Hope for haploinsufficiency diseases

Genetic conditions like Dravet syndrome, which causes severe childhood epilepsy, are hard to tackle with traditional gene therapy. New approaches in the works include using antisense therapy to boost mRNA splicing.

By Elie Dolgin

The seizures started when Samantha Gundel was just four months old. By her first birthday, she was taking a cocktail of three different anticonvulsant medicines. A vicious cycle of recurrent pneumonia, spurred on by seizure-induced inhalation of regurgitated food, landed the young toddler in and out of the hospital near her Westchester County home in New York State.

Genetic testing soon confirmed her doctors’ suspicions: Samantha, now age 4, has Dravet syndrome, an incurable form of epilepsy. Her brain was misfiring because of a mutation that is unlike those responsible for most genetic diseases; it’s a type that has long eluded the possibility of correction. Available drugs could help alleviate symptoms, but there was nothing that could address the root cause of her disease.

That’s because the mutation at the heart of Dravet creates a phenomenon known as haploinsufficiency, in which a person falls ill if they have only a single working copy of a gene. That lone gene simply can’t produce enough protein to serve its molecular purpose. In the case of Dravet, that means that electrical signaling between nerve cells gets thrown out of whack, leading to the kinds of neuronal shock waves that trigger seizures.

Most genes are not like this. Though the human genome contains two copies of almost every gene, one inherited from each parent, the body can generally do fine with just one.

Not so for genes such as SCN1A, the main culprit behind Dravet. For SCN1A and hundreds of other known genes like it, there’s a delicate balance of molecular activity that is needed to ensure proper function. Too little activity is a problem — and oftentimes, so is too much.

This Goldilocks paradigm partially explains why conventional gene therapy strategies are ill-suited to the task of haploinsufficiency correction. With therapies of this kind — several of which are now available to treat “recessive” genetic diseases such as the blood disorder beta thalassemia and a form of inherited vision loss — the amount of protein made by an introduced gene just needs to cross a minimum threshold to undo the disease process.

In those contexts, it’s not a problem if the added gene is overactive — there’s a floor, but no ceiling, to therapeutic protein levels. That is simply not the case with many dosage-sensitive diseases like Dravet, especially for brain disorders in which too much protein can overexcite neuronal activity, says Gopi Shanker, who served as chief scientific officer of Tevard Biosciences in Cambridge, Massachusetts, until earlier this year. “That’s what makes it more challenging,” he says.

Adding to the challenge: The special types of modified viruses that are used to ferry therapeutic genes into human cells can handle only so much extra DNA — and the genes at the heart of Dravet and many related haploinsufficiency disorders are much too big to fit inside of these delivery vehicles.

Overlooked no more

Faced with these technical and molecular hurdles, the biotechnology industry long ignored haploinsufficiencies. For more than 30 years, companies jostled to get a piece of the drug development action in other areas of rare genetic disease — for cystic fibrosis, say, or for hemophilia — but conditions like Dravet got short shrift. “It’s one of the most neglected classes of disorder,” says Navneet Matharu, cofounder and chief scientific officer of Regel Therapeutics, based in Berkeley, California, and Boston.

Not anymore. Thanks to new therapeutic ideas and a better understanding of disease processes, Regel, Tevard and a group of other biotech startups are taking aim at Dravet, with experimental treatments and technologies that they say should serve as testing grounds for going after haploinsufficiency diseases more broadly.

Currently, there’s little to offer patients with these maladies other than drugs to aid with symptom control, says Kenneth Myers, a pediatric neurologist at Montreal Children’s Hospital who cowrote an article about emerging therapies for Dravet and similar genetic epilepsies in the 2022 issue of the Annual Review of Pharmacology and Toxicology. But thanks to new advances, he says, “there’s a huge reason for optimism.”

Samantha, for one, now seems to have her disease under control because of a drug called STK-001; it is the first ever to be evaluated clinically that addresses the root cause of Dravet.

Between February and April 2022, doctors thrice inserted a long needle into the young girl’s lower spine and injected the investigational therapy, which is designed to bump up levels of the sodium-shuttling protein whose deficiency is responsible for Dravet. It seemed to work. For a time, Samantha lived nearly seizure-free — presumably because the increased protein levels helped correct electrical imbalances in her brain.

Conventional gene therapy strategies are ill-suited to the task of haploinsufficiency correction.

She went from epileptic attacks every 7 to 10 days, on average, to nothing for months on end. Her verbal skills improved, as did her physical capabilities. Her gait improved and her tremors disappeared.

Eventually, as the therapy wore off, Samantha began to backslide, with seizures returning every couple of weeks or so. But she started receiving additional doses of STK-001 under a new trial protocol in October 2022, and since then has experienced only two epileptic episodes over the span of six months. “It’s really pretty amazing,” says her mother, Jenni Barnao.

“Is it a cure? No.… But this is absolutely our best shot,” Barnao says. “There’s definitely something with this drug that’s very good. Her brain is just working better.”

Give a boost

The STK-001 treatment relies on the fact that the normal activity of genes is somewhat inefficient and wasteful. When genes get decoded into mRNA, the resulting sequences require further cutting and splicing before they’re mature and ready to serve as guides for making protein. But often, this process is sloppy and doesn’t result in usable product.

Which is where STK-001 comes in.

A kind of “antisense” therapy, STK-001 consists of short, synthetic pieces of RNA that are tailor-made to stick to part of the SCN1A gene transcript and, as a result, make productive cutting and splicing more efficient. The synthetic pieces glom on to mRNA from the one working version of the gene that people with Dravet have and help to ensure that unwanted bits of the mRNA sequence are spliced out, just as a movie editor might cut scenes that detract from a film’s story. As a result, more functional ion channel protein gets made than would otherwise happen.

Protein levels don’t get completely back to normal. According to mouse studies, there’s a 50 percent to 60 percent boost, not a full doubling of the relevant protein in the brain. But that bump seems to be enough to make a real impact on patients’ lives.

Stoke Therapeutics, the company in Bedford, Massachusetts, that is behind STK-001, reported at the American Epilepsy Society’s 2022 Annual Meeting that 20 of the first 27 Dravet patients to receive multiple doses of the therapy in early trials experienced reductions in seizure frequency. The greatest benefits were observed among young children like Samantha whose brains have accumulated less damage from years of debilitating seizures and abnormal cell function. Larger confirmatory trials that could lead to marketing approval are scheduled to begin next year.

