.Putns. @ 28.07.2021 18:14
Man izskatās, ka Tev ir kautkāds bias attiecībā uz fastingu.
Internets pilns ar dažādām publikācijām un apkopojumiem, bet Tu vēlies izrakt to, kur pētījums neapstiprina.
https://siimland.com/does-fasting-make-you-live-longer/
Es no savas pieredzes varu pateikt, ka fastings mani ir paglābis no veselas kaudzes medikamentu un tādēļ paildzinājis mūžu.
Fastings mani izglāba no autoimūnās lēkmes, kas radās pēc baltmaizes ēšanas. Es nevarēju paelpot. Bet redzi pāris dienas bez ēdiena un viss bumbās. Nekādu medikamentu.
Fastings mani glāba no kuņģa dedzināšanas. Ja es turpinātu visu laiku ēst, tad tā arī nevarētu ilgi no tā atbrīvoties un būtu jādzer zāles.
strīdēties mēs varam ilgi un dikti, bet tiešu pētījumu par cilvēka dzīves ilgumu nebūs, jo cilvēki dzīvo ļoti ilgi!putns @ 28.07.2021 22:21Come on... Tur vienkārši random čalis uzskaita dažādus pētījumus. Tā nav ne meta, ne kāda cita analīze. Jau arī redzēju, ka ir minēta virkne pētījumu, kas ir minēti arī analīzē - ka tajos normāli dzīvnieki tika salīdzināti ar kontrolgrupu, kas bija aptaukojušies dzīvnieki. Jā, aptaukošanās ved pie daudz īsāka mūža nekā sugai ir normāls.
arī tas raksts apkopo lielu skaitu pētījumu. Saites apakšāputns @ 28.07.2021 22:12
Tā ir ļoti liela skaita pētījumu datu analīze, nevis viens pētījums. Pēc tam likt linku uz random cilvēka rakstu, kur viņš apgalvo, ka 'peles, kas ēd mazāk, dzīvo ilgāk' ir bezjēdzīgi, ņemot vērā visu šajā analīzē rakstīto.
Ar to es nestrīdos, ka, ja cilvēkam pie normāla uztura, kas der 99% citu cilvēku, sākas veselības problēmas, tad ir jāmēģina kaut kādas alternatīvas. Bet visiem nav jāēd tā, kā ēd cilvēki ar veselības problēmām.
Internets pilns ar dažādām publikācijām un apkopojumiem, bet Tu vēlies izrakt to, kur pētījums neapstiprina.
Fastings mani izglāba no autoimūnās lēkmes .. Fastings mani glāba no kuņģa dedzināšanas
Putns Pameklēju kādu analīzi par dzīvnieku pētījumiem. Piemēram, viena, atkal raksta to pašu, ko iepriekšējā citētā:
Kamēr tomēr ir veikta izpēte uz dzīvniekiem un citiem organismiem. Kur patērējot par 30% mazāk uztura tie dzīvo arī par 30% ilgāk.
A further misgiving is that the control animals, fed ad libitum (AL), become overweight and prone to early onset of diseases and death, and thus may not be the ideal control animals for studies concerned with comparisons of longevity. Reexamination of body weight and longevity data from a study involving over 60,000 mice and rats, conducted by a National Institute on Aging-sponsored project, suggests that CR-related increase in life span of specific genotypes is directly related to the gain in body weight under the AL feeding regimen.
According to Martin et al. , failure to recognize that “control rats and mice used in biomedical research are sedentary, obese, glucose intolerant and on a trajectory to premature death, may confound data interpretation and outcomes of human studies.” Overeating and the resultant energy imbalance are known to enhance oxidative stress, inflammation, diabetes, kidney disease, and cancer, among others, leading to an abridgement of potential life span
Swindell has discussed several examples in the literature in which the effects of CR on longevity do not uphold the assertion of universality. Particularly, studies by Liao et al. on several different strains of mice have demonstrated that under 40% CR, longevity of individual strains is either decreased or increased or remains unaffected, thereby suggesting that the nature of the CR effect on life span is genotype-specific.
