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Starting Fasting Every Other Day


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#1 kevin

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Posted 29 April 2003 - 05:27 AM


A recent study has found that mice who fasted one day and then fed well the next, fared better under experimental neurological stress than those on a calorie restricted diet, indicating that there may be more benefits to occasional fasting than those obtained from following a strict CR oriented regime.

Link to article..

http://story.news.ya...meals_health_dc

#2 hughbristic

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Posted 30 April 2003 - 07:28 PM

Based on the recent study that shows that mice who alternate daily between fasting and binging are able to attain health benefits similar to CR ( http://www.betterhum...ID=2003-04-29-4 ), I'm going to start on the yo-yo diet. I'm going try fasting every other day and see if I have any better luck maintaining that than I have at doing standard CR. I'm hoping it will better suit my extremist temperment (I've never been good with moderation). I'll try to keep track of my diet and exercise, as well as my weight, blood pressure, resting heart rate, temperature, and cholesterol levels. I'll try to keep you posted with weekly reports on my progress. Wish me luck.

Hugh

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#3 kevin

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Posted 01 May 2003 - 04:42 AM

I've never tried fasting myself... I have a feeling I wouldn't have much luck... I'm the type who eats an entire box of chocolate covered almonds at once... yeesh.. guess I'll be hoping for a good mimetic with few side effects..

#4 fruitimmortal

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Posted 01 May 2003 - 07:35 AM

I fasted several times, the last time was 2 yrs. ago.
Once i fasted under supervision at a Health Resort. A cleansing Diet before a water fast is often recommended.

The desire for food dies after 2-3 days;
i'm getting hungry...........

#5 fruitimmortal

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Posted 07 May 2003 - 05:08 PM

Hughbristic

I recently saw a Website(lost the adress) on fasting.
The Members fast on specific dates; the "tune-up" is easier when we know others are doing the same.

It would be benefical to have a fasting club here.

#6 Lazarus Long

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Posted 08 May 2003 - 11:09 AM

I fast as a kind of seasonal and demand oriented approach that I find too haphazard and random to be as effective as I like. I have the problem of single parenting and I do need to prepare meals for my children and this creates an additional stress, and "need" to eat. Also I am under normal circumstances very fond of the traditional gathering of the "meal". I think it serves a very important function socially and beyond mere ingestion of calories.

But I also do not indulge. I would rather eat well then excessively, or trash. Fast (convenient) foods have generally disappeared from my stocks and I favor a more omnivorous diet focused on flavor and alternatives to meat then using meat as staple. I think whole grains, fresh vegetables, and legumes are more satisfying anyway but I find I must vary my diet a little to adapt to seasons. Food prep is also something that requires real attention especially in a group setting.

I routinely gain and lose ten pounds going into and out of winter. This doesn't necessarilly relate to activity. I am active outdoors in the winter and as my "types" of crafts have moved over to the more cerebral I am less physically active then I should be in summer.

This is an aspect of "seasonal response" that I think is both genetically encrypted as well as socially/behaviorally reflective. I suspect for instance the supposed "obesity gene" is an example of a "seasonal clock" that may work through subtle feedback such as a circadian (daylight duration) rhythm to regulate both demand and storage rates for fats in the body but that the "modern lifestyle" plays havoc with the regulator the way a child playing with a thermostat can.

I would love to see this entire "system" for metabolic feeding and feed-back laid out more comprehesively. Remember one of the arguments, is that for those of us that carry the feast/famine genes that leads to obesity is, it is the famine cycle which triggers the fat storage.

But back to a diet for a small planet, how do we regulate our intake when the demands of the individuals in a given feeding group differ widely?

And as for a "Fasting Club" all that is required is the "will" and then the "support" from one another. This is as simple as creating a set of alternative activities to "eating" and also to offsetting any craving with a a functional distraction. But I also think there is a need for "monitoring".

