The case is the first human illness detected in Colorado in connection with an ongoing outbreak in cattle. It follows one human case in Texas and two in Michigan. The second case in Michigan caused mild respiratory symptoms, such as coughing, but the other three cases — including the most recent in Colorado — have only included eye symptoms, such as redness.

The culprit behind these infections is a bird flu virus called influenza A(H5N1). This subtype of flu was first spotted among U.S. dairy cows in March. Since then, dozens of herds across the country have tested positive for the virus.

Recent research suggests that, when it infects cows, the virus can end up in the animals' milk and remain infectious in unpasteurized milk for at least an hour after harvest. This poses a significant risk to dairy workers, who may come into contact with contaminated milk through contact with cows or with milking equipment. The pasteurized milk supply, on the other hand, is safe because the pasteurization process inactivates any viruses in the milk. 

Related: 'Playing Russian roulette with your health': Officials warn that social media trend of consuming raw milk will not protect you from bird flu

Because of the risk posed by raw milk, the CDC recommends that dairy workers wear personal protective equipment.

In the recent Colorado case, the individual was being monitored because they'd been exposed to H5N1-infected cattle at work. Clinical samples from the person were sent to the CDC, who confirmed an infection with an influenza A(H5) virus. The agency is continuing to analyze the sample to confirm that the virus is in fact H5N1.

The infected person was treated with a common drug for seasonal flu, called oseltamivir; Tamiflu is a well-known, brand-name version of the drug. The person recovered following this treatment. 

All three people previously infected in the outbreak also recovered from their mild infections. In the past, though, H5N1 has been known to sometimes kill people.

Overall, the Colorado case doesn't change the CDC's overall assessment of the unfolding outbreak.

"CDC has been watching influenza surveillance systems closely, particularly in affected states, and there has been no sign of unusual influenza activity in people," the agency reported. "Based on the information available at this time, this infection does not change CDC's current H5N1 bird flu human health risk assessment for the U.S. general public, which the agency considers to be low."

Nonetheless, the CDC will continue to monitor for unusual flu activity. There's a possibility that, in time, H5N1 could pick up mutations that enable the virus to spread easily from person to person — something it hasn't yet been able to do. Such a change in the virus' genetics would be concerning because the pathogen could then potentially spark a widespread outbreak, or even a pandemic.

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Waiting for Amazon Prime Day to save some bucks on a new rowing machine? There's no need. Right now, retailers far and wide are stepping up their game against Amazon with some truly unmissable deals. Like Echelon, for example.

This compact, foldable rowing machine is one of our all-time favorites, which is why we included it in our roundup of the best rowing machines as the best option for small spaces. During our Echelon Smart Rower review, it impressed us with its sleek design, sturdiness and smooth, near-silent magnetic resistance. We enjoyed the engaging fitness classes available on the Echelon Fit app, too. True, you have to watch them on your own device, and they require a monthly subscription — but it is money well spent. Especially when you can knock a hefty $400 off the price of the rower in the first place.

Key features: 32 levels of magnetic resistance, foldable design, Bluetooth connectivity and a device holder.

Price history: For the most part of this year, the price of the Echelon Smart Rower at Amazon fluctuated between $700 and $800. The last time we saw it dip below $600 was in late April when it stood at $523.99.  

Price comparison: The Echelon Smart Rower is currently discounted to $699.99 at both Amazon and Best Buy, while at Walmart it stands at $685. 

Reviews consensus: The online reviews for the Echelon Smart Rowers are overwhelmingly positive, with most rating it at 4 or 4.5 out of 5 stars. The rowing machine is universally praised for its near-silent operation, sturdiness, space-savvy design and ease of use. Many reviewers, however, complain about its high price given the lack of an integrated screen, and that the Echelon Fit app requires a monthly subscription.      

Buy it if: You are looking for a well-made, thoughtfully designed rowing machine that offers engaging workouts and does not take up much space. The Echelon Smart Rower is a quiet, sturdy and good-looking piece of kit. 

Don't buy it if: You want a built-in touchscreen and other frills typical of more premium rowing machines. 

More than 1 billion people each year will have a migraine, and about one-quarter of those migraines will be accompanied by an aura. These sensory symptoms can include seeing lights and hearing sounds that aren't there or feeling tingling or numbness. 

Scientists have known that these auras are associated with "cortical spreading depression," waves of abnormal activity that wash over the brain and temporarily inactivate certain neurons. The waves are thought to somehow trip pain-detecting nerves outside the brain, in part by releasing chemicals into the cerebrospinal fluid (CSF), a substance that surrounds and cushions the organ. 

Exactly how the chemicals reached the nerves was a mystery. Now, scientists have uncovered a route by which some molecules can escape the brain's protective barrier. 