Stoke is hardly alone in its quest to fix Dravet and haploinsufficiency disorders more generally. Several other biotech startups are nearing clinical trials with their own technological approaches to enhancing what working gene activity remains. Encoded Therapeutics, for example, will soon begin enrolling participants for a trial of its experimental Dravet therapy, ETX-001; it uses an engineered virus to deliver a protein that ramps up SCN1A gene activity so that many more mRNA copies are made of the single, functional gene.

And if any of these companies succeed in reversing the course of Dravet, their technologies could then be adapted to take on any comparable disease, says Orrin Devinsky, a neurologist at NYU Langone Health who works with several of the firms and is involved in Samantha’s care. “An effective therapy would provide a potential platform to address other haploinsufficiencies,” he says.

New targets, new tactics

Stoke will soon put that idea to the test.

Buoyed by the early promise of its Dravet therapeutic, the company developed a second drug candidate, STK-002, that similarly targets splicing to turn nonproductive gene transcripts into constructive ones. But in this case, it’s designed to tackle an inherited vision disorder known as autosomal dominant optic atrophy, caused by haploinsufficiency of a gene called OPA1. In this disease, a single working copy of OPA1 is not enough to sustain proper nerve signaling from the eyes to the brain.

Clinical evaluation of STK-002 is expected to start next year. Meanwhile, in partnership with Acadia Pharmaceuticals of San Diego, Stoke is also exploring treatments for Rett syndrome and SYNGAP1-related intellectual disability, both severe brain disorders caused by insufficient protein levels.

“There’s definitely something with this drug that’s very good. Her brain is just working better.”

Jenni Barnao

Stoke’s splice-modulating approach flows naturally from the success of another antisense drug, Spinraza. Developed by Ionis Pharmaceuticals in collaboration with Biogen, Spinraza also works on splicing of mRNA transcripts to promote production of a missing protein. In 2016, it became the first therapy approved for treating a rare neuromuscular disorder called spinal muscular atrophy (SMA).

SMA is somewhat different, though. It isn’t a haploinsufficiency — it occurs when both gene copies are defective, not just one — but it’s an unusual disease from a genetics standpoint. Because of a quirk in the human genome, it turns out that people have a kind of backup gene that doesn’t normally function because its mRNA undergoes faulty splicing. With Spinraza acting as a guide to help the mRNA splice correctly, that backup gene can be made operational and do the job that the damaged gene copies can’t do.

Few diseases are like this. But Stoke’s scientific cofounders, molecular geneticist Adrian Krainer of Cold Spring Harbor Laboratory in New York (who helped to develop Spinraza) and his former postdoctoral researcher Isabel Aznarez, realized that there was a whole world of other ailments — haploinsufficiencies — for which this type of splice modulation could be beneficial.

Spinraza was the prototype. Stoke’s portfolio is full of the next-generation editions. “We brought it to the next level,” says Aznarez, who now serves as head of discovery research at Stoke.

Striking a balance

There was a time when Dravet researchers were more focused on traditional gene replacement therapies. They aimed to insert a working version of the SCN1A gene into the genome of a virus and then introduce the engineered virus into brain cells. The problems proved manifold, though.

For starters, the virus vehicles generally used in gene therapy strategies — adeno-associated viruses (AAVs) — are too small to hold all 6,030 of the DNA letters that constitute the SCN1A gene sequence.

Researchers tried a few potential workarounds. At University College London, for example, gene therapist Rajvinder Karda and her colleagues split the SCN1A gene in half and delivered both parts into mice in different virus carriers. And at the University of Toronto, neuroscientist David Hampson and his group tried introducing a smaller gene that would fit in a single AAV vector and compensate for the SCN1A deficiency in an indirect way.

But none of those efforts advanced past mouse experiments. And while it is technically feasible to deliver the entire SCN1A gene into cells if you use other kinds of viral vectors, as researchers at the University of Navarra in Spain showed in mice, those viruses are generally considered unsafe for use in people.

To get protein levels just right, scientists say, it is best to follow the cell’s own lead.

What is more, even if gene replacement could be made to work, there are many reasons to think it would not be ideal for diseases like Dravet in which the underlying defect is mediated by an imbalance of protein levels. The amount of protein produced by those kinds of gene therapies can be unpredictable, and so are the types of cells that end up manufacturing the proteins.

To get protein levels just right, scientists say, it is best to follow the cell’s own lead, tapping into the ways that it naturally produces the protein of interest only in certain tissues of the body, and then providing a therapeutic nudge to aid the process along.

CAMP4 Therapeutics, for example, is using antisense therapies, like Stoke. But instead of targeting the splicing of gene transcripts, CAMP4’s drugs are directed at regulatory molecules that act like rheostats to control how much of those transcripts are made in the first place. By blocking or stabilizing different regulatory molecules, the company claims it can ramp up the activity of target genes in a precise and tunable way.

“It’s basically teaching the body to do it a little bit better,” says Josh Mandel-Brehm, president and CEO of CAMP4, which is based in Cambridge, Massachusetts.

In theory, the gene-editing technology known as CRISPR could obviate the need for all of these therapeutic approaches. Gene editing allows you to perfectly correct a mistake in a gene — so one could edit a faulty DNA sequence to correct it and render kids with Dravet or some other haploinsufficiency disease as good as new.

But the technology is nowhere near ready for prime time. (Some of the first CRISPR therapies to be tested in children have failed to demonstrate much benefit.) Plus, any gene-correction therapy would have to be tailored to the unique nature of a given patient’s mutations — and there are more than 1,200 Dravet-causing mutations in the SCN1A gene alone.

That’s why Jeff Coller, an RNA biologist at Johns Hopkins University and a scientific cofounder of Tevard, prefers therapeutic strategies that can address all manner of disease-causing alterations in a gene of interest, as most companies are doing now. “Having a mutation-agnostic technology is a way of going after the entire cohort of patients,” he says.

“We’re open to any approach that would help our daughters.”

Daniel Fischer

Tevard, whose mission is to “reverse” Dravet syndrome (the company’s name is Dravet spelled backward), is approaching this challenge in various ways. Some involve engineered versions of other RNAs that are key for protein production; known as “transfer” RNAs, they help to ferry amino acid building blocks to the growing protein strands. Others are intended to help bring beneficial regulatory molecules to sites of SCN1A gene activity.

