNF ma lona faʻamaumauga TrkB na faʻaalia i genomes lata mai talu ai nei o loʻo i ai i vertebrates, ae o loʻo i ai i anufe, lago ma mea lalo ifo (Chao, 2000). O matafaioi iloga a le BDNF i le faatonutonuina o le malosi o taumafa ma tupe alu i mamame 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).

O le fiaʻai o se tali faʻafefe i le faʻaaogaina o meaai lea e aofia ai suiga faʻapitoa, mafaufau ma le neuroendocrine lea e faaosofia ai ma mafai ai ona sailia le sailia o amioga. Na folasia atu o fesoʻotaʻiga o le neuronal e aʻafia ai le fiaai, neuropeptides ma 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.

Anapogi, Tuai, ma le Maʻi i le Rodent Mala

Eseese auala o anapogi ma le matua

O le eseesega tele i le va o le IF ma le PF i mumua o le umi ma le taimi o le faasologa vave. AFAI E masani lava ona tutupu le taamilosaga i 24 itula ma e tasi i ni nai aso, ae o le PF e mulimuli i le 2 mulimuli po o le sili atu foi o aso ma e le itiiti ifo i le 1 vaiaso le vavaeeseina, lea e tatau mo le maunu ona toe maua lo latou mamafa masani. E tasi le eseesega i suiga mole mole e mafua mai i le eseese o pulega o anapogi o le aafiaga lea i luga o mea eseese o le tuputupu ae ma faailoga o le gataifale, faatasi ai ma IF e mafua ai suiga e masani ona le masani ai ae le sili atu nai lo le PF. O le a taua tele le fuafuaina pe faʻafefea ona faʻafefe taimi ole suiga faʻapitoa e pei o le faʻaitiitia o le IGF-1 ma le kulukose e aʻafia ai le puipuia o cellular, faʻamaʻi ma umi le ola. O le metotia aupito sili ona suʻesuʻeina IF i le suʻesuʻeina o meaola i le soifuaga o le matua, o se aso e tasi (anapogi faʻasolosolo mo 24 itula i isi aso, faatasi ai ma le vai e maua ai ad libitum) (Varady ma Hellerstein, 2007). O le tele o aʻafiaga o le aso e tasi e anapogi ai i le umi o le ola i meaola e faalagolago ile ituaiga ma le matutua i le faigamalo amataga, ma e mafai ona aʻafia mai se aafiaga le lelei e pei o le 80% faʻaopoopoga faʻaopoopoga (Arum et al., 2009; Goodrick et al., 1990). AFAI o isi aso uma e faʻalautele le pusa o kiota nai lo le anapogi i aso 3rd poʻo 4th (Carlson ma Hoelzel, 1946). O le anapogi mo 24 itula e faalua vaiaso i le taimi atoa o le olaga matua na mafua ai ona maualuga le faateleina o le vaeluaina o kuli paʻu (Kendrick, 1973). I kulumu, o le tuufaatasiga o le isi aso o anapogi ma le gaioiga faamalosi na iu ai ina sili atu le tausiga o le musika nai lo le IF pe na o le faamalositino na o ia (Sakamoto ma Grunewald, 1987). O le mea e mataʻina ai, pe a fai e tausia le rato mo le 10 vaiaso i se taumafataga PF lea na latou anapopogi ai 3 i aso taʻitasi i vaiaso taitasi, latou te le maualalo i le hypoglycemia i itula 2 o le malosi o le aau e mafua mai i lo latou faaputuputuina o fale tele o glycogen ma triglycerides (Favier ma Koubi, 1988). O nisi o tali taua i le anapogi e talitutusa ma mea e mafua mai i faamalositino masani e aofia ai le faateleina o le lagona o le inisalini ma le malosi o le cellular stress, faaitiitia le toto toto ma le fatu, ma faateleina le fesuisuiaʻi o le fatu e mafua mai i le faateleina o le mafaufau (Figure 2) (Anson et al., 2003; Mager et al., 2006; Wan et al., 2003). O faʻamatalaga faʻaalia e fautuaina ai le faʻamalositino ma le IF ua leva ona matua ma nisi o faʻamaʻi e mafua i le matutua e ala i fefaʻasoaʻiga e aofia ai le faʻaleleia atili o le suiga o le telefoni (Stranahan ma Mattson, 2012). Ae ui i lea, i ni eseesega eseese o le kosi, IF e leʻi faʻalauteleina le ola ma e oʻo lava i le faʻaitiitia o le ola pe a amata i 10 masina (Goodrick et al., 1990). Aʻo amataina i 1.5 masina, AF pe faʻalautele le umi pe leai foi (Ata 1D) (Goodrick et al., 1990). O nei mea e mafua ai ona maua e togavao ia aafiaga o le anapogi i taimi uma, ae faʻapea foʻi le manaʻoga mo se malamalama sili atu i le ituaiga o anapogi lea e mafai ona faʻateleina ai ona faʻamaunuʻuga o le uumi ma auala e aʻafia ai aʻafiaga e ono aʻafia ai lona tauleʻaleʻa aafiaga. Mo se faʻataʻitaʻiga, se tasi o mea e ono mafai ona puipuia i taimi uma i talavou ma matua lapisi o fale suesue e maua pe tausia se tino o le tino, ae atonu e ono afaina i manu matutua, pei o tagata, amata ona leiloa le mamafa ao lei maliu. E le gata i lea, ae o siama, o le fefete ma tagata e mafai ona ola mo le tele o vaiaso pe sili atu foi e aunoa ma ni meaʻai, o le tele o aʻa o naifo e le mafai ona ola nai lo le 3 aso e aunoa ma se meaai. O le pa'ū o le mamafa o le tausaga e mafai ona faʻaalia ai lenei lagona i taimi uumi o le anapogi e sili atu le leaga.

