Life at the bottom of the Pacific Ocean is slow, dark and quiet. Strange creatures glitter and glow. Oxygen seeps mysteriously from lumpy, metallic rocks. There is little to disturb these deep-ocean denizens.

“There’s weird life down here,” said Bethany Orcutt, a geomicrobiologist at Bigelow Laboratory for Ocean Sciences.

Research in the deep sea is incredibly difficult given the extreme conditions, and rare given the price tag.

On Thursday, President Trump signed an executive order that aims to permit, for the first time, industrial mining of the seabed for minerals. Scientists have expressed deep reservations that mining could irreversibly harm these deep-sea ecosystems before their value and workings are fully understood.

What’s down there, anyway?

Seafloor mining could target three kinds of metal-rich deposits: nodules, crusts and mounds. But right now, it’s all about the nodules. Nodules are of particular value because they contain metals used in the making of electronics, sophisticated weaponry, electric-vehicle batteries and other technologies needed for human development. Nodules are also the easiest seafloor mineral deposit to collect.

Economically viable nodules take millions of years to form, sitting on the seafloor the whole time. A nodule is born when a resilient bit of matter, such as a shark tooth, winds up on the ocean floor. Minerals with iron, manganese and other metals slowly accumulate like a snowball. The largest are the size of a grapefruit.

Life accumulates on the nodules, too. Microbial organisms, invertebrates, corals and sponges all live on the nodules, and sea stars, crustaceans, worms and other life-forms scuttle around them.

About half of the known life in flat, vast expanses of seafloor called the abyssal plain live on these nodules, said Lisa Levin, an oceanographer at the Scripps Institution of Oceanography. But “we don’t know how widespread species are, or whether if you mine one area, there would be individuals that could recolonize another place,” she said. “That’s a big unknown.”

How do you mine the sea?

Two main approaches to nodule mining are being developed. One is basically a claw, scraping along the seabed and collecting nodules as it goes. Another is essentially an industrial vacuum for the sea.

In both, the nodules would be brought up to ships on the surface, miles above the ocean floor. Leftover water, rock and other debris would be dropped back into the ocean.

Both dredging and vacuuming would greatly disturb, if not destroy, the seafloor habitat itself. Removing the nodules also means removing what scientists think is the main habitat for organisms on the abyssal plain.

Mining activities would also introduce light and noise pollution not only to the seafloor, but also to the ocean surface where the ship would be.

Of central concern are the plumes of sediment that mining would create, both at the seafloor and at depths around 1,000 meters, which have “some of the clearest ocean waters,” said Jeffrey Drazen, an oceanographer at the University of Hawaii at Manoa. Sediment plumes, which could travel vast distances, could throw life off in unpredictable ways.

Sediment could choke fish and smother filter-feeders like shrimp and sponges. It could block what little light gets transmitted in the ocean, preventing lanternfish from finding mates and anglerfish from luring prey. And laden with discarded metals, there’s also a chance it could pollute the seafood that people eat.

“How likely is it that we would contaminate our food supply?” Dr. Drazen said. Before mining begins, “I really would like an answer to that question. And we don’t have one now.”

What do mining companies say?

Mining companies say that they are developing sustainable, environmentally friendly deep-sea mining approaches through research and engagement with the scientific community.

Their research has included basic studies of seafloor geology, biology and chemistry, documenting thousands of species and providing valuable deep-sea photos and video. Interest in seafloor mining has supported research that might have been challenging to fund otherwise, Dr. Drazen said.

Preliminary tests of recovery equipment have provided some insights into foreseeable effects of their practices like sediment plumes, although modeling can only go so far in predicting what would happen once mining reached a commercial scale.

Impossible Metals, a seafloor mining company based in California, is developing an underwater robot the size of a shipping container that uses artificial intelligence to hand pick nodules without larger organisms, an approach it claims minimizes sediment plumes and biological disturbance. The Metals Company, a Canadian deep-sea mining company, in 2022 successfully recovered roughly 3,000 tons of nodules from the seafloor, collecting data on the plume and other effects in the process.

The Metals Company in March announced that it would seek a permit for seafloor mining through NOAA, circumventing the International Seabed Authority, the United Nations-affiliated organization set up to regulate seafloor mining.

Gerard Barron, the company’s chief executive, said in an interview on Thursday that the executive order was “not a shortcut” past environmental reviews and that the company had “completed more than a decade of environmental research.”

