Meteorologists call them “mammary clouds” – nebulous, celestial udders that portend looming change. So called for their resemblance to breasts, a gang of these big-bosomed ladies thundered into town late this afternoon like roller-derby queens, hip-checking the last remnants of summer and letting everybody know who was boss. With the dog days out of play, fifty shades of gray heavens and a notable chill followed.
The clouds didn’t really look like breasts to me, at least not the pair I know best, so the moniker seems ill fitting. No, they resembled a sea – the underside of one. The clouds’ crests and troughs undulated in billowing mounds, like waves suspended in the sky, pearly gray, and brushed in a soft, matte finish. It seemed an entire ocean had ascended into the firmament.
The lyrics of a song from the 70s came to mind:
The ocean is a desert with its life underground And a perfect disguise above…
Of course, the lyricists were probably stoned and experiencing a hallucinogenic event, but it’s a wondrous, cerebral concept to consider.
I’m not the first person to look to the heavens for inspiration. Ancient peoples worshiped celestial bodies – sun, moon, stars – dancing in goat leggings and sacrificing their children in rapturous praise. And, although clouds figured prominently in many religious stories, with spiritual beings appearing in vapors and such, nobody, it seems, worshiped the nebulous mists. Too flighty, too unpredictable, too risky? Perhaps that’s why I like clouds so much. They seem to suffer from a sort of atmospheric ADHD. Never a dull moment with clouds, I say.
As the afternoon waned, I marked the passing of time by the clouds’ changing hues and roiling shapes, subtly back-lit by a heavily veiled sun. But true to form, the heavenly tide began to turn by evening, and when I searched the skies this morning, my sea of clouds was gone, leaving behind a cliché blue sky.
They’ll be back.
This blog is dedicated to my grandmother – “Granny” – with whom I used to cloud gaze.
In the early morning darkness of the moss-draped forests of the Florida Panhandle, teenager Bob Baxter hobbled down a dusty, one-lane gravel road. Blood soaked the back of his jeans and trickled down into his coarse leather shoes. A few hours earlier, he’d been caught running away from the Florida Industrial School for Boys, a reform school in the small, Jackson County town of Marianna. His punishment: a beating with a wooden paddle. “I got twenty-five or twenty-six licks,” recalls Baxter.
The year was 1950, corporal punishment was legal in state-run institutions, and this was no ordinary paddle. Roughly two feet long and three inches wide, the three-quarter-inch thick board was pocked with a network of holes that reduced drag during the disciplinarian’s downward stroke – more bang for the buck, so to speak. The board scraped the rough plaster ceiling with each strike. “You could hear that board coming across the ceiling, click-click-click. Then they hit you right on your butt,” says Baxter. “After about four or five licks, you were numb.”
Halfway to the low brick cottage that served as his temporary home, the boy made a decision: Run. Once again, he escaped into the thick underbrush.
The first time Baxter ran away he managed to last four days until hunger forced him out of the snake-infested swamps east of the school. But this time, already weak and exhausted, his bloodied buttocks painful and raw, he lasted only two days. School officials found him, took him back to the school, and beat him again. He woke up in the school infirmary. He never ran away again.
Baxter, now 83, lives in Ocala, Florida, just a few hours’ drive from Marianna. He spent ten months in the school, until an aunt arranged his release. The official Record of Inmates from 1950 lists the names of all the boys sent to the school during that period and the reasons for their incarceration. Offenses ranged from the serious (armed robbery) to the mundane (incorrigibility). The entry next to Baxter’s name, in beautiful looped penmanship, reads, “Growing up in idleness and crime.” Baxter maintains that his alcoholic mother married a man who didn’t want Baxter around, so the two fabricated a story to have the boy – then sixteen – sent to the school. Under the column titled “Term,” it reads, “Until legally discharged.” In other words, indefinitely.
Dubbed “the place where Satan has his seat” by former slaves and Civil War-era Reconstructionists, Jackson County, Florida, had a dark past. A vibrant culture of meanness lurked and thrived in the towns and woods there, and the Ku Klux Klan was pervasive. In 1934, Marianna was the scene of one of the most horrific lynchings in the history of the state, when a young black man, Claude Neal, was castrated, murdered, dismembered, and hung up for display in the town square. Marianna seemed an unlikely place for a reform school.
Later named the Arthur G. Dozier School for Boys, in honor of one of the school’s superintendents, the Florida Industrial School for Boys had a similar dark past. Whistleblowers – past employees, state psychologists, and former inmates – had come and gone for more than a century with no enduring change. But in 2008, a Miami Herald reporter broke the story on the school’s century-long abuses, and a series of follow-up articles in the St. Petersburg Times [now the Tampa Bay Times] revealed even more atrocities – beatings, whippings, forced labor, and rapes – committed in the name of “reform.” The school finally closed in 2011, after investigations by the Florida Department of Law Enforcement and the United States Department of Justice confirmed the allegations.
What kind of person does these things to another human being?
Quite often, it’s the sadists among us.
These “everyday sadists” are part of a constellation of malevolent personalities that exists in society. Collectively known as the Dark Tetrad, a term coined by University of British Columbia psychologist Del Paulhus, this nasty quartet includes the narcissist, the Machiavellian, the psychopath, and the everyday sadist. Paulhus explains that these monsters aren’t necessarily in jail or therapy (although they might benefit from the latter) and they survive, even thrive, in everyday society.
Sadists, however, stand out from the group because they live to cause pain. They hurt others, emotionally or physically, just for the self-indulgent pleasure it provides.