But all of Tevard’s therapeutic candidates remain at least a year away from clinical testing, whereas STK-001 is in human trials today. So the company’s chief executive, Daniel Fischer — who, along with board chair and cofounder Warren Lammert, has a daughter affected by Dravet — is considering enrolling his child, now 13, in the Stoke trial rather than waiting for his own company’s efforts to bear fruit.

“We’re open to any approach that would help our daughters,” Fischer said over lunch last November at the company’s headquarters.

“And help people with Dravet generally,” added Lammert. “We’d love to see many of these things succeed.”

Editor’s note: This article was amended on April 14, 2023, to correct Gopi Shanker’s relationship with Tevard Biosciences. Shanker is Tevard’s former chief scientific officer; he is now chief scientific officer with Beam Therapeutics.

Elie Dolgin is a science journalist in Somerville, Massachusetts.

This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews.

A brief history of colorful presidential relatives, from Alice Roosevelt to Hunter Biden

Hunter Biden embraces his father, President Joe Biden, and his stepmother, Jill, at Biden’s 2021 inauguration. Drew Angerer/Getty Images

Shannon Bow O'Brien, The University of Texas at Austin

Hunter Biden, the younger son of U.S. President Joe Biden, is expected to plead guilty to two misdemeanor tax charges as part of a recently announced deal with the Justice Department that will help him avoid the federal charges for possessing a gun while using illegal drugs.

Joe Biden has long defended his son amid his drug addiction and other personal issues, including a paternity scandal and ongoing court battle over child support.

The president responded to the news of Hunter’s charges, saying on June 20, 2023, that he is “very proud of my son”.

I am a scholar of the American presidency and have looked at how the children and other family members of presidents have been thrust into the nation’s spotlight, often unwittingly. Their shortcomings, vices and sometimes even physical appearance have been fodder for gossip columns, political opponents and comedians.

Hunter Biden is not the first child of a president to be charged with a crime. Jenna and Barbara Bush pleaded “no contest” in 2001 to misdemeanor charges of underage drinking and using a false ID. Amy Carter was arrested for protesting in 1985, and before his father was president, Donald Trump Jr. was arrested for public drunkenness in 2001.

But nearly all presidents have had incidents involving their kids and other family members that attracted public scrutiny. Some of the events fall into questionable prank category, like when Tad Lincoln, the son of Abraham Lincoln, sprayed dignitaries with fire hoses.

Other incidents are less innocuous and amusing.

A colorized portrait of former President Theodore Roosevelt’s family features his oldest daughter, Alice, in the center. Stock Montage/Getty Images

Youthful indiscretions

James Madison raised his troubled stepson, John Payne Todd, as his own. Todd regularly engaged in gambling, drinking and womanizing. Madison went deeply into debt trying to pay off Todd’s vices, including once bailing him out of debtor’s prison. In the mid-1800s, Todd’s debts eventually forced his widowed mother to sell the family estate, Montpelier.

Todd even had a lawyer visit his mother on her deathbed to rewrite her will, making himself her sole heir.

Alice Roosevelt, the oldest child of Theodore Roosevelt, also presented some complications for her father during his presidency in the early 1900s.

Alice had a strained relationship with her father and his second wife, Edith. When her parents suggested sending her to a boarding school, Alice responded: “If you send me, I will humiliate you. I will do something that will shame you. I tell you I will.”

In a time when women were expected to be demur, Alice smoked, drank, partied and even sometimes wore a pet snake as an accessory.

Theodore Roosevelt once said, “I can do one of two things: I can be president of the United States or I can control Alice Roosevelt. I cannot possibly do both.”

Alice was later banned from the Taft White House after burying a voodoo doll in the likeness of the new first lady, Helen Herron Taft, on the property.

Neil Bush, son of George H.W. Bush and brother to George W. Bush, also has a colorful history.

Neil was the director of a large savings and loans company that collapsed in 1988, after it made improper and illegal loans. This cost taxpayers more than US$1 billion at the time and resulted in an embarrassing payout to federal banking regulators.

People also criticized Neil because of his ties to Chinese investors and his limited knowledge about industries that employed him, leading to accusations of influence peddling.

Neil Bush, like Hunter Biden, was also the subject of paternity accusations during his divorce.

That’s my brother

Presidential brothers have been another particular sore point for some presidents.

Lyndon Johnson’s brother, Sam Houston Johnson, was often quite talkative after he had a few drinks. The president eventually had to use the Secret Service to follow his brother to ensure he didn’t disclose any embarrassing information to the press .

Billy Carter, former President Jimmy Carter’s brother, reveled in his notoriety. As the president’s brother, he toured the country to make money and hawk his own Billy Beer.

He urinated on a runway before the press corps while waiting for people.

When Carter was running for reelection in 1980, Billy took money from the Libyan government and became a foreign agent for the country – while also making inflammatory and antisemitic statements to justify his behavior.

Billy’s association with Libya ultimately led to a Senate investigation and complicated his brother’s failed reelection campaign.

Former President Bill Clinton comforts his half-brother Roger in 1994, shortly after their mother’s death. POOL/AFP via Getty Images

Roger Clinton, the younger half-brother of former President Bill Clinton, also engaged in questionable activities. In the 1980s, before the Clinton presidency, Roger sold cocaine to an undercover officer.

Later, during the Clinton administration, Roger’s Secret Service codename was “Headache.”

Bill Clinton pardoned Roger for his drug offenses right before leaving office in January 2001.

Hunter Biden stands next to his father, President Joe Biden, at an event in 2016. Kris Connor/WireImage

Keeping it in the family

Presidents are like everyone else. They, too, have family members who do or say things that eventually become stories for the dinner table – or tales people want to push under the rug.

A federal judge still needs to approve Hunter Biden’s deal with the Justice Department that would allow him to avoid prison time for paying $1 million in taxes late and possessing a gun.

And he is still not free of other controversies. The Republican-controlled House continues to investigate his bank records, as well as lingering questions about money he received from foreign organizations.

Hunter himself has said that he is accountable for his actions, and I do not think it is fair to conflate the administration with the activities of an adult son.

He is not the first presidential relative who has caused turmoil, and he won’t be the last.

Shannon Bow O'Brien, Associate Professor of Instruction, The University of Texas at Austin

This article is republished from The Conversation under a Creative Commons license.

3 Healthy Habits to Protect Your Skin

(Family Features) As the first line of defense against the outside world, skin is the body’s largest organ and takes on an important role in maintaining overall health. While products like sunscreen and moisturizer can help skin thrive, healthy skin starts from within where food and beverage choices can play a key role.

