Eat Less, Buzz Longer?
In late 2000, researchers at the
University of Connecticut Health Center announced that they had
found an altered gene that effectively doubled the life span of
certain flies. Some flies in the study lived as long as 110 days
— three times their normal life span. And perhaps more importantly,
these flies appeared to stay "middle aged" and active
for most of their lives. Female flies were able to reproduce almost
until the time they died.
The gene change — a mutation on a single fly chromosome — seems to work by preventing individual fly cells from using too many calories. Odd as this sounds, this finding agrees with decades-old research that shows that some mammals, such as mice and rats, live longer, healthier lives when they eat less. This isn't the same as a person going on a diet to lose weight, although weight loss might be a welcome side-effect. The lab animals were fed the same amount of nutrients, such as vitamins and minerals. The difference is that the experimental diet had 30 percent fewer calories. Early results of experiments on rhesus monkeys appear to confirm the earlier experiments with rodents. And now, a genetic mutation discovered in flies seems to duplicate both process and result.
"Great," your students might say. "Does the world really need flies, mice, or even monkeys that live twice as long?" Remind them that all animals are genetically similar. The same gene that makes flies live longer also exists in humans. With this gene identified, future drug therapies could attempt to extend the life span of humans to 150 active years or longer.
No More Long Division
What causes aging? There isn't
a simple answer to that. But one important aspect of aging was discovered
in the early 1960s by Leonard Hayflick. Hayflick discovered that
aging occurs on the cellular level. Cells divide and replicate themselves
over the course of our lives. However, each cell has a built-in
clock that says how many times it can divide. Beyond a certain point,
the cell ceases to be able to divide or repair itself. This loss
of the ability to divide is called cellular senescence.
An interesting aspect of research into cellular senescence has shown that the ticks on a cell's internal clock seem predetermined. This is separate from chronological time. Slowing down or stopping the cell divisions does not change the number of times the cell can divide. Cells frozen in liquid nitrogen pick up where they left off and complete the same number of divisions as unfrozen cells, as if they remember the count.
One possible cause of aging is the degradation of the telomeres, pieces of DNA that cap the ends of each chromosome. As the cell divides over and over, these telomeres become shorter and shorter. Eventually, they become so short that the cell can no longer reproduce.
Cancer cells seem to have "discovered" a way to avoid aging. Cancer cells produce their own telomerase, an enzyme that a cell can use to rebuild its telomeres and continue dividing — ignoring their own clocks. Could other cells be made "immortal" by replenishing their telomeres with telomerase?
The genetic mutation of the long-lived flies appears to have slowed down the ticking of the cell's built-in clock. Could a drug be developed that would slow down the human metabolism and mimic the effect observed in the flies?
Results of a study announced in August suggest that the "eat less, live longer" idea may actually be at work in humans. In a preliminary study of men aging in Baltimore, researchers found that men who shared the same biological "markers" as the long-lived rodents on restricted diets — lower temperatures than normal, lower insulin levels, and a steady level of a hormone called DHEAS — were dying at a slower rate than men who did not have those "markers." These men are not on a restricted diet; something about them, probably something in their DNA, makes their bodies function in a manner similar to the rats on a restricted diet or the flies with the altered gene.
For more on the Baltimore study, read the CBSNews.com story, "Eat
Less, live longer, study says."
The following Riverdeep activities can help your students understand the concepts involved in genetics and cell replication:
- Logal Science, Biology Gateways, Genes and Dominance, in which you explore genes, alleles, and the physical appearance of traits.
- Logal Science, Biology Gateways, Sex-Linked Genes, in which you follow generations of fruit flies and observe trait inheritance.
- Logal Science, Biology Explorer, From Protein to DNA, in which you find a DNA sequence from a given protein using the genetic code and investigate how genes degenerate.
- Logal Science, Biology Explorer, The Human Genome Database, in which you retrieve and analyze data from the Human Genome Database.
Think About the Problem
Have a class discussion about the social, economic, and
ethical issues surrounding aging as it exists now and as it might
exist if human life spans were lengthened. Students may not realize
that the average human only lived to around 25 years of age 1000
years ago — roughly one third the life expectancy in the United
States today. Has that increase in life span been good or bad? Is
aging natural and something to accept or is it something that either
changes naturally over time or can be changed artificially? Other
questions to consider include:
- What is the difference between a population of long-lived individuals (older, but still vital like the flies) and an aging population (older, not active, etc.)?
- What might happen if no one died?
- What if an "anti-aging" treatment were found, but was very expensive and only available to those people rich enough to afford the procedure?
Extending the Problem
This article from MEDLINEplus at the National Library of Medicine
discusses the changes in human organs, tissues, and cells during
the aging process. Some cells atrophy, or waste away, while others
enlarge or increase in number.
