Nearly two decades ago, during a Thanksgiving gathering in New York’s Finger Lakes, my family went to a local tavern for our last dinner. I have a hazy memory of my father ordering either fried shrimp or chicken. What’s vivid, however, is him pushing the plate away, claiming he felt unwell and couldn’t eat. Across the table, his face seemed ashen. It was a meal he didn’t touch, a foreshadowing, perhaps, of how something unseen was beginning to consume him.
Shortly after, my parents returned to their Florida home. About two months later, in February 2001, my father struggled to swallow a simple glass of orange juice. A doctor’s visit, a series of tests, and then the stark diagnosis: esophageal cancer. My sister, in an attempt to offer some solace, emailed the family a link to an American Cancer Society page. The clinical words on the screen were anything but comforting: esophageal cancer, rare and stealthy, often undetected until it reaches an advanced, difficult-to-treat stage.
The news hit me like a physical blow. I spent that entire weekend in tears, my eyes swollen shut. My father wasn’t just my parent; he was my confidant, my closest friend.
His medical team, initially optimistic, outlined a rigorous plan: chemotherapy and radiation to reduce the tumors, followed by surgery two months later. The surgery took place in May, but by June, a horrifying development – tumors were erupting across his body, both internally and externally, resembling angry mosquito bites. One particularly large tumor appeared on his chin, which we morbidly nicknamed “the nipple.”
Courtesy of the Chesler family
In February 2001, Edwin “Eddie” Chesler, my father, encountered difficulty swallowing a glass of orange juice, leading to a diagnosis of esophageal cancer. He had less than a year to live.
In a desperate attempt, my father enrolled in a Phase I clinical trial at Memorial Sloan Kettering Cancer Center in New York City. He commuted from Long Island, where he was staying with my aunt, several times a week. By September, the doctors delivered the devastating news – the trial wasn’t working. Three months later, he was gone. He was only 62.
The medical explanation for his adenocarcinoma, a type of cancer typically found in the lower esophagus, was gastroesophageal reflux disease (GERD), or chronic heartburn. When the sphincter between the stomach and esophagus weakens, stomach acid can backflow into the esophagus. This repeated acid exposure irritates the esophageal lining, causing cellular changes. In this transformation, cell division can become erratic, leading to tumors that initially wreak havoc in the esophagus, then spread to lymph nodes, and eventually to organs like the lungs, liver, and brain.
Seventeen years have passed since my father’s death, and as I approach his age at passing (I’m now 55), a chilling fear grips me: the same illness that claimed him might claim me. I, too, suffer from acid reflux, a condition alarmingly common in America. Heartburn, in fact, is almost epidemic, with over 60 million Americans experiencing reflux at least once a month, according to the American College of Gastroenterology. Some studies suggest that more than 15 million Americans endure heartburn symptoms daily.
Globally, squamous cell carcinoma, linked to alcohol and tobacco use and usually occurring in the upper and middle esophagus, is the predominant form of esophageal cancer. This was once the case in the U.S., but around 1997, a shift occurred. Americans diagnosed with esophageal cancer became significantly more likely to have adenocarcinoma, the type associated with GERD. The National Cancer Institute reports that esophageal adenocarcinoma is one of the fastest-growing cancers in the nation. In 1973, it affected just 3 in a million Americans; by 2014, that number had surged to 26 per million – a staggering increase of over 600%.
Dr. Michael Ebright, a thoracic surgeon in Connecticut, notes that many patients, like my father, seek medical help when they experience difficulty swallowing. “Some patients can’t even swallow their own saliva,” he explains. The image of my father internally suffocating sends a shiver down my spine.
One major risk factor for esophageal cancer is Barrett’s esophagus. This condition develops when chronic acid exposure alters the esophageal lining at a cellular level, transforming it to resemble the lining of the stomach or intestines, which are adapted to acidic environments. This biological progression, known as metaplasia, starts with squamous cells, the normal esophageal lining, being replaced by glandular cells – normal cells, but in the wrong location. This can progress to dysplasia, where these glandular cells become abnormal due to DNA changes. Neoplasia, the next stage, is when cells become so distorted and fragmented they are barely recognizable, marking the beginning of potential spread.
