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In Brief
- For decades researchers assumed that highly reactive molecules called free radicals caused aging by damaging cells and thus undermining the functioning of tissues and organs.
- Recent experiments, however, show that increases in certain free radicals in mice and worms correlate with longer life span. Indeed, in some circumstances, free radicals seem to signal cellular repair networks.
- If these results are confirmed, they may suggest that taking antioxidants in the form of vitamins or other supplements can do more harm than good in otherwise healthy individuals.
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David Gems's life was turned upside down in 2006 by a group of worms that kept on living when they were supposed to die. As assistant director of the Institute of Healthy Aging at University College London, Gems regularly runs experiments on Caenorhabditis elegans, a roundworm that is often used to study the biology of aging. In this case, he was testing the idea that a buildup of cellular damage caused by oxidation—technically, the chemical removal of electrons from a molecule by highly reactive compounds, such as free radicals—is the main mechanism behind aging. According to this theory, rampant oxidation mangles more and more lipids, proteins, snippets of DNA and other key components of cells over time, eventually compromising tissues and organs and thus the functioning of the body as a whole.
Gems genetically engineered the roundworms so they no longer produced certain enzymes that act as naturally occurring antioxidants by deactivating free radicals. Sure enough, in the absence of the antioxidants, levels of free radicals in the worms skyrocketed and triggered potentially damaging oxidative reactions throughout the worms' bodies.
This article was originally published with the title The Myth of Antioxidants.
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14 Comments
Add CommentThis is really important news. Free radicals can potentially reduce the chance of developing type 2 diabetes? AND we shouldn't be taking antioxidant supplements, unless we have a demonstrated nutritional need? Damn, but that's relevant.
Reply | Report Abuse | Link to thisI've often wondered about the absolute idea that all anti-oxidants were harmful. If there is one thing I have learned from Sci-Am over the years is that most all conditions have exceptions. It would be ironic, that after thousands upon thousands of man-hours of study and billions of dollars spent on diets, that the best thing a person could do is "get plenty of rest, pleny of excercise, and eat a balanced diet" (author unknown, but encouraged by mothers everywhere).
Reply | Report Abuse | Link to thisI wonder if Ray Kurzweil or any of the other life extension gurus know about this?
Reply | Report Abuse | Link to thisAllow me
Reply | Report Abuse | Link to thisA bit about my discovery of CELL DIVISION! …
The cell has a nucleus with chips (nuclei) of itself in orbit.
Horizontally to the nuclei orbit, chips are flung out to produce a pole on each side of the orbit.
The cell and all its chips contain the complete make up of the species.
The nuclei orbit speed and maturity will determine the strength needed for the poles to pull the cell apart. The nuclei at a pole with all the information of the nucleus of the cell centers to the mass producing a new nucleus with its orbiting chips.
The cell Earth with one orbit, rock with two some minerals and all life with three and a new species (BRAIN) with four.
Cells are separated by their aura and will maintain to be in a packed state. In the case of giving three gallons of blood to the Red Cross the blood cells that are left are no longer packed and cell division takes place replacing what was taken (thank goodness)!
A child that does not have fast orbiting cell nuclei promoting growth will suffer from the disease ?? and will at a young age, age to old age.
The cell Earth with one orbit, rock with two some minerals and all life with three and a new species (BRAIN) with four.
Reply | Report Abuse | Link to this------
Here we go;
Quote
'Quadruple helix' DNA discovered in human cells
January 20, 2013
In 1953, Cambridge researchers Watson and Crick published a paper describing the interweaving 'double helix' DNA structure - the chemical code for all life. Now, in the year of that scientific landmark's 60th Anniversary, Cambridge researchers have published a paper proving that four-stranded 'quadruple helix' DNA structures - known as G-quadruplexes - also exist within the human genome. They form in regions of DNA that are rich in the building block guanine, usually abbreviated to 'G'.
As fas as taking the 'antioxidant' 'vitimins' goes, it was always nonsense. There has never been a proven link, nor even science that suggests the oral consumption of antioxidants results in their delivery to cells. It's as though you could eat cartilage and it would build up your cartilage. Nonsense.
Reply | Report Abuse | Link to thisBruce,
Reply | Report Abuse | Link to thisHysterical. 2013 candidate for best pseudo-scientific nonsense award. Really good stuff. I suggest adding some quantum mechanics terms. Seriously. LOL
Firstly, thanks to Quantum Biophysical Semeiotics we are able for a decade to bedside assess free radical level in every biological tissue.
Reply | Report Abuse | Link to thisSecondly, free-radicals contribute to damage mit-DNA and n-DNA, as well as cell membranes, bedside evaluated by means of assessing cell glycocalix in any biological systems.