One example is grapes: Emerging research suggests consuming grapes may help protect healthy skin even when exposed to UV light, which is known to be damaging. A study published in the journal “Antioxidants,” in which people consumed 2 1/4 cups of grapes every day for two weeks, showed increased resistance to sunburn and reduced markers of UV damage at the cellular level.

This study reinforced previous and similar findings published in the “Journal of the American Academy of Dermatology.” Grapes are also a hydrating food with 82% water content; hydration is essential to healthy skin.

To take care of your skin, consider these skin-friendly health tips.

Protect Skin While Outdoors
While perhaps an obvious step to some, one of the most direct ways you can protect skin is by applying sunscreen – most experts recommend 30 SPF or higher – before heading outdoors and reapplying every 1-2 hours. Additionally, consider wearing protective clothing, such as a hat large enough to shade your face and neck. If you plan to spend extended time in the sun, opt for a lightweight, long-sleeve shirt and pants for maximum skin coverage.

Fill Your Plate with Healthy, Hydrating Foods
Nutritious foods, including fruits and vegetables, can play an important role in achieving an overall balanced diet with adequate hydration. Enjoying the goodness of fresh or frozen Grapes from California can provide extra hydration and a boost of beneficial antioxidants and other polyphenols that help protect the health and function of the body’s cells, including those in the skin.

Drink water throughout the day, and for added flavor, infuse with fruits like frozen grapes. Simply rinse, pat dry, remove from the stems and freeze the grapes for 2 hours in a single layer on a sheet pan for flavorful ice cube replacements.

For an easy, refreshing way to add grapes to your menu and stay hydrated on warm days, try this Frosty Grape Hibiscus Slush for a subtly sweet, fruity tea in frozen form.

Manage Stress
Whether it’s caused by a lengthy to-do list or general anxieties, stress can negatively impact skin health while even exacerbating certain conditions. Managing stress can offer a reprieve in multiple ways, including encouraging healthier skin. Some simple ways to relieve stress include exercising, getting enough sleep, lightening or limiting your workload, scaling back on to-do lists and making time for things you enjoy.

Visit GrapesFromCalifornia.com for more information on grapes and health and delicious recipes.

Frosty Grape Hibiscus Slush
Prep time: 15 minutes, plus freezing overnight
Servings: 6 (1 cup each)

9          hibiscus tea bags
6          cups boiling water
3          cups Grapes from California puree (green, red, black or mixture)
4 1/2    tablespoons frozen lemonade concentrate, thawed
1 1/2    tablespoons lime juice (optional)

Steep tea bags in boiling water. Remove tea bags and stir in grape puree, lemonade concentrate and lime juice, if desired. 

Pour into ice cube trays and freeze overnight until firm. 

In blender, blend until slushy, stirring as needed.

Notes: If no ice cube trays, freeze mixture in large container about 1 1/2 inches deep. Let soften slightly then break into pieces with knife before blending and serving.

Nutritional information per serving: 80 calories; 1 g protein; 21 g carbohydrates; 0 g fat; 0 g saturated fat; 0 mg cholesterol; 0 mg sodium; 1 g fiber.

SOURCE:
California Table Grape Commission

Ocean heat is off the charts – here’s what that means for humans and ecosystems around the world

The Indian Ocean’s heat is having effects on land, too. NOAA Coral Reef Watch

Annalisa Bracco, Georgia Institute of Technology

Ocean temperatures have been off the charts since mid-March 2023, with the highest average levels in 40 years of satellite monitoring, and the impact is breaking through in disruptive ways around the world.

The sea of Japan is more than 7 degrees Fahrenheit (4 degrees Celsius) warmer than average. The Indian monsoon, closely tied to conditions in the warm Indian Ocean, has been well below its expected strength.

Spain, France, England and the whole Scandinavian Peninsula are also seeing rainfall far below normal, likely connected to an extraordinary marine heat wave in the eastern North Atlantic. Sea surface temperatures there have been 1.8 to 5 F (1 to 3 C) above average from the coast of Africa all the way to Iceland.

So, what’s going on?

Sea surface temperatures are running well above the average since satellite monitoring began. The thick black line is 2023. The orange line is 2022. The 1982-2011 average is the middle dashed line. ClimateReanalyzer.org/NOAA OISST v2.1

El Niño is partly to blame. This climate phenomenon, now developing in the equatorial Pacific Ocean, is characterized by warm waters in the central and eastern Pacific, which generally weakens the trade winds in the tropics. This weakening of those winds can affect oceans and land around the world.

But there are other forces at work on ocean temperatures.

Underlying everything is global warming – the continuing rising trend of sea surface and land temperatures for the past several decades as human activities have increased greenhouse gas concentrations in the atmosphere.

The world just came off three straight years of La Niña – El Niño’s opposite, characterized by cooler waters rising in the equatorial Pacific. La Niña has a cooling effect globally that helps keep global sea surface temperatures in check but can also mask global warming. With that cooling effect turned off, the heat is increasingly evident.

Arctic sea ice was also unusually low in May and early June, and it may play a role. Losing ice cover can increase water temperatures, because dark open water absorbs solar radiation that white ice had reflected back into space.

These influences are playing out in various ways around the world.

The effects of extraordinary Atlantic heat

In early June 2023, I visited the NORCE climate center in Bergen, Norway, for two weeks to meet with other ocean scientists. The warm waters and mild winds across the eastern North Atlantic brought a long stretch of sunny, warm weather in a month when more than 70% of days normally would have been downpours.

The whole agricultural sector of Norway is now bracing for a drought as bad as the one in 2018, when yield was 40% below normal. Our train from Bergen to Oslo had a two-hour delay because the brakes of one car overheated and the 90 F (32 C) temperatures approaching the capital were too high to allow them to cool down.

Many scientists have speculated on the causes of the eastern North Atlantic’s unusually high temperatures, and several studies are underway.

Weakened winds caused the Azores high, a semi-permanent high pressure system over the Atlantic that affects Europe’s weather, to be especially weak and brought less dust from the Sahara over the ocean during the spring, which may have increased the amount of solar radiation reaching the water. A decrease in human-produced aerosol emissions in Europe and in the United States over the past few years – which has succeeded in improving air quality – may also have reduced the cooling effect such aerosols have.