Not everyone with GERD develops Barrett’s esophagus; Dr. Ebright estimates about 10%. And even with Barrett’s, the risk of progressing to esophageal cancer is less than 1% per year. Yet, data from the National Cancer Institute reveals a disturbing trend: the incidence of esophageal adenocarcinoma has increased across all age groups over 30 since the 1970s. While the disease disproportionately affects older white men, squamous cell carcinoma remains more prevalent in African Americans. For individuals my father’s age, the incidence rate increased fivefold between 1975 and 2015. While rising obesity and poor diet are strongly suspected links, they don’t fully account for this dramatic rise.
“There’s another risk factor, or maybe multiple risk factors, we’re missing, that’s likely contributing. We just don’t know what it is,” Dr. Ebright admits.
This uncertainty leaves millions of Americans desperately searching for relief from heartburn symptoms, turning to pills, specialized pillows, and chewing gum. For a growing number, these symptoms are not just uncomfortable but potentially lethal. Researchers are intensely investigating the mechanics of this rapidly escalating cancer, exploring theories that range from the underappreciated bacterial ecosystem within our guts to the very medications designed to treat reflux.
Despite doctors assuring me my esophageal cancer risk is low, worry persists. Heartburn is a frequent companion. Swallowing sometimes feels labored, food momentarily halting in my throat. My dentist confirms acid reflux is impacting my teeth – tangible evidence of its unwelcome presence.
The complete picture behind this malignant surge remains elusive. Like many Americans, and acutely aware of my father’s fate, I crave understanding and reassurance.
Courtesy of the Mayo Clinic
Barrett’s esophagus, a significant risk factor for esophageal cancer, occurs when the esophageal lining changes due to persistent acid exposure.
Seeking answers, I visited Dr. Russell Hales, a radiation oncologist specializing in esophageal cancer at Johns Hopkins University School of Medicine in Baltimore. Entering the Sidney Kimmel Comprehensive Cancer Center, I was struck by a wave of sadness, imagining the hopes of those seeking to overcome this disease, a disease that had ultimately defeated my father. A memory surfaced: shortly after my father’s diagnosis, I confided in an ex-boyfriend whose father had died of cancer years prior. “These doctors make you think they can save them,” he’d said, “but they can’t.” His words, intended to comfort, felt horrifyingly bleak.
In Dr. Hales’ office, we discussed the mechanics of acid reflux. Acid itself isn’t inherently problematic when confined to the stomach. The issue arises when the lower esophageal sphincter, the muscular ring between the stomach and esophagus, malfunctions, allowing acid to escape and irritate the esophageal lining.
Heartburn sufferers are generally aware of factors that can weaken this sphincter, including caffeine, alcohol, smoking, obesity, pregnancy, and hiatal hernias. However, Dr. Hales pointed out another less-known factor: cortisol. Excess cortisol, a stress hormone regulating various bodily processes, can also relax the sphincter. Its effect is so predictable that Dr. Hales routinely prescribes antacids alongside steroids, anticipating heartburn as a side effect.
Dr. Hales reiterated obesity as a significant risk factor for esophageal adenocarcinoma. I countered, “I must be the exception then.” “What do you mean exception? You’re not going to get this, okay?” he reassured me, snapping me back to the present.
We delved into the differences between squamous cell carcinoma and adenocarcinoma, noting their distinct risk factors and treatment responses. “Adenocarcinomas are more prone to spread,” Dr. Hales explained, “while squamous cell carcinomas tend to cause more localized problems.” When I asked which was “better,” his response was sobering: “Well, they’re both problematic. Ultimately, you can die from localized disease or distant disease. It’s a problem either way.”
The typical patient profiles also differ. While cautious about generalizations, Dr. Hales described the squamous cell cancer patient as often thin, a heavy smoker and/or drinker, and generally presenting with more advanced disease due to delayed medical attention – “the type of person who puts duct tape over the ‘service engine soon’ light in the car.”
