A Diet of Old Tissues Modestly Shortens Life Span

In an interesting series of experiments, researchers found evidence for a diet of old tissues to modestly reduce life span in flies and mice. If speculating on specific mechanisms, we might look to the various forms of metabolic waste and damaged proteins that accumulate with age; some of that might find its way past the digestive process to be incorporated into tissues and thereby accelerate the aging process. This sort of dietary influence on aging is already a much-debated topic regarding advanced glycation end-products, for example. The results of the studies here offer reinforcement for the SENS approach of damage repair to create rejuvenation, but sadly that is not the conclusion reached by the researchers involved. They instead look ahead to a much harder task with the prospect of only marginal benefits, which is to say safely altering cellular metabolism in order to slow down damage accumulation. This is an inferior approach to periodic damage repair, requiring far more research to realize, and capable of producing only lesser gains in health and life span.

A study offers evidence bolstering one long-held theory: that aging is caused, at least in part, by molecular damage accumulating in the cells. This damage is generated by nearly every cellular process by the work of enzymes and proteins and the life-sustaining metabolic processes that occur at every level of complexity, from simple molecules and cell components to whole cells and entire organs. Over time we have many, many damage forms, byproducts of enzyme function, for example, or of protein-to-protein interactions, errors in DNA transcription or translation. As a function of age, they accumulate, and eventually, it's more than the body can cope with.

Researchers found that feeding a diet of "old" organisms to yeast, fruit flies, and mice shortened their lifespans by roughly 10 percent. Here's how it worked: for yeast, the researchers formulated one cell-culture medium composed of extracts from young yeast cells and another of extracts from old ones. They then grew new yeast cells on each medium and watched to see which set would live longer. "Our hypothesis was that as yeast ages, it accumulates certain damage forms, and we wanted to test that specific damage and find out if it is deleterious for yeast."­­­­ The team replicated the same basic procedure in fruit flies and mice: they collected 5,000 freshly dead flies that had lived an average of 45 days, and sacrificed 5,000 others that were three to five days old. Then they prepared two homogenized diets, one composed of young flies and the other using the old ones. They fed these diets to young female fruit flies. The mice were fed diets of skeletal muscle from young and old farmed red deer (three years old versus 25) that replaced the animal-product components (insects, carrion, worms, etc.) of a normal mouse diet. Using mouse tissue was not feasible because of the large quantities needed for the experiment; deer meat was a suitably close match.

The experiments raise new questions - in a field that's full of them - and some of the results were a little unexpected. The researchers had expected to see larger differences in the test organisms' relative lifespans. The effect was consistent, however, across all three species. In the study, the authors interpret the minor-but-consistent effect to mean that damage accumulation may be only one contributing factor in aging, and also that damage caused by internal molecular changes may have a stronger effect than damage introduced through the diet. It's also likely that the damage arises from many processes. "And they all work together in a deleterious way. So the question is, how do we slow down this process? How do we restructure cellular metabolism so that this damage accumulates at a slower rate?"

Link: http://harvardmagazine.com/2017/02/old-food-reduces-lifespan

Comments

Not exactly related to the post, but I saw that David Spiegel was awarded a grant of up to 1.625 million by the American Diabetes Association for his research on targeting glucosepane crosslinks. It's nice to see more than just the SENS foundation funding his work. Hopefully we see more of this in the future. Here's the link to the story: http://www.diabetes.org/newsroom/press-releases/2017/american-diabetes-association-2017-pathway-winners.html

And here's a link to the grant description:

http://www.diabetes.org/pathway/recipients/

Posted by: Empirical at February 20th, 2017 9:27 AM

I think they'll never get it.
Articles like these can only serve as proof towards the inability of mainstream academia to make a simple deduction even-though the answer is plain to see for everyone else.

Posted by: Anonymoose at February 20th, 2017 3:08 PM

Wow, very good news, Empirical! I read somewhere that they needed around $100k per year to continue their research on glucosepane at full speed. So this grant should be more than enough.

Posted by: Antonio at February 20th, 2017 4:15 PM

I theorised this a few years ago. Based on that the body accumulates damage, I also thought that the meat we eat have accumulated damage and that this might add up to our own damage. I also understood that in vitro meat will be more healthy.
Luckily there are a few companies working on in vitro meat, Modern Meadow, New Harvest, Memphis Meat.

Posted by: Norse at February 20th, 2017 4:31 PM

@Norse
The old meat in the study was from 25 year old red deer, which I estimate to be equivalent to a human in their 70s or 80s (I can only speculate this was a zoo animal or something similar). It seems reasonable to assume that the damaged proteins would accumulate in the meat in a somewhat linear manner, and that the farmed meat we buy is a lot closer to "young" then it is to "old" since Cows, Hogs, chicken, etc are generally slaughtered shortly after reaching full size, long before they would be considered old. So I am not seeing a big difference (accumulated damage wise) between in vitro meat and our current farmed meat.

I would like to see a comparable study using the same young meat as a control, vs. the same meat cooked at high temperature, I would speculate that there is more damage done to the meat via cooking that from just aging. Which is why I eat almost all my meat rare, and steamed.

Posted by: JohnD at February 21st, 2017 2:37 PM

AFAIK, proteins are broken into small peptides (2-3 aminoacids) before being absorbed by intestinal tract cells, and further broken into aminoacids before being released into the bloodstream. So what is this damage made of?

Posted by: Antonio at February 21st, 2017 3:09 PM

@Antonio: Good questions. Asked myself. I guess it is lipofuscin and the 7 damages that SENS postulates?

Posted by: Norse at February 21st, 2017 4:35 PM

The 7 damages?? Senescent cells? Telomeres?

Posted by: Antonio at February 21st, 2017 4:55 PM

@Antonio
It is a good question. Probably something the animals couldn't digest.
Depending on what digestive enzymes the animals in question have, seeing how all three of the species couldn't digest whatever it is that made them age faster it should be a pretty easy thing to answer for a specialist.

If the test animals are a close analogue to humans then the answer is easy - we have a hard time digesting fibrous proteins and some sugars. So - some AGEs and cross-linked proteins and quite possibly some protein plaques with a fibrous structure as well.

Posted by: Anonymoose at February 22nd, 2017 3:33 AM

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