The common view of sadism associates the behavior solely with aberrant sexual practices or violent criminal activities. But finding pleasure in cruelty is far more humdrum and frequently manifested among normal, everyday people. In reality, many people exhibit some degree of sadism, albeit on a continuum. These workplace tormenters, school bullies, and Internet trolls lust after cruelty and actively expend time and resources to execute their harms. “Every dark personality’s motivation is usually power, ego, status, or recognition,” says Dan Jones, a psychologist at the University of Texas at El Paso who studies the Dark Tetrad. “But the sadist’s [motivation] is to watch other people be in pain.”
Most of the dark personalities endure across cultures and age groups and seem to hold some evolutionary leverage even in today’s world. But sadism doesn’t bring any unique clout to the evolutionary table, according to Jones. “Sadists are engaged in the suffering of others. That is their end goal.”
Eventually, nearly every discussion of sadism comes back to the Gordian knot of nature versus nurture. That is, are sadists born or made?
Behavioral genetic studies suggest that heredity plays a significant role in sadism, according to Paulhus. And brain scans reveal differences in neurobiological structures and in activity patterns in the sadist’s brain.
Why have sadists persisted in the gene pool? Paulhus thinks that the sadist’s lack of empathy likely conferred early social advantages whose dividends resulted in reproductive – and therefore evolutionary – success. An openly cruel, vicious person would gain the upper hand in a group, allowing him or her to rise in social, political, and sexual power.
But interplay between a person’s natural predispositions and how they choose to cope with challenges and adversity plays a role in sculpting personality, according to clinical psychologist George K. Simon. “The same thing can happen to two different individuals and, depending on how they’re wired, they’ll turn out differently.” Simon adds that the brain is amazingly adaptable, even into adulthood, so it’s difficult to say how much of adult behavior, including sadism, is due to nature and how much is nurture.
Whether they’re born or made, sadists often seek out certain types of “enforcer” jobs, such as police officers, school deans, prison guards, and military personnel. That’s a troubling thought for Paulhus. “Sadistic types might gravitate toward [these jobs] because they would have the power to hurt others,” says Paulhus. “They could even be assigned roles where the idea is to hurt people, but they might push it too far.” Paulhus suggests that recent incidents involving police brutality and misconduct underscore the need for appropriate screening for sadistic tendencies in law enforcement job applicants. Most sadists live dual existences, compartmentalizing their mean streaks from their more socially acceptable lives, making identifying them difficult.
University of Texas at El Paso psychologist Dan Jones’ research focuses on finding ways to protect people from the harmful effects of the sadists among us. “Understanding [sadists] is the first step in trying to empower people to prevent exploitation.” Jones hopes to identify ways to deal with these characters so innocent people don’t fall prey to them, but he’s a long way from formulating any conclusive strategies.
Many of the boys who went to the Arthur G. Dozier School for Boys turned to lives of violent crime and horrific abuse, punctuated by long periods of jail time and homelessness. Baxter, however, joined the Marine Corps, served in the Korean War, and was honorably discharged. During that time, he married and started a family. But the terrors of Marianna never left his thoughts and eventually reached a tipping point. “When I came back from Korea, I made up my mind – I was going to [the school] and I was going to kill everybody.”
As Baxter packed his things to go, he looked at his children playing nearby. Not everyone who falls prey to a sadist’s treatment is scarred by the experience; the human psyche has an immense capacity for healing and even growth. Baxter changed his mind. “I never had a childhood to speak of. By God, I wasn’t going to deprive my children of one. They deserved better than that.”
As Basel walked toward me, he swayed, listing slightly to his left. His face contorted into a crooked smile. Just a few weeks earlier, I’d heard that he “got his feet all tangled up” and fell, requiring eight staples in his head, but his injury had since healed. He shook my hand. That’s when I noticed a subtle pulsing in his grip – what doctors refer to as “milkmaid’s grip,” the alternate contraction and relaxation of the tiny muscles in his hand.
Basel Queen and his wife, Teresa, live down the street from my parents in the small Florida panhandle town of Freeport. Basel retired there after serving in the military for two decades, a heavy equipment operator for the Air Force’s elite heavy construction unit, RED HORSE. He operated immense cranes, drove powerful bulldozers and dump trucks, and built runways and other key structures in Korea during the Vietnam War and later in the United States. These days Basel’s driving is limited to around town. “I can’t drive on the interstate because I don’t know what I’m doing,” he said.
When I first met Basel a few years ago, he had the appearance of a guy who had spent much of his life working outdoors: lean and lanky with a weathered face and tanned, sinewy arms. His salt-and-pepper hair was neatly trimmed, a holdover from his military days. He stood quietly as Teresa and I spoke, one arm folded and clutching his opposite elbow. He seemed shy. I didn’t think much about his unusual stance at the time, but often over the years I have seen him in this position at home or around town, his arms locked in a self-imposed vise.
Basel wasn’t always given to such constraint. As a teenager growing up in Texas in the 1960s, Basel loved to dance, especially the Twist, his hips swiveling and arms waving to the rousing tempo of dance phenom Chubby Checker. Now 66, Basel does a different dance, directed by a cruel, inner choreographer over which he has no control: Huntington’s disease.
Sometimes referred to as Huntington’s chorea (chorea is Greek for “dance”) because of the dance-like movements associated with the condition, Huntington’s disease is a hereditary disorder that affects the brain, causing uncontrolled movements, speech problems, personality changes, and dementia. Although symptoms usually begin around age 40, Basel didn’t show signs until his late 50s.