Describing the adenocarcinoma patient, Dr. Hales offered a contrasting sketch: “The adenos are well-dressed, a bit younger, slightly overweight, or even quite overweight. They look like business guys who’ve gotten a little pudgy… like Donald Trump.” Squamous patients, in contrast, tend to be thinner and “might smell of cigarette smoke. Sometimes, there are alcohol dependence issues.”
He emphasized that these were broad caricatures, and both diseases are profoundly complex, affecting diverse individuals. “Most cancers are random events,” he concluded. “Sometimes there aren’t simple answers.”
His words weren’t entirely comforting, prompting more questions. I brought up antibiotics, recalling my own six-month course of antibiotics for a recurring bladder infection 25 years prior, around my initial reflux diagnosis. Could antibiotic overuse be contributing to the rise in esophageal adenocarcinoma? Dr. Hales acknowledged it wasn’t a top risk factor currently but admitted this could change. “Ten years from now, I may be saying something different, but currently, data shows a small association with antibiotics,” he stated.
Some studies have hinted at a link between antibiotics and esophageal and other cancers, but the evidence remains preliminary. Even Dr. Ben Boursi, an expert in clinical oncology and radiotherapy and co-author of some of these studies, cautioned against making a definitive link between esophageal adenocarcinoma and antibiotics, calling it a “giant leap.”
Before leaving Baltimore, I walked by the Inner Harbor, pausing on the steps of the Maryland Science Center. Observing the people around me – schoolchildren, adults, cyclists, police officers, groups of women, ice cream eaters – a recurring pattern emerged: many were overweight.
The link between rising obesity and heartburn-related cancer seemed undeniable. Yet, obesity’s inability to explain every case of esophageal adenocarcinoma still troubled me, leading me to contact Dr. Martin Blaser, a microbiologist and director of the Center for Advanced Biotechnology and Medicine at Rutgers University, who has spent a decade studying the gut microbiome. Dr. Blaser believes the rise in esophageal adenocarcinoma is at least partially attributable to the decline of Helicobacter pylori (H. pylori) bacteria.
Courtesy of the Chesler family
My father was my closest confidant and best friend. I often contemplate when cancer began its silent takeover and what, if anything, could have been done differently.
In his book, “Missing Microbes,” Dr. Blaser proposes that our bodies harbor ancient microbes with beneficial roles, and disruptions to this ecosystem have consequences. “One consequence,” he explained, “is the decrease in some diseases, like stomach cancer, and the increase in others, like esophageal adenocarcinoma.”
He attributes this partly to H. pylori, “once the dominant organism in the human stomach, which has been gradually disappearing throughout the 20th century.” While this decline predates antibiotics, medications contribute to H. pylori’s disappearance, which Dr. Blaser believes fuels esophageal adenocarcinoma.
“In short,” Dr. Blaser summarized, “I think the rise in esophageal cancer likely began in the 1960s and 1970s, and the initial trigger was the loss of Helicobacter pylori.”
He explained that in the past, when H. pylori was ubiquitous, acid production naturally decreased around age 40 as the bacteria damaged acid-producing cells. “Without H. pylori,” he stated, “people are reaching 40, 50, 60, and still producing high levels of acid.”
This constant high acid exposure is unprecedented in human history. Dr. Blaser added a fascinating detail: “The strongest predictor of H. pylori presence is whether your mother had it. It’s passed down through generations.”
Dr. Jason Mills, a gastroenterology professor at Washington University School of Medicine, further elucidated the H. pylori-acid dynamic. He explained that H. pylori, while acid-tolerant, prefers the less acidic end of the stomach and, in some individuals, can trigger events that kill acid-secreting cells, potentially leading to gastric cancer. However, on average, less H. pylori in a population correlates with higher acid levels and increased esophageal acid exposure.
Some researchers propose that the rise in esophageal adenocarcinoma is partly due to the decreasing prevalence of Helicobacter pylori (H. pylori), shown here with multiple flagella.
What’s driving the decline of H. pylori? Improved sanitation in developed countries is one factor. However, Dr. Mills, speaking from a European Helicobacter & Microbiota Study Group meeting, suggested antibiotic overuse also plays a role. “My H. pylori colleagues here believe increased antibiotic use might contribute to decreased H. pylori,” he noted.