A weakened monsoon in South Asia

In the Indian Ocean, El Niño tends to cause a warming of the water in April and May that can dampen the crucial Indian monsoon.

That may be happening – the monsoon was much weaker than normal from mid-May to mid-June 2023. That can be a problem for a large part of South Asia, where most of the agriculture is still rain-fed and depends heavily on the summer monsoon.

India saw sweltering temperatures in May and June 2023. Sanjeev Verma/Hindustan Times via Getty Images

The Indian Ocean also saw an intense, slow-moving cyclone in the Arabian Sea this year that deprived land of moisture and rainfall for weeks. Studies suggest storms can sit for longer over warmer waters, gaining strength and pulling moisture to their core, and that can deprive surrounding land masses of water, increasing the risk of droughts, wildfires and marine heat waves.

North American hurricane season up in the air

In the Atlantic, the weakening trade winds with El Niño tend to tamp down hurricane activity, but warm Atlantic temperatures can supercharge those storms. Whether the ocean heat, if it persists into fall, will override El Niño’s effects remains to be seen.

Risk of marine heat waves in South America

Marine heat waves can also have huge impacts on marine ecosystems, bleaching coral reefs and causing the death or movement of entire species. Coral-based ecosystems are nurseries for fish that provide food for 1 billion people around the world.

The reefs of the Galapagos Islands and those along the coastlines of Colombia, Panama and Ecuador are already at risk of severe bleaching and mortality from this year’s El Nino. Meanwhile, the Japan Sea and the eastern Mediterranean Sea are both losing their biodiversity to invasive species – giant jellyfish in Asia and lionfish in the Mediterranean – that can thrive in warmer waters.

These kinds of risks are increasing

Spring 2023 was exceptional, with several chaotic weather events accompanying the formation of El Niño and the exceptionally warmer temperatures in many parts of the world. At the same time, the warming of the oceans and atmosphere increase the chances for this kind of ocean warming.

To lower the risk, the world needs to reduce baseline warming by limiting excess greenhouse gas emissions, like fossil fuels, and move to a carbon-neutral planet. People will have to adapt to a warming climate in which extreme events are more likely and learn how to mitigate their impact.

Annalisa Bracco, Professor of Ocean and Climate Dynamics, Georgia Institute of Technology

This article is republished from The Conversation under a Creative Commons license. 

Like hungry locusts, humans can easily be tricked into overeating

Our bodies crave more food if we haven’t had enough protein, and this can lead to a vicious cycle — especially if we’re reaching for ultraprocessed instead of high-fiber whole foods

By Tim Vernimmen

This story starts in an unusual place for an article about human nutrition: a cramped, humid and hot room somewhere in the Zoology building of the University of Oxford in England, filled with a couple hundred migratory locusts, each in its own plastic box.

It was there, in the late 1980s, that entomologists Stephen Simpson and David Raubenheimer began working together on a curious job: rearing these notoriously voracious insects, to try and find out whether they were picky eaters.

Every day, Simpson and Raubenheimer would weigh each locust and feed it precise amounts of powdered foods containing varying proportions of proteins and carbohydrates. To their surprise, the young scientists found that whatever food the insects were fed, they ended up eating almost exactly the same amount of protein.

In fact, locusts feeding on food that was low in protein ate so much extra in order to reach their protein target that they ended up overweight — not chubby on the outside, since their exoskeleton doesn’t allow for bulges, but chock-full of fat on the inside.

Inevitably, this made Simpson and Raubenheimer wonder whether something similar might be causing the documented rise in obesity among humans. Many studies had reported that even as our consumption of fats and carbohydrates increased, our consumption of protein did not.

Might it be that, like locusts, we are tricked into overeating, in our case by the irresistible, low-protein, ultraprocessed foods on the shelves of the stores where we do most of our foraging? That’s what Raubenheimer and Simpson, both now at the University of Sydney, argue in their recent book “ Eat Like the Animals” and in an overview in the Annual Review of Nutrition.

Simpson took us through the reasoning and the data in an interview with Knowable Magazine. This conversation has been edited for length and clarity.

How does an entomologist end up studying nutrition in humans?

My interest in feeding behavior goes all the way back to my undergraduate years in Australia, where I was studying the food choices of sheep blowfly maggots, which are laid in the wool of sheep and eat the sheep alive. For my PhD, I took an opportunity at the University of London, England, to study appetite and food intake control in migratory locusts, which exist in two extreme forms — one solitary and one aggregating in swarms that create devastating plagues.

Since they had this reputation for being absolutely voracious, we surely did not expect them to have a lot of nuance in the way they control what they eat. But I started to explore whether they could sense the requirement for different nutrients and use it to regulate their intake. That led to experiments with artificial diets of different nutrient compositions, which showed that locusts have nutrient-specific appetites for protein and carbohydrate: Their food tastes differently to them depending on what they need, and that enables them to balance their diets.

In 1987, I started working with David Raubenheimer at Oxford to find out what happens if you put locusts on a diet that forces different appetites to compete, by feeding the animals mixtures of proteins and carbohydrates in relative amounts that do not match their intake target. We made 25 different diets, measured how much the locusts ate, how quickly they developed, and how big they grew, and found that when protein and carbohydrate appetites compete, protein wins.

What that means is that if you put animals on a low-protein, high-carb diet, they’ll eat more calories to get that limiting protein, and they’ll end up obese. Likewise, if you put them on a high-protein, low-carb diet, they don’t need to eat as much to get to their protein target, and they end up losing weight. It was at that point that we knew we had discovered a powerful new way of looking at nutrition.

We started looking at lots of different species of insects, and found that they, too, had the capacity to regulate their intake of protein and carbohydrate, and that protein was often, but not always, the prioritized nutrient.

By now, we have studied species from cats, dogs and free-ranging primates to fish in aquaculture to slime molds to humans, in a variety of contexts — from understanding health and disease to optimizing animal feed to conservation biology.

You’ve found that the nutrient levels that animals aim for are the ones at which they grow, survive or reproduce best. Just by following their appetite, they eat exactly what they need. Why don’t we?

There are two possibilities. Either our biology is broken, or it still works but we’re in the wrong environment. What we’ve shown in our studies is the latter. What has happened is our appetites, which evolved in natural environments, have now been subjected to highly engineered food environments which have been designed, in many ways, to hack our biology, to subvert our appetites.

One of our favorite examples came from a study we did in Sydney. We confined people in a sleep center for three four-day periods and provided them with foods and menus which were varied and matched in palatability, but were all of the same nutrient composition for a given week.