Basel is one of roughly 30,000 people in the United States currently living with Huntington’s; his daughter and granddaughter are among nearly 200,000 at risk of inheriting it. Huntington’s bears striking similarity to other neurodegenerative diseases, such as Alzheimer’s and Parkinson’s, which target specific areas of a person’s brain and often appear late in life.
Many people who have Huntington’s disease retreat from the world, self-conscious about their uncontrollable movements, odd grimaces, and strange speech patterns. As I’ve come to know Basel, I’ve learned that he isn’t embarrassed by his condition. He still socializes with friends in his neighborhood and at his church, and he often goes shopping with Teresa. The reactions of people around him don’t go unnoticed, however. “Sometimes I can tell that people are staring at me, curious,” he said.
Because Huntington’s disease is so rare, few people have seen or met someone with the condition, although occasionally it surfaces in literature or pop culture. A character in the popular television show House, MD, had the disease; in one episode, she helped her brother, who also had Huntington’s, commit suicide rather than succumb to its eventualities. Perhaps the most famous person with the disease was folk singer Woody Guthrie, who died from its complications in 1967. Guthrie once wrote a letter to his wife, Marjorie, describing its effects: “No bodily pains; just like my arms and legs and hands and feet and my whole body belongs to somebody else and not to me.”
Basel loves the outdoors, but the physical manifestations of his condition keep him from doing his favorite activities. He and my dad hunted together for many years, trekking through palmetto and pine forests dressed in camouflage and snake boots in search of white-tailed deer. Since his diagnosis, Basel doesn’t hunt anymore; carrying a gun would be a bad idea.
He’s still active in his church, however, where he serves as a deacon. Basel organizes visits to church members who are sick or have special needs. But he gets anxious about things that wouldn’t have bothered him before. “He used to lead the most beautiful prayers,” my mother told me. Now he can’t speak in front of a group because he’s too nervous. Plus, he’s hard to understand. Basel’s speech slurs slightly, and he often struggles to form words, a consequence of the loss of muscle control and language processing skills.
Ordinary activities like eating and drinking are perilous for Basel. Teresa adds thickening agents to his drinks to prevent one of the more common risks people with Huntington’s disease face: aspiration – inhaling thin liquids or foods into the lungs, putting them at risk for pneumonia. But a greater danger is weight loss due to changes in the way the body metabolizes foods and the inability to swallow. Teresa said that Basel has lost more than 35 pounds since his diagnosis, a lot for an already slender guy.
“Right now I can still eat,” said Basel. “I love hamburgers and fish sandwiches, but I can’t eat them anymore. I can eat soft foods like pudding and applesauce.” Occasionally, he coughs or chokes while eating; eventually, he’ll need a feeding tube to help him meet his nutritional needs. Basel hopes to delay that as long as possible.
Last summer, I sat down with Basel and Teresa, and we talked about the fundamental cause of his condition – a single genetic mutation, or change, in his DNA, called a CAG repeat. The mutation repeats the genetic information in his DNA too many times, a sort of “genetic stutter,” like a stuck key on a keyboard. The end result: tortuous twisted clumps of protein that wreak havoc on his brain, producing the condition’s telltale symptoms.
Basel was quiet for a moment. Then he asked, “Will I become a vegetable?”
That’s a difficult question to answer. People with Huntington’s disease typically die within 15 to 20 years of diagnosis, usually from complications such as pneumonia, injuries from a fall, or starvation due to swallowing difficulties. If Basel is typical, he has about 5 to 10 years left.
Although Huntington’s is the focus of much study, including the application of new techniques like gene editing and protein visualization, none of the research will help Basel. The damage to his brain is irreversible. But it might help Basel’s daughter, Keri, who has a 50 percent chance of developing the disease. She had never heard of Huntington’s disease before her father’s diagnosis, even though other family members showed signs of having the condition. “I noticed that Dad’s aunt, grandmother, and cousin moved a lot, but I never really thought about it,” she said.
Keri doesn’t know whether she has inherited the disease, and she doesn’t want to be tested. She’s not alone. Fewer than 5 percent of people at risk for Huntington’s disease choose to undergo genetic testing to learn if they will get the disease or if they might be carriers. “My in-laws, my husband, even my friends want me to get DNA testing,” she said. “But I think that what I don’t know won’t hurt me. I don’t want to know because if I do know that my daughter or I have it, then that’s going to be a constant burden. I will always be looking around the corner, wondering, what was that? Was that a sign? What was that movement?”
Basel has a keen understanding of the mental and physical changes that accompany his illness, but many people who have Huntington’s disease demonstrate poor self-awareness, oblivious to the changes that are often obvious to those around them. His sister, whose symptoms are far worse than Basel’s, is either unaware or unwilling to admit that she has the disease. Basel believes it’s the latter. “She won’t go to the doctor. She’s in denial.”
When I asked Basel what he sees in his future, he was matter-of-fact. “Well, there’s no cure for Huntington’s disease. I guess I’ll just have to deal with life as it progresses.” Medications help. Basel takes tetrabenazine to reduce his involuntary movements and Ativan to help with his anxiety. Both seem to be working for now, although neither is 100 percent effective in reducing his symptoms. “He doesn’t move constantly,” Teresa said, “but when he gets anxious or aggravated, his movements get worse.”
