Lee Friedlander coined a term for the subject of his work: the “social landscape.”

The great American documentary photographer, now 89, gives each row house and strip mall and mass-produced car a living and breathing personality. He frames places so as to imbue them with strangeness, movement, intrigue. He often makes what would normally be the background of a photograph the subject of a photograph. He does not treat American cityscapes as another photographer might treat a static mountain or an ancient river. He treats them like main characters—confused, chaotic, tragicomic, all-American characters.

More than 150 such images, captured from 1961 to 2022, are collected in the epic new retrospective Real Estate, published this month by the Eakins Press Foundation. The book ends with a play on a rider-on-the-trail image: a whole house being towed on a western highway, off to its next adventure. It begins with a play on a classic American beauty-queen photograph: A girl in a crown, sash, and white stole beams and waves at the camera. But she’s out of focus. Friedlander has us looking at the asphalt-shingle one-story home behind her.

Many of the images in this book contain such layering and texturing, characteristic of Friedlander’s photography: a child or an errant bit of debris in the foreground, a procession or an animal or a poster in the middle ground, a building under construction or a skyline or a grove of trees in the background, framed by a highway, riven by a telephone pole, hugged by a statue, seen most clearly in a mirror or through a window. Some of the images are stark: Places that are home to millions of people seem empty. Many are awkward. I am not sure how he manages to make a home look as if it’s posing awkwardly, but he does it again and again. This has the effect of making the houses look alive.

While soaking in the book’s images, I kept noting how often the only clue to when Friedlander might have taken the photo was the cut of a person’s pants or the style of their hat. (The boxy, low cars were a dead giveaway too.) Looking at the buildings, I was never quite sure. They have a timeless quality. That’s a credit to Friedlander, who makes every image feel jarring, fresh. But it was also a reminder of how many of those buildings are still among us today. This decades- and continent-spanning documentary of change reveals an American stasis. Our current housing crisis is due to our unwillingness to build, grow, and allow new life to come into our cities. Friedlander made the built environment look dynamic and alive; we cast it in amber. If only we saw those neighborhoods like he did.

Seaside, Oregon, 1972 (copyright Lee Friedlander, courtesy of Eakins Press Foundation and Fraenkel Gallery) Knoxville, Tennessee, 1971 (copyright Lee Friedlander, courtesy of Eakins Press Foundation and Fraenkel Gallery) Atlantic City, New Jersey, 1971 (copyright Lee Friedlander, courtesy of Eakins Press Foundation and Fraenkel Gallery) Left: Dallas, Texas, 2003. Right: Ridgewood, New Jersey, 2006. (© copyright Lee Friedlander, courtesy of Eakins Press Foundation and Fraenkel Gallery) California, 1961 (copyright Lee Friedlander, courtesy of Eakins Press Foundation and Fraenkel Gallery) Oxford, Ohio, 1976 (copyright Lee Friedlander, courtesy of Eakins Press Foundation and Fraenkel Gallery) Left: Victor, Colorado, 2001. Right: Boston, Massachusetts, 1975. (copyright Lee Friedlander, courtesy of Eakins Press Foundation and Fraenkel Gallery) New England, 1981 (copyright Lee Friedlander, courtesy of Eakins Press Foundation and Fraenkel Gallery) Buffalo, New York, 1962 (copyright Lee Friedlander, courtesy of Eakins Press Foundation and Fraenkel Gallery) San Francisco, California, 1977 (copyright Lee Friedlander, courtesy of Eakins Press Foundation and Fraenkel Gallery)

At first, doctors didn’t believe that bacteria could live in the stomach at all. Too acidic, they thought. But in 1984, a young Australian physician named Barry Marshall gulped down an infamous concoction of beef broth laced with Helicobacter pylori bacteria. On day eight, he started vomiting. On day 10, an endoscopy revealed that H. pylori had colonized his stomach, their characteristic spiral shape unmistakeable under the microscope.  

Left untreated, H. pylori usually establishes infections that persist for an entire lifetime, and they’re common: Half of the world’s population harbors H. pylori inside their stomach, as do more than one in three Americans. In most cases, the microbe settles into an asymptomatic chronic infection, but in some, it becomes far more troublesome. It can, for example, cause enough damage to the stomach lining to create ulcers. Worse still, H. pylori can lead to cancer. This single bacterium is by far the No. 1 risk factor in stomach cancers worldwide. By one estimate, some 70 percent can be attributed to H. pylori.