Anapogi ma le Cfaʻatau

O le anapogi e mafai ona i ai ni aafiaga lelei in kanesa ma togafitiga. I pepe, o isi aso na anapogi na mafua ai le faʻaitiitia o le faʻaititia o le lymphomas (Descamps et al., 2005) ma le anapogi mo le 1 aso i le vaiaso na faʻatuai ai le tumoigenesis tuusaʻo i mice p53-deficient (Berrigan et al., 2002). Ae peitai, o le paʻu tele o le kulukose, insulin ma le IGF-1 e mafua mai i le anapogi, lea eo mai faatasi ma le oti ma le / or atrophy i le tele o meaola ma okeni e aofia ai le ate ma fatuga, ona mulimulitaʻia lea o se vaitau masani faʻalauteleina i totonu o nei masini e faʻamalosi i se vaega e ala i le toe faʻaleleia o tulaga tuputupu aʻe ao faagasolo le toe totoina. Pe a tuʻufaʻatasia ma meaʻai i le taimi o le toe totoina, o lenei faʻatupulaia o le gaioiga e mafai moni ona faʻateleina le carcinogenesis ma / poʻo ni faʻamaʻi faʻamuamua i totonu o masini e aofia ai le ate ma le kolone (Tessitore et al., 1996). E ui lava o nei suʻesuʻega o loʻo vaseina ai le manaʻoga mo se loloto Malamalama i le faiga o gaoioiga, o le anapogi e tatau ona i ai ni aʻafiaga o le kanesa e pei ona faʻaalia e suʻesuʻega o loʻo i luga ma faʻamatalaga o le tele o poloka o le anapogi faʻavaitaimi e mafai ona aoga e pei o le chemotherapy i le togafitiga o ni kanesa i mumumu (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, atonu e naʻo se vaega moni, a itiiti mai mo nisi ituaiga o kanesa, ae e faʻamoemoe e le aoga mo isi ituaiga o kanesa. O le aoga o le anapogi tumau (2 vaiaso poʻo le umi) i togafitiga o le kanesa e tatau ona tofotofoina i le faʻatinoina o togafitiga o falemaʻi e aʻafia ai aʻafiaga e aofia ai le malnourishment ma atonu o se faʻafitauli faʻavaivaia ma le faateleina o le faʻafitauli i nisi o siama. I le eseesega, o faʻamatalaga mai manu mai le tele o falemaʻi ua taʻu mai ai o le tuufaatasiga o le anapogi anapogi faatasi ai ma le chemotherapy e maualuga ma aoga i le faaleleia o le chimotherapeutic index ma e maualuga le faaliliuga o faaliliuga. O le tele o faʻataʻitaʻiga faifaipea e tatau ona vave amata ona fuafua le aoga o le anapogi i le faʻaleleia o togafitiga o le kanesa i le falemaʻi.