Basel’s symptoms will progressively worsen over time, and the drugs will be less effective. Although some scientists hope to find new drugs to better treat the symptoms of Huntington’s disease, some doctors have mixed feelings about the research and express concern about their patients’ quality of life. Drugs that could reduce Basel’s unnatural movements and muscle problems also might extend his life and prolong his suffering – what one researcher referred to as “unpalatable trade-offs.”
The progressive physical decline associated with Huntington’s disease typically ushers in a loss of independence. But the mental changes, such as depression, irritability, anxiety, and memory problems lead to a loss of self. Even so, Basel remains upbeat. When he visits church members or hears of neighbors whose health is much worse, he’s thankful that he is still able to do so much. Eventually, he will need around-the-clock medical care.
Keri sees Basel about twice a week and notices small changes in his health, but she thinks her father is doing okay. “I know a little bit of his memory isn’t as sharp as it used to be. But we still laugh about things that have been running jokes in our family for a really long time,” she said. “He’s still Daddy to me.”
Basel stopped by my parents’ home recently. “Basel was twisting and turning like he does,” my mother said. “I told him, ‘I can do the Twist just as good as you, Basel!’” And she began twisting her 83-year-old hips. Basel laughed and grabbed her, as if ready to dance.
Coral cores reveal truths about the earth’s climate history – and provide insights about its possible future.
I picked up the foot-long, cream-colored slab, a stony missive carved from a coral reef, far from its former home in the tropical Atlantic Ocean. It felt cool in my hands. About two inches across and just under a quarter of an inch thick, the slice, a vertical cross-section excised from a cylindrical coral core, resembled a piece of rough-sawn tile, bordered on one end with the lumpy edge of now-dead coral polyps – the tiny creatures’ most recent skeletal layer.
Lying on a table nearby was the printed image of the slab’s X-ray, an account of the corals’ internal layers, revealed in alternating bands of black and white. “The X-ray allows me to count the bands,” said paleoclimatologist Hali Kilbourne. “This is 2004, 2003, 2002, 2001,” she said, sliding her finger down the image and pointing out each layer with her finger. “I do the chemistry down-core and then I can [identify] exactly what year it was.” When the slab and the image were perfectly aligned, I could clearly pinpoint the years, decades, and centuries. Here in front of me was a timeline of the earth’s history, hard evidence of the past’s climate, etched in limestone.
I met Kilbourne during a recent visit to the University of Maryland Center for Environmental Science’s Chesapeake Biological Laboratory, a clutch of brick buildings that sits alongside the Patuxent River, in Solomon’s Island, Maryland. Kilbourne studies the earth’s climate from the past, before instruments for measuring and recording the weather were available. We talked about how she and her colleagues conduct their research – how they get to the truth about the earth’s past climate.
Kilbourne’s scientific background is in geology, but her interests lie in climate change, a subject she’s been studying for more than fifteen years. “I use natural archives of past environmental conditions to understand climate variability,” she said. Those natural archives can be found in ice caps, peat bogs, or tree rings – nature keeps very good records – but Kilbourne prefers the records found in coral reefs.
A coral reef is a collection of the external skeletons of millions of corals, tiny, soft-bodied creatures called polyps that claim distant kinship to jellyfish and anemones. Coral polyps prefer warm water that’s clear and shallow, so most reefs can be found in the tropical and subtropical oceans. The polyps draw on the stew of nutrients around them to excrete seasonal layers of calcium carbonate, the principal ingredient in their skeletons.
Despite their hard, sturdy appearance, corals are aquatic prima donnas. They possess a narrow range of tolerance to changes in their environment, making them excellent barometers for climate change.
Corals’ sensitivity manifests in their growth rate, which is faster or slower depending on variations in the surrounding ocean temperature, salinity, or clarity. These variable rates create thicker or thinner layers within the coral skeletons, producing an identifiable pattern of light and dark stripes – the black and white bands I observed on the X-ray – much like the concentric rings of a tree trunk or the stacked ribbons of lake sediments. The layers provide a record, a seasonal imprint of the passing of time that allows scientists to look back in history, from the very recent past to millions of years ago.
The use of corals in the search for answers about the earth’s climate is relatively new. “The recognition that corals could be used for reconstructing past temperatures occurred in the 1970s,” said Kilbourne, “but the analytical capability to measure some of the important chemistry inexpensively and with the precision needed didn’t catch up until the 1990s.”
Kilbourne analyzes the chemical properties of the coral skeletons’ layers to “read” their natural histories. “If I can understand some [chemical] process in the modern world, then I can understand how it occurred in the past,” Kilbourne said. That’s because chemistry doesn’t change. Specifically, she looks at the ratio of two minerals – strontium and calcium – to determine the climate conditions in which the corals grew.
Strontium shares many chemical and physical characteristics with calcium and can even serve as a stand-in for some of the calcium in a coral skeleton, depending on the surrounding ocean temperature. Corals incorporate less strontium into their skeletons when ocean temperatures are warm, and more when temperatures are cool.
“Let’s say we have a coral that grew in the 2000s. We had thermometers in the 2000s! So, I look at what the temperature was [when it was growing], and I look at what the strontium concentration was, and I can make a relationship between the two because they’re correlated,” Kilbourne said. “One drives the other.” The modern-day coral strontium-calcium ratios and temperature observations create a reference data set that allows Kilbourne to extend the correlation backward in history before thermometers were available. “And that’s how I can get a temperature record back in 1492 when Columbus sailed the ocean blue.”