Not everybody responds to hunger the same way. I have found a number of people that become violently irritatble when hungry. Actually I sense this to be one root of violence among many poorer societites. I wonder what aspect of this anger/anxiety/hunger reflex is also a simple genetic response mechanism designed to activate the hunter/gatherer reflex for survival? Remember too that seasonal also refers to a routine "spring famine" and "harvest bounty" that has been the biological experience for our species since the beginning.

In other words we are also influenced negatively by hunger, not just positively. But once the metabolic mechanism of this is better understood it may be possible to just interfere carefully with the gene based signal response to remove the anxiety and this would eliminate the psychological stress of fasting for these personality types.

Opinions and observations please; as well as suggestions. :)

Edited by Lazarus Long, 09 May 2003 - 11:09 PM.


#7 Saille Willow

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Posted 09 May 2003 - 10:37 PM

I used to fast on a regular basis once a week. I did find an increse in my energy levels. What I really enjoyed about it, was that it increased my taste sensations. You just can't eat junkfood then, it tastes like cardboard.

As Lazarus said, it is not easy with a family. Meal times forms an important part in the unity of a family. It is a time of sharing and togetherness. We eat a high percentage of fresh/raw food. The seasonal element then comes in naturally I vary meals seasonally. During hot weather you feel like eating lighter meals than colder months. It is much easier to fast during summer time.

I have maintained a consistent weight this way, throughout my adult life. I have founf that the trick in maintaining a CR is to satisfy the tastebuds. I always add fresh herbs to meals and eat fresh chilli with most meals. Herbs like watercress, rocket and coriander just rounds the tastebuds and you don't feel hungry. Fresh soups like Gazpacho and Minted Cucumber soup are quick to make and satisfy the tastebuds. Even my children enjoy eating fresh.

#8 dademurphy

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Posted 26 August 2003 - 09:14 PM

any updates on fasting diet progress?

#9 Bruce Klein

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Posted 26 August 2003 - 09:54 PM

Check:

Fasting and Calorie Restriction
With Dietary and Supplemental Suggestions To Increase Life Span
Updated: 08/05/2003

Because of the parallel between the two models, fasting and calorie restriction will be presented in the same protocol.

Claims that various nutritional interventions can extend life span are manifold, but some are grounded in greater credibility than others. Among regimens debated, gerontologists often agree that Caloric Restriction with Optimal Nutrition (CRON) offers the greatest likelihood of succeeding.

The concept of restricting calories to improve health was first introduced in the early 1900s, but Clive McCay (Cornell University) advanced the theory significantly when (in the 1930s) he found that calorie-restricted rats lived longer than those allowed to eat ad libitum. Though decades have passed since McCay's initial findings, the exact mechanisms whereby dietary restriction retards aging and extends life span are still not fully understood. Much of the emerging data suggest that McCay's calorie-restricted rodents lived longer and aged more slowly because they were more resistant to stress and their cells appeared protected against damaging agents (Van Remmen et al. 2001).

* * *

http://www.lef.org/p...Fasting#fasting

#10 Michael

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Posted 13 April 2004 - 05:19 PM

All:

This is a summary of some posts I've made on the CR Society < http//www.calorierestriction.org > forum on Every Other Day (EOD) AL feeding, as vs. Limited Daily Feeding (LDF -- "conventional" CR), esp as regards the suggestion -- based on the metabolic effects observed in some new studies by Mark Mattson et al (1,2) -- that EOD, even in the absence of overall CR (ie, in the presence of compensatory overeating on the feeding day) might still slow aging and extend LS. I'd like to bring the subject in again, advance my reasons for rejecting this conclusion, & esp for thinking that EOD is not a promising life-extension strategy, especially for implementation in adult animals.

The question is important. CR is, at present, the only intervention available which is proven to retard aging in mammals -- and a large body of evidence strongly suggests that it does so in humans as well. CR might make the difference between your catching the first wave of anti-aging biomedical interventions and missing them by a few months or years; it might also be crucial for your ability to actually use those interventions, as it will not just keep you alive, but biologically young. Biological youth might well be key to either implementing those technologies (especially if they merely slow down, as opposed to arrest or reverse, the aging process) or to your ability to survive them without complications (if they are invasive, physically ardurous, or prone to side-effects). Based on the evidence reviewed below, this means you'll have to adapt to a lifestyle of tracking and reducing your Calories; simply adapting an EOD or "food window" strategy is unlikely to work.

