Some people with depression sleep far more than average, wake up exhausted, habitually stay up late, and experience mood shifts with the seasons. A new study suggests that these symptoms may cluster in a distinct subtype of depression that's tied to the body's internal clock.

While research has long linked a scrambled circadian rhythm to a risk of mood disorders, neuroscientists are now proposing that these disruptions define a specific form of depression that they call "circadian depression." First conceptualized in 2021, the body-clock subtype may affect about 1 in 4 people with severe, recurrent or persistent depression, the researchers estimate.

In their new study, published Wednesday (Oct. 21) in The British Journal of Psychiatry, the team identified the subtype in about 2,600 people out of over 11,000 evaluated.

"Circadian depression is a biologically informed subtype," said study co-author Emiliana Tonini, a neuroscientist at the University of Sydney. "Unlike subtypes defined mainly by symptoms, the core feature here is a disturbed circadian system, which common antidepressants may not fully address," Tonini told Live Science in an email.

The researchers think treatments that target the sleep-wake system, such as the sleep hormone melatonin or bright light therapy, might be beneficial for people with this subtype. However, because the subtype is still a proposal and not formally established yet, other experts say that further research is needed before the findings can inform clinical practice.

More than just bad sleep

Tonini and her team analyzed data from 11,380 adults ages 18 to 90 who took part in the Australian Genetics of Depression Study (AGDS), a nationwide study exploring how genes and life experiences influence depression and responses to treatment. They classified participants under the "circadian" umbrella if they had at least three of six features: seasonal mood swings, late sleep schedules, social jet lag (a mismatch between sleep routine during workdays and free days), night-owl habits, excessive sleep (hypersomnia), and fatigue upon waking.

A total of 2,604 people fit the proposed subtype. Compared with others in the AGDS cohort, this group was younger and developed depression earlier in life — around 19, compared with about 23 for the rest of the cohort.

The group also skewed female, and individuals reported greater psychological distress, frequent suicidal thoughts and more physical complaints than people who didn't fit the proposed subtype. Some experienced weight gain during depressive episodes and symptoms resembling hypomania, a revved-up state of elevated mood and energy that's milder than full-blown mania.

However, having this constellation of symptoms doesn't mean someone's biological clock is disrupted, said Brant Hasler, a psychologist and sleep researcher at the University of Pittsburgh who was not involved in the study. The researchers relied on the participants' self-reports of their sleep patterns; that data correlates only modestly with direct measures of circadian timing, such as measurements of melatonin in saliva, he said in an email.

"One can identify as an evening-type, and report later sleep timing, and still have physiological circadian timing that is not particularly delayed," he said.

So, in addition to checking symptoms, the team hunted for genetic clues underlying the proposed subtype. They analyzed DNA from participants' saliva samples and calculated "polygenic risk scores," which add up the influence of thousands of different genetic variants to estimate how likely someone is to develop a given condition.

"Mental health conditions are shaped by hundreds or thousands of variants that each add a small amount of risk, so everyone carries a unique 'portfolio' of risk," Tonini explained.

People in the circadian group had a higher genetic risk for depression, anxiety, attention-deficit/hyperactivity disorder (ADHD) and bipolar disorder, the analysis suggested. They also had a greater genetic risk of higher body weight, insulin resistance, inflammation, insomnia and late-night sleep habits, compared with the other study participants.

This suggests "circadian depression is more than just 'depression with bad sleep,'" Tonini said. "It involves a mix of metabolic, inflammatory, circadian, and mood-related processes."

Could this change depression treatment?

The researchers looked at the participants' past experiences with antidepressants, finding that the circadian group reported less benefit from common medications, such as selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs). Common examples include the SSRI Lexapro and the SNRI Cymbalta.

The circadian group also experienced more side effects from these treatments, such as drowsiness, nausea, anxiety and weight gain.

"If circadian disruption is a core biological mechanism in these individuals, treatments that fail to address those abnormalities may naturally be less effective," said Dr. Ruth Benca, a psychiatrist and sleep researcher at Wake Forest University School of Medicine who was not involved in the study. However, Benca cautioned that body-clock disruption may not be the only reason standard drugs fall short for these patients.

"People with more pronounced circadian disturbances often have more severe illness and other psychiatric conditions, which can contribute to treatment resistance," Benca told Live Science in an email.