Based on the differences in the strontium-calcium ratio, scientists can calculate ocean temperatures with great accuracy. “A single measurement by itself might have an uncertainty of plus or minus one degree Celsius,” said Kilbourne. But the coral-based climate records she and her colleagues rely on are made up of hundreds to thousands of measurements. With such large datasets, the results become much more certain – to within one-tenth of one degree Celsius.
Measuring other elements in the skeletons, such as different varieties of oxygen (“heavy” or “light” oxygen, called isotopes), Kilbourne back-calculates levels of the ocean’s salinity. A higher concentration of light oxygen is a sign of heavy rainfall, which results in lower salinity. “So, with the strontium-calcium [ratio] and that salinity information, I can see floods, I can see droughts.” Kilbourne can even identify years in which El Niño events, intense hurricanes, or large volcanic eruptions occurred.
Choosing the dive site where Kilbourne will collect the coral samples is an important part of the research. “We want to [collect from] several sites in order to get the bigger picture more confidently,” said Kilbourne. “If you have a really enclosed lagoon, you might have processes that alter the seawater chemistry. It’s not reflective of the open ocean conditions, which is what we’re trying to look at in the [global] perspective.” Although she and her colleagues have been as far south as islands off the coast of Brazil, Kilbourne spends most of her time in the Caribbean and the tropical Atlantic, in places like Grenada and the Lesser Antilles. “It’s easier to count the islands I haven’t been to,” she said.
Even though Kilbourne studies coral reefs in balmy waters far from where I live, in northern Virginia, she makes an excellent case for why tropical ocean temperatures should matter to me. “The Caribbean and tropical Atlantic are like a pot of warm water letting off steam. That steam is the moisture that provides rain for North America, South America, Africa, and Europe. If you live in one of those four continents, and a lot of people do, including us, it’s pretty important,” she said. That’s because we really have only one ocean, and it’s a global one, a massive, interconnected reservoir of heat and the principle regulator of the globe’s weather.
The type of coral Kilbourne samples is important, too. The delicate arms and fanned sprays of branching corals that most people are familiar with don’t provide the long, continuous records that Kilbourne needs for her research, so she looks for coral species that tend to form solid boulder-like formations. “In the Pacific, we go after the Porites genus, but in the Atlantic, we are more often looking at the Orbicella, which is the boulder star coral.” Orbicellas grow in massive stony mounds with dome-like tops or ruffled, skirted edges, in shades of green, orange, brownish yellow, and gray. The mounds cluster in colonies that may reach ten feet in diameter.
Outfitted in scuba gear and using a hand-held hydraulic drill with a long, hollow, cylindrical coring bit attached, Kilbourne removes two-and-a-half feet-long segments of the coral skeleton, roughly the diameter of a soup can, at a time. Kilbourne is petite, and working underwater for long periods of time is grueling, but she has grown accustomed to the physical demands of her profession. She breaks off each segment, removes it from the bit, and then continues drilling. The largest coral core Kilbourne drilled was more than eight feet long. When pieced back together, she said, it served as a stony, cylindrical “biopsy” of the reef.
Keeping accurate records of where the cores come from allows Kilbourne to collaborate with other scientists who drill in nearby locations and to analyze the data within the broader context of weather around the globe. “We take GPS coordinates at the site,” said Kilbourne. “Then we bring [the cores] onboard and use a waterproof marker to label them with the GPS coordinates and our depth. We take extensive field notes as to where we are and take pictures.” When Kilbourne returns to her lab, she uses a tile saw to cut the cores into slabs and X-rays them to observe the growth patterns, she said.
Corals are natural products, however. They aren’t perfect proxies for past climate change, but they’re the gold standard in tropical regions for now. “A very rigorous quality control analysis must be applied to each record to ensure that it represents climate and not other factors,” said Kilbourne.
In cooler parts of the world, where corals are unable to grow, paleoclimatologists rely on temperature and rainfall records preserved in land archives such as ice (from high-latitude polar regions) or trees (from mid-latitude regions) to complement the data from tropical region coral cores. Piecing together the data from these complementary sources, Kilbourne and her fellow paleoclimatologists, a consortium of climate scientists from around the world, have observed a significant cooling trend in the Indian, western Pacific, and Atlantic oceans over the past 2000 years, with the steepest drop occurring between 1400 and 1800 of the Current Era. Their findings, published in the August 2016 issue of the journal Nature, reveal that the cooling trend came to an abrupt halt around 1830 – the infancy of the Industrial Age and the widespread production of greenhouse gases from fossil fuels, especially coal – some 20 years earlier than most climate change models suggest, an indication that even small amounts of the gases can change the earth’s climate.
The data gleaned from Kilbourne’s lab support and expand on what scientists already know about climate change: The trend toward increasing global temperatures has already altered local and regional weather patterns, incurring threats to food production, freshwater supplies, and the safety and welfare of people living in coastal areas. “It’s not a trend that’s going to change unless humans change the carbon dioxide content of the atmosphere in a different way other way than up,” said Kilbourne. But the findings also suggest that the earth’s climate can respond to even small changes in greenhouse gas emissions, perhaps offering humans a means of slowing down the warming process.
Despite the bad news about changes in the world’s climate, Kilbourne is optimistic. “To me, the important [thing] is that it’s not too late and that we need to change our ways now. Smart people have thought about solutions to this; I’m trying to understand the problem, but we already understand it enough to take action.”
