This means that when a telescope captures the light from a distant galaxy, the image does not reveal where that galaxy is today. It shows the galaxy as it appeared when the light began its journey. To estimate its present distance, astronomers must use a cosmological model that accounts for how the universe has expanded over time.

The leading model used today is called LCDM. It includes dark matter (different episode) and dark energy (different episode). The strengths and limitations of LCDM are worth discussing separately (different episode), but alternative models do not significantly change the overall picture described here.

The Edge of the Observable Universe

The universe is about 13.77 billion years old, but the most distant regions we can observe are now roughly 45 billion light-years away. Space expanded during the entire time that their light was traveling toward us.

This boundary is known as the particle horizon, the cosmological horizon, or the comoving horizon, depending on how stylish you feel in the moment. It defines the outer edge of our observable bubble and marks the greatest distance we can see today.

At first, the numbers seem contradictory. How can the observable universe extend 45 billion light years when the universe is only 13.77 billion years old? The answer is that the universe can expand faster than light.

Why Faster Than Light Expansion Is Allowed

This does not violate the laws of physics. The speed of light limits how quickly objects can move through space in a local region. An observer will never see a nearby rocket ship pass by faster than light.

Cosmic expansion is different. Faraway galaxies are not necessarily speeding through space in the usual sense. Instead, the space between us and those galaxies is growing. Special relativity does not place the same restriction on how quickly large distances can increase across the universe.

Astronomers can estimate how quickly a galaxy is receding by measuring its redshift. As a galaxy moves away, its light is stretched toward redder wavelengths in the electromagnetic spectrum. Edwin Hubble used this effect to uncover evidence that the universe is expanding.

In an expanding universe, more distant galaxies generally recede more quickly because a greater amount of space lies between them and us. More space means more distance that can expand.

The point at which galaxies begin receding faster than light is called the Hubble distance. It lies about 13.77 billion light-years away.

Why We Can Still See Faster Moving Galaxies

We can observe galaxies beyond the Hubble distance because the light reaching us today was emitted long ago, when those galaxies were much closer. We may also eventually receive light from some galaxies located even farther away, provided that the light began traveling toward us when the galaxies were nearer.

However, there is an ultimate limit called the cosmological event horizon (which is ever so slightly different from the black hole event horizon). It is currently about 17 billion light years away.

Any light emitted RIGHT NOW from beyond that boundary will NEVER reach us, ever, no matter how long we wait. The expansion of space will prevent it from crossing the growing distance.

Dark Energy and the Vanishing Universe

The accelerating expansion driven by dark energy makes this separation even more extreme. The cosmological event horizon will continue to expand in the future, but it will eventually approach a maximum distance of about 60 billion light years.

Even then, observers will not be able to see everything within that distance. Light from the most remote galaxies will become stretched to such enormous wavelengths that it will effectively disappear from view.

In about 100 billion years, every galaxy beyond the Local Group of galaxies will fade from sight, forever. Future observers will live in a universe that appears far smaller and emptier than the one we can see today.

In mice, the medications reduced hedonic feeding, which means eating for enjoyment rather than because the body needs energy. The drugs appeared to do this by changing activity in a reward circuit located deep inside the brain.

This newly mapped pathway is separate from the appetite-control systems previously linked to drugs such as semaglutide. Researchers say it may also offer clues about whether GLP-1 medications could eventually be used to address other problems involving reward and craving, including substance use disorder.

Oral Alternatives to Injectable GLP-1 Drugs

The University of Virginia team studied small-molecule GLP-1 receptor agonists. These compounds differ from larger peptide medications such as semaglutide, which is used in well-known drugs including Ozempic, Wegovy, and Rybelsus.

The researchers focused on orforglipron, a Food and Drug Administration (FDA)-approved oral medication, as well as the experimental small-molecule drug danuglipron. Oral compounds of this kind can be taken as pills and may cost less to manufacture than injectable GLP-1 drugs.

“As the accessibility of these medications continues to rise and patient uptake increases, it’s crucial that we understand the neural mechanisms underlying the effects we’re seeing,” said Lorenzo Leggio, M.D., Ph.D., Clinical Director of NIH’s National Institute on Drug Abuse (NIDA).

How Semaglutide and Other GLP-1 Drugs Affect Hunger

Scientists have already studied the effects of larger peptide GLP-1 drugs, such as semaglutide, extensively. Research has shown that these medications reduce hunger-driven eating by acting on networks in the hypothalamus and hindbrain.

Much less was known about what small-molecule oral GLP-1 drugs do after they enter the brain.

To investigate, the researchers used gene-editing techniques to modify GLP-1 receptors in mice, making the receptors more similar to those found in humans.

A Surprising Signal Deep in the Brain

The team gave the mice either orforglipron or danuglipron and then examined which parts of the brain became active.

As expected, the drugs affected regions already associated with appetite regulation. However, they also activated the central amygdala, an area involved in desire and reward.