Even so, tracking sleep, measurements of circadian rhythm, and seasonal shifts in mood could help clinicians identify at-risk patients earlier and select more effective treatments sooner in the course of illness, Benca suggested. "Potential approaches include behavioral routines, structured sleep schedules, or chronotherapy," in which the timing of medication or light exposure is strategically coordinated with internal body rhythms, she added.

Clinical trials are still needed to draw firm conclusions about potential treatments, Tonini noted. The findings also must be validated in broader populations, since the study drew on a single Australian cohort and its genetic analysis included only people of European ancestry.

For now, "the study is an important step toward a more personalized treatment approach," she said.

This article is for informational purposes only and is not meant to offer medical advice.

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Many people are familiar with melatonin, a hormone that helps ready the body for sleep. But there's another, lesser-known chemical in the brain, called orexin, that tips the scale in the other direction: waking the body up.

In 1999, two scientists independently uncovered the function of orexin and published papers about it. Dr. Masashi Yanagisawa, a molecular biologist and physician now at the University of Tsukuba in Japan, came across orexin while studying the interaction of receptors and chemicals in the brain. Dr. Emmanuel Mignot, now the director of the Stanford Center for Narcolepsy, homed in on orexin while studying narcoleptic dogs. (His Chihuahua, named Watson, has narcolepsy, and he previously had another dog with the condition, named Bear.)

This year, the pair of researchers won the coveted Albert Lasker Basic Medical Research Award for this fundamental finding that helped reshape our understanding of sleep. Their work has since led to the development of drugs for insomnia and narcolepsy.

Yanagisawa told Live Science that, at the start of his research career, he didn't expect to end up studying sleep. Mignot, on the other hand, had an early interest in understanding narcolepsy so that better treatments for the neurological disorder could be developed. Live Science spoke with Mignot about the discovery of orexin and how the field might progress in the future.

Nicoletta Lanese: What initially drew you to studying narcolepsy?

Dr. Emmanuel Mignot: There were three things that attracted me to narcolepsy: Number one, it was a human problem. It was already known [at the time] that it was not super rare. I'm not saying it's super common, but 1 person per 3,000, 0.03% ‪—‬ it's reasonably common. And nobody cared about it. I would talk to neurologists and they'd say, "Oh, I've never seen one case in my entire life." So I would say, "Yes, of course; you miss them all." That was the state of the play at the time.

Number two, was what this was a quintessential sleep disorder [in which sleep itself is disrupted]. I thought that if we found the cause of this disease, we could potentially discover something totally new about sleep — a fantastic entry point to a mystery.

The third thing that made me ready to go there was that it was tractable. A lot of problems are not tractable.

NL: Why did you start working with the dogs with narcolepsy?

EM: I studied the pharmacological basis because I was trained in pharmacology, and as a psychiatrist, and I discovered how this drug modafinil [a stimulant-based narcolepsy treatment] was working. But quickly, I realized I'm not going to find the cause by doing pharmacology. I'm only going to explore what's known.

That's when I started to fall in love with genetics, even though I was not trained as a geneticist. I said, "We have to find this gene in the dogs." It looks like they have all the symptoms. It was a huge bet, and it took me 10 years because I was definitely … overoptimistic. But it was worth the price at the end.

NL: And scientists already knew about narcolepsy in dogs at that time?

EM: The guy at Stanford that started the sleep program was called Dr. [William] Dement. He was a graduate student in Chicago in the 1950s, when [Eugene] Aserinsky and [Nathaniel] Kleitman discovered REM sleep. He had the foresight to understand that this was an important discovery.

[Later], he discovered that narcolepsy was really a disorder where people go into REM sleep and have this very abnormal dreaming. He came in 1970 to Stanford, and the first thing he did after his medical school was to start a clinic to see patients with narcolepsy. Around then, he spoke at an American Medical Association conference in San Francisco, and he discussed different sleep disorders, including narcolepsy. And then there was someone in the audience that said, "Oh my god; I have a dog with your disease. Every time it gets excited — boom — it collapses. And it sleeps all the time."

That dog had already been euthanized, but it still gave him the idea that these dogs have narcolepsy — maybe we should try to get some. So he went to a lot of veterinarians to talk to them about it, and they identified a whole series of dogs, including the first poodle, Monique, who had narcolepsy. And they started this little colony of dogs. Initially, they tried to breed them, but most cases of narcolepsy are actually not genetic. Then, in 1977, they got a whole litter of Dobermans, and then Labradors, that had some form that was genetic.

So when I arrived, it was in 1987. They already had the dog colony. I came to study the pharmacology, to try to find a better treatment for narcolepsy. But I did stand on the shoulders of giants.