Abram, N. J., McGregor, H. V., Tierney, J. E., Evans, M. N., McKay, N. P., Kaufman, D. S., & PAGES 2k Consortium. (2016). Early onset of industrial-era warming across the oceans and continents. Nature, 536(7617), 411-418.
Tierney, J. E., Abram, N. J., Anchukaitis, K. J., Evans, M. N., Giry, C., Kilbourne, K. H., & Zinke, J. (2015). Tropical sea surface temperatures for the past four centuries reconstructed from coral archives. Paleoceanography, 30(3), 226-252.
One of the tenets of exercise nutrition is the importance of the pre-workout meal: a small snack, eaten about 15-30 minutes before exercising, to maintain normal blood sugar levels during the workout and to promote muscle recovery afterward. But findings from a new study published in American Journal of Physiology-Endocrinology and Metabolism (paywall) flips that idea on its head, at least for one group of people – overweight men.
The study took place over a period of about four weeks. First, the researchers measured the maximum amount of oxygen the men needed during intense exercise, called VO2max. Then they asked the men to walk for one hour on a treadmill at 60 percent of their VO2max – equivalent to moderately intense exercise, such as a brisk walk or a slow bike ride – two hours after eating a large meal (about 650 calories). The scientists took blood samples before, during, and after the exercise.
About four weeks later, the researchers repeated the experiment, but this time they asked the men to fast for at least 12 hours prior to the exercise. Again, blood samples were taken before, during, and after the exercise.
The results of the study showed that when overweight men exercised two hours after eating, their utilization of fat stores dropped by as much as 45 percent compared to when the men exercised after fasting. This means that instead of using stored fat to fuel their exercise, the men’s bodies relied on the carbohydrates from their recently eaten meal (in the form of blood glucose).
These findings suggest that eating before exercise may alter the beneficial effects of exercise such as weight loss and metabolic improvements in overweight men.
Chen YC, Travers RL, Walhin JP, Gonzalez JT, Koumanov F, Betts JA, Thompson D. Feeding Influences Adipose Tissue Responses to Exercise in Overweight Men. American Journal of Physiology-Endocrinology and Metabolism. 2017 Mar 14:ajpendo-00006.
Some popular diet plans suggest that eating too many acid-forming foods, such as dairy products or grains, harms your health and damages your bones. Proponents of the theory argue that you need to ”alkalize” your body by eating alkaline foods, such as fruits and vegetables.
But is your body actually “acidic” after eating? Not really.
Here’s why: During digestion, foods are broken down into various components, some of which are acidic. But for most healthy people, the stomach, gall bladder, liver, and kidneys are very efficient at handling acids and do a great job of maintaining the perfect balance of acidity to alkalinity.
Although eating alkaline foods such as fruits and vegetables is always a good idea, excluding dairy products or grains can hurt, rather than help, your health and bones. For overall health, strong bones, and optimal performance, choose calcium-rich foods such as low-fat dairy products, fortified soy or nut milks, leafy green vegetables, and calcium-fortified orange juice. Opt for whole grain foods such as brown rice, pasta, and cereals.
Bonjour, Jean-Philippe. “Nutritional disturbance in acid–base balance and osteoporosis: a hypothesis that disregards the essential homeostatic role of the kidney.” British Journal of Nutrition 110.07 (2013): 1168-1177.
Fenton, Tanis R., and Andrew W. Lyon. “Milk and acid-base balance: proposed hypothesis versus scientific evidence.” Journal of the American College of Nutrition 30.sup5 (2011): 471S-475S.
Tang, Minghua, Lauren E. O’Connor, and Wayne W. Campbell. “Diet-Induced Weight Loss: The Effect of Dietary Protein on Bone.” Journal of the Academy of Nutrition and Dietetics 114.1 (2014): 72-85.
Many of our people died from [scurvy] every day, and we saw the bodies thrown into the sea constantly, three or four at a time. For the most part they died without aid given to them, expiring behind some case or chest, their eyes and the soles of their feet gnawed away by rats.
~16th century English sea surgeon
Pondering the effects of a poor diet is an awesome and terrible thing. Consider for a moment the fictitious Pirates of the Caribbean.
The dashing image of Captain Jack Sparrow was a far cry from the haggard, infirm figure of a real-life sailor in the 18th century. The hardships of sea life knew no bias: Warfare, shipwreck, injury, and drowning killed thousands. None of those threats, however, were responsible for as many deaths as the dreaded disease scurvy.
Scurvy is a condition characterized by fatigue, bleeding gums and skin, fragile bones, and muscle and joint pain. The body of a person with scurvy begins to break down and rot while they’re still alive. They become like a dead man walking.
Nearly 2 million sailors died from scurvy between the 15th and 18th centuries. During the Seven Years War, from 1756 to 1763, scurvy likely claimed the lives of nearly three-fourths of Great Britain’s Royal Navy – more than 133,000 men. Loss of life was only one of scurvy’s threats to the Navy. A little more than a decade earlier, mutiny ensued after the East India Company ship The Wager, her crew decimated and demoralized by nutritional deficits like scurvy, wrecked on the Patagonian archipelago.
Near the end of the 18th century, however, the discovery that citrus fruits could prevent or cure the disease prompted the Royal Navy to implement a prevention program that included a daily ration of lemon juice, eradicating the illness. The source of the juice’s health-giving effects was ascorbic acid, later known as vitamin C.