Anna Kelly, a White House spokeswoman, said the United States would abide by two American laws that govern deep-sea exploration and commercial activities in U.S. waters and beyond. “Both of these laws require comprehensive environmental impact assessments and compliance with strong environmental protection standards,” she said.

What are the long-term risks?

Many scientists remain skeptical that enough is known about seafloor mining’s environmental effects to move forward. They can only hypothesize about the long-term consequences.

Disrupting the bottom of the food chain could have ripple effects throughout the ocean environment. An extreme example, Dr. Drazen said, would be if sediment diluted the food supply of plankton. In that case they could starve, unable to scavenge enough organic matter from a cloud of sea dust.

Tiny plankton are a fundamental food source, directly or indirectly, for almost every creature in the ocean, up to and including whales.

Part of the challenge in understanding potential effects is that the pace of life is slow on the seafloor. Deep-sea fish can live hundreds of years. Corals can live thousands.

“It’s a different time scale of life,” Dr. Levin said. “That underpins some of the unknowns about responses to disturbances.” It’s hard for humans to do 500-year-long experiments to understand if or when ecosystems like these can bounce back or adapt.

And there are no guarantees of restoring destroyed habitats or mitigating damage on the seafloor. Unlike mining on land, “we don’t have those strategies for the deep sea,” Dr. Orcutt said. “There’s not currently scientific evidence that we can restore the ecosystem after we’ve damaged it.”

Some scientists question the need for seafloor mining at all, saying that mines on land could meet growing demand for metals.

Proponents of deep-sea mining have claimed that its environmental or carbon footprint would be smaller than traditional mining for those same minerals.

“There has been no actual recovery of minerals to date,” said Amy Gartman, an ocean researcher who leads the United States Geological Survey seabed minerals team, referring to commercial-scale mining. “We’re comparing theoretical versus actual, land-based mining practices. If and when someone actually breaks ground on one of these projects, we’ll get a better idea.”

Eric Lipton contributed reporting.

Do we really have free will when it comes to eating? It’s a vexing question that is at the heart of why so many people find it so difficult to stick to a diet.

To get answers, one neuroscientist, Harvey J. Grill of the University of Pennsylvania, turned to rats and asked what would happen if he removed all of their brains except their brainstems. The brainstem controls basic functions like heart rate and breathing. But the animals could not smell, could not see, could not remember.

Would they know when they had consumed enough calories?

To find out, Dr. Grill dripped liquid food into their mouths.

“When they reached a stopping point, they allowed the food to drain out of their mouths,” he said.

Those studies, initiated decades ago, were a starting point for a body of research that has continually surprised scientists and driven home that how full animals feel has nothing to do with consciousness. The work has gained more relevance as scientists puzzle out how exactly the new drugs that cause weight loss, commonly called GLP-1s and including Ozempic, affect the brain’s eating-control systems.

The story that is emerging does not explain why some people get obese and others do not. Instead, it offers clues about what makes us start eating, and when we stop.

While most of the studies were in rodents, it defies belief to think that humans are somehow different, said Dr. Jeffrey Friedman, an obesity researcher at Rockefeller University in New York. Humans, he said, are subject to billions of years of evolution leading to elaborate neural pathways that control when to eat and when to stop eating.

As they have probed how eating is controlled, researchers learned that the brain is steadily getting signals that hint at how calorically dense a food is. There’s a certain amount of calories that the body needs, and these signals make sure the body gets them.

The process begins before a lab animal takes a single bite. Just the sight of food spurs neurons to anticipate whether a lot of calories will be packed into that food. The neurons respond more strongly to a food like peanut butter — loaded with calories — than to a low-calorie one like mouse chow.

The next control point occurs when the animal tastes the food: Neurons calculate the caloric density again from signals sent from the mouth to the brainstem.

Finally, when the food makes its way to the gut, a new set of signals to the brain lets the neurons again ascertain the caloric content.

And it is actually the calorie content that the gut assesses, as Zachary Knight, a neuroscientist at the University of California San Francisco, learned.

He saw this when he directly infused three types of food into the stomachs of mice. One infusion was of fatty food, another of carbohydrates and the third of protein. Each infusion had the same number of calories.

In each case, the message to the brain was the same: The neurons were signaling the amount of energy, in the form of calories, and not the source of the calories.

When the brain determines enough calories were consumed, neurons send a signal to stop eating.

Dr. Knight said these discoveries surprised him. He’d always thought that the signal to stop eating would be “a communication between the gut and the brain,” he said. There would be a sensation of having a full stomach and a deliberate decision to stop eating.