NL: At that time, it's not like you had a complete dog genome. Did that make studying their genetics challenging?

EM: It was crazy. A couple of human genes had been isolated, and mouse genes, but it was a handful. We didn't even have the full genome map in humans. And meanwhile, dogs — no pun intended — were in no man's land. Very little was known.

It took me 10 years. I had times where some people didn't believe that the dogs had narcolepsy. There were a few depressing moments, but I was convinced that was the right thing to do.

NL: When you ultimately found the receptor for orexin, did it surprise you? It strikes me as surprising that there would be a discrete "switch" in the brain that controls wakefulness.

EM: I was lucky. Honestly, I had no idea. I got enamored with genetics because what I love [about it] is you can find something without any hypothesis. You just search for it, and what you find tells you what it is. You have no prerequisite for knowing what you would find.

I could have found something much less significant. That was a dream, to find a GPCR [G-protein coupled receptor, a protein on the outside of cells]. Can you imagine? A drug target.

Then, it turned out to be immediately applicable to humans. That, too, was a lot of luck; let's be honest. I was just trying to find the cause of one thing and one step at a time; it could have been something very complicated. It turned out to be simple.

Was I surprised? No, because I was not expecting one or another.

NL: Do you recall what the reception was like when the initial finding was published?

EM: It had an immediate effect, for several reasons. For example, I was seeing a lot of patients with narcolepsy at the time, but they were all old folks that had had narcolepsy forever. A lot of people would tell me, "I think I had it from when I was born, because I don't remember." We were never seeing children.

But after narcolepsy was described — the dog gene — suddenly narcolepsy became much more famous. And what happened is that people started to pay attention to narcolepsy, and we started to see kids. In kids, the picture is so much different. They gain an enormous amount of weight; it's very abrupt. It's a little bit different than what you see in adults, where they have adapted to it.

That was, I think, a practical consequence of the discovery. It really put narcolepsy on the map.

The second thing that happened is, all the drug companies started to develop hypnotics [sleeping pills], trying to block the orexin. They developed hypnotics relatively quickly, and they are very effective. They are probably safer than benzos [benzodiazepines] and so forth.

NL: Is it considered safer because the orexin blockers better replicate natural sleep?

EM: We know that the orexin definitely drops during sleep, so blocking it is definitely a way to recapitulate that drop; that's true. It's an awake-promoting system, so if you remove something that makes you more awake, it's safer than inducing sleep by shutting down the brain.

NL: As you moved to studying narcolepsy in humans, you found evidence that there might be an autoimmune response involved; it's been suggested that such a response may be harming the cells that make orexin in the brain. Was there suspicion that the condition had an autoimmune element previously?

EM: It's not something I 100% discovered. In 1983, before I came to study narcolepsy, there was a guy in Japan who I met, called Yutaka Honda. [Editor's note: Honda's research linked narcolepsy to the human leukocyte antigen (HLA) region of the genome, which helps regulate immune responses.]

The HLA is the way the immune system sees the world. That had just been discovered as very important for transplantation, because it's very polymorphic [takes on different forms] from one person to the next. They [Honda's group] found that all narcoleptics had a particular genetic variant, called HLA-DR2. This was a total surprise.

When I came, that was already known. But then people really looked and tried to see if the disease was autoimmune, but they couldn't find anything — no autoantibody, nothing. It was all negative.

I did a study with African Americans, and in African Americans, I found that this DR2 marker was not the best marker for narcolepsy. It was a gene just next to it that was called DQB1*06:02. [Editor's note: That HLA variant is now recognized as a strong risk factor for narcolepsy, particularly for narcolepsy type 1 (which involves a symptom called cataplexy).]

I'm very proud of that study because I think it's the first time that people used human diversity to actually map down a genetic factor more precisely, which now is used commonly. It's called transethnic mapping.

NL: New treatments that target orexin have just been approved. Do you see those therapies as an extension of your earlier findings?

EM: Of course. I was trained as a pharmacologist originally, so obviously, I do a lot of clinical trials. I see my patients totally transformed by this medication. It's just amazing. I'm so fortunate. How could you get a better reward than seeing your patients totally transformed by this medication?

It's going to have a lot of other applications [beyond narcolepsy]. Some people think it's going to be very helpful for ADHD; some people think it could be very helpful for depressed people with excessive sleepiness. We don't know, really; there's a lot of possibilities.