Vitamin C serves as a sort of molecular martyr. It donates electrons to other molecules in the human body to prevent oxidation from occurring – earning vitamin C the moniker “antioxidant” – and, in turn, undergoes oxidation itself. Vitamin C sacrifices itself this way in many reactions in the body, including those that produce key structural and chemical components like collagen, carnitine, and norepinephrine. The complications associated with the absence or deficiency of these components provide a framework for understanding the true curse of the Black Pearl.
A toothless grin
Collagen is a structural protein found in skin, bones, tendons, and cartilage. Vitamin C is involved in nearly every step of collagen formation, yielding a highly resilient triple-braided molecule, essential to every tissue in the body. So, the toothless image of Captain Barbossa’s crew was pretty accurate – without adequate vitamin C, collagen’s strength and rigidity fails, and the teeth are among the first to jump ship.
Carnitine, a compound produced in the liver, facilitates fat metabolism. Without vitamin C for carnitine synthesis, fats can’t be transported into the cellular machinery where they get processed. This can cause hepatic encephalopathy, a condition where ammonia builds up in the bloodstream, resulting in dulled, even psychotic, thinking. Carnitine deficiency can also induce a reversal of day-night behavior, driving sleepiness during the day and wakefulness at night, perhaps explaining the proclivity of the Black Pearl’s crew for nocturnal activities.
A rolling stone
Normal brain function relies on norepinephrine, a type of neurotransmitter. The chemical reaction that produces norepinephrine starts when vitamin C binds to another brain chemical, dopamine, and converts it to norepinephrine. A person with low levels of norepinephrine in their brain might experience depression, mood swings, and other psychiatric symptoms – such as the Keith Richards-like behavior of Captain Sparrow following his exile on a remote, ostensibly citrus-free island.
Rewriting medical history (or a Hollywood movie script) is problematic without a proper physical exam, but many of the symptoms manifested by Captain Jack and his scabby cohorts point to one conclusion.
Retrodiagnosis: hypovitaminosis C (scurvy).
Brown, S., Scurvy: How a Surgeon, a Mariner, and a Gentlemen Solved the Greatest Medical Mystery of the Age of Sail, St. Martin’s Press, New York 2003.
Pimentel, L., Scurvy: historical review and current diagnostic approach. Am J Emerg Med 2003, 21, 328-332.
Thomas, D. P., Sailors, scurvy and science. J R Soc Med 1997, 90, 50-54.
Levine, M., Rumsey, S., Wang, Y., Park, J., Kwon, O., Xu, W., Amano, N., in: Ziegler, E. E., Filer, L.J. (Ed.), Present Knowledge in Nutrition, ILSI Press, Washington 1996, pp. 146-159.
Amat di San Filippo, C., Taylor, M. R., Mestroni, L., Botto, L. D., Longo, N., Cardiomyopathy and carnitine deficiency. Mol Genet Metab 2008, 94, 162-166.
Rebouche, C. J., in: Shils, M. E., Olson, J.A., Shike, M., Ross, A.C. (Ed.), Nutrition in Health and Disease, Williams & Wilkins, Baltimore 1999, pp. 505-512.
Carr, A. C., Frei, B., Toward a new recommended dietary allowance for vitamin C based on antioxidant and health effects in humans. Am J Clin Nutr 1999, 69, 1086-1107.
Researchers at the National Institutes of Health have found that measuring tau, a brain protein found in the blood, might help doctors identify athletes who need a longer recovery time after a sports-related concussion, according to a new report in the medical journal Neurology.
Tau is linked to the development of Alzheimer’s and Parkinson’s diseases and serves as an indicator of nerve cell damage following traumatic brain injuries, commonly referred to as concussion.
According to the Centers for Disease Control and Prevention, nearly 1.3 million concussions occur each year in the United States. Athletes who participate in contact sports have nearly a one in five chance of suffering a sports-related concussion per year of play.
Concussion damages the delicate tissues and blood vessels of the brain and can result in altered brain function that can last for days, weeks, or months. About 15 percent of concussed athletes experience symptoms as long as one year after their injury, a condition called persistent post-concussion syndrome, or PPCS—typically after returning to play too quickly.
Determining when an athlete can return to play presents many challenges. Doctors and athletic trainers currently rely on a variety of measures, including physical examination, cognitive performance, and interviews with the patient and his or her family. Balance tests and computer-generated assessments can gauge an athlete’s mental performance before and after a brain injury.
Some athletes, however, have found work-arounds for the tests, blaming poor ankle strength for failed balance tests and intentionally underperforming on the preseason computerized assessments so that their baseline test scores (what they’re compared against if they have a concussion) are falsely low.
Measuring tau levels could be an objective means of preventing athletes from returning to physical activity too soon and risking further brain injury.
In the study, researchers measured preseason tau levels in blood samples from more than 600 male and female University of Rochester athletes who participate in contact sports, including football, basketball, hockey, and lacrosse.
Then the researchers measured tau levels in those athletes who experienced a concussion during the season – 43 athletes in all – at multiple time points: within 6, 24, and 72 hours of the injury, and again at seven days post-injury and compared them with samples from uninjured athletes and non-athletes.
Tau was higher in the blood of male and female athletes who needed a longer recovery time, regardless of sport played. Measuring tau in concussed athletes might be a useful way to determine how long an athlete needs to be on the bench.
Current tests for measuring tau take weeks, not hours, to come back from the lab, however, and are expensive. Experts believe it might be many years before tau testing for concussion becomes routine.
Gill, Jessica, et al. “Acute plasma tau relates to prolonged return to play after concussion.” Neurology (2017): 10-1212.