Using that reasoning, some dieters try to drink a big glass of water before a meal, or fill up on low-calorie foods, like celery.

But those tricks have not worked for most people because they don’t account for how the brain controls eating. In fact, Dr. Knight found that mice do not even send satiety signals to the brain when all they are getting is water.

It is true that people can decide to eat even when they are sated, or can decide not to eat when they are trying to lose weight. And, Dr. Grill said, in an intact brain — not just a brainstem — other areas of the brain also exert control.

But, Dr. Friedman said, in the end the brain’s controls typically override a person’s conscious decisions about whether they feel a need to eat. He said, by analogy, you can hold your breath — but only for so long. And you can suppress a cough — but only up to a point.

Scott Sternson, a neuroscientist with the University of California in San Diego and Howard Hughes Medical Institute, agreed.

“There is a very large proportion of appetite control that is automatic,” said Dr. Sternson, who is also a co-founder of a startup company, Penguin Bio, that is developing obesity treatments. People can decide to eat or not at a given moment. But, he added, maintaining that sort of control uses a lot of mental resources.

“Eventually, attention goes to other things and the automatic process will wind up dominating,” he said.

As they probed the brain’s eating-control systems, researchers were continually surprised.

They learned, for example, about the brain’s rapid response to just the sight of food.

Neuroscientists had found in mice a few thousand neurons in the hypothalamus, deep in the brain, that responded to hunger. But how are they regulated? They knew from previous studies that fasting turned these hunger neurons on and that the neurons were less active when an animal was well fed.

Their theory was that the neurons were responding to the body’s fat stores. When fat stores were low — as happens when an animal fasts, for example — levels of leptin, a hormone released from fat, also are low. That would turn the hunger neurons on. As an animal eats, its fat stores are replenished, leptin levels go up, and the neurons, it was assumed, would quiet down.

The whole system was thought to respond only slowly to the state of energy storage in the body.

But then three groups of researchers, independently led by Dr. Knight, Dr. Sternson and Mark Andermann of Beth Israel Deaconess Medical Center, examined the moment-to-moment activity of the hunger neurons.

They began with hungry mice. Their hunger neurons were firing rapidly, a sign the animals needed food.

The surprise happened when the investigators showed the animals food.

“Even before the first bite of food, the activity of those neurons shut off,” Dr. Knight said. “The neurons were making a prediction. The mouse looks at food. The mouse predicts how many calories it will eat.”

The more calorie-rich the food, the more neurons turn off.

“All three labs were shocked,” said Dr. Bradford B. Lowell, who worked with Dr. Andermann at Beth Israel Deaconess. “It was very unexpected.”

Dr. Lowell then asked what might happen if he deliberately turned off the hunger neurons even though the mice hadn’t had much to eat. Researchers can do this with genetic manipulations that mark neurons so they can turn them on and off with either a drug or with a blue light.

These mice would not eat for hours, even with food right in front of them.

Dr. Lowell and Dr. Sternson independently did the opposite experiment, turning the neurons on in mice that had just had a huge meal, the mouse equivalent of a Thanksgiving dinner. The animals were reclining, feeling stuffed.

But, said Dr. Andermann, who repeated the experiment, when they turned the hunger neurons on, “The mouse gets up and eats another 10 to 15 percent of its body weight.” He added, “The neurons are saying, ‘Just focus on food.’”

Researchers continue to be amazed by what they are finding — layers of controls in the brain that ensure eating is rigorously regulated. And hints of new ways to develop drugs to control eating.

One line of evidence was discovered by Amber Alhadeff, a neuroscientist at the Monell Chemical Senses Center and the University of Pennsylvania. She recently found two separate groups of neurons in the brainstem that respond to the GLP-1 obesity drugs.

One group of neurons signaled that the animals have had enough to eat. The other group caused the rodent equivalent of nausea. The current obesity drugs hit both groups of neurons, she reports, which may be a factor in the side effects many feel. She proposes that it might be possible to develop drugs that hit the satiety neurons but not the nausea ones.

Alexander Nectow, of Columbia University, has another surprise discovery. He identified a group of neurons in the brainstem that regulate how big a meal is desired, tracking each bite of food. “We don’t know how they do it,” he said.

“I’ve been studying this brainstem region for a decade and a half,” Dr. Nectow said, “but when we went and used all of our fancy tools, we found this population of neurons we had never studied.”

He’s now asking if the neurons could be targets for a class of weight loss drugs that could upstage the GLP-1s.

“That would be really amazing,” Dr. Nectow said.