Eating heavy isotopes to prevent aging.

[Mr Skeptic]

According to Newscientist, it may be possible to reduce aging by eating heavier isotopes, such as deuterium and carbon-13. The mechanism is a reduction in free radical damage, as it is harder to break the bonds with heavier isotopes. Also, the isotopes could be incorporated into essential foods that our body cannot synthesize, which would ensure that they are used by the body.

 

A warning: having 20% deuterium or more in your body is bad for you, and 35% deuterium can kill. However, it seems that small quantities are safe, and in some tests increased lifespan of fruit flies. Also, it seems babies are born with an unusually high proportion of heavier isotopes.

[SkepticLance]

A recent study suggests that free radicals are not the cause of ageing. Rather spoils the heavy isotope idea.

http://www.sciencedaily.com/releases/2008/12/081201105711.htm

[npts2020]

Mr Skeptic: What is your definition of a "heavier" isotope? I am not an expert at physics or chemistry but it seems to me that deuterium and carbon-13 are among the lightest isotopes out there.

[insane_alien]

npts, yes deuterium is a light isotope when compared with things like U-238 or something but its twice as heavy as protium (H-1) which it would be replacing. smae can be applied to carbon-13.

 

I suspect that the heavier the element the less difference there will be between the different isotopes.

[iNow]

A recent study suggests that free radicals are not the cause of ageing. Rather spoils the heavy isotope idea.

http://www.sciencedaily.com/releases/2008/12/081201105711.htm

 

Indeed. Very well timed article. Thanks for sharing it, Lance.

 

In 1956, Denham Harman proposed the theory that aging is caused by an accumulation of molecular damage caused by "oxidative stress", the action of reactive forms of oxygen, such as superoxide, on cells. This theory has dominated the field of aging research for over fifty years. But now, a study published online today in the journal Genes & Development suggests that this theory is probably incorrect and that superoxide is not a major cause of aging.

 

"The fact is that we don't understand much about the fundamental mechanisms of aging," says Dr David Gems from UCL. "The free radical theory of aging has filled a knowledge vacuum for over fifty years now, but it just doesn't stand up to the evidence."

 

Dr Gems and colleagues at the Institute of Healthy aging studied the action of key genes involved in removing superoxide from the bodies of the nematode worm C. elegans, a commonly-used model for research into aging. By manipulating these genes, they were able to control the worm's ability to "mop up" surplus superoxide and limit potential damage caused by oxidation.

 

Contrary to the result predicted by the free radical theory of aging, the researchers found that the lifespan of the worm was relatively unaffected by its ability to tackle the surplus superoxide. The findings, combined with similar recent findings from the University of Texas using mice, imply that this theory is incorrect.

[Mr Skeptic]

Thanks for the info, SkepticLance.

 

From the original study: http://www.springerlink.com/content/p5654j43237g5878/

"The senescent decline that leads inevitably to death in most animal species is accompanied by a massive increase in molecular damage. Yet, the chain of events that initially causes this process, and the determinants of the rate at which it happens, remain poorly understood. For many years, much research on this topic has been guided by an interrelated set of theories that view oxidative damage as a potential primary cause of aging. These theories have framed the construction and interpretation of many studies in the nematode Caenorhabditis elegans. In this chapter, we critically survey these studies. Overall, these investigations have either disproved or, at least, failed to find clear evidence for many of the oxidative damage theories. In particular, they have failed to demonstrate any role of metabolic rate or mitochondrial superoxide (O2 •−) in aging. However, they have revealed a powerful influence of mitochondria on the rate of aging in C. elegans. This may or may not have something to do with mitochondrial O2 •− production. "

 

They only tested superoxide, but there are many more free radicals than that. I don't think the free radical theory is dead yet, but no one has considered it as the only cause of aging for ages now. Anything that causes cumulative damage would be a cause of aging.

 

Oh, I should mention, in the heavy isotope study they said an alternate explanation was that the heavy isotopes made the food less tasty, and that the increased lifespan may have been due to caloric restriction instead. It seems that heavy water tastes kind of sweet, so it is possible that the fruit flies could taste the difference too.

[SkepticLance]

There is another possible explanation also, if the isotopes are radioactive at all. Radio-hormesis is somewhat controversial, but the idea has its advocates. This suggests that a slight increase in damage to genetic material by a slight increase in background radioactivity stimulates the genetic repair mechanisms, leading to lower cancer risk and longer lifespan. Not proved, though there is some impressive evidence. The problem is that we need to carry out experiments currently classed as unethical to prove it.

[iNow]

They only tested superoxide, but there are many more free radicals than that. I don't think the free radical theory is dead yet, but no one has considered it as the only cause of aging for ages now.