Interleukin 1-beta, or IL-1β, a protein produced by white blood cells, promotes your body’s production of insulin in response to eating. Together, IL-1β and insulin activate your body’s immune response and enhance its ability to utilize glucose, according to a new report published in the journal Nature Immunology (paywall).
If you’ve ever endured the fallout from a bad dietary decision at your local food truck, then you’ve experienced first hand how your body maintains the delicate balance between acquiring the necessary calories and nutrients for your day-to-day existence and simultaneously protecting you from serious, sometimes deadly, infection.
Every time you eat, you ingest bacteria – fellow travelers that hitch rides on your food.
Fortunately, your body has a defense mechanism that rivals most nations’ early tactical response teams – the innate immune system, a collection of cells and proteins always on alert and ready to respond to foreign attack. The end result of immune system activation is inflammation.
Some research suggests that eating is associated with mild, short-lived inflammation. The principal activator of this inflammation is IL-1β, a tiny protein produced by white blood cells called macrophages.
In a recent study, researchers at the University Hospital Basel in Switzerland hypothesized that IL-1β not only drives post-meal immune system activation and inflammation, it also promotes the production of insulin, which helps your body utilize glucose. Why? To fuel the immune cells actively engaged in containing the bacteria in the foods you eat.
Using an animal model with ordinary (“wild type”) mice, the researchers discovered that the number of macrophages in the guts of the wild type mice increased after feeding. In turn, the macrophages produced IL-1β, which led to immune system activation and an increase in insulin production. The insulin bolstered the inflammatory response by stimulating the macrophages to produce more IL-1β.
They also discovered that the macrophages in the wild type mice only produced IL-1β if they had been exposed to bacteria and if their blood glucose was elevated due to eating.
The researchers noted that although IL-1β and insulin worked together to help the mice utilize glucose, IL-1β favored the immune cells – increasing their ability to take in more glucose (compared to other cells).
Activation of the innate immune system is important for our survival. But eating too much can cause prolonged activation, eventually leading to the development of metabolic disorders, such as diabetes, gout, and cardiovascular disease. And, in a strange paradox, IL-1β is both beneficial and toxic to certain cells in the pancreas. Short-term exposure to IL-1β helps the pancreatic cells regenerate, but long-term exposure to IL-1β destroys the cells.
This synergistic cooperation between your immune system and your gut is what keeps you healthy and well fed.
Dror, E., Dalmas, E., Meier, D. T., Wueest, S., Thévenet, J., Thienel, C., … & Item, F. (2017). Postprandial macrophage-derived IL-1 [beta] stimulates insulin, and both synergistically promote glucose disposal and inflammation. Nature Immunology.
They put arsenic in his meat And stared aghast to watch him eat; They poured strychnine in his cup And shook to see him drink it up: They shook, they stared, as white’s their shirt: Them it was their poison hurt. –I tell the tale that I heard told. Mithridates*, he died old.
~A. E. Housman
In what might have been the first recorded account of biological warfare, the Roman army of Pompey the Great succumbed to intentional poisoning due to ingestion of “mad honey” – wild honey contaminated with grayanotoxin, a toxic substance found in the pollen and nectar of some rhododendron species. The sinister sweet, hidden in honeycombs placed along the soldiers’ route, produced a sudden drop in blood pressure, slowed heart rate, and impaired vision in those who ate. So weakened, the Romans were easy prey.
The perpetrator of the crime was Mithradates VI, king of Pontus on the Black Sea – now present-day Turkey – from 119 to 63 BC. Mithradates was a brilliant ruler, warrior, orator, and, by some accounts, a psychopath. Better known as “The Poison King,” Mithradates was also a phytochemist – a student of the chemical and medicinal properties of plants – and an early visionary in the field of clinical toxicology. Unfortunately, the concept of research ethics had not yet reached Pontus, and many a death row prisoner died in the name of scientific exploration, involuntary subjects in Mithradates’ laboratory.
Mithradates lived in constant fear of poisoning by his enemies. In a brilliant preemptive measure, the king concocted a special potion – now referred to as a mithradatum – of nearly three-dozen edible plants mixed with honey that would inure him to toxic harm. He took an almond-sized portion of the mithradatum daily, with a little wine. According to legend, Mithradates’ shrewd precautionary measures were so successful that when he attempted suicide by poisoning, no toxin was equal to the task. The last line of an A. E. Housman poem describes the outcome: “I tell the tale that I heard told. Mithridates, he died old.”
The upshot suggests that Mithradates had found the ultimate antidote: the inherent value of fighting poison with poison. Modern chemical analysis and medical practice have since confirmed the therapeutic, preventive effects of many of the compounds in Mithradates’ self-prescribed remedy.
Much of Mithradates’ tale is the stuff of legends and poetry. His mithradatum – his daily challenge to his body’s defense mechanisms – fulfilled the Nietzschean philosophy that suggests what doesn’t kill you really can make you stronger.
This blog is a mithradatum. An antidote. A challenge to your brain to read and learn about the world of science that is in, on, and around us. If science is presented poorly, boringly, or inaccurately, we run the risk of being poisoned by the piles of non-scientific discussion that surround us. Let’s engage in a discussion of the amazing, scary, thrilling, wacky, bizarre, logical, paradoxical world of science.
*Pronounced “mith-ruh-DAY-teez,” two spellings of the king’s name appear in ancient writings: Mithridates (Greek) and Mithradates (Roman).