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Smell of food cancels CR's benefits in fruit flies


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#1 JLL

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Posted 30 October 2008 - 06:55 PM


Just ran into this one, though it's more than a year old:

Evidence began mounting as long as 70 years ago that restricting calories while consuming necessary amounts of sustenance could increase one's life span. Since then, a group called the North Carolina-based Calorie Restriction Society has sprouted whose 1,800 members routinely down about half of the daily caloric intake recommended by the Food and Drug Administration (FDA) in the hope of living to the ripe old age of 120. New research may prompt the organization to send out nose plugs with its next newsletter.

A team of scientists at the Baylor College of Medicine in Houston, New Mexico State University at Las Cruces and the University of Houston found that the average life span of fruit flies on restricted diets decreased when they were exposed to food odors. The findings, according to lead researcher Scott Pletcher of Baylor's Huffington Center on Aging, suggest that the flies are "actually perceiving the environment," thinking they are in a nutrient-rich place and then their bodies are "adaptively responding to it." The results imply there is likely some olfactory component affecting humans on caloric restriction diets as well.

Pletcher's group exposed two lab strains of fruit flies on caloric restriction to smells created by live yeast, an important constituent of the fly's diet. These flies died three to 10 days sooner—a 6 to 18 percent reduction in life span—than flies on the same diet that did not get a whiff of the yeast. Their life spans were further shortened if the flies actually ate the yeast paste.


Pletcher says the smell of yeast only had an effect on the life spans of dieting flies and not on those that were fully fed and likely already perceived their immediate environment to be nutrient-rich. "If you're in what might be considered an alternative physiological state that is associated with long life span under diet restriction, then the foods have some effect," he says, noting "that suggests that there's some interaction because the odorants aren't having the same effect in all environments."

To determine if smell alone has an effect on longevity, Pletcher's team created a fruit fly strain that had a particularly sensitive olfactory receptor inhibited. Fully fed female flies with an impaired sense of smell exhibited an average life span increase of 56 percent compared with unaltered wild females. Males also lived longer than their wild counterparts. Pletcher says this indicates that odor-mediated aging and dietary effects on aging probably share some of the same physiological pathways.

Brown University ecologist Marc Tatar says the current study, published in this week's Science, provides "really profound evidence" that longevity is controlled not by actual resources but rather by hormones that are cued to resources (such as the way plants sense winter by sunlight changes). "It's like the whole system doesn't actually function on the currency of resources anymore, it all functions on virtual data about what the resources should be like," he says. "It's mind over matter."

Pletcher agrees with that analysis, at least in part. "Some component is due to perception," he says, "and another large component is actually consumption." But given the effect that eating versus smelling yeast had on longevity, he says, "Overall, I would guess consumption has a bigger effect than perception, that's for sure."


http://www.sciam.com...of-a-calorie-wh

I've been wondering whether smelling or being around food has an effect on the benefits of CR/IF; like the researchers hypothesize, maybe the smell signal is enough to trick the brain into thinking there's plenty of food around, and thus the stress response from adaptation is negated.

Then again, if a smell of food is enough to do that, what about the fact that anyone not living in a cave in the middle of the forest would always know that if they truly needed food, it's there for the taking? Would that fool (or rather, un-fool) the brain as well?

Any thoughts?

#2 Michael

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Posted 30 October 2008 - 07:54 PM

I would ignore studies on aging -- and CR in particular -- in non-mammalian species, despite all the hype they've received in recent years.

Drosophila, for instance, don't develop cancer, their entire bodies being composed of post-mitotic cells, and also don't accumulate mitochondrial mutations as they age (1); moreover, there are a zillion things (including many dietary and genetic antioxidant manipulations, or even putting the little bastids in the 'fridge!) that extend their lives that definitely do not work in mammals.

Similarly in C. elegans: again, they have bodies that when mature are composed entirely of postmitotic cells, so they don't develop cancer; they have little to no turnover of their mitochondria (a feature in our own cells that is central to Dr. de Grey's mitochondrial free radical theory of aging); with aging, they therefore end up often apparently dying of muscle failure, leading to the inability to eat and subsequent starvation -- and to take the distinction even further, this is apparently not due to the kind of stochastic factors that contribute to mammalian sarcopenia, but to developmental transitions leading to an ultimately functionally unsustainable process (2).

There is of course a substantial phylogenetic distance between either of those organisms and humans, which is why drug research, even when it involves C. elegans or Drosophila for early screening, always goes through mice before advancing to even early clinical trials. This is particularly so for most diseases genuinely involving aging (as opposed, eg, to finding cognitive enhancers that exploit mechanisms of learning & memory that could in principle be applied to correct failing memory, but equally might work in the young -- ie, make up for decrements, but aren't actually disease-modifying (in this case, the disease being biological aging). So, for instance, vaccines to remove beta-amyloid were never tested in these to begin with, because they were just never a good model for the disease, and are now already in advanced (Phase III) human clinical trials; we certainly can't include them in any fly longevity program, because they just don't have Abeta plaque or toxic oligomers to remove. Etc.

References
1. de Grey AD. Mitochondrial mutations in vertebrate aging. In Cutler RG, Rodriguez H (eds). Critical Reviews of Oxidative Stress and Aging: Advances in Basic Science, Diagnostics and Intervention. 2002; River Edge, NJ: World Scientific Publishing, 437-451.

2. Herndon LA, Schmeissner PJ, Dudaronek JM, Brown PA, Listner KM, Sakano Y, Paupard MC, Hall DH, Driscoll M.
Stochastic and genetic factors influence tissue-specific decline in ageing C. elegans.
Nature. 2002 Oct 24;419(6909):808-14.
PMID: 12397350 [PubMed - indexed for MEDLINE]

3. Johnston J, Iser WB, Chow DK, Goldberg IG, Wolkow CA.
Quantitative image analysis reveals distinct structural transitions during aging in Caenorhabditis elegans tissues.
PLoS ONE. 2008 Jul 30;3(7):e2821.
PMID: 18665238 [PubMed - in process]




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