This region lies deeper in the brain than scientists had previously thought GLP-1 drugs could reach directly.

Additional experiments showed that activation of the central amygdala reduced dopamine release in important parts of the brain’s reward system while the mice were eating for pleasure.

Turning Down the Reward of Food

“We’ve known that GLP-1 drugs suppress feeding behavior driven by energy demand. Now it seems oral small-molecule GLP-1s also dial back eating for pleasure by engaging a brain reward circuit,” said co-corresponding author Ali Guler, Ph.D, a professor of biology at the University of Virginia.

The findings suggest that oral GLP-1 drugs may influence more than physical hunger. They may also weaken the pleasurable reward signals that make certain foods especially tempting.

Researchers now want to determine whether these next-generation medications can reduce cravings for substances other than food. Follow-up studies will specifically examine their possible effects on substance use disorder.

Funding and Regulatory Details

NIH supported this research through the National Institute of Neurological Disorders and Stroke (NINDS) grants R01NS111220, R01NS122834, and R01NS120702, the National Institute of General Medical Sciences (NIGMS) grant R35GM140854, the National Heart, Blood, and Lung Institute (NHLBI) grant R01HL153916, and the National Cancer Institute (NCI) grant P30CA044579.

This study was not completed as a clinical trial associated with an application and has not been assessed by FDA for product approval for stated indications.

Researchers at the University of Nottingham led the INSPIRE clinical trial, which tested inulin, a natural dietary fiber found in chicory root, Jerusalem artichokes, and other vegetables. Taking inulin each day significantly reduced pain among participants with OA.

Published in the journal Nutrients, the findings indicate that supporting gut health could provide a new way to manage a widespread and disabling condition that commonly affects older adults.

A Simpler Approach to Knee Osteoarthritis

Hundreds of millions of people worldwide live with knee OA, which is a major cause of chronic pain and disability, especially later in life. Treatment often involves pain medication, which can produce side effects, or exercise programs that some patients find difficult to continue over time.

“This study raises the exciting possibility that a simple dietary change — adding a fiber supplement to your breakfast or yogurt — could meaningfully reduce pain and improve physical function,” said Dr. Afroditi Kouraki, lead author of the study from the School of Medicine at the University of Nottingham.

How Prebiotic Fiber May Influence Pain

The gut microbiome consists of trillions of bacteria that live in the digestive system and affect many aspects of health, including the way the body experiences pain. Inulin is a prebiotic, which means it provides nourishment for beneficial gut bacteria.

When these bacteria consume inulin, they produce short-chain fatty acids (SCFAs). One of the most important is butyrate, a compound that can affect inflammation and the biological pathways involved in pain throughout the body.

Participants who received inulin had higher levels of both butyrate and glucagon-like peptide-1 (GLP-1) — a gut hormone associated with pain regulation and muscle health. Increased GLP-1 levels were also linked to better grip strength, suggesting a possible connection between gut health and muscle function that researchers believe deserves further study.

Inulin and Physiotherapy Reduced Pain

The six-week randomized controlled trial included 117 adults with knee OA. Participants were divided into four groups that received inulin alone, digital physiotherapy-supported exercise (PSE) alone, both treatments together, or a placebo.

Inulin and physiotherapy each reduced knee pain independently. However, only the inulin group experienced improved grip strength and lower pain sensitivity. These measurements can reflect how the nervous system detects and processes painful signals.

The inulin group also had a much lower dropout rate. Only 3.6% of participants taking the supplement left the study, compared with 21% of those in the physiotherapy group. The difference suggests that adding a supplement to a daily routine may be easier for many patients to maintain than following an exercise program.

Dr. Kouraki said: “Our findings suggest that targeting gut health with a prebiotic supplement is a safe, well-tolerated, and effective way to reduce pain in people with knee osteoarthritis. The very low dropout rate compared to the exercise group is also encouraging from a public health perspective — people were able to fit this supplement easily into their daily lives.”

A Possible Gut-Muscle-Pain Connection

Senior author Professor Ana Valdes from the School of Medicine added: “The link we observed between GLP-1 and grip strength is particularly intriguing and points to a broader gut-muscle-pain axis that warrants further investigation. This could have implications not just for osteoarthritis, but for understanding how gut health influences ageing and physical resilience more broadly.”

Professor Lucy Donaldson, Director of Research at Arthritis UK said: “The pain of arthritis can severely impact quality of life. Our recent lived experience survey showed that six in ten people are living in pain most or all of the time due to their arthritis.

“Researchers are starting to explore the role of the gut microbiome in our experience of pain. This exciting preliminary research highlights how diet and physiotherapy can act in different ways to have benefits for people with arthritis. We know a variety and balance of healthy foods, including fiber, and regular physical activity matter, and we’re glad to be supporting research that explores how they work to help people with arthritis.”