The irony is stark: H. pylori increases stomach cancer risk, once the leading cause of cancer death in the U.S. up to the 1930s. By reducing H. pylori, we aimed to lower stomach cancer rates, but inadvertently created a scenario with excessive stomach acid, elevating the risk of esophageal cancer. “We’ve essentially traded stomach cancer for esophageal cancer,” Dr. Mills summarized.
A key puzzle for cancer researchers is why metaplasia becomes a cancer risk. Dr. Mills, who organized a symposium on this very topic, believes it’s because cells in hostile environments (acid and bile in the esophagus, bacterial inflammation in the stomach) revert to fetal or embryonic states focused solely on reproduction. Understanding this “paligenosis” process, as his lab terms it, could unlock pathways to halt or reverse metaplasia and potentially regenerate lost tissue.
While scientists delve into cellular mechanisms, reflux sufferers seek immediate symptom relief. Home remedies abound. Chewing gum, for example, has shown some promise in small studies. A writing group member, Delia O’Hara, swears by sugarless gum, claiming it eliminated her GERD years ago.
Health food stores offer raft-forming alginates, mixtures that expand in the stomach, creating a pH-neutral foam barrier that prevents acid reflux. A company in Australia, KFSU, produces dietary fiber from sugarcane. Initially intended for general gut health, pharmacists noticed customers using it for reflux. The managing director, Gordon Edwards, theorizes the fiber reduces acid bubbling.
For my own reflux, I rely on apple cider vinegar and a foam wedge pillow. The vinegar’s efficacy lacks scientific backing, but gravity explains the wedge’s benefit. Elevating the body during sleep prevents stomach contents from flowing into the esophagus, akin to a pitched sewer pipe.
I interviewed Aaron Clark, developer of an improved wedge pillow, MedCline. He collaborated with Dr. Carl Melcher, a Barrett’s esophagus patient, who believed positional therapy could be therapeutic. After years of development, Clark created a pillow allowing comfortable left-side sleeping, the optimal position to minimize acid reflux.
Intrigued, I purchased a MedCline pillow for $238 (a “bargain” at 40% off, I rationalized). The cost, I told myself, was a small price to protect my esophagus. Yet, even conventional reflux treatments, H-2-receptor blockers (Zantac, Pepcid) and proton pump inhibitors (PPIs, like Prilosec, Nexium), face scrutiny. H-2 blockers reduce acid production but can cause side effects. PPIs, while stronger, have been linked to infections, bone fractures, vitamin B12 deficiency, and ironically, increased stomach cancer risk.
Concerned about PPI overuse, the Lexington VA Medical Center implemented a PPI stewardship program to reduce their use. A 2017 meta-analysis even questioned PPIs’ effectiveness in preventing cancer in Barrett’s esophagus patients. Some researchers now propose PPIs might cause Barrett’s by reducing stomach acidity, leading to bile reflux into the esophagus, potentially inducing metaplasia.
However, Dr. Stuart Spechler, a gastroenterologist at Baylor Scott & White Center for Esophageal Diseases, argues against this anti-PPI bias. He cites methodological issues in studies linking PPIs to adverse effects, emphasizing the difficulty in establishing cause-and-effect in retrospective studies. He stresses the importance of appropriate PPI use for severe reflux, stating, “If you have severe reflux disease and don’t take PPIs, your disease will return.” He acknowledges PPI overuse but maintains their benefits outweigh risks when used correctly.
For those seeking PPI alternatives, surgical options exist. Hiatal hernias can be surgically repaired with fundoplication. The LINX Reflux Management System, a magnetic ring placed around the lower esophagus, tightens the sphincter. Both aim to reduce or eliminate reflux medication.
For Barrett’s esophagus with dysplasia, radiofrequency ablation or cryotherapy can destroy abnormal tissue. Endoscopic mucosal resection can remove tumors not yet invading the esophageal muscle. Esophagectomy, surgical removal of cancerous tissue, is an option for more advanced, operable cancers.
My father underwent an esophagectomy. Eight inches of his esophagus were removed, his stomach repositioned. The surgeon initially declared the surgery a success, almost casually mentioning a “small black spot” on his lung, likely insignificant.