Anapogi ma NEurodegeneration

Compared to ad libitum-fed controls, rats and mice maintained on an IF diet exhibit less neuronal dysfunction and degeneration, and fewer clinical symptoms in models of Alzheimer�s disease (AD), Parkinson�s disease (PD) and Huntington�s disease (HD). These models include transgenic mice expressing mutant human genes that cause dominantly inherited AD (amyloid precursor protein and presenilin-1) and frontotemporal lobe dementia (Tau) (Halagappa et al., 2007), PD (?-synuclein) (Griffioen et al., 2012) and HD (huntingtin) (Duan et al., 2003), as well as neurotoxin-based models pertinent to AD, PD and HD (Bruce-Keller et al., 1999; Duan and Mattson, 1999). Animals on an IF diet also fare better than ad libitum-fed controls after acute injury including severe epileptic seizures, stroke, and traumatic brain and spinal cord injuries (Arumugam et al., 2010; Bruce-Keller et al., 1999; Plunet et al., 2008).

E tele fesoʻotaʻiga telefoni feaveaʻi e fesoasoani i aʻafiaga aoga o le IF i luga o le faʻalavelave faʻalavelave e aofia ai le faʻaitiitia o le faʻapupulaina o molelaʻau faʻamaʻi, faʻaleleia atili meaola eletise, faʻamalosia le faʻalauiloaina o aʻafiaga, ma faʻaitiitia le mumū (Mattson, 2012a). O loʻo faʻalagolago le faʻaaogaina o le neuroprotective mechanisms e ala i suʻesuʻega e faʻaalia ai le IF e maua ai le maualuga o le malosi o puipuiga o antioxidants, o mea e leʻo faʻasolosolo (BDNF ma FGF2) ma cape (HSP-70 ma GRP-78), ma faʻaitiitia ai le maualuga faʻamalamalamaga cytokines (TNF?, IL-1? ma le IL-6) (Ata 4) (Arumugam et al., 2010). IF mafai foi faʻalauiloa le toe faʻaleleia o le faʻaleagaina neula sela faataamilo e ala i le faʻaosofia o le synaps fausiaina ma le gaosiaina o fou neo mai neural mafuaʻaga sela (neurogenesis) (Lee et al., 2002). O le mea e mataʻina ai, e ui o le aoga i faʻataʻitaʻiga o le tele o tulaga o le neurodegenerative, o loʻo iai le faʻamaoniga o le anapogi e mafai ona faʻavavevaveina le neurodegeneration i nisi faʻataʻitaʻiga o le tofi amyotrophic lateral sclerosis, atonu ona o le afi neurons aʻafia i na faʻataʻitaʻiga e le mafai ona tali faʻafetauiina i le feololo le faʻafitauli na faʻatupuina e le anapogi Mattson et al., 2007; Pedersen ma Mattson, 1999).

Anapogi ma le Metabolic Smaʻi

Metabolic syndrome (MS), faʻamalamalamaina o le manava o le manava, faʻatasi ma le insulin resistance, maualuga faʻamaʻi ma / poʻo le maualuga maualuga, e faʻapupulaina ai le lamatiaga o le maʻi cardiovascular, diabetes, stroke ma AD. O'oti ma mice e tausia i lalo o le masani masani o le fafagaina o le libitum e faʻaleleia ai se foliga o le MS pei o latou tausaga. E mafai foʻi ona faʻaosoina MS i manu laiti e ala i le fafagaina o se meaai maualuga i gaʻo gaʻo ma faigofie (Martin et al., 2010). AFA e mafai ona puipuia ma fesuiaiga uma vaega o le MS ile togavaʻa: gaʻo o le manava o le manava, mumu ma 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 e faalagolago i le amino acid sensing kinase Gcn2 (Peng et al., 2012).

