Are veterinarians embracing anti-aging drugs?
Published: June 1, 2009
Updated: June 1, 2009
Q: Anti-Aging medicine is the newest clinical medical specialty offered to physicians. Human medicine is moving from a disease-based model to a preventive, proactive approach. Shouldn’t veterinarians move in this direction as well?
A: The fact is movement is already occurring. In recent years, advances in veterinary medicine have nearly doubled the lifespans of our pets. Many veterinarians have shifted towards wellness protocols that get our pets into their offices two, three or even four times a year. More visits mean more chances to find small issues before they become big problems! But, just seeing your veterinarian more often is only part of the solution.
When scientists unraveled the genetic code of dogs, they discovered humans and their canine counterparts share similar mechanisms relative to aging. As we grow older, adverse changes in our cells increase the risk of death. About a third of these changes are genetic in nature. Most, however, are due to lifestyle and environmental factors.
As systems slow down, cells deteriorate faster than the body can repair them, leading to a decline in function and changes in appearance. The American Academy of Anti-Aging Medicine states that up to 90 percent of diseases are due to the degenerative process associated with aging. So, earlier intervention by veterinarians might provide your pet with a longer, happier life.
Currently, one aging theory has become almost universally accepted. The theory states that cells accumulate damage from the presence of molecules with an unpaired electron, or free radical. This cellular damage is cumulative and leads to a loss of functionality and death. By finding ways to reduce the chaos caused by free radicals, scientists hope to lengthen the average lifespan.
Some experts point towards antioxidants as the answer to free radical damage. Antioxidants slow or even prevent the changes to cells by removing intermediary chemicals in the oxidation reaction of free radicals. Once the intermediate steps are stopped, damage is reduced or avoided. Antioxidants include compounds such as Vitamins C and E, beta carotene, retinol and melatonin. Many fruits and vegetables contain high levels of these antioxidants.
However, diet alone cannot provide the levels of antioxidants needed without seriously affecting caloric intake and causing obesity. As with most things in life, more is not always better and in some cases, excess supplementation can result in adverse side effects.
Antioxidant benefits are numerous, but the lack of standard dosages and clear research is a big concern. More studies are sorely needed. Despite this uncertainty, many pet food companies are marketing new lines of pet foods enhanced by antioxidants or touting “fresh fruits and vegetables” in their diets. “Nutraceutical” supplements are also available that add antioxidants to the pet’s diet with promises of better health.
Another way to reduce the damage from free radicals is caloric restriction, or maintaining lean body weight. Many different models, from mice and rats to fruit flies, have shown that reducing the amount of calories fed can increase life span. Even dogs have benefitted. One landmark study showed dogs kept lean using calorie restriction actually lived almost 2 years longer than their free fed counterparts. Human studies show lower cholesterol, lower blood pressure and a lower body fat percentage as benefits of limiting caloric intake.
So, what does this all mean to you and your pet? Simply put, there is no magic bullet, but veterinary science continues to investigate novel therapies and ideas to help keep our pets with us even longer. As with any medication or diet change, you should always discuss use of antioxidants or anti-aging therapy with your veterinarian. Prevention, early disease detection and prompt intervention, combined with good nutrition, exercise and regular veterinary visits are the cornerstones of your pet’s good health.
The Veterinary News Network contributed material for this week’s column.
Dr. Watts is a companion animal general practitioner and owner of Clevengers Corner Veterinary Care. He can be reached through ClevengersCorner.com or by calling 428-1000.
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Reader Reactions
This article likely contains information that is about to become obsolete. Recently this free-radical oxidation aging stuff has largely given way to aging is from mostly genetics, which is highly supported by a lot of disease and longevity is clearly genetic and inherited.
See here:
This was and is highly debatable and recently has progressed into probably being flat out wrong.