Let me first point out the obvious, tho' it seems to be often overlooked in discussions on the subject. Contrary to the impression many people seem to've gotten from pop press acounts, Mattson's studies (1,2) do not provide any lifespan data. All they have shown is that EOD animals undergo a variety of favorable-looking metabolic shifts, such as lower insulin and glucose levels. These shifts, while consistent with the effects of LDF, do not themselves constitute evidence that EOD will lead to life extension in the absence of actual Calorie restriction.

Many studies in which EOD has been implemented in juvenile animals have demonstrated LS extension (3-7) (most of them coauthored by Ingram (a coauthor of (2)) -- but in all of these studies, EOD animals have undergone decreases in the ballpark of ~30% in body weight in response to EOD feeding, which suggests that their overall Caloric intake has indeed been reduced -- an inference which (when measured) has been confirmed. (NB that (1), unlike (2), reported just this change).

Of these studies, (5) is of special interest. In this study,

-----------------
Beginning at either 1.5, 6 or 10 months of age, male mice from the A/J and C57BL/6J strains and their F1 hybrid, B6AF1/J were fed a diet (4.2 kcal/g) either ad libitum every day or in a restricted fashion by ad libitum feeding every other day.

Relative to estimates for ad libitum controls, the body weights of the intermittently-fed restricted C57BL/6J and hybrid mice were reduced and mean and maximum life span were incremented when the every-other-day regimen was initiated at 1.5 or 6 months of age. When every-other-day feeding was introduced at 10 months of age, again both these genotypes lost body weight relative to controls; however, mean life span was not significantly affected although maximum life span was increased.

Among A/J mice, intermittent feeding did not reduce body weight relative to ad libitum controls when introduced at 1.5 or 10 months of age; however, this treatment did increase mean and maximum life span when begun at 1.5 months, while it decreased mean and maximum life span when begun at 10 months.

--------------

That is: the one strain that did not undergo a reduction in BW (& thus, by implication, a reduction in overall Caloric intake) in response to EOD was the same one in which this regimen -- when implemented in adulthood -- not only failed to increase mean & max LS, but actually shortened them.

At the same time, the strains in which EOD did reduce BW (& thus, by implication overall Caloric intake) DID extend LS -- but not robustly. Indeed, the lack of an increase in mean LS observed in these strains when implemented in adulthood, despite a (presumed) reduction in Caloric intake, suggests a lot of early mortality (otherwise the max LS increase would, by simple arithmetic, increase av'g LS), again suggesting that this is not a promising strategy.

Also of note is that one of these 'successful' strains was, in fact, the very same strain (C57BL/6) which (2) reported not to show reduced BW. It seems reasonable to assume that the statistically nonsignificant reduction in BW observed in (2) is simply the result of the brevity of the experiment to date, and that -- extended over a lifespan -- the small Caloric deficit slowly manifests itself, leading to the loss of BW observed in (5). Thus, even (2)'s results may actually be the result of CR.

Second, in studies in which the timing of feeding has been manipulated (single day feeding vs. several smaller feeding sessions/day) while keeping Caloric intake constant, no differences in LS have been observed: the survival curves overlap, almost perfectly (8-10). This again suggests that the life-extending effects of EOD, when observed, are simply the result of reduced Caloric intake. This is a direct experimental refutation of the whole notion IMO, and certainly refutes the increasingly-widespread notion that just concentrating the same amount of food into one meal per day or a window of a few hours will have any substantial impact on long-term health or LS.