That night, our family sought solace in marijuana, attempting to banish the words “spot” and “lung” from our thoughts, robotically repeating, “The surgery went well.” We didn’t want to cry, or appear intoxicated to concerned neighbors.
This was May 2001. By June, tumors emerged on my father’s arms – unusual for esophageal cancer. His surgeon, upon hearing of the cancer’s progression, was visibly shocked. A month later, the news worsened: liver metastasis. My cry of “Noooooo!” was misinterpreted as a joke by a coworker. I fled to a nearby park, watching clouds morph into shapes – a bunny, a dog – realizing my father wouldn’t see many more. He didn’t.
During Yom Kippur last year, at the Yizkor memorial service, a father and daughter performed a musical interlude. The slightly chubby, nervous girl played clarinet harmony. I was reminded of my junior high band days, always third clarinet, playing whole notes, overshadowed by the first clarinet melodies. Third clarinet held no glory.
Yet, after their performance, the father’s fist bump to his daughter triggered a sudden memory of my own father, my unwavering cheerleader. Awkward in junior high, with frizzy hair and thick glasses, my father always listened to my teenage woes, reminding me of my inherent worth. In our home movies, there’s one of me, broccoli-haired and bespectacled, playing those whole notes, the song unrecognizable.
The GERD treatment dilemma lies in balancing medication and surgery. Dr. David Spector, director of bariatric and anti-reflux surgery at Brigham and Women’s Faulkner Hospital, believes too many rely on medication, neglecting surgical options. PPIs, he notes, don’t always halt esophageal deterioration. Early intervention is crucial in progressive conditions like GERD. Gastrointestinal surgeons are advocating for a shift in approach.
“If we can eliminate the irritating factor, reflux, we could potentially stop the progression from reflux to Barrett’s to dysplasia to cancer,” Dr. Spector asserts. Despite some publications downplaying surgery’s role in Barrett’s management, he argues a subset of patients would benefit significantly.
“Many patients with severe reflux are never referred for proper treatment, remaining on medication for years,” he explains. He sees patients referred only after years of PPI use when concerns about long-term effects surface.
Dr. Spector stratifies reflux based on duration, regurgitation symptoms, and medication dependence. He considers my father a prime example of someone with long-term reflux who developed esophageal changes that ultimately led to fatal cancer.
Courtesy of the Chesler family
My father and I in happier times. Looking back at old photos, I wonder: was his body already deteriorating? What was his esophagus like then?
Dr. Spector anticipates a shift in perspective within the next decade or two, where anti-reflux surgery becomes a more considered option, recognizing that “Barrett’s can regress if we remove the offending problem, reflux.”
Cancer, like environmental changes like rising sea levels, can be a slow, insidious progression. As a doctor friend put it, “It’s not like you’re cancer-free one day and have cancer the next. It’s that one day you find out.” An insidious force subtly invades, whispering to cells, turning them against themselves.
Looking at old photos of my father, I wonder: was his body already failing him at my brother’s 1991 wedding? He had only a decade left. What was the state of his esophagus then?
Dr. Spector’s questions turn to my own health.
“I was diagnosed with reflux at 29,” I tell him.
“Wow,” he responds – a doctor’s “wow” that never bodes well.
“I had chest pains, like a heart attack,” I explain. After diagnosis, “they put me on the purple pill, but after a year, I refused to take a pill for life.”
Dr. Spector probes my symptoms: chest pain radiating to my ear or jaw, “distractingly uncomfortable.”
“Do you ever have content rise into your throat – a bitter, burning feeling?” he asks.
“Yes,” I confirm.
“Bile-ish taste – at night?”
“More in the morning. My worst reflux might be overnight or early morning.”
“Wake up coughing or choking?”
“No,” but “I often wake with a sore throat.”
“A sore throat?” he repeats.
“I always fear throat cancer, imagining acid constantly reaching my throat,” I admit.
“When was your last gastroenterologist visit?”
Three years ago, I confess, but determined to schedule one soon.
This article was originally published on Undark. Read the original article.
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Caren Chesler
Caren Chesler is an award winning journalist whose work has appeared in The New York Times, Scientific American, Slate, Salon, and Popular Mechanics.