Faʻafeiloaʻiga faʻasagaga e tele e faʻaalia ai MS i totonu o tagata a toe matau i le tootoo na tumau pea i luga o gaʻo maualuga ma gaʻo suka e aofia ai le maualuga o le inisalini ma le leptin ma faʻaitiitia ai le maualuga o le adiponectin ma le vevelin. O maualuga maualuga o le leptin e masani lava o le atagia o a faʻamalamalamaga tulaga, ae o le adiponectin ma le vetelin e mafai ona taofia le mumū ma faateleina ai le lagona o le insulin (Baatar et al., 2011, Yamauchi et al., 2001). O le mumusu i le lotoifale i le vavalo o le mafaufau lea e pulea ai le malosi o le malosi ma tupe faʻaalu e mafai ona fesoasoani i le paleni malosi o le malosi i MS (Milanski et al., 2012). O le anapogi e mafua ai le faaitiitia o le inisalini ma le leptin maualuga ma le maualuga o le adiponectin ma le maualuga o le tino. O le faateleina o le inisalini ma le leptin sensitivity, o le taofiofia o le mumū ma le faʻaleleia o le autophagy, o le anapogi e faʻaleagaina ai le tele o faʻalavelave faʻafuaseʻi o le MS i togavao (Singh et al., 2009, Wan et al., 2010). Ma le mea mulimuli, i le faaopoopo atu i le tele o aafiaga i luga o siama i le tino atoa ma le faiʻai, IF atonu e mafai ona suia suiga i le pepe microbiota e puipuia mai le MS (Tremaroli ma Backback, 2012). E masani lava, o le luʻitau o le faʻaaogaina o faʻaoga anapogi e togafitia ai MS i tagata, o se mea taua tele, e pei o nisi o tagata pagatia e ono i ai faigata i le mulimulitaia IF mo taimi uumi.

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. O le FMD e mafai ona faʻateleina le umi.

Dr. Alex Jimenez DC, CCST Insight

Anapogi, Tuai, ma le faamaʻi i Humans

Anapogi ma Faʻailoga Faigata i le Tupulagaina

O faʻamatalaga faʻamaʻi ma faʻamaʻi pipisi e tumau ma le h se gafatia o le anapogi e toe faʻafoʻi le faagasologa o le matua ma faʻamaʻi pipisi. O mea taua e mafua mai i le matua o le augatupulaga ua faanatinatiina e le tele o ituaiga soifuaga ma ua faagesegese i le malosi o le malosi i totonu o tagata e aofia ai: 1) le faaleagaina o meaola, proteins, DNA ma lipids; 2) mumu; 3) faʻatoʻateleina o aʻafiaga ma organelles; ma le 4) maualuga le kulukose, insulin ma IGF-I, e ui lava o IGF-1decreas ma le matua ma lona faaletonu matuia e mafai ona fesootaʻi ma nisi o maʻi (Patriarchs ma al., 2010; Fontana ma Klein, 2007). Faʻailoga o meaʻai faʻamaʻi faʻamaʻi ma le afaina faʻapea foʻi ma faʻamatalaga faʻapitoa 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).

Faatasi ai ma le tele o aafiaga o le anapogi e talafeagai i le matua ma faʻamaʻi o suiga ia i le maualuga o le IGF-1, IGFBP1, glucose, ma le inisalini. O le anapogi mo le 3 poʻo le sili atu aso e mafua ai le 30% pe sili atu le faʻaitiitia i le faʻasalalauina o le inisalini ma le kulukose, faʻapea foʻi ma le vave faʻaitiitia o le maualuga o le insulin-pei le tuputupu ae 1 (IGF-1), o le autu o le tuputupu aʻe o mammals, lea e faʻatasi ma le insulin e fesoʻotaʻi ma le faʻateleina o le matua ma le kanesa (Fontana et al., 2010). I totonu o tagata, e lima aso o le anapogi e mafua ai le sili atu i le 60% faʻaititia i le IGF-1and 5 poʻo le maualuga maualuga ile tasi o le IGF-1-inhibiting proteins: IGFBP1 (Thissen et al., 1994a). O lenei aafiaga o le anapogi i le IGF-1is tele ona o le puipuia o le palatini, ae maise lava i le tapulaa o mea aoga amino taua, ae e lagolagoina foi e le calorie tapulaa ona o le faaitiitia o le insulin i le taimi o le anapogi e faalauiloa ai faʻaitiitia i le IGF-1 (Thissen et al., 1994a). E le gata i lea, i totonu o tagata, o le faʻatapulaʻaina o calorie masani e le faʻaitiitia ai le IGF-1unless faʻatasi ma le faʻatagaina o le protein (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 ma isi taufaaleaga e oʻo lava i le matua. O le fafagaina o mataupu e mafai ona ausia e ala i le faʻafesoʻotaʻi IF poʻo le PF faʻatasi ma suʻesuʻega mole micro-ma macro e faʻataʻitaʻi ai le aafiaga o le IF poʻo le PF i luga o faailoga o le soifua matua, cancer, cognition ma O loʻo iai le gasegase (V. Longo ma M. Mattson).