Third, while Mattson's group is promulgating the idea that hormesis (the adaptive response to a specific stressor (such as hunger) with an overall upregulation of nonspecific stress-resistance ("that which does not kill you makes you stronger")) plays a key role in the effects of CR/EOD/LDF, so that a more 'stressful' dietary pattern (such as simply concentrating the same number of Calories into a single meal or window) will simulate CR under isocaloric feeding or enhance "regular" LDF, & while these may very well be involved in some of the health benefits of these regimens (including, especially, the neuroprotective effects, via a preconditioning mechanism), (15) provides several lines of evidence which strongly suggest that it is not, at least in mammals:

(a) hormesis induced by a multitude of other mechanisms (exercise, cold, heat shock, irradiation) has repeatedly failed to extend max ls in mammals (tho' an ambiguity in (13), combined with other evidence, continues to intrigue me about exposure to cold -- but that other evidence implies mechanisms other than hormesis are also at work), & doesn't clearly do so even in flies, worms etc (where most of the hormesis work has been done);

(b) most of the evidence is in poikilotherms, in whom the stressors apparently lower metabolic rate; this would (per simple-minded rate-of-living mechanisms) slow aging in such organisms -- but would be unlikely to be relevant to mammalian aging;

© there's inconsistency in the hormesis work, per strain & gender & other factors, which make hormesis per se questionable as a causal agent in the observed effect & certainly a poor place to directly place one's bet (ie, thru' ignoring Calories in favor of EOD AL, per (2-7)'s protocols; and in particular

(d) it isn't clear that hormesis extends longevity at all, except in adverse conditions where longevity is cut short by environmental hardship (addressing extrinsic rather than intrinsic mortality; curve-squaring, not slowing aging). Where the control group is longevous, hormetic interventions seem to have little or no impact on LS. (Cf Sohal's recent analysis (16) and new results (17) using SOD-transgenic flies).

Another line of evidence cited in favor of the benefits of EOD is the fact that it seems to provide some neuroprotection against a variety of hideous neurotoxins -- for instance, kainate excitotoxicity in (2) (& other excitotoxins in previous EOD studies from Mattson's lab). I don't think that injecting the brain with hideous toxins tells us much about the kinds of challenges that the human brain is likely to experience on a day-to-day basis, or as part of "normal" aging, and I certainly don't think they tell us much about the impact of this regimen on the aging process. In any case, I suggest that the observed results are best explained as a mixture of the increased ketone body production noted in (2) and a preconditioning hormetic mechanism. As (2) notes -- but fails to emphasize -- ketogenic diets, per se, independent of CR, are widely experimentally & clinically demonstrated to have neuroprotective effects & reduce seizures ((11-14), including against kainate (eg. (11)). The mechanism is apparently NOT any direct neuroprotective effect, nor a change in excitatory signalling; it may be a simple matter of providing an alternative energy source, which could rescue neurons in excitotoxic crisis:

"[E]pileptic patients undergoing cortical resection, demonstrated abnormal expression of [blood-brain barrier] glucose transporter molecules (GLUT1) ... Diminished ion homeostasis together with increased metabolic demand of hyperactive neurons may further aggravate the neuropathological consequences of BBB loss of glucose uptake mechanisms. Since ketone bodies can provide an alternative to glucose to support brain energy requirements, it is hypothesized that one of the mechanisms of the ketogenic diet in epilepsy may relate to increased availability of beta-hydroxybutyrate, a ketone body readily transported at the BBB." (14)

Finally, even looking at the metabolic results of (1,2) seems IMO to argue against the EOD paradigm (in the absence of overall energy restriction) as a fully effective alternative to CR. Because while glycemia and resistance to excitotoxins were improved, they seem to report that EOD doesn't lower IGF1 -- even when actual Caloric restriction is associated therewith.

The cardiovascular study (2), in which 4 mo old rats on an EOD "regimen consumed 30% less food over time and had reduced body weights compared with rats fed ad libitum" found that wehn "The levels of .. IGF-1 in plasma were assessed at 3 and 6 months after diet initiation. ... [T]here were no significant differences in plasma IGF-1 levels among the three groups [AL, EOD, and 2-DG] at either time point, although IGF-1 levels in group IF were lower after 6 months on the diet (Table 1)" -- ie, there was a nominal reduction, if you want to play voodoo, but not statistically significant, at 6 mo, and no change at all at 3 mo -- hardly a robust-sounding response.

