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.”
I lay down on the hard, gray flagstones of my backyard patio and stretched out the kinks and coils that lingered after my early morning exercise. My dog and I had just returned from a long walk, and she lounged in the cool waters of her wading pool, panting contentedly. Without warning, a violent, invisible whirlpool seemed to engulf me, dragging me into its swirling maelstrom. I grappled for an anchor on the smooth stones but came up empty-handed. Waves of fear and nausea washed over me for nearly a minute. Slowly, the storm subsided.
I sat up, baffled but relieved that the episode had passed. Suddenly, a different sensation ensued: Unseen forces gripped me, propelling me forward in the continuous loop of a nightmarish waterpark ride. The earth’s gravitational pull seemed to double, triple, and the watercoaster in my head took off, faster, faster. My eyes shut tight against the tumult. I cried out, startling my dog, who came to comfort me, panting and dripping wet. As all wet dogs do, she shook. The discordant jingle of her license tags and the cool spray of water launched me into a backyard version of sensory waterboarding.
My heart raced, my breathing quickened, and I broke into a sweat. On an intellectual level, I recognized the event as vertigo, a condition I’d heard of (and dismissed as minor). But on a more primal level, my brain recognized it as a serious threat to my survival.
Despite what we learn in school about the earth’s rotation, the common wisdom asserts that the ground under our feet remains immobile while we do the moving. We don’t call it terra firma for nothing. But vertigo defies those assertions and fools us into doubting our strongest convictions about the world around us.
Vertigo makes you feel like you’re spinning, swaying, or tilting when you’re not. Basically, it’s a type of hallucination – a mismatch between reality and the signals our eyes, inner ears, and sense of touch send our brain. Whereas some people with vertigo sense their bodies moving in space (even though they’re standing still), others sense their surroundings moving around them. Either way, something isn’t right.
A visit to my doctor revealed no epiphanies. “Your ears are full of fluid,” she announced. “Fluid” seemed to define my condition. I felt like I was walking on water, and if I tapped my ears, the light drumming produced a sodden, muffled sound like I was under water. “You probably have benign paroxysmal positional vertigo.”
It didn’t feel “benign,” or harmless, to me, but it did feel “paroxysmal,” a mouthful of a word that means violent and sudden. She suggested I take an over-the-counter decongestant, and she prescribed Meclizine®, an anti-vertigo medication, and Augmentin®, an antibiotic. “Just in case,” she added cryptically.
Nearly a third of all adults over the age of 40 in the United States – roughly 69 million people – will experience vertigo at least once in their lives. Most cases of vertigo are transient, lasting only a few weeks to months, while some last for years.
Although vertigo is a serious health condition, it’s a symptom, not a disease. It’s an indication that something is wrong somewhere else in the body. Doctors classify vertigo as either central (originating in the brain) or peripheral (originating in the inner ears). Benign paroxysmal positional vertigo, or BPPV, is the most common form of the condition and is usually peripheral. Professional golfer Jason Day collapsed after a bout of BPPV during the U.S. Open during the summer of 2015, and basketball legend LeBron James has recurrent BPPV. Walking my dog doesn’t exactly qualify as a professional sport, but at least I was in good company.
In BPPV, certain head movements, like tipping it back or rotating it to one side, can trigger the episodes, which usually last less than a minute. The onset is often so sudden that people sometimes think they’re having a stroke. Others become disoriented and stumble while walking, and some even fall out of bed. People of all ages can get BPPV, but it’s much more common in older adults – as much as seven times more common in adults over the age of 60. And experts aren’t sure why, but women are almost twice as likely to experience BPPV than men.
I asked my doctor what caused my BPPV. Her bedside manner left a lot to be desired: “It can be caused by a tumor,” she replied. I blanched. Sensing my alarm, she added, “Or a virus. Or a bacterial infection.” Her last answer explained the “just in case” remark and the rationale for prescribing antibiotics. “But usually it’s caused by little stones in your ear that move.” Wait,I have rocks in my head? I wondered, but I was too rattled to ask. She handed me a piece of paper that described special exercises designed to treat BPPV and sent me home.
While BPPV can be related to some serious medical conditions, David Zee, a neurologist at the Johns Hopkins University and a specialist in treating balance disorders, says, “Vertigo can also be caused by a knock on the head, riding on a bumpy road, or even migraine headaches.” Even lying in the magnetic field of an MRI machine can cause vertigo for many people. Most cases, however, are due to those pesky little stones, called otoconia. “Otoconia create a lot of mischief,” says Zee. “They can get dislodged and kind of float around, producing a powerful false sense of spinning.”
Otoconia are tiny limestone and protein crystals that live deep in your inner ear, in an area called the vestibule. In the vestibule, the otoconia attach to the gel-like surfaces of two tiny organs, the utricle and saccule, which help you sense gravity and movement in vertical or horizontal directions, such as riding in an elevator or moving in a car. The otoconia slide back and forth over the surfaces of the utricle and saccule in response to these movements and send the information to your brain.