Anapogi ma le Cfaʻatau

O le anapogi o loʻo i ai le avanoa mo talosaga i le puipuia ma le togafitiga o le kanesa. E ui lava e leai se faʻamaumauga a le tagata e aʻafia i le IF poʻo le PF i le puipuia o le kanesa, o le aʻafiaga i le faʻaitiitia o le IGF-1, insulin ma le kulukose, ma le faateleina o le IGFBP1 ma le tino o le ketone e mafai ona maua ai se siosiomaga puipuia e faʻaitiitia ai le faaleagaina o DNA ma carcinogenesis, i le taimi lava lea e fatuina ai tulaga faʻafefe mo tumutumu o le paʻu ma le mualaʻi (Figure 5). O le mea moni, o le maualuga o le faasalalauina o le IGF-1 e fesootaʻi atu i le faateleina o le lamatiaga o le atiaeina o nisi o kanesa (Chan & al., 2000, Giovannucci et al., 2000) ma tagata taitoatasi i le IGF-1deficiency ogaoga e mafua mai i le tuputupu ae o le senate o le hormone, Guevara-Aguirre et al., 2011; Sheva ma Laron, 2007, Steuerman et al., 2011). E le gata i lea, o le lauga mai nei IGF-1deficient mataupu na puipuia ai le ola o tagata mai le epithelial cell from oxidative stress-induced DNA damage. E le gata i lea, a oʻo loa ina faaleagaina le DNA, o le a sili atu ona lamatia le tino i le tino (Guevara-Aguirre et al., 2011). O le mea lea, o le anapogi e mafai ona puipuia mai le kanesa e ala i le faʻaitiitia o le cellular ma le DNA ae faʻapea foi i le faʻaleleia o le oti o sela muamua.

I se suʻesuʻega muamua o le 10 mataupu ma le tele o feusuaiga, o le tuufaatasiga o le chemotherapy ma le anapogi na mafua ai ona paʻu i le tele o aʻafiaga masani masani a le tagata lava ia e mafua mai i le chemotherapy pe a faatusatusa i mataupu lava e tasi e maua ai le chemotherapy ae i luga o se fua masani (Safdie et al., 2009). O le aʻafiaga o le anapogi i le faʻamaʻi o le chemotherapy ma le alualu i luma o le kanesa o loʻo tofotofoina nei i faamasinoga i totonu o Europa atoa ma le US (0S-08-9, 0S-10-3).

Anapogi ma NEurodegeneration

O lo tatou malamalamaaga nei o le aʻafiaga o IF i luga o le faʻalavelave o le tino ma galuega faʻamalosia e tele lava ina faʻaalia mai suesuega a manu (silasila i luga). O suʻesuʻega faʻasalalau e fuafua ai le aʻafiaga o le anapogi i luga o faiʻai ma gaioiga o faʻamaʻi neurodegenerative ua leai.

After 3�4 month, CR improved cognitive function (verbal memory) in overweight women (Kretsch et al., 1997) and in elderly subjects (Witte et al., 2009). Similarly, when subjects with mild cognitive impairment were maintained for 1 month on a low glycemic diet, they exhibited improved delayed visual memory, cerebrospinal fluid biomarkers of A? metabolism and brain bioenergetics (Bayer-Carter et al., 2011). Studies in which cognitive function, regional brain volumes, neural network activity, and biochemical analyses of cerebrospinal fluid are measured in human subjects before and during an extended period of IF should clarify the impact of IF on human brain structure and function.