Another thing I'm excited about is that I have a few patients with [both] narcolepsy and schizophrenia. You cannot give them stimulants. If you give them modafinil or another dopamine stimulant [for narcolepsy], they have even more hallucinations. Often, they are sedated by their medication, and we are very poor at making people more motivated and active. These [orexin-activating] drugs seem to have effects beyond just waking people up. They seem to increase motivation.

You don't know until you try, but I'm sure it's going to have other applications.

This interview has been condensed and edited lightly for clarity. It is for informational purposes only and is not meant to offer medical advice.

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A poop transplant — otherwise known as a fecal microbiota transplant (FMT) — may help adults with long-term insomnia sleep better, a small study suggests.

After the transplant, study participants' gut bacteria became more diverse than an untreated group of people with insomnia. Their sleep efficiency, meaning the percentage of time they spent asleep while in bed, also increased, researchers reported July 22 in the Journal of Internal Medicine.

If future studies confirm that FMT is safe and effective for the treatment of insomnia, it could become another tool against the sleep disorder, joining sleeping pills and cognitive behavioral therapy (CBT).

The findings "are aligned with a recent body of work over the last five years indicating that the gut microbiome may play a role in sleep-wake regulation," said Dr. David Gozal, a pediatric sleep specialist at Marshall University in West Virginia who wasn't involved in this study.

However, "these results should be regarded as promising proof-of-concept evidence rather than confirmation that FMT is ready for routine treatment of insomnia," Kenji Hashimoto, a forensic mental health researcher at Chiba University in China who wasn't involved with the study, told Live Science in an email.

Improving sleep with "poop pills"

The study included 80 adult women and men with chronic insomnia from seven hospitals in China; the participants did not have other health problems, such as migraine or obstructive sleep apnea, that could interfere with the results.

Half of the participants took antibiotics for two days to clear out some of their existing gut bacteria. Then, they swallowed 60 FMT capsules chockfull of gut bacteria from healthy donors who had been confirmed to be good sleepers. These bacteria were isolated from fecal samples from the donors. Two weeks later, this group took a booster dose of 20 capsules.

The other half of the participants instead took placebo pills in place of the antibiotics and FMT capsules.

The researchers used an overnight sleep assessment called a polysomnography, which records brain waves, eye movements, heart rate, oxygen levels and breathing patterns, to assess the participants. The results showed that sleep efficiency in the FMT group jumped from 79% before the transplant to 93% one month after treatment, on average. The placebo group's sleep efficiency barely changed, shifting from about 85% to 87%.

Additionally, the treated group woke up less throughout the night. Their time spent awake after initially falling asleep fell from 79 to 17 minutes, while the same metric increased from 37 to 42 minutes in the placebo group.

On questionnaires, the FMT group continued reporting better sleep from two all the way to six months after treatment.

It is "encouraging" that FMT treatment seemed to improve sleep not only on objective tests, but also in how the participants themselves rated their insomnia, added Harriët Schellekens, a neuroscientist and microbiome researcher at University College Cork in Ireland, who wasn't involved in the work.

Gut-sleep connection

The results also suggest that the treatment is safe. In the FMT group, only three out of 40 participants had side effects, and they were mild, such as nausea and transient fever.

However, experts noted several caveats. The trial was small and limited to relatively healthy adults in China, so the results may not apply broadly. Sleep was measured only once after treatment, at the one‑month mark, Hashimoto said. And because the treatment combined antibiotics with FMT, it's unclear how much of the benefit came from the donor microbes alone, Schellekens and Hashimoto noted.

Hashimoto added that the study focused exclusively on the gut microbiota. "Microbial communities in other body sites, particularly the oral and nasal cavities, may also influence sleep regulation through immune, metabolic, and neural pathways and through oral-gut-brain or nasal-gut-brain communication," he said.

The gut and brain communicate in various ways, including via chemicals made by gut microbes that travel to the brain via the bloodstream, Hashimoto explained. These chemicals may steer inflammation, stress responses and the body's sleep-wake control.

Shifts in certain microbes can alter these gut chemicals and gut barrier function in ways that ripple out to the brain and change sleep patterns, Gozal said. Conversely, disrupted sleep can reshape the microbiome. "The question is, what came first?" he said — a disordered microbiome driving insomnia, or insomnia reshaping the microbiome and worsening symptoms.

In the study, the mix of gut microbes in the FMT group shifted between the start and end of the study, but the placebo group's microbiomes stayed the same. Several types of bacteria became more abundant after FMT, while others decreased, suggesting that FMT reshapes the gut microbiome.