Even more surprisingly, the excitotoxin study (1), in which EOD did not lead to any reduction in weight or overall food intake, actually reported that EOD *increased* IGF1: "Levels of circulating IGF-1 were decreased in mice on the [LDF] diet but increased in mice on the [EOD] diet".

Granted the extensive evidence that interfering with IGF1 signalling exerts anti-aging effects in a variety of species -- including several rodent models (Ames and Snell dwarves, IGF1-receptor heterozygous knockouts, etc) -- & that LDF lowers IGF1, it seems reasonable to assert (and many do) that many of the benefits of LDF may arise from reduced IGF1. If this is the case, then EOD without CR would be predicted to flop. This may be one reason for the failure of EOD to increase LS when implemented in adulthood in the A/J strain.

As has been pointed out to me, however, it is possible that the significant reductions in insulin observed in EOD might result in sufficiently elevated IGFBPs as to reduce actual IGF1 signalling. I would call out to Mattson et al to test this parameter.

However, whatever the actual impact on EOD on this particular metabolic parameter, the weight of the evidence on LS (3-10) seems to me to strongly argue against an anti-aging effect of EOD in the absence of overall CR.


-Michael


1. Wan R, Camandola S, Mattson MP.
Intermittent fasting and dietary supplementation with
2-deoxy-D-glucose improve
functional and metabolic cardiovascular risk factors in rats.
FASEB J. 2003 Apr 22 [epub ahead of print]
PMID: 12709404 [PubMed - as supplied by publisher]

2: Anson RM, Guo Z, De Cabo R, Iyun T, Rios M, Hagepanos A, Ingram DK,
Lane MA, Mattson MP.
Intermittent fasting dissociates beneficial effects of dietary
restriction on
glucose metabolism and neuronal resistance to injury from calorie intake.
Proc Natl Acad Sci U S A. 2003 Apr 30 [epub ahead of print]
PMID: 12724520 [PubMed - as supplied by publisher]

3: Beauchene RE, Bales CW, Bragg CS, Hawkins ST, Mason RL.
Effect of age of initiation of feed restriction on growth, body composition,
and longevity of rats.
J Gerontol. 1986 Jan;41(1):13-9.
PMID: 3941250 [PubMed - indexed for MEDLINE]

4: Goodrick CL, Ingram DK, Reynolds MA, Freeman JR, Cider NL.
Differential effects of intermittent feeding and voluntary exercise on body
weight and lifespan in adult rats.
J Gerontol. 1983 Jan;38(1):36-45.
PMID: 6848584 [PubMed - indexed for MEDLINE]

5: Goodrick CL, Ingram DK, Reynolds MA, Freeman JR, Cider N.
Effects of intermittent feeding upon body weight and lifespan in
inbred mice:
interaction of genotype and age.
Mech Ageing Dev. 1990 Jul;55(1):69-87.
PMID: 2402168 [PubMed - indexed for MEDLINE]

6: Goodrick CL, Ingram DK, Reynolds MA, Freeman JR, Cider NL.
Effects of intermittent feeding upon growth, activity, and lifespan in rats
allowed voluntary exercise.
Exp Aging Res. 1983 Fall;9(3):203-9.
PMID: 6641783 [PubMed - indexed for MEDLINE]

7: Goodrick CL, Ingram DK, Reynolds MA, Freeman JR, Cider NL.
Effects of intermittent feeding upon growth and life span in rats.
Gerontology. 1982;28(4):233-41.
PMID: 7117847 [PubMed - indexed for MEDLINE]

8. Masoro EJ, Shimokawa I, Higami Y, McMahan CA, Yu BP.
Temporal pattern of food intake not a factor in the retardation of aging
processes by dietary restriction.
J Gerontol A Biol Sci Med Sci. 1995 Jan;50A(1):B48-53.
PMID: 7814779; UI: 95114284