Anapogi, Inflammation ma Hogaoga

I tagata, o se tasi o faʻataʻitaʻiga sili ona lelei o aoga aoga o le anapogi umi tumau tasi i le 3 vaiaso o i le togafitiga o rheumatoid gugu (RA). I maliega ma iʻuga i rodents, e i ai sina masalosalo o le vaitaimi o le anapogi uma mumu ma tiga ua faʻaititia i RA tagata mama (Muller et al., 2001). Peitai, a maeʻa ona toe amata le taumafataga masani, e toe foʻi le fula seʻi vagana ua mulimuli mai le vaitaimi o le anapogi e le vegetarian diet (Kjeldsen-Kragh et al., 1991), o se vailaʻau e mafai ona aoga mo le lua tausaga pe sili atu (Kjeldsen-Kragh et al., 1994). O le aoga o lenei auala e lagolagoina e le fa eseʻese faʻatonutonu suʻesuʻega, e aofia ai lua randomized tofotofoga (Muller et al., 2001). O le mea lea, o le anapogi faʻatasi ma se taumafataga vegetarian ma ono maua ma isi teuteuina meaai maua ai aoga aoga i le togafitiga o RA. Faʻafesuiaʻi aso IF na mafua ai foi le taua faʻaititia o le serum TNF? ma ceramides i tagata mamaʻi sela i le 2 masina vaitaimi (Johnson et al., 2007). O le suʻesuʻega mulimuli na faʻaalia ai foi, o faʻailoga o le faʻamamaina o le oxidative e masani ona fesoʻotaʻi ma le fulafula (protein ma lipid oxidation) na matua faʻaititia lava ile tali atu ia IF. O le mea lea, mo le tele o tagata gasegase mafai ma naunau e onosaia umi-anapogi ma ia suia fesuiaʻi a latou taumafataga, anapogi taʻamilosaga ono i ai le ono mafai e le gata faʻaopoopo ae suia foi faʻafomai togafitiga nei.

Na o le vai ma isi ituaiga o anapogi umi ua uma ona tusia ina ia i ai ni aʻafiaga i luga o le maualuga. O le umi o 13 aso o le vai naʻo le anapogi na mafua ai le ausia o se faiga faʻavae 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.

Mo le lua maualuga ma RA o le a taua tele le atinaʻeina o le PF i mea taumafa e sili ona lelei e pei o le anapogi anapogi o loʻo faʻamatalaina i luga ae e mafai foi ona talileleia e le toatele o tagata maʻi.

Anapogi ma le Metabolic Smaʻi

O le anapogi anapogi e mafai ona faʻafeiloaʻi ai le tele o foliga o le faʻamaʻi pipisi i le tino: e faʻaleleia le lagona o le inisalini, faʻaosofia le lipolysis ma faʻaitiitia ai le toto maualuga. Na faʻaitiitia le toto o le tino ma le toto maualuga ma ua faʻaleleia atili le metabolosis i mea e sili ona leaga i le tali atu i se isi aso na vave faʻafouina (Klempel et al., 2013, Varady et al., 2009). O mataupu mamafa e tumau mo 6 masina ile a faalua vaiaso 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 mamafa masani o alii ma tamaitai (Heilbronn et al., 2005) ma anapogi Ramadan (2 taumafataga / aso na vavaeese e tusa ma le 12 itula) i mataupu ma MS na mafua ai le faaitiitia o le malosi i aso taitasi, faaitiitia le maualuga o kulukose plasma ma le faateleina o le lagona o le insulin (Shariatpanahi et al., 2008). O mataupu o loʻo i ai faʻataʻitaʻiga o le matelaina oe na lipotia mai o latou anapopogi e masani ona faʻaalia le maualalo o le maʻisuka pe a faatusatusa i tagata e leai ni tagata faʻatau (Horne et al., 2012). O aʻafiaga faʻaleagaina o le faʻaleagaina o le faʻaleagaina o le IF, na maitauina foi i alii talavou soifua maloloina (BMI o le 25) i le maeʻa o 15 aso o le aso anapogi: o la latou tino atoa o le kulūkose ua maualuga tele, o maualuga o plasma body citone and adiponectin ua maualuga, na tupu e aunoa ma se faaitiitia tele o le mamafa o le tino (Halberg et al., 2005). O faʻamatalaga mulimuli e talitutusa ma faʻamatalaga mai suʻesuʻega a manu o loʻo faʻaalia ai e mafai e le IF ona faʻaleleia le metabolism o le glucose e tusa lava pe laitiiti pe leai se suiga (Anson et al., 2003). O le a taua le iloa pe o le umi o le anapogi anapogi e faʻateleina ai le malosi o le paʻu o le gaʻo ma le faʻamautuina o le tino, e ono mafua ai le tumau umi ma sili atu ona aʻafia.