We had a 25 percent protein week, a 15 percent protein week, and a 10 percent protein week, and the subjects didn’t know that was going on. As far as they were concerned, they were allowed to eat what they wanted, everything tasted equally well and there were lots of choices. But it turned out that during the low-protein week, people ate more, because their protein appetite would drive them to eat more calories, to try and get enough protein. They largely did this by increasing snacking between meals, and selectively on savory-flavored snacks.

We’ve subsequently discovered that when you’re low in protein, as is the case on a 10 percent protein diet, you have elevated levels of a hormone called FGF21, which is mainly released from the liver. What we’ve shown in mouse experiments and confirmed in humans is that FGF21 switches on savory-seeking behavior, which is a proxy for eating protein.

Now, if you have that response and the nearest savory thing is a bag of barbecue-flavored potato crisps, that’s a protein decoy. You’ll be misdirected to eat that, but you’ll not get any substantial amount of protein. You’ll remain protein-hungry, and you’ll have to eat more to satisfy that protein appetite. That means you’re accumulating excess calories, and that is precisely what happens to us in our modern food environment.

You argue that ultraprocessed foods are especially likely to make us consume too many calories. Why would that be so?

Over the last couple of years, population survey data have shown that the average person in the US, Australia or the UK gets more than half their calories from highly processed foods — in some cases it’s 90 percent or more. As the proportion of ultraprocessed food in the diet increases, protein intake remains largely the same, but energy intake goes up steeply because of the dilution of protein by the fats and carbs in these foods. So this protein appetite we discovered initially in locusts operates in us too. In our modern food environment, it drives us to overconsume energy, and that sets up a vicious cycle.

What we find is that as people become overweight, their metabolism becomes dysregulated. Their tissues become less responsive to insulin, which normally regulates protein metabolism. This makes protein metabolism less efficient, causing the body to break down lean tissues like muscle and bone and burn protein to produce energy.

That increases people’s protein target, so they’ll eat even more, put on more weight, become even more metabolically dysregulated, start craving more protein, and so on.

We’ve since taken that basic idea and used it in a paper at the end of last year to propose a new understanding of why women are prone to put on weight during menopause. That’s a period when protein breakdown rates go steeply upwards in bone and muscle because of the decline in reproductive hormones. And it is driving the same sort of outcome that I just described.

You also see it in aging, you see it in people who smoke, you see it with excess alcohol intake — these are all circumstances in which FGF21 goes up, protein appetite goes up, protein breakdown goes up, and you’ll end up in this sort of vicious cycle.

As an entomologist, how did you manage to convince colleagues in nutrition science this matters?

It’s just the accumulation of evidence. Last fall, we spoke at the Royal Society in London at a big obesity conference, and the response to our talk indicated to me that protein leverage is now accepted as one of the main, credible underlying explanations for obesity. Our evidence comes from pre-clinical studies, it comes from clinical studies, it comes from cohort studies, it comes from population-level analyses, it comes from deep mechanistic biology — it’s now unanswerably there. The remaining question is: Of the various influences that drive obesity, is protein appetite a main one? We think it probably is.

Why would protein be the strongest driver of our appetites? What would be the biological logic?

All three macronutrients — fat, carbs and protein — contain calories, so we can burn any of them to yield energy, and we can use any of them to make glucose, which is the preferred fuel for our cells and brain.

But only protein has nitrogen, which we need for many other purposes, from maintaining our cells to producing offspring. You don’t want to eat too little protein.

That leaves the question of why we don’t overeat it. Why do we eat fewer calories than we need on a high-protein diet, rather than eat excess protein? To us, that implied there is a cost to eating too much protein, and we set out to discover that cost in fruit flies. We designed a large experiment where we confined a thousand flies to one of 28 diets varying in the ratio of protein and carbohydrate, the two major macronutrients for flies. What we found was that flies lived longest on a lower-protein, high-carbohydrate diet, but laid most eggs on a higher-protein, lower-carbohydrate diet. A really-high-protein diet, finally, wasn’t better for either outcome.

That overturned a hundred years of thinking around restricting calories and aging: The dominant view was that reduced calories were what prolonged life, but our data showed that the type of calories matter, notably the ratio of protein to carbs. And it created quite a stir at the time — the paper came out in 2008.

We set out to do the same experiment in mice. To do that, we had to add fat as a third nutrient dimension to the dietary design. That involved an enormous study. We took more than 700 mice and put them on one of 25 different diets varying in the concentration and ratio of protein, carbohydrate and fat. It took 6 metric tons of experimental diet to run that study across the 3 or 4 years it took before the oldest mice died.

That was the first of a whole series of huge mouse experiments where we looked at different types of carbohydrate, different ratios of amino acids, and so on. The long and the short of it was that the mice lived longer on low-protein, high-carbohydrate diets, but reproduced better on high-protein, low-carbohydrate diets — very similar to the flies.

Importantly, the benefit of low protein was only realized when the carbohydrates were harder-to-digest complex carbohydrates like fiber and starch, not simple sugars. If you translate that into human populations and look across the world for human populations that live the longest, lo and behold they’re the ones on diets low in protein and high in healthy carbohydrates and fats, such as Mediterranean-style diets and the traditional Okinawan diet.

I’m sure they’re all very healthy, but how do people on these diets manage their appetites?

That’s a really interesting question. The Okinawans certainly are hungry for protein. In traditional Japanese cuisine, there is an almost religious prominence given to umami flavors, which are the signature of protein, the savory characteristic in foods. So that’s like a societal protein appetite.

The other question is: On a 10 percent protein diet like the Okinawan diet, why aren’t they all suffering obesity because they have to eat far more to get their protein? The answer is that the traditional diet is low in energy, and high in fiber. By eating more to try and attain their protein target, they get more fiber instead of more calories, until their stomach is full. That’s a crucial distinction with the modern industrialized food environment, which isn’t just low in protein, but also low in fiber — and high in fats and carbs.

If low protein and low fiber content are the main problem, would it help to just increase them in ultraprocessed foods? Or would that not be sufficient?

Science has already nudged the industry in that direction in a couple of ways that are not altogether helpful. The high-protein snack industry is a phenomenon which reflects this science. Their response was: We’ve got a new market now for high-protein bars. Whether or not that’s ultimately going to help the world’s waistline is less clear at the moment, as the food environment as a whole remains replete with low-protein, low-fiber, ultrapalatable processed foods.