But what still puzzles doctors years later is why H. pylori has such different consequences for different people. Why is it asymptomatic in most but carcinogenic in others? Although the full answer is complex, one key factor seems to be mutations in H. pylori itself. Not every strain is created equal. The presence of select genes intensifies H. pylori’s pathogenicity, and even a single mutation in a single gene, scientists recently found, enhances the link to cancer. A small genetic tweak in a common stomach bug could have profound consequences for us, its unwitting hosts.

H. pylori has lived inside of us for a long time. Our ancestors who left Africa likely carried it inside them as they crossed continents and oceans, built and felled civilizations. And over the course of what some scientists hypothesize to be more than 100,000 years of co-evolution, H. pylori has exquisitely adapted to the harsh, acidic conditions of the human stomach.

It survives, for example, by producing “copious amounts” of an enzyme that neutralizes stomach acid, Richard Peek, a gastroenterologist at Vanderbilt, told me. H. pylori can also burrow into the mucus-gel lining of the stomach using powerful, whiplike flagella. The mucus lining offers a relative haven from stomach acid, but another prize lies underneath too: stomach cells, rich in nutrients that the bacteria needs to survive.

The way that H. pylori steals nutrients could be the key to how it ends up causing cancer. The bacterium isn’t necessarily out to hurt its human host. “H. pylori doesn’t want you to get an ulcer or to get cancer, but it needs to replicate to high enough levels in the stomach that it can be transmitted to another person,” Nina Salama, a biologist at Fred Hutchinson Cancer Center, told me. (The bacteria seem to spread through an infected person’s saliva, vomit, or feces.) But to replicate, it needs nutrients, in particular iron, which our cells probably hoard to starve pathogens.

In response, certain strains of H. pylori have evolved genetic changes that might make its iron-mining more efficient. But this also causes more collateral damage to the host’s stomach, enough damage, perhaps, to eventually trigger cancer. First, the bacteria uses a protein called HtrA—essentially “a pair of molecular scissors,” Peek said—to cut the bonds that hold stomach cells together, so the microbes can slip between. A single mutation in this scissor protein makes it better at cutting, a group based in Germany found in a recent study, and this mutation is disproportionately found in H. pylori strains isolated from people who developed stomach cancer.

Once H. pylori has wedged itself in between cells, it also has clever ways of accessing the nutrients inside. Certain strains carry a set of about 18 genes that collectively encode a molecular needle through which H. pylori injects bacterial proteins, triggering a cascade of changes to the cell. These hijacked cells end up giving up their iron more easily, but they also become worse at essential functions such as fixing damaged DNA. This set of approximately 18 genes, collectively called the “cag pathogenicity island,” are in fact disproportionately found in strains from cancer patients. Stomach cancer thus might be a secondary consequence of the microbe’s aggressive search for nutrients. For the H. pylori, “there’s no selective pressure to cause cancer in 80 years. The selective pressure is to acquire iron now,” Karen Guillemin, a microbiologist at the University of Oregon, said.

But not everyone infected with one of these cancer-linked strains will develop cancer. Other factors likely play a role too: diet, environment, and genetics of the individual patient  Stomach-cancer rates vary quite widely around the world, with the highest prevalence in East Asia. In Japan, doctors routinely test for H. pylori in people with no symptoms, and prescribe antibiotics if the tests come back positive. But some scientists have argued against aggressive treatment, pointing at hints that humans derive some benefits from living with H. pylori too. Those infected, for example, tend to have lower rates of asthma and allergy. Genetic signatures associated with more pathogenic H. pylori strains, Peek told me, would help identify those at highest risk, who could most benefit from antibiotics.

Marshall, the Australian doctor who infected himself with H. pylori, ultimately recovered just fine. His self-experiment, in addition to other studies with his collaborator Robin Warren, proved that the bacterium does indeed infect the stomach and does indeed cause stomach ulcers, which later spurred the work linking H. pylori to cancer. Understanding exactly how and why H. pylori becomes pathogenic is still key to finding the way to treat it, but in the past 40 years the significance of H. pylori to human health has become indisputable—so much so that in 2005, Marshall and Warren won the Nobel Prize in Medicine.