See here:
http://www.dailygalaxy.com/my_weblog/2009/05/is-aging-an-acc.html
Is Aging an Accident of Evolution? -A Galaxy Classic
“Everyone has assumed we age by rust. But how do you explain animals that don’t age? Some tortoises lay eggs at the age of 100, there are whales that live to be 200 and clams that make it past 400 years.“
Stuart Kim, PhD, Stanford University professor of developmental biology and genetics
Prevailing theory of aging challenged by Stanford University Medical School researchers. Their discovery contradicts the prevailing theory that aging is a buildup of tissue damage similar to rust. The Stanford findings suggest specific genetic instructions drive the process. If they are right, science might one day find ways of switching the signals off and halting or even reversing aging.
“We were really surprised,” said Stuart Kim, who is the senior author of the research.
Kim’s lab examined the regulation of aging in C. elegans, a millimeter-long nematode worm whose simple body and small number of genes make it a useful tool for biologists. The worms age rapidly: their maximum life span is about two weeks.
Comparing young worms to old worms, Kim’s team discovered age-related shifts in levels of three transcription factors, the molecular switches that turn genes on and off. These shifts trigger genetic pathways that transform young worms into social security candidates.
The question of what causes aging has spawned competing schools, with one side claiming that inborn genetic programs make organisms grow old. This theory has had trouble gaining traction because it implies that aging evolved, that natural selection pushed older organisms down a path of deterioration. However, natural selection works by favoring genes that help organisms produce lots of offspring. After reproduction ends, genes are beyond natural selection’s reach, so scientists argued that aging couldn’t be genetically programmed.
The alternate, competing theory holds that aging is an inevitable consequence of accumulated wear and tear: toxins, free-radical molecules, DNA-damaging radiation, disease and stress ravage the body to the point it can’t rebound. So far, this theory has dominated aging research.
But the Stanford team’s findings told a different story. “Our data just didn’t fit the current model of damage accumulation, and so we had to consider the alternative model of developmental drift,” Kim said.
The scientists used microarrays—silicon chips that detect changes in gene expression—to hunt for genes that were turned on differently in young and old worms. They found hundreds of age-regulated genes switched on and off by a single transcription factor called elt-3, which becomes more abundant with age. Two other transcription factors that regulate elt-3 also changed with age.
To see whether these signal molecules were part of a wear-and-tear aging mechanism, the researchers exposed worms to stresses thought to cause aging, such as heat (a known stressor for nematode worms), free-radical oxidation, radiation and disease. But none of the stressors affected the genes that make the worms get old.
So it looked as though worm aging wasn’t a storm of chemical damage. Instead, Kim said, key regulatory pathways optimized for youth have drifted off track in older animals. Natural selection can’t fix problems that arise late in the animals’ life spans, so the genetic pathways for aging become entrenched by mistake. Kim’s team refers to this slide as “developmental drift.”
“We found a normal developmental program that works in young animals, but becomes unbalanced as the worm gets older,” he said. “It accounts for the lion’s share of molecular differences between young and old worms.”
Kim can’t say for sure whether the same process of drift happens in humans, but said scientists can begin searching for this new aging mechanism now that it has been discovered in a model organism. And he said developmental drift makes a lot of sense as a reason why creatures get old.
“Everyone has assumed we age by rust,” Kim said. “But then how do you explain animals that don’t age?”
Some tortoises lay eggs at the age of 100, he points out. There are whales that live to be 200, and clams that make it past 400. Those species use the same building blocks for their DNA, proteins and fats as humans, mice and nematode worms. The chemistry of the wear-and-tear process, including damage from oxygen free-radicals, should be the same in all cells, which makes it hard to explain why species have dramatically different life spans.
“A free radical doesn’t care if it’s in a human cell or a worm cell,” Kim said.
If aging is not a cost of unavoidable chemistry but is instead driven by changes in regulatory genes, the aging process may not be inevitable. It is at least theoretically possible to slow down or stop developmental drift.
“The take-home message is that aging can be slowed and managed by manipulating signaling circuits within cells,” said Marc Tatar, PhD, a professor of biology and medicine at Brown University who was not involved in the research. “This is a new and potentially powerful circuit that has just been discovered for doing that.”
Kim added, “It’s a new way to think about how to slow the aging process.”
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