A whale shark off the coast of Donsol.
- Scientists have finally determined the age of whale sharks using radioactive elements from bomb tests.
- Using the new data, the age range of the animals' bones has now been determined.
- The findings will help conservationists better maintain whale shark populations.
There are some things that you presume science already knows and may be surprised to learn it doesn't. One seemingly simple thing was resolved this week, as scientists finally put an age range on whale sharks by dating the slightly radioactive carbon-14 isotope their bones collected after Cold War atomic bomb tests.
Majestic whale sharks, the gentle giants of the shark family.
Weighing in at 9 tons (20,000 pounds) and typically growing to around 10 meters (32 feet) long, the whale shark is the largest living species of fish. Despite the name, it is not a whale, though it is the size of one. Like many kinds of whales, it filter feeds on plankton.
Many things about the whale shark have remained unknown to science; how long they can live, their mortality rate, and how exactly to determine the age of a specimen from its remains was chief among them. However, these questions are now a little closer to being settled. In a study recently published in Frontiers in Marine Science, scientists explain how they were able to date the bones of two whale sharks who met their fate earlier than they may have expected.
Like trees, whale sharks' bones have growth rings. Scientists have known about these rings for a while, but how quickly the rings grow has been unknown. It is difficult to use them to estimate the age of a shark if you aren't sure how much time each ring represents.
A whale shark vertebra from Pakistan, in cross section, showing 50 growth bands
Image: © Paul Fanning, Pakistan node of the UN Food and Agricultural Organisation
This is where carbon-14 comes in. As a result of nuclear bomb tests during the Cold War, large quantities of carbon-14 were put into the oceans. The isotope slowly made its way up the food web and into the bodies of larger animals. Knowing the yearly changes in the amount of carbon-14 in the oceans due to bomb testing, scientists merely had to compare that data with the changes seen in the sharks' bones.
"We found that one growth ring was definitely deposited every year," said Dr. Mark Meekan of the Australian Institute of Marine Science in Perth, a co-lead on the study. "This is very important, because if you over- or under-estimate growth rates you will inevitably end up with a management strategy that doesn't work, and you'll see the population crash." This means the sharks used in this study were around 35 and 50 years old at the time of their deaths.
Working forward from there, the scientists were able conclude that the animals may have an age range of 100-150 years. "Earlier modelling studies have suggested that the largest whale sharks may live as long as 100 years," Dr. Meekan explained in a statement. "However, although our understanding of the movements, behaviour, connectivity and distribution of whale sharks have improved dramatically over the last 10 years, basic life history traits such as age, longevity and mortality remain largely unknown. Our study shows that adult sharks can indeed attain great age and that long lifespans are probably a feature of the species. Now we have another piece of the jigsaw added."
Whale sharks are an interesting species that many eco-tourists want to see. Conservation efforts for them rely on having accurate data on their longevity, mortality rate, and the age of specific animals. This information will help those managing ocean preserves keep the population stable for future generations to enjoy.
Reactive oxygen species (ROS) accumulate in the gut of sleep-deprived fruit flies, one (left), seven (center) and ten (right) days without sleep.
- A study provides further confirmation that a prolonged lack of sleep can result in early mortality.
- Surprisingly, the direct cause seems to be a buildup of Reactive Oxygen Species in the gut produced by sleeplessness.
- When the buildup is neutralized, a normal lifespan is restored.
We don't have to tell you what it feels like when you don't get enough sleep. A night or two of that can be miserable; long-term sleeplessness is out-and-out debilitating. Though we know from personal experience that we need sleep — our cognitive, metabolic, cardiovascular, and immune functioning depend on it — a lack of it does more than just make you feel like you want to die. It can actually kill you, according to study of rats published in 1989. But why?
A new study answers that question, and in an unexpected way. It appears that the sleeplessness/death connection has nothing to do with the brain or nervous system as many have assumed — it happens in your gut. Equally amazing, the study's authors were able to reverse the ill effects with antioxidants.
The study, from researchers at Harvard Medical School (HMS), is published in the journal Cell.