Faaiuga ma Fautuaga

E tusa ai ma faʻamatalaga o loʻo i ai nei mai manu ma suʻesuʻega a le tagata ua faʻamatalaina, matou te manatu o loʻo i ai le malosi tele mo le soifuaga lelei e aofia ai le anapogi masani i le taimi o le olaga matua e faʻamalosia ai le soifua maloloina lelei ma faʻaitiitia le lamatiaga o le tele o faʻamaʻi faʻamaʻi, aemaise lava mo i latou o loʻo mamafa tele ma nonofo mamao. O suʻesuʻega a manu na tusia ai ni aʻafiaga mamafa ma le faʻaaogaina o faʻamaʻi anapogi i luga o le soifua maloloina, ma le faʻaitiitia o le maualuga o le toto, tino o le IGF-I, insulin, glucose, lipine atherogenic ma le mumū. O le anapogi e mafai ona faʻaleleia ai faʻamaʻi faʻamaʻi ma faʻaleleia ai le faʻatinoina o galuega i mamanu o meaola e aofia ai le faʻaleagaina o le myocardial, diabetes, stroke, AD ma le PD. O le tasi auala masani o le faʻatinoina o le anapogi, o le faʻaaogaina lea o tali faʻaogaina i le telefoni feaveai, lea e mafua ai le faʻaleleia atili o le tomai e taulimaina ai faʻafitauli matuia ma faʻafefe ai togafitiga faʻamaʻi. E le gata i lea, i le puipuia o siama mai le faaleagaina o DNA, faʻaitiitia o le tuputupu aʻe o le cell ma faʻaleleia apoptosis o sela na faʻatuina, o le anapogi e mafai ona vave ma / poʻo le puipuia o le faʻavae ma le tuputupu ae o kanesa.

However, studies of fasting regimens have not been performed in children, the very old and underweight individuals, and it is possible that IF and PF would be harmful to these populations. Fasting periods lasting longer than 24 hours and particularly those lasting 3 or more days should be done under the supervision of a physician and preferably in a clinic. IF- and PF-based approaches towards combating the current epidemics of overweight, diabetes and related diseases should be pursued in human research studies and medical treatment plans. Several variations of potential �fasting prescriptions� that have been adopted for overweight subjects revolve around the common theme of abstaining from food and caloric beverages for at least 12 � 24 hours on one or more days each week or month, depending on the length, combined with regular exercise. For those who are overweight, physicians could ask their patients to choose a fasting-based intervention that they believe they could comply with based upon their daily and weekly schedules. Examples include the �5:2� IF diet (Harvie et al., 2011), the alternate day modified fasting diet (Johnson et al., 2007; Varady et al., 2009), a 4�5 day fast or low calorie but high nourishment fasting mimicking diets once every 1�3 months followed by the skipping of one major meal every day if needed (V. Longo, clinical trial in progress). One of the concerns with unbalanced alternating diets such as those in which low calorie intake is only observed for 2 days a week are the potential effects on circadian rhythm and the endocrine and gastrointestinal systems, which are known to be influenced by eating habits. During the first 4 � 6 weeks of implementation of the fasting regimen, a physician or registered dietitian should be in regular contact with the patient to monitor their progress and to provide advice and supervision.

Fasting regimens could also be tailored for specific diseases as stand-alone or adjunct therapies. Results of initial trials of IF (fasting 2 days per week or every other day) in human subjects suggest that there is a critical transition period of 3 � 6 weeks during which time the brain and body adapt to the new eating pattern and mood is enhanced (Harvie et al., 2011; Johnson et al., 2007). Though speculative, it is likely that during the latter transition period brain neurochemistry changes so that the �addiction� to regular consumption of food throughout the day is overcome. Notably, the various fasting approaches are likely to have limited efficacy particularly on aging and conditions other than obesity unless combined with diets such as the moderate calorie intake and mostly plant-based Mediterranean or Okinawa low protein diets (0.8 g protein/Kg of body weight), consistently associated with health and longevity.

I le lumanaʻi, o le a taua tele le tuʻufaʻatasia o faʻamaumauga o le epidemiological, o suʻesuʻega o faitau aofaʻi ola ma a latou meaʻai, o taunuuga mai meaola faʻapitoa e fesoʻotaʻi atu i vaega o mea taumafa faʻapitoa mo mea faʻamuamua ma faʻamaʻi, faatasi ai ma faʻamaumauga mai suʻesuʻega e uiga i le anapogi i totonu o tagata , ia mamanuina ni suʻesuʻega faʻapitoa o suʻesuʻega o loʻo faʻapipiʻi ai le anapogi ma meaai faʻamauina e puipuia ma fiafia. O se malamalamaaga sili atu e uiga i mea mole mole fualaau lea e aʻafia ai le anapogi i ituaiga eseese o le tino ma faʻaʻauʻau e tatau ona taʻitaʻia ai le atinaʻeina o tala faʻasolosolo ma togafitiga faʻafomaʻi mo le tele o faʻafitauli.