The principal driver for reducing protein content in ultraprocessed foods was that protein is more expensive than fats and carbohydrates. It was cheaper to take some of the protein out and add a little more fat and carbs, particularly when you can make things taste fantastic by mixing sugar and fat and a bit of salt together.

Some of the big providers of lifestyle interventions have shifted towards increasing the percent protein in the diet. And of course, all of the commercially successful fad diets of recent decades have been high-protein diets. But none of them takes account of the fact that there’s potentially a cost to a higher-protein diet.

As we’ve shown originally in flies and mice, a higher protein-to-carbohydrate ratio than we need speeds up aging in our tissues. That being said, if you’re suffering obesity and diabetes, the benefits of a high-protein diet in terms of weight loss may outweigh the costs. It’s a matter of understanding the relative costs and benefits associated with different diet compositions, relating them to personal goals and breaking away from some of the crazy diet zealotry that goes on online and is promoted by many of the fad diet industries.

So you’d recommend eating more fiber and fewer carbs and fats rather than eating more protein? How does that affect your own choice of snacks outside of mealtimes?

I have a deep love of food, cooking, and even hunting and gathering — I’m a fisherman. But I’m as susceptible to the siren call of ultraprocessed foods and beverages as everyone else. These products have been designed to be irresistible, so I avoid them, except on occasions. They are not in the house or my shopping trolley.

As a family, we eat whole foods, plenty of fruits and vegetables, pulses, nuts and grains, as well as dairy and high-quality meat, fish and poultry. There are many ways to mix a nutritionally balanced and delicious diet without the use of apps or computer programs. After all, no species in the history of life on Earth ever needed those.

The trick is to take advantage of our evolved biology of appetite by creating an environment in which our appetites can guide us to a healthy and balanced diet. We need to help our appetites work for ourselves and our health, not the profits of the food and beverage industries.

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Tim Vernimmen, a freelance science journalist based near Antwerp, Belgium, has always had a healthy appetite, but now wonders how fitting that term really is. He does like to cook, which helps him steer clear of highly processed foods most of the time.

This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews.

Mission trips are an evangelical rite of passage for US teens – but why?

Where to? georgemuresan/iStock via Getty Images Plus

Caroline R. Nagel, University of South Carolina

As tourists head to airports this summer, American travelers are likely to see groups of young people in matching T-shirts awaiting flights to Latin America or further afield. Their T-shirts sport biblical verses or phrases like “Here I am, send me” or “Called to serve,” and the teens may gather for prayer before boarding.

These young people are heading off to be short-term missionaries: an experience that has become a rite of passage in some corners of Protestant Christianity as overseas travel has become more affordable for Americans. According to some estimates, as many as 2 million youth and adults per year participated in Christian mission trips before the pandemic, including overseas trips and trips to poor communities at home.

While it is difficult to confirm these numbers, mission trips are now especially commonplace within evangelical churches, with larger and more affluent churches offering multiple trips throughout the year. Some congregations plan their mission trips in-house. Others enlist the services of mission companies with names like World Race, He Said Go and World Gospel Mission. Typically, these companies combine humanitarian service, development projects and faith. They promise participants adventure, spiritual growth and an opportunity to serve as Jesus’ hands and feet in the world.

I have been studying short-term missionaries for the past six years. I have interviewed dozens of pastors, trip leaders and young missionaries, and I have had the opportunity to participate in a mission trip in Central America. Through this research, I have learned about why so many young Christians want to go on mission trips and have been struck by their desire to “serve.” Yet, as a geographer, I am concerned by their lack of knowledge about the people and places they visit.

‘White man’s burden’

The missionary impulse within Christianity comes from the Great Commission, a Gospel verse in which Jesus instructs his disciples “to go and make disciples of all nations, baptizing them in the name of the Father and of the Son and of the Holy Spirit.”

The spirit of evangelism thrived among European and American Christians in the 19th century, fueled by frontier expansion and colonization. Protestant missionaries spread throughout Africa, Asia, Latin America and the Pacific, seeking to win souls for Christ. Also important, in many of these men’s and women’s eyes, was something often referred to as the “white man’s burden”: the imperialist idea that they had a duty to introduce Western civilization to supposedly “backward” people.

Missionaries had mixed success in converting so-called natives to Christianity. But they left lasting impacts through the many institutions they established around the world, including schools, universities and hospitals.

A teacher and students at a Christian missionary school in Shanghai around 1855. William Jocelyn/Getty Images

Missions 2.0

Contemporary missionaries are the inheritors of these earlier waves. Yet they also have some distinctive characteristics.

Historically, mission work was a lifelong calling and profession, one that often meant never coming home. Career missionaries continue to have a role in missions today, sometimes financially supported by denominational organizations like the Southern Baptist Convention’s International Missions Board or by donations from individual churches.

But the movement is now dominated by short-termers who are in the “mission field” for a couple of weeks or months. Some trips go to destinations where Christians are a minority, such as the Middle East, India or Southeast Asia. More commonly, they take place in countries with a sizable Christian population and partner with local evangelical organizations and churches “planted” by long-term missionaries. Trip organizers I interviewed emphasized that the mission teams are there to serve and to take direction from their local partners.

Another distinctive feature of short-term missions is their approach to faith. Rather than push “conversion” as a goal, today’s mission leaders emphasize “relationship building” in hopes that connections will gradually lead people closer to Christian beliefs.

Trips are oriented not just around the spiritual transformation of the local community but also the spiritual transformation of missionaries themselves. Pastors and organizers say that trips are meant to teach young American Christians what it means to live as a disciple of Jesus, to share the gospel and to love people who are not like them. Organizers talk about young people learning to “live missionally” and to see opportunities to build God’s kingdom in their ordinary lives.

Sacred and secular

Short-term missions, however, also appeal to young people’s desire to see the world and to be adventurous. The language used to describe and promote trips is remarkably similar to secular overseas volunteering or “voluntourism,” as well as gap-year programs before college.

Both experiences are built around the idea of getting out of your comfort zone and experiencing cultural differences in the name of self-improvement, preparing for life in a globalized, diverse world.

Another similarity is that both Christian and secular programs usually involve some kind of service project: building a house, digging a well or leading recreational activities for children. Such activities are meant to give young people confidence in their ability to “make a difference” in the world, while developing resilience and gratitude.