Thirdly we can nowaday use potent free radical scavengers and substrates that are acting succesfully on both genomes, normalizing them. I think that scientists should finally talk about the function of the DNA-antenna, which I documented by the clinical method, using a simple stethoscope. This fascinating event, made possible by the presence of non-local reality, beside local reality, in biological systems, I have discovered clinically, allows us to understand why the dual mechanism of action of hormones, which irreparably undermines the dogma of Western Medicine, according to which "Corpora not agunt nisi conjuncta": (1) Stagnaro Sergio and Paul Manzelli. Semiotics Endocrinology Biophysics: Quantum Mechanics and Mechanisms of Hormone Action. December 2007, http://www.fce.it,
http://www.fcenews.it/index.php?option=com_content&task=view&id=816&Itemid=45.
To these facts, unfortunately till now overlooked, is linked the demonstration of the scientific truth of the Fractal Genome Recursive Function Principle, according to Andras Pellionisz, which I demonstrated clinically, as shows the birth of Manuel (2-3), as well as an awful number of clinical Medicine advances (4-5).
References on request.
It's old hat- has been known for decades that supplements can be a health risk. It was shown that Cancer patients can shorten their lives by taking antioxidant -supplements.
Reply | Report Abuse | Link to thisWhy not get logical, bio-logical,to be precise, and eat the REAL thing:
such as in-vivo plant pigments.
think: orange, as in: oranges, carrots, turmeric, with proven health benefits, for plants as well as humans.
Youthevity.com
Why DO those with KNOWN oxidative stress , get older , quicker.
Reply | Report Abuse | Link to thisWhite hair in those with iron excess , for example.
The conclusion , the hallowed notion that oxidative damage causes aging is being proven wrong , is partially incorrect. There is more than one cause of oxidative stress , and the mouse or worm model of oxidative stress 'may' only cover one or more of the causes of oxidative stress. Lack of vitamins causes lack of oxidation quenching potential in the body , UV radiation causes oxidation and if lacking in vitamins oxidation is not quenched , heavy metal poisoning causes oxidation and if not removed continues to cause oxidation . The documented evidence has pointed to oxidation in ageing , and so the 'type' of oxidation represented in the worm or mouse would not completely exhonerate oxidative stress.
Was mitochondrial oxidative stress in the worm model or mouse model ruled out ?
Reply | Report Abuse | Link to thisThe 'oxidative stress' in the mouse or worm tested might actually be 'superficial', in that it never actually reaches the mitochondria ?
"NOS1 is a mitochondrial NOS that reduces ROS levels, mitigates oxidative damage, and acts as an antisenescence agent"
"Self-amplifying cycle between mitochondrial and telomeric DNA damage during cellular senescence"
It 'could' be there is a 'chicken or the egg' in the oxidative stress hypothesis equation.
Reply | Report Abuse | Link to this"Increased lipofuscinogenesis"
"Consequence of lipid peroxidation, mitochondrial damage and iron accumulation"
Lipofuscin is used as THE 'marker' for ageing.
"Lipofuscin quantification is used for age determination"
The mouse or worm most likely are NOT accumulating , mitochondrial iron.
""Lipofuscin-associated iron"
Therefore the mouse or worm do not manifest 'ageing' , lipofuscin deposition , BECAUSE , the oxidative stress is not induced BY iron , but by genetic means ?
The source of the mitochondrial iron may BE , body iron levels achieved by meat eaters .
Low , moderate and high levels.
Fish and other meats allow the absorption of the metal iron.
"Enhancing effect of fish on nonheme iron uptake"
NORMALLY the body 'shuts down' absorption of iron from plants , nonheme iron but it doesn't or can't control heme iron absorption.
"Absorption of Nonheme, But Not Heme Iron, Is Substantially Reduced with High Iron Stores"
Soo , would a vegetarian have lower lipofuscin accumulation ?
"Lipofuscin-bound iron is a major intracellular source of oxidants: role in senescent cells"
"It is suggested that pulse doses of iron chelators that easily penetrate membranes could be used to diminish lipofuscinogenesis"
The theory is iron overload from meat eating.
Reply | Report Abuse | Link to this"Non-transferrin-bound iron, commonly found in the plasma of iron-overloaded individuals, permeates into cells via pathways independent of the transferrin receptor. This may lead to excessive cellular accumulation of labile iron followed by oxidative damage and eventually organ failure."
"The physiological role of occluded iron transfer might be to confer cells with a “safe and efficient cytosolic iron corridor” to mitochondria. However, such a mechanism might be deleterious in iron-overload conditions, because it could lead to surplus accumulation of iron in these critical organelles."
Instead of genetically modifying mice and worms to boost free radical levels, can free radical supplements serve to extend the lifespans of those lab animals?
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