 

In case you're interested, I'm pretty sure the below is the University of Texas study on mice referenced by the article:

 

 

http://dx.doi.org/10.1016/j.freeradbiomed.2007.03.034

The early observations on the rate-of-living theory by Max Rubner and the report by Gershman that oxygen free radicals exist in vivo culminated in the seminal proposal in the 1950s by Denham Harman that reactive oxygen species are a cause of aging (free radical theory of aging). The goal of this review is to analyze recent findings relevant in evaluating Harman’s theory using experimental results as grouped by model organisms (i.e., invertebrate models and mice). In this regard, we have focused primarily on recent work involving genetic manipulations. Because the free radical theory of aging is not the only theorem proposed to explain the mechanism(s) involved in aging at the molecular level, we also discuss how this theory is related to other areas of research in biogerontology, specifically, telomere/cell senescence, genomic instability, and the mitochondrial hypothesis of aging. We also discuss where we think the free radical theory is headed. It is now possible to give at least a partial answer to the question whether oxidative stress determines life span as Harman posed so long ago. Based on studies to date, we argue that a tentative case for oxidative stress as a life-span determinant can be made in Drosophila melanogaster. Studies in mice argue for a role of oxidative stress in age-related disease, especially cancer; however, with regard to aging per se, the data either do not support or remain inconclusive on whether oxidative stress determines life span.

[npts2020]

npts, yes deuterium is a light isotope when compared with things like U-238 or something but its twice as heavy as protium (H-1) which it would be replacing. smae can be applied to carbon-13.

 

I suspect that the heavier the element the less difference there will be between the different isotopes.

 

Ahhh. Thanks for the further explanation.

 

IMO if what you are saying is true at all, it is only true for certain (and probably few) elements. As mentioned many isotopes are radioactive, most of those enough to negate any positive effect they might have. eg. strontium-90, if present in large enough amounts, preferentially takes over for calcium in bone building and can cause leukemia and other bone and blood related disorders. The list of isotopes causing similarly deleterious effects is quite long.

[vampares]

having 20% deuterium or more in your body is bad for you, and 35% deuterium can kill.

 

I was completely unaware of that. I knew it could **** up a bicycle race ...

[John Cuthber]

This is an interesting notion. It seems to rest on the idea that the reactions associated with aging are slowed down by deuteration of the molecules.

That might be true- I' don't know.

However, most of the reactions in the body are associated with living, rather than aging.

Do these reactions get slowed down too? Is the relative slowing the same for the two sorts of reactions?

Would it just be a case of live fast; die young vs live slow; die old?

 

If anything, the toxicity of heavy water might be because some reactions are slowed down more than others and things get out of step.

Since the so called kinetic isotope effects are reasonably well documented and are very variable this is entirely reasonable.

[Mr Skeptic]

Well, most of the hydrogen in the body is either in water or in fairly unused parts of proteins. If you replaced the hydrogen in the active site of a protein with deuterium though, that would likely mess up the enzyme. He claims that if the deuterium is ingested as certain molecules that the deuterium would remain in the same location as a stronger bond, which he says might lower the toxicity. So long as his idea lowers the amount of damage to biomolecules without ruining their usefulness, it seems like a good idea even if it doesn't prevent aging.

[Mokele]

It's not worth getting excited about yet - it's just a hypothesis. Once there's experimental evidence, then we can all break out the C-14 cake. It shouldn't be too hard - six populations of standard-bred lab mice, 3 control and 3 experimental, with the experimental mice fed isotope-laced food. Given the short lifespan of mice, it would be very feasible experiment, and even with the cost of isotope-laced food, would cost less than many, many other studies.

 

Mokele

[Mr Skeptic]

Well, they already did it with fruit flies. Still, a lot more testing would be required, especially in mammals. Also, I'm pretty sure that 6 mice is not enough for statistical experiments. They are planning on doing more testing, and I will keep an eye out for it.

[Mokele]

Well, they already did it with fruit flies. Still, a lot more testing would be required, especially in mammals. Also, I'm pretty sure that 6 mice is not enough for statistical experiments. They are planning on doing more testing, and I will keep an eye out for it.

 

6 populations, not 6 mice, in order to keep them in different buildings and such and thereby reduce the risk of psuedoreplication (a weird statistical problem).

 

Flies are suggestive, but yes, mammals would be better.

 

Mokele

[John Cuthber]

It's not worth getting excited about yet - it's just a hypothesis. Once there's experimental evidence, then we can all break out the C-14 cake. It shouldn't be too hard - six populations of standard-bred lab mice, 3 control and 3 experimental, with the experimental mice fed isotope-laced food. Given the short lifespan of mice, it would be very feasible experiment, and even with the cost of isotope-laced food, would cost less than many, many other studies.

 

Mokele

 

I will stick to C13 cake thanks. I might not live as long, but I won't glow in the dark.

But you are right, without a lot of long term study this is almost pure speculation.