Related: Migraines and blood sugar issues share common genetic risk factors

In a study published Thursday (July 4) in the journal Science, researchers examined the route CSF takes to exit the brain by zooming in on a cluster of neurons called the trigeminal ganglion. This bundle of cells transmits signals from the nerves of the face and jaw to the brain, plugging in around the brainstem. 

The scientists discovered that this nerve bundle also provides a route for CSF and the molecules within it to reach the world beyond the brain.

They learned this by using genetically engineered mice whose neurons make a protein that glows in the presence of calcium. Calcium is a key element that brain cells use to send electrical signals. While observing the trigeminal ganglion, the researchers would inject a tracer into the mouse's brain to track the flow of its CSF. They also introduced a substance that allows calcium to flow into neurons, activating them.

The experiment revealed that CSF appeared in the trigeminal ganglion about four minutes after injection, followed by a sharp increase in calcium-driven activity. This provided direct evidence that CSF can carry molecules outside the brain via this channel. 

The fluid likely makes contact with the ganglion near the brainstem. There, the ganglion lacks the tightly fused outer barrier that can be seen elsewhere along its length, the team found.

To connect the dots to migraine, the team looked at the effects of cortical spreading depression. They demonstrated that it can increase the flow of CSF in the affected area, carrying more proteins and other molecules to the trigeminal ganglion than it normally would. Many of those proteins were drivers of pain and inflammation.

"We found that during aura, proteins that can activate and sensitize sensory nerves are released to the CSF and transported to the trigeminal ganglion, where they activate pain-mediating sensory nerves," study author Martin Kaag Rasmussen, a postdoctoral scholar at the University of Copenhagen, told Live Science in an email. 

"This is what drives the migraine headache, and it is what links the aura phase to the headache," he said.

Related: Does caffeine help or cause headaches?

Of the 12 proteins found to activate pain-sensing nerves, only one — calcitonin gene-related peptide (CGRP) — is a current target for migraine therapies. Medications that block CGRP function relieve migraine symptoms in about half of patients, but that still leaves millions of people without effective treatment. 

Rasmussen is optimistic that the additional molecules uncovered in the study could offer new treatment options. "I believe that, when patients do not respond well to currently available therapies, it is because we have not identified what molecule is responsible for their headache," he said. 

"I find it really exciting because it's a new pathway for delivery of molecules from the brain to peripheral ganglia," Andrew Russo, a professor of neurology at the University of Iowa who was not involved in the study, told Live Science. That could have relevance well beyond migraines, he said.

The caveat, however, is that all of the group's experiments were performed in mice. In comparison to the human brain, "the mouse brain is very smooth," Russo said. Humans' brain tissue has more folds so the abnormal waves tied to migraine can't travel as efficiently. That might affect how fast CSF flows out of the brain and whether or not it triggers the pain-sensing nerves, Russo noted.

The next step will be to answer that question by examining the same processes in humans or more human-like animal models. The researchers also want to take a closer look at the new pain-triggering proteins they identified, both in migraines and other headache disorders. This could potentially lead to new diagnostic tests and treatments for a variety of patients.

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The findings support current guidelines on the use of this class of drugs, which caution against using benzodiazepines for extended periods of time. 

Benzodiazepines, also known as "benzos," are sedative drugs commonly prescribed to treat numerous conditions, including insomnia, anxiety and seizure disorders. They work by slowing down the activity of the central nervous system, meaning the brain and spinal cord. This can relax a person's mood, relieve muscle spasms and also cause people to feel sleepy. 

These drugs, which include Xanax, are highly addictive and previous research has shown that long-term use comes with a risk of memory and movement issues. As such, the U.S. Food and Drug Administration (FDA) recommends that benzodiazepines are prescribed at the lowest dose possible and for the minimum time required to achieve the desired clinical effects — usually around two to four weeks. 

Despite these concerns, evidence suggests that between 6% and 15% of patients prescribed benzodiazepines use the drugs for more than six months.

In the new study, published Monday (July 1) in the journal BMC Medicine, researchers have revealed another reason to be cautious about prolonged benzo use: it use may speed up the natural age-related dwindling of two regions of the brain involved in memory and mood regulation, called the hippocampus and the amygdala. 

Related: Scientists debunk myth that human brains are 'underdeveloped' at birth

The researchers reviewed the medical records of 5,443 adults in the Netherlands who initially had no reported cognitive impairment. The scientists scanned the medical records to determine if, and how many, benzodiazepines the individuals had taken daily between 1991 and 2008. On average, people took their prescribed daily dose 37 times within this time frame. 

The team found that around 50% of study participants had used benzodiazepines at some point up to 2008, and approximately 13% of the overall group went on to be diagnosed with dementia by 2020. Notably, the people who took benzodiazepines were no more likely to develop dementia than those who'd never taken them, regardless of how much they took and for how long, the team found. 