9. Nelson W.
Food restriction, circadian disorder and longevity of rats and mice.
J Nutr. 1988 Mar;118(3):286-9. Review.
PMID: 3280755; UI: 88171757

10. Nelson W, Halberg F.
Meal-timing, circadian rhythms and life span of mice.
J Nutr. 1986 Nov;116(11):2244-53.
PMID: 3794831; UI: 87085847

11. Noh HS, Kim YS, Lee HP, Chung KM, Kim DW, Kang SS, Cho GJ, Choi WS.
The protective effect of a ketogenic diet on kainic acid-induced hippocampal
cell death in the male ICR mice.
Epilepsy Res. 2003 Feb;53(1-2):119-28.
PMID: 12576173 [PubMed - indexed for MEDLINE]

12. Lefevre F, Aronson N.
Ketogenic diet for the treatment of refractory epilepsy in children: A
systematic review of efficacy.
Pediatrics. 2000 Apr;105(4):E46. Review.
PMID: 10742367 [PubMed - indexed for MEDLINE]

13. Stafstrom CE.
Animal models of the ketogenic diet: what have we learned, what can we learn?
Epilepsy Res. 1999 Dec;37(3):241-59. Review.
PMID: 10584974 [PubMed - indexed for MEDLINE]

14. Janigro D.
Blood-brain barrier, ion homeostatis and epilepsy: possible implications
towards the understanding of ketogenic diet mechanisms.
Epilepsy Res. 1999 Dec;37(3):223-32. Review.
PMID: 10584972 [PubMed - indexed for MEDLINE]

15. Minois N.
Longevity and aging: beneficial effects of exposure to mild stress.
Biogerontology. 2000;1(1):15-29. Review.
PMID: 11707916 [PubMed - indexed for MEDLINE]

16. Orr WC, Sohal RS.
Does overexpression of Cu,Zn-SOD extend life span in Drosophila melanogaster?
Exp Gerontol. 2003 Mar;38(3):227-30.
PMID: 12581785 [PubMed - indexed for MEDLINE]

17: Orr WC, Mockett RJ, Benes JJ, Sohal RS.
Effects of overexpression of copper-zinc and manganese superoxide dismutases,
catalase, and thioredoxin reductase genes on longevity in Drosophila
melanogaster.
J Biol Chem. 2003 Jul 18;278(29):26418-22. Epub 2003 May 12.
PMID: 12743125 [PubMed - in process]

#11 DrEvil

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Posted 08 June 2009 - 10:39 PM

Michael thanks for your review on EOD and CR.
Certainly CR has been proven to be effective in extending mean and max lifespan and EOD not or not yet.

However not all beneficial IF effects are jsut due to some CR effect:
The IF profile of rats is very different than that of the AL (eat a lib profile) .
http://www.pubmedcen...gi?artid=156352

The IF profile of insulin levels are even stronger than those for CR and the same goes for neuroprotection mechanism.

So perhaps IF can increase mean age in humans and prevent Alzheimers, cancer etc., if not maxmium age.
Maybe humans are more prone to die from Cancer and Alzheimers. Certainly my parents and grand parents suffer and eventually die from either cancer,Heart problems and Alzheimer after the age of 75, not sure what rats die off. I would be happy to live to 100 years instead of 80 by EOD with a 10% weight reduction. EOD with 10% weight reduction is fairly easy to do . 25% weight reduction by CR not.

#12 russianBEAR

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Posted 09 June 2009 - 02:03 AM

I gotta commend those who can pull this fasting thing off.

Just the word alone makes me ridiculously hungry, plus I'm already skinny as a stick as it is - I'll probably get blown away by the wind if I do fast.

^
The above is an excuse because I can't pull it off ;)

Working on my diet now though, got to have more discipline in that.

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#13 JLL

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Posted 09 June 2009 - 07:11 AM

It's not that difficult, really. I've been doing intermittent fasting for a while now and tracked my progress on my blog. I've been doing the 24/24 version, but yesterday I started the condensed eating window version as a short experiment. Currently, I eat from about 5 PM to midnight and then fast during the night and next workday.




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