Nevertheless, comparisons between the CR-responsive, C57BL/6 mice and the CR-unresponsive, DBA/2 mice have pointed to the role of energy imbalance in determining the nature of the effect of CR on longevity , , , . A major difference between the C57BL/6 and the DBA/2 mice was that during 4 to 23 months of age, the AL-fed C57BL/6 mice maintained a mean body weight that was 20% greater than their weight at 4.5 months of age, whereas the comparable gain in body weight was insignificant in the DBA/2 mice. The DBA/2 mice also had a higher rate of energy expenditure than the C57BL/6 mice, as indicated by resting and in vitro rates of oxygen consumption and the core body temperature , , , . Thus, although the amount of energy (food) consumption was similar in the two strains, the C57BL/6 mice, whose longevity is extended by CR, had a relatively lower metabolic rate and gained more weight with age, whereas the DBA/2 mice had a higher metabolic rate and did not exhibit a significant gain in the mean body mass during adult life, and their longevity was not extended by CR. These associations support the hypothesis that CR-induced increase in life span occurs in those genotypes that display weight gain or positive energy balance when fed AL. Rikke et al. have also noted that fuel efficiency, determined as the ability to maintain growth and body weight, was correlated with longevity of their inbred mice, a finding that is compatible with our analysis.
The association between energy imbalance and the effect of CR on longevity, summarized in Fig. 4, is also compatible with findings in rhesus monkeys, reported from the Wisconsin National Primate Center (WNPC) and the National Institutes of Health (NIH) . Caloric restriction was reported to decrease mortality from age-related as well as aggregate causes at the WNPC , whereas no significant differences in the life spans of control and CR groups were observed at the NIH site. However, a crucial variation in the experimental design at the two sites was that the control monkeys at the NIH were fed a diet that did not permit excessive weight gain, whereas the AL-fed controls in the WNPC study ate more liberally. Consequently, the body weights of the age-matched control groups at WNPC were greater than those in the NIH study, suggesting that a comparatively higher degree of energy imbalance is associated with longevity extension under CR. Comparisons of the body weights of the control groups at these two sites with those available from a national database indicated that control monkeys at WNPC were approximately 7–10% heavier than the national average, whereas controls in the NIH study were 9–17% below the average
It is often asserted that CR prolongs the maximum life span, which is regarded as a more critical indicator of the rate of aging than the average life span. However, it has not yet been specifically shown that CR increases longevity beyond the maximum species life span Perhaps, in counterpoint, it can also be argued that CR does not increase longevity per se: rather the AL feeding shortens the life span, because it causes a deleterious energy imbalance, which prevents the animals from reaching their potential longevity.
Vispār jā - cilvēks ar vidēju svaru dzīvos daudz ilgāk nekā cilvēks, kurš sver ap 300kg un bieži vien mirst jau ap 30. Bet nav pierādījumu, ka tas pats attiecas uz normāla svara kategoriju, un tie, kas pie normāla svara ēd mazāk, arī dzīvo ilgāk un veselīgāk utt.
Piem., ja palasa nesenu 29 pētījumu metaanalīzi, izrādās, ka 50% no visu šādu pētījumu subjektiem ir 'overweight or obese'. Protams, ka viņus uzsēdinot uz diētas, viņiem uzlabosies veselība. Tur jebkura diēta, kas ved pie svara nomešanas, palīdzētu un uzlabotu arī citus rādītājus, kas parasti ir slikti pie ļoti augsta svara, un ved pie agrākas nāves.
Nu, viens no 'uzkrājumiem', ko organisms mēdz sākt ēst bada apstākļos, ir smadzenes. Protams, ja ir daudz liekā svara, tad smadzenes vēl ilgi netiks izmantotas uzturam. Bet ja tāda nav, tad tās kļūst par vienu no enerģijas avotiem.
Ja mēs skatāmies zinātnē, tad tie kas ēd mazāk un vai retāk dzīvo arī ilgāk
Together, our findings recollect and consolidate current evidence on the link between CR and markers relating to health-span and longevity. Hypothetically, these results could hint at the therapeutic implications of CR in non-pharmacological management of a many chronic diseases and cardiometabolic problems originating from inadequate lifestyle habits.
However, additional evidence is needed to support to clinical practice and/or prevention and health promotion during lifespan. This SR underlined that, excluding body composition, blood lipids and blood pressure, trials reporting data on hormones and glucose metabolism, osteoporosis and bone health and inflammatory markers are few to support strong conclusion in favor to caloric restriction for healthy aging.
We showed that CR of 10–25% of the total caloric intake was efficacious on some markers of health relatively to metabolism, endocrine system, and inflammation without main adverse events. However, these findings are limited to a short period of observation, in people mostly aged 70 years, and overweight. The effect on normal-weight subjects, the potential deprivation of nutritional agents on the long-term, and the need of food supplement are not investigated at all. Although increasing data on animals are encouraging, there is not enough evidence to suggest CR for a long time at any age, any weight, any diseases.
Tā nav mocīšana, jo cilvēkam ir (uzkrājumi).
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