These findings contradict two prior analyses conducted by different groups of researchers. These past analyses summed up the findings of numerous studies on the topic — however, those studies differed in how they were conducted, and their differences might have muddied the results, the team said. 

Although the new study didn't find that benzos boosted dementia risk, it did uncover physical brain changes tied to the drugs. The researchers looked at brain scans that were taken at least once from roughly 4,800 of the 5,443 participants. These scans showed changes in the volume of different structures in the brain over time. 

Based on these scans, the researchers concluded that benzodiazepine use was associated with an accelerated reduction in the volume of the hippocampus and amygdala. In other words, these structures shrunk faster in the group who took benzos, compared to the group who had not used the drugs. 

In addition to these changes in overall brain volume, the team uncovered differences in white matter, the brain tissue that contains the passageways that transmit signals between neurons. Participants who took benzodiazepines specifically for sleep issues — known as sedative-hypnotics — showed a faster reduction in white matter volume than those who took benzodiazepines for anxiety, called anxiolytics.

"Our results underline guidelines that say that you shouldn't take benzodiazepines for a very long period of time," Ilse vom Hofe, co-senior study author and a doctoral candidate at Erasmus University Medical Center in The Netherlands, told Live Science. "Also, I think it motivates health clinicians to look into other therapies to address the problems that people are experiencing, instead of just riding out the benzodiazepines."

The team acknowledged several limitations of the new study. For instance, they only looked at people who started out "cognitively healthy," so it's unclear whether benzos might have more or less profound impacts in people with cognitive impairment. Participants were also mainly white, which may limit how well the findings apply to additional groups. 

As they stand, though, the findings support the need for more research investigating the impact of long-term benzodiazepine use on brain health, the team said. 

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

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While Black people constitute only 12% of the U.S. population, they account for 35% of those with kidney failure. The reason is due in part to the prevalence of diabetes and high blood pressure — the two largest contributors to kidney disease — in the Black community.

Almost 100,000 people in the U.S. are awaiting kidney transplantation. Though Black Americans are more likely to need transplants, they are also less likely to receive them.

Making matters worse, kidneys from Black donors in the U.S. are more likely to be thrown away as a result of a flawed system that erroneously considers all Black donor kidneys as more likely to stop working after a transplant than kidneys from donors of other races.

As a scholar of bioethics, health and philosophy, I believe this flawed system raises serious ethical concerns about justice, fairness and good stewardship of a scarce resource — kidneys.

How did we get here?

The U.S. organ transplantation system rates donor kidneys using the kidney donor profile index, an algorithm that includes 10 factors, including the donor’s age, height, weight and history of hypertension and diabetes.

Another factor in the algorithm is race.

Research on previous transplants shows that some kidneys donated by Black people are more likely to stop working sooner after transplantation than kidneys donated by people from other races.

This brings down the average time a transplanted kidney from a Black donor can last for a patient.

As a result, kidneys donated by Black people are discarded at higher rates because the algorithm downgrades their quality based on the donor’s race.

This means that some good kidneys may be wasted, raising several ethical and practical concerns.

Risk, race and genetics

Scientists have shown that races are social constructs that are poor indicators of human genetic diversity.

Using a donor’s race assumed people who belong to the same socially constructed group share important biological characteristics despite evidence that there is more genetic variation within racial groups than between other racial groups. Such is the case for Black Americans.

RELATED: 'Racism is a global public health crisis': Author Layal Liverpool says racist ideas still pervade medicine, and that hurts all of us

It is possible that the explanation for observed differences in outcomes lies in genetics and not in race.

People who have two copies of certain forms or variants of the APOL1 gene are more likely to develop kidney disease.

About 85% of people with those variants never develop kidney disease, but 15% do. Medical researchers do not yet understand what is behind this difference, but genetics is likely only part of the story. Environment and exposure to certain viruses are also possible explanations.

People who have two copies of the riskier forms of the APOL1 gene almost all have ancestors who came from Africa, especially from West and sub-Saharan Africa. In the U.S., such people typically are categorized as Black or African American.

Research on kidney transplants suggests that kidneys from donors with two copies of the higher-risk APOL1 variants fail at higher rates after transplantation. This could explain the data on Black donor kidney failure rate.

How might this practice change?

Health care professionals decide how limited resources are used and distributed. With that comes an ethical responsibility to steward resources fairly and wisely, which includes preventing unnecessary loss of transplantable kidneys.

Reducing the number of wasted kidneys is important for another reason.

Many people agree to organ donations to help others. Black donors may be disturbed to learn that their kidneys are more likely to be discarded because they came from a Black person.

This practice can further decrease the trust of Black Americans in a health care system that has a long history of mistreating Black people.

Making organ transplantation more equitable could be as simple as ignoring race when evaluating donor kidneys, as some medical researchers have proposed.