Not everyone responded to the treatment, and they mostly differed in what their gut microbiota looked like before FMT, not after. That suggests that a person's initial microbial makeup may help determine how well they respond to the treatment.

Gozal said he would have liked the study to measure the chemicals made by gut microbes before treatment and then show how those same chemicals changed after FMT.

More research is needed to understand the biological mechanisms underlying the improvements, Schellekens said. For now, "FMT remains an experimental approach for insomnia and is not something that should be used outside carefully controlled clinical studies."

The study's researchers did not respond to a request for comment by the time of publication.

This article is for informational purposes only and is not meant to offer medical advice.

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Oura Ring 5: Two minute review

I've been going around in circles writing this Oura Ring 5 review. On the one hand, I find the health insights equally fascinating and motivating just like the best smart rings, and its discreet design is without a doubt comfortable to wear all day long.

But it's worth noting that Oura has been facing increasing backlash after deepening its partnership with the Department of Defense in the US last year, which is something ethically-conscious buyers may want to look into before purchasing.

That said, its ability to track more than 50 health and wellness metrics, such as sleep quality and stress levels, is undeniably enticing for anyone wanting to be more aware of their body — and the launch of this newest model brought a whole host of new insights.

What I will say is that the Oura app does try to include a lot of context about how these measurements can be interpreted and how they contribute to‚ for example, determining how prepared your body is for the day ahead based on a range of metrics, which Oura calls your 'Resilience Score'. But, again, this only scratches the surface of understanding how your body actually functions.

The best example of these assessments triggering misguided concern was when I got warnings from a feature called 'Symptom Radar', which tracks your respiratory rate and body temperature to flag signs of strain. What it didn't take into account was that a woman's body temperature naturally rises after ovulation, making its assessment unnecessarily worrying for anyone who didn't know that.

I can't deny that its claim to be the world's smallest smart ring at launch really does hold up — its lightness makes it disappear on your finger, making it ideal for everyday wear. With six stylish finishes and an even more scratch-resistant titanium surface, it's no wonder it's made headlines in the wearable tech space, with plenty of influencer reviewers fawning over the all-new Oura Ring 5.

By now you've definitely noticed my to-ing and fro-ing as I work through every side of the Oura Ring 5 to reach an honest and fair review. I won't say it's the most perfect smart ring on the market — that would be ignoring too much — but I will say it comes close. I can't argue with its premium build and the level of tech packed into those tiny sensors, which manage to achieve high levels of accuracy. That's impressive in itself, and

Oura has been facing increasing backlash after deepening its partnership with the Department of Defense in the US last year, although it doesn't use data from any of its users other than specific military personnel as part of this arrangement. It's also worth keeping in mind that there have been studies raising concerns about 'health data anxiety', and Oura's attempt to bring new biomarkers into play have given us a whole new category to worry about. But at the end of the day, I'm a sucker for brilliant tech — which the Oura Ring 5 definitely is.

Oura Ring 5: Price and availability

• $399 / £399 / AU$649 (each) for two base finishes
• $499 / £499 / AU$799 (each) for four premium styles
• $5.99 monthly subscription (priced in USD across all regions)
• $99 / £99 / AU$159 for the Oura Ring 5 travel case

The Oura Ring 5 costs an extra $50 / £50 / AU$80 — or $100 / £100 for a premium finish — compared with the Oura Ring 4, which launched in 2024. (Australian pricing doesn't appear to carry the same premium finish gap.)

Beyond the high-gloss gold and silver finishes, you're paying an extra $100 / £100 / AU$150 for any of the four premium styles: a softer gold, brushed silver, matte black, and — the color I tried — deep copper rose.

Add the $5.99 monthly subscription, and you're looking at up to $670 / £670 / AU$1,029.88 to own an Oura Ring 5 for a year, if you go for the most expensive finish plus the travel case.

That's no small sum when most smart rings on the market cost less and many don't require a recurring subscription. There are also plenty of wearable alternatives that track the same health vitals, which makes this very much a luxury purchase.

• Value score: 2/5

Oura Ring 5: Design

• The closest a smart ring has come to looking like luxury jewellery
• Extremely low-profile and light, making it comfortable to wear all day
• An easy-to-use companion app with a clean UI

By far the best justification for the Oura Ring 5's high price tag is that it could easily pass for a piece of jewellery. That's largely down to a 40% decrease in size from the previous model, the result of Oura redesigning the entire core.