An unexpected culprit
The new research examines the mechanisms at play in sleep-deprived fruit flies and in mice — long-term sleep-deprivation experiments with humans are considered ethically iffy.
What the scientists found is that death from sleep deprivation is always preceded by a buildup of Reactive Oxygen Species (ROS) in the gut. These are not, as their name implies, living organisms. ROS are reactive molecules that are part of the immune system's response to invading microbes, and recent research suggests they're paradoxically key players in normal cell signal transduction and cell cycling as well. However, having an excess of ROS leads to oxidative stress, which is linked to "macromolecular damage and is implicated in various disease states such as atherosclerosis, diabetes, cancer, neurodegeneration, and aging." To prevent this, cellular defenses typically maintain a balance between ROS production and removal.
"We took an unbiased approach and searched throughout the body for indicators of damage from sleep deprivation," says senior study author Dragana Rogulja, admitting, "We were surprised to find it was the gut that plays a key role in causing death." The accumulation occurred in both sleep-deprived fruit flies and mice.
"Even more surprising," Rogulja recalls, "we found that premature death could be prevented. Each morning, we would all gather around to look at the flies, with disbelief to be honest. What we saw is that every time we could neutralize ROS in the gut, we could rescue the flies." Fruit flies given any of 11 antioxidant compounds — including melatonin, lipoic acid and NAD — that neutralize ROS buildups remained active and lived a normal length of time in spite of sleep deprivation. (The researchers note that these antioxidants did not extend the lifespans of non-sleep deprived control subjects.)
Image source: Tomasz Klejdysz/Shutterstock/Big Think
The experiments
The study's tests were managed by co-first authors Alexandra Vaccaro and Yosef Kaplan Dor, both research fellows at HMS.
You may wonder how you compel a fruit fly to sleep, or for that matter, how you keep one awake. The researchers ascertained that fruit flies doze off in response to being shaken, and thus were the control subjects induced to snooze in their individual, warmed tubes. Each subject occupied its own 29 °C (84F) tube.
For their sleepless cohort, fruit flies were genetically manipulated to express a heat-sensitive protein in specific neurons. These neurons are known to suppress sleep, and did so — the fruit flies' activity levels, or lack thereof, were tracked using infrared beams.
Starting at Day 10 of sleep deprivation, fruit flies began dying, with all of them dead by Day 20. Control flies lived up to 40 days.
The scientists sought out markers that would indicate cell damage in their sleepless subjects. They saw no difference in brain tissue and elsewhere between the well-rested and sleep-deprived fruit flies, with the exception of one fruit fly.
However, in the guts of sleep-deprived fruit flies was a massive accumulation of ROS, which peaked around Day 10. Says Vaccaro, "We found that sleep-deprived flies were dying at the same pace, every time, and when we looked at markers of cell damage and death, the one tissue that really stood out was the gut." She adds, "I remember when we did the first experiment, you could immediately tell under the microscope that there was a striking difference. That almost never happens in lab research."
The experiments were repeated with mice who were gently kept awake for five days. Again, ROS built up over time in their small and large intestines but nowhere else.
As noted above, the administering of antioxidants alleviated the effect of the ROS buildup. In addition, flies that were modified to overproduce gut antioxidant enzymes were found to be immune to the damaging effects of sleep deprivation.
The research leaves some important questions unanswered. Says Kaplan Dor, "We still don't know why sleep loss causes ROS accumulation in the gut, and why this is lethal." He hypothesizes, "Sleep deprivation could directly affect the gut, but the trigger may also originate in the brain. Similarly, death could be due to damage in the gut or because high levels of ROS have systemic effects, or some combination of these."
The HMS researchers are now investigating the chemical pathways by which sleep-deprivation triggers the ROS buildup, and the means by which the ROS wreak cell havoc.
"We need to understand the biology of how sleep deprivation damages the body so that we can find ways to prevent this harm," says Rogulja.
Referring to the value of this study to humans, she notes,"So many of us are chronically sleep deprived. Even if we know staying up late every night is bad, we still do it. We believe we've identified a central issue that, when eliminated, allows for survival without sleep, at least in fruit flies."