Not far from the utricle and saccule lies a series of three looped tunnels, like waterpark tube slides, known as the semicircular canals. These fluid-filled canals sit at right angles to each other and sense speed and spinning motion. When you move, the fluid moves across hair-like structures in the canals called cilia. The cilia move the way wheat stalks swish in the wind and tell your brain you’ve turned your head and whether the movement was fast or slow.
The semicircular canals, the utricle, and saccule work jointly to keep you balanced. Together, they’re known as the vestibular system. Most of the time the vestibular system works without problem. Occasionally, however, rogue stones escape the utricles’ surface and wash up into one of the semicircular canals. Why the stones dislodge and relocate remains a mystery, and often doctors can’t pinpoint a specific cause. “As we get older, the otoconia are probably more easily sheered off,” says Zee. Most of us likely have a few renegade stones floating around in our semicircular canals, he adds, but it’s only when large clumps form that there’s a problem. The clumps aggregate in the canals, effectively converting the speed-sensing semicircular canals to gravity-sensing ones.
This is vertigo, and it’s enough to turn your world upside down.
Vertigo can cause anxiety, depression, and panic attacks. Some people with vertigo lose their jobs and can’t care for their children and families. At the very least, vertigo robs a person of their physical freedom. “The vestibular system is fundamental to our survival,” says Zee. “We wouldn’t exist without it. The brain needs to know where we are, relative to our enemies, and whether we are moving or still.” Vertigo threatens our sense of security.
I certainly felt threatened, but I also wanted to wretch every moment. “A person with BPPV can feel ill with nausea, vomiting, and other motion sickness-like symptoms,” says Zee. “[Drugs] like Meclizine®, or its generic form, Antivert®, might make you feel better if you have nausea, but they won’t cure your BPPV. You have to treat it with physical therapy.”
The physical therapy for BPPV is simple and involves exercises like the ones my doctor suggested. A few variations of the exercises exist, and some variants work better than others. The version I completed, a series of head movements referred to as “modified Epley maneuvers,” resolve vertigo in about two-thirds or more of people with BPPV.
Essentially, the exercises are human versions of those ball-in-a-maze games you played as a kid, where you roll a bead around in a maze, trying to get the bead to go into a hole. The goal is to roll the renegade stone (the bead) through the maze of canals and return it to the vestibule (the hole), where it can be recycled in a sort of inner-ear sustainability program. Of course, you can’t see the otoconia rolling around, so you hope for the best.
I faithfully performed my physical therapy for three days, and then, as suddenly as they appeared, my symptoms went away. When I rested my head on my pillow that night, I realized the tide had receded. Finally, I was symptom-free.
I’m not off scot-free, though. About one third of people who’ve had BPPV will get it again. As I get older I’m at greater risk for other types of vertigo, too, and my sense of balance will gradually diminish. According to Zee, as we age we lose neurons in our inner ears and in the part of our brain that controls coordination, we lose sensation in our feet, and we lose visual acuity. This trifecta of losses creates a perfect storm for balance problems. “It’s amazing we do as well as we do,” says Zee. But activities that challenge the vestibular system and improve balance, like tai chi, or dancing (especially the tango), or yoga, help maintain balance as we age.
When it comes to Zee’s advice, I’m all ears. I’ve added some balance exercises to my morning routine on the flagstones, and I’ve begun shadow boxing – the closest I’ll come to dancing.
My world is right side up now, and I hope to keep it that way.
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.
A quick internet search of the terms “pregnancy” and “DHA” (commonly known as fish oil) yields nearly half a million results, most of them either extolling the latter for its virtues or (more likely) peddling it. Although many physicians advise their patients to increase DHA intake during pregnancy, little scientific evidence supports this advice. Now findings from a study published on March 21 in the Journal of the American Medical Association (paywall) suggest that DHA has little benefit during pregnancy.
The study, dubbed DOMInO for short (DHA to Optimize Mother Infant Outcome), was conducted in five Australian maternity hospitals between October 31, 2005, and January 11, 2008, and involved nearly 2,400 pregnant women. It was a double-blind, multicenter, randomized controlled trial – considered the gold standard in research study designs because it helps scientists determine whether a cause-effect relationship exists.
The researchers set out to determine whether increasing women’s DHA intake during the last half of pregnancy would improve their children’s neurological development. The pregnant women were divided in two groups: One group received 800 milligrams of DHA, and the other received a placebo (vegetable oil) daily. The women’s children participated in follow-up studies (at 18 months, 4 years, and 7 years of age) to assess the long-term effects of DHA.
At 18 months and 4 years of age, the two groups of children showed no differences in cognitive, language, or motor development.
At the seven-year point, the researchers assessed the children’s intelligence based on age-appropriate IQ tests. They found no differences between the two groups. In other words, the kids whose moms took DHA during pregnancy were no smarter than those whose moms didn’t.
Although DHA plays many roles in infant development, little evidence supports the need for increased DHA intake during pregnancy.
Gould JF, Treyvaud K, Yelland LN, Anderson PJ, Smithers LG, McPhee AJ, Makrides M. Seven-Year Follow-up of Children Born to Women in a Randomized Trial of Prenatal DHA Supplementation. Jama. 2017 Mar 21;317(11):1173-5.
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 really “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.