That freed up space to drop multiple sensors, but it hasn't made the Ring 5 any less accurate — Oura has increased the efficiency of the remaining sensors to offset the loss. The titanium surface is also more scratch-resistant; I can't compare it directly to a previous model, but it hasn't picked up a nick yet.

What I can say is that the Oura Ring 5 is significantly smaller than the Ring 4. Holding it up against a previous-generation ring (admittedly the bulkier ceramic finish), I was shocked at how noticeable the size difference is. It's lighter and far more comfortable to wear, since it doesn't protrude — and therefore doesn't rub against — my finger as much.

That same design ethos carries through to the Oura app, which has a minimalist interface that isn't cluttered with numbers and graphs. Instead, data is presented as scores with percentages and ratings for each health vital. It's easy to use, though it's worth noting that the app needs a certain amount of data to establish your health baseline, so you won't have access to every feature right away.

• Design score: 5/5

Oura Ring 5: Features

• Tracks vitals including body temperature, heart rate, and respiratory rate
• AI wellness assessments for sleep, stress, resilience, and more
• Activity tracking lags behind more dedicated fitness wearables

After two weeks of wearing the Oura Ring 5, I've unlocked most features — sleep, resilience, and activity scores — which now populate what was once a fairly bare home screen.

The Oura app works best with more data, so it's constantly prompting you to add new "tags" to your day's timeline. Some are automatic, like detecting exercise, while others — what you ate, or what kind of activity you did — require manual logging.

The app's other three main sections cover your vitals, a health assessment area, and an LLM chatbot you can talk to about your data. That last part matters, because as I mentioned above, there's plenty of room for misleading interpretations if you don't understand the many factors behind your body's vitals.

I got a lot out of learning more about my sleep quality and general heart health (the app has a neat feature that lets you feel your heartbeat throughout the day via your phone's haptic feedback), but what I'm most interested in unlocking next are the new women's health features, such as Hormonal Birth Control, which builds on the existing Cycle Insights dashboard with what Oura calls a "first-of-its-kind" view into how biometrics shift across hormonal and hormone-free days.

While I find the wellness insights genuinely useful, the ring is nowhere near as practical as a dedicated fitness tracker. Without GPS — it relies on a paired device for location — and limited to activities compatible with wearing jewellery on your hand (so no weightlifting without a third-party silicone band over the top), it falls short, even with the addition of real-time tracking — which, again, you can only view through a paired device).

• Features score: 4/5

Oura Ring 5: Performance

• Battery life has increased to seven days
• Automatic activity tracking has been accurate
• Sleep and heart rate tracking data is in line with our benchmark device

One of the biggest improvements that the Oura Ring 5 brings over the Ring 4 is that has managed to squeeze out a whole extra day of battery life, despite the ring itself being redesigned to be 40% smaller.

During my testing, I found it lasted a whole seven days on one full charge. But I was more impressed with was how quickly you can charge the smart ring. From a fully drained battery, it took less than an hour until it was all way back up to 100%, which means it's very easy to top it up throughout the week whenever you're, say, washing dishes or having a shower.

For the most part, I kept the Oura Ring 5 on throughout the day, allowing it to track my vitals as I moved from home to work to seeing friends, exercising and cooking, which it does very well. Most of the automated tracking suggestions were accurate, allowing me to quickly confirm all of the day's activities when I next checked into the app.

This same accuracy extends to the sleep data, which is the absolute highlight of the Oura Ring 5's feature set. I found the insights both enlightening and motivating, especially after getting my first sleep score as (like any gamification effect) I began trying to reach a new higher level. My testing also confirmed this when my readouts for my average heart rate managed to be within 3 BPM of the Polar H10 chest strap, which is the gold standard for consumer heart rate and workout accuracy as it uses actual ECG (electrocardiogram) technology.

Average heart rate

Oura Ring 5

115

Polar H10

112

037.575112.5150

Average heart rate Data

Product	Value
Oura Ring 5	115
Polar H10	112

• Performance score: 5/5

Oura Ring 5: Scorecard

Oura Ring 5: Should I buy?

Buy it if...

Don't buy it if...

Also consider

How I tested

I wore the Oura Ring 5 for two weeks, draining the battery completely (despite the app advising against letting it go below 30%). I have some gaps in my data from forgetting to put it back on, but I mostly didn't take it off. I tested the ring's heart rate monitoring accuracy against the Polar H10 chest strap, and compared its design to a ceramic Oura Ring 4.