- The Chicago Public Library found that a third of their economically disadvantaged members had been denied borrowing privileges due to overdue books.
- Overdue fines account for a tiny fraction of library funding, so the ramifications of ending them are more social than financial.
- Though 92% of U.S. libraries still charge late fees, the number is shrinking.
Whether we're out to quench a thirst for information or lose ourselves in story, checking out a book from a public library may start the first tick of a worrisome clock. It's the time interval in which the book has to be read and returned before the imposition of a rapidly accumulating late-return fee begins. Though the fees are generally fairly small, the threat of them does introduce a measure of pressure that can be just enough to make some — especially those stretching each dollar — decide not to bother in the first place. This is especially true for people who would also have to lay out money to get themselves to the library in the first place.
Late fees conflict with the reason we have public libraries as stated at the opening of the first public library in the U.S.:
"Above all…the first regard should be shown…to the wants of those, who can, in no other way supply themselves with the interesting and healthy reading necessary for their farther education."
With wealth inequality continuing to accelerate in the U.S., more and more libraries around the country are reconsidering the negative effect of late fees. In October, the largest public library in the U.S., the Chicago Public Library, announced they were doing away with them. (92% of U.S. libraries still have late fees.)
The purpose and history of public libraries
The Boston Public Library
Image source: Mark Zhu/Shutterstock
"Of all the human arts, that of writing, as it was one of the earliest invented, is also one of the most important. Perhaps it would be safe to pronounce it, without exception, the most useful and important. It is the great medium of communication between mind and mind, as respects different individuals, countries, and periods of time. We know from history that only those portions of the human family have made any considerable and permanent progress in civilization, which have possessed and used this great instrument of improvement." — First trustees report, Boston Public Library, 1854.
The first public library in the U.S. was the Boston Public library, and the quote immediately above laying out its purpose — as well as the quote in the previous section — were written in its report to library trustees as the library opened its doors to the general population in 1854.
Prior to this, libraries were mostly personal book collections, at best available only to an owner's family, friends, and associates.
Benjamin Franklin owned over 4,000 books, and in 1731 created the first subscription library, or "social library," as a means of exchanging books within Philadelphia's literary society. In 1762, William Rind in Annapolis, Maryland, opened the first circulation library, an innovation that saw print shops and bookstores renting out books. School libraries provided reading materials to their students.
In 1833, the first organization we might recognize as a public library was started in Peterborough, New Hampshire, as the result of an unexpected windfall. New Hampshire had raised tax money for a state college that never made it off the ground and had to find something education-related to do with the money — they disbursed it to towns around the state. Peterborough used its share for a library for its citizens. It was a well-received idea, and in 1849, the state became the first to enact a law empowering municipalities to raise tax money for libraries.
Just five years later the first truly public library opened in Boston.
Chicago Public Library’s announcement
Mural on Chicago's South Side
Image source: Terence Faircloth/Flickr
Chicago Public Library Commissioner Andrea Telli told the Chicago Sun-Times, "I think our staff members are going to be practically jumping over their circulation desks to tell people that fines have been eliminated."
They'll also want to get word out to the 343,208 former patrons who've lost their library privileges to overdue fines. Data recently collected by the library reveals that one in three cardholders in the city's low-income South District is among that number. One in five of those is under 14, children who would benefit from access to the library's books. In more affluent areas, by contrast, just one in six cardholders has been penalized.
Eliminating the fines aims to return the library system to those most in need of it. Telli said, "We're removing one of the most important barriers."
Mayor Lori Lightfoot, who supports the change, said in a statement, "Like too many Chicagoans, I know what it is like to grow up in financially challenging circumstances and understand what it is like to be just one bill or one mistake away from crushing debt."
Chicago is not alone in finding late fees disproportionately affecting its less-monied cardholders. In San Francisco, whose own San Francisco Public Library got rid of late fees last month, 5% of members could no longer borrow, with the majority of them living in low-income communities, African-American communities, and areas with fewer college graduates. Each of those who'd lost library privileges, on average, owed about $24 in late fees.
Curtis Rogers of the Urban Libraries Council told CityLab's Linda Poon, "Overdue fines are not distinguishing between people who are responsible and who are not. They're distinguishing between people who can and cannot use money to overcome a common oversight."
Why bother charging late fees anyway?
Image source: Thought Catalog/Unsplash
Libraries cost money. Books must be purchased, facilities paid for, and staff compensated. Nonetheless, late fees constitute just a tiny fraction of a library's budget. As a big library system, the Chicago Public Library collects nearly a million dollars each year through fines, but that represents less than 1% of their annual budget. Rogers says the impact of fees' elimination has proven negligible for other libraries, and may even save them money since personnel and time no longer need to be allocated to collecting them.
Some consider overdue fees a form of discipline that can reduce the number of books lost to people who never return them, though a 1983 study found that this isn't so over time. And, in any event, says Dawn Wacekof of La Crosse Public Library in Wisconsin, "I don't think it's our task, or that it's mission-centric, any more than teaching people manners is. Our role is to provide access to information."
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."