‘Walk with the poor’

Not all evangelicals see the value of mission trips. Critics have argued that American short-term mission teams dump unwanted goods on host communities, are culturally insensitive and commonly assume that locals need American “expertise.” Construction projects push out local workers and often result in shoddily built structures – suggesting the enormous sums of money spent on mission trips might be better spent if donated directly to local organizations.

Helping or, ultimately, hurting? kali9/E+ via Getty Images

Books like “When Helping Hurts,” by evangelical authors Brian Fikkert and Steve Corbett, aim to explain how leaders can make mission trips more effective, both in terms of alleviating poverty and in terms of evangelism.

Warning against a “white savior” attitude, they suggest that the purpose of short-term missions is to “walk with the poor” and build lasting relationships that will lead people to Christ.

Beyond the bubble

In my research, I have met mission trip leaders who are trying to put these ideas into practice without harming the communities they visit. But troubling elements persist.

Trip organizers want to open American Christians’ eyes to realities of the world outside of their bubbles. Yet their messages tends to imply the effects of poverty can be overcome through personal faith in Christ. Short-term missionaries I interviewed did not blame people for being poor but were reluctant to describe the hardship they witnessed in terms of social injustice.

The mission teams I studied learned almost nothing about the impacts of corruption, violence and social inequality on the communities they believed they were there to help. Trip leaders felt that such information would bore participants and detract from the spiritual aims of the trip. In effect, what mattered to the volunteers and organizers was simply that places were poor and foreign rather than the reasons poverty was so entrenched.

Many of the short-term missionaries I interviewed described feeling changed by their trip and becoming more aware of their own privilege. But the focus on spiritual fulfillment means that these young people may be missing out on opportunities to deepen their understandings of the world and to build solidarity with the communities they visit.

Caroline R. Nagel, Professor of Geography, University of South Carolina

This article is republished from The Conversation under a Creative Commons license. 

Big money bought the PGA Tour, but can it make golf a popular sport in Saudi Arabia?

The kingdom hopes to have 135,000 kids playing golf in school by 2025 and plans to build 23 new courses by 2030. JulyVelchev/iStock via Getty Images

Josh Woods, West Virginia University

The recent merger between the PGA Tour, DP World Tour and Saudi-funded LIV Golf – now being reviewed by the U.S. Department of Justice over antitrust concerns – stunned the golf community.

A year ago, the idea that Saudi Arabia – an absolute monarchy with few golf courses, scant public interest in the sport and a notorious human rights record – could suddenly leap to the top of the global golf hierarchy seemed impossible. Now, the new company will be chaired by Yasir Al-Rumayyan, the governor of Saudi Arabia’s sovereign wealth fund, or PIF.

Most observers explained the surprising merger with a simple principle: Cash is king. As professional golfer Rory McIlroy put it, “At the end of the day, money talks.”

PIF, an investment fund with more than US$700 billion in Saudi government money, can certainly wield immense influence.

But even PIF’s deep pockets may not be deep enough to achieve the Saudi grand vision of bringing golf to the Arab masses.

An ambitious vision

The fund’s venture into golf, according to Golf Saudi, a division of PIF, is part of a broader economic growth plan aimed at reducing the country’s reliance on oil and enacting sweeping societal and lifestyle transformations.

One of the driest nations in the world hopes to build new golf courses, “spread the sport of golf among the Saudi society” and “enhance the Kingdom’s position in the game of golf locally and internationally,” as Golf Saudi noted on its website.

The organization has outlined the country’s grand plans for growing the game: 250,000 Saudis trying golf in 2023, 135,000 kids playing it in school by 2025, 23 new courses built by 2030 and 37,000 registered golfers by 2040.

American golfer Matthew Wolff competes at the PIF Saudi International at Royal Greens Golf & Country Club in Al Murooj, Saudi Arabia, in February 2023. Luke Walker/WME via Getty Images

If you build it, will they come?

The strategies for achieving these goals – state funding for new infrastructure, school programs, ambassadors and global golf clout – involve a top-down economic approach.

But as I argue in my recent book, “Emerging Sports as Social Movements,” such an approach to sports often falls short.

Similar cases in the U.S. point to an uphill battle for Saudi golf promoters. Heady predictions about emerging American sports have been just as optimistic – and potentially flawed – as those coming out of Saudi Arabia about golf.

Lacrosse was once the poster child of fast-growing sports in the U.S., but the number of players declined from 2.1 million in 2015 to 1.8 million in 2022, according to the Sports Business Research Network.

The same data source dubs pickleball the fastest-growing sport in America, but its total number of players is tiny compared with dozens of well-known sports and recreational activities in the U.S., and its quest for mainstream status will likely encounter stumbling blocks, despite having wealthy benefactors and celebrity sponsors like NBA superstar LeBron James.

In recent years, cornhole, drone racing, mountain biking, disc golf and ax throwing have established professional leagues, appeared on ESPN and attracted major corporate sponsors. But they haven’t achieved anywhere near the participation levels, fandoms or cultural foundation that football, basketball, baseball, or hockey possess in the U.S.

Meanwhile, soccer, as the joke goes, is America’s sport of the future — and always will be.

What money can’t buy

The kingdom’s plans for growing golf resemble its efforts to promote soccer. Lured by the promise of making fortunes, some of the world’s best-known soccer players, including the Portuguese star Cristiano Ronaldo and French sensation Karim Benzema, have joined the Saudi Pro League.

Soccer, however, is already the most popular sport in Saudi Arabia. The Saudi national team has been competitive in Asia for decades and has qualified for six FIFA World Cup tournaments. Its run in 2020 included a stunning victory over Argentina, the eventual winner.

In contrast, programs to develop professional golf talent in Saudi Arabia are still in an early stage of development.

The history of sports is filled with stories of visionary business people taking big financial risks to grow their sports.

But emerging sports are more like social movements than business enterprises. Like social movements, sports rarely experience substantial, sustained growth unless countless individuals and groups come together, create a community, share an identity and foster a culturally meaningful sporting experience.

With vast oil wealth, Saudi Arabia showed the world how easy it is to buy a seat at the table of an elite sport. It appears equally poised to construct a new golf infrastructure at home. And yet, even if it built a string of world-class courses from the Red Sea to the Persian Gulf, golf still may not bloom in the desert without a golf culture and the one thing money alone cannot buy: a love of the game.

Josh Woods, Professor of Sociology, West Virginia University

This article is republished from The Conversation under a Creative Commons license.

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