Ave le Savali a le Aiga

O le anapogi e faʻatatau ai taumafa e maua ai tutusa lelei o le masani masani ile anapogi e ala i le taofiofia o lau kalori mo le lima aso mai le masina ae le o le faʻaaogaina uma o meaai mo ni nai aso poʻo ni vaiaso foi. Le ProLon O le taumafa anapogi e ofoina atu ai le polokalama o le taumafataga o le 5 lea na faaputuputuina taitoatasi ma faaigoaina i aofaiga saʻo ma tuufaatasiga mo aso taitasi. E ui o le suʻesuʻega suʻesuʻega i luga ua faʻaalia ai le soifua manuia o le anapogi, faamolemole ia mautinoa e te talanoa i se fomai tausi soifua aʻo leʻi amataina ProLon` anapogi mimicking meaai, 5-aso taumafataga polokalama ia iloa pe o le FMD, poʻo soʻo se isi lava meaai, e saʻo mo oe.

O le lomiga lolomiina, faaiu mulimuli o le suesuega sailiiliga na faasinomia i luga na maua i le NIH Public Access Author Tusitala i le PMC Fepuari 4, 2015. O le lautele o a tatou faʻamatalaga e faʻamapulaʻaina i faʻamaʻi faʻasalalau, mataupu faʻalesoifua maloloina o le toto, ma mataupu tau vailaʻau faʻaaogaina. Ina ia toe talanoaina le mataupu, faamolemole ia lagona le saoloto e fesili ia Dr. Alex Jimenez pe faʻafesoʻotaʻi mai i matou 915-850-0900 .

Faʻailoina e Dr. Alex Jimenez

Faʻamatala mai: Nih.gov

Faʻaopoopo Autu Talanoaga: Matuitui Paʻu Paʻu

Paʻu tua o se tasi o mafuaʻaga sili ona taatele o le le atoatoa ma aso ua misia i galuega i le lalolagi atoa. Faʻasologa o tiga i le mea lona lua e sili ona taatele mo asiasiga o le ofisa o le fomaʻi, naʻo naʻo faʻamaʻi pipisi pito i luga. E tusa ma le 80 pasene o le faitau aofaʻi o le a maua le tiga i le itiiti ifo ma le tasi i le taimi atoa o lo latou olaga. O lau tuila o se fausaga faʻapitoa e faia i ponaivi, sooga, ligaments, ma maso, faatasi ai ma isi mea vaivai. Manua ma / poʻo tulaga faʻamalosia, pei o siaki faʻasolosolo, e mafai ona oʻo atu ai i faʻamaoniga o le tigā mulimuli. O manuʻa o le taʻavale poʻo faʻalavelave faʻafuaseʻi faʻafuaseʻi faʻafuaseʻi o manuʻa e tele lava ina mafua ona o tiga i tua, ae ui i lea, o nisi taimi o le faigofie o gaioiga e mafai ona i ai ni taunuuga tiga. O le mea e lelei ai, o isi togafitiga togafitiga, e pei o le togafitiga o le chiropractic, e mafai ona fesoasoani e faʻafilemu ai le tiga e ala i le faʻaaogaina o fetuunaiga o le ogatotonu ma le faʻaaogaina o le tusi lesona, faʻamalosia ai le faʻamalosi o le tiga.

XYMOGEN's Ole Polokalame Tomai Faapitoa e avanoa e ala i le filifilia o tagata tomai faapitoa ile soifua maloloina. Ole faʻatau ile initaneti ma le faʻaititia o XYMOGEN faʻataʻitaʻiga e matua faʻasaina.

Ma le fiafia, Dr. Alexander Jimenez faia faʻataʻitaʻiga XYMOGEN na o maʻi i lalo o la matou tausiga.

Faʻamolemole valaʻau i le matou ofisa ina ia matou tofia se fomaʻi mo faʻamatalaga vave.

Afai o oe o se tagata maʻi Manua Fomaʻi & Chiropractic Clinic, e mafai ona e fesili e uiga i le XYMOGEN ile valaʻau 915-850-0900.

Mo lou faigofie ma iloiloga o le XYMOGEN oloa faamolemole toe iloilo le sootaga lenei. *XYMOGEN-Catalog-Download

* O tuʻutuʻuga uma o XYMOGEN o loʻo i luga e tumau pea le faʻamalosia.

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