But this approach would not account for the observed difference in transplantation outcomes and could result in transplanting some kidneys that are at increased risk for early failure due to a genetic issue.

And since Black kidney recipients are more likely to receive kidneys from Black donors, this approach could perpetuate transplant disparities.

Another option that would improve public health and reduce racial health disparities is to identify the factors that lead to some kidneys donated by Black people to fail at higher rates.

One way researchers are working to identify higher risk kidneys is using the APOLLO study, which assesses the impact of key variants on donated kidneys.

In my view, using the variant instead of race likely would decrease the number of kidneys wasted while protecting recipients from kidneys that are likely to stop working sooner after transplantation.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

It turns out that, on a cellular level, there do seem to be inherent differences in how males and females process painful stimuli. But the question of which sex — if either — has a higher pain tolerance has a fuzzier answer.

For a person to feel pain, sensory neurons called nociceptors detect painful stimuli and then send a signal to the brain for interpretation. These painful stimuli include extreme temperatures, mechanical pressure and inflammation. People show differences in how they perceive each stimulus, and these differences stem from various factors, including a person's sex. 

Several studies have reported that women have higher pain sensitivity and a lower pain threshold than men. For instance, a 2012 study that examined how men and women respond to physical pressure found that women are more sensitive to mechanical pain than men are. In another study, men and women were asked to indicate when they felt a heat stimulus and judge its intensity. It suggested women have lower pain thresholds to heat than men. 

"It is well known that females are more sensitive to pain than males," said Jeffrey Mogil, a professor of behavioral neuroscience at McGill University who studies sex differences in pain. "This has been shown in humans in hundreds of studies; not all of them are statistically significant, but essentially all of them go in the same direction," Mogil told Live Science. 

However, some studies actually show the opposite. 

Related: Do women get cold more easily than men?

In a study published in 2023, researchers recruited 22 adolescents — 12 females and 10 males — for a thermal pain sensitivity test. These participants were exposed to hot and cold stimuli and then asked to rate the intensity of their pain. The males rated higher pain intensity to both stimuli than the females did. 

Still other studies have suggested that there are no differences in how males and females respond to pain-inducing heat.

This dissensus exists among scientists because there are no "meaningful" metrics for measuring pain tolerance, said Frank Porreca, a professor of neuroscience at the University of Arizona. A given person's pain threshold and tolerance tend to vary across tests and environments; plus, some studies find that females are more reliable test subjects than males, providing more consistent ratings of their pain. 

Porreca studies mechanisms that can promote pain, and he and his team recently discovered that males' and females' nociceptors are activated by different substances. That is, the first step for pain perception differs between the sexes. 

Mogil told Live Science that it had not previously been shown that features of the nociceptors themselves are sex-dependent.

It was known that pain stimuli need to surpass certain thresholds to activate nociceptors. Usually, a low-intensity stimulus, like drinking cold water, would not activate nociceptors — but if you have a sore in your mouth, the nociceptors there would be activated. Porreca explained that, in this scenario, the threshold for nociceptor activation is lowered, and his team wanted to know if this "sensitization" was sex-dependent. 

To investigate, they sampled nociceptor cells from the dorsal root ganglion, a terminal near the spinal cord through which sensory information passes to the central nervous system. The team took cells from male and female mice, nonhuman primates and humans and exposed the cells to various substances. 

Previous studies have implicated the hormone prolactin in females' response to pain and a chemical messenger called orexin in males' pain responses, so these seemed like the perfect agents for the experiment. The results showed that the cells behaved differently when exposed to either substance across all of the sampled species. 

Prolactin lowered the threshold for nociceptor activation in females but didn't affect males. Conversely, orexin sensitized male cells but had no effect on the female cells. Both substances naturally occur in both sexes but in different concentrations.

"The nociceptors that we derive from either male or female animals or postmortem human donors are quite different in what processes produce this lowering of thresholds," Porreca said. 

He added that this discovery could help devise pain therapies that would be optimized for men and women, especially as "most of the world's pain patients are women." For example, the chronic-pain condition fibromyalgia is more common in women than men in the U.S.

"Regardless of which sex is more sensitive to pain, there's increasing evidence, like this paper here, that the circuitry going on behind the scenes is different circuitry in males and females," Mogil said. "The system is actually a different system in males versus females, and that's actually the more interesting part."

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But what is BVO, and what is it found in?

BVO is vegetable oil modified with bromine, a naturally occurring chemical element that's dark-reddish-brown and liquid at room temperature. Bromine is denser than water and sinks when added to it, and when combined with a vegetable oil, the element makes that oil denser than water. This effect makes BVO useful for emulsifying certain ingredients in water, ensuring that they're evenly distributed throughout the liquid and don't separate from it.

In the past 50 years, BVO has primarily been used to help stabilize citrus flavorings within sodas, sports drinks and energy drinks. That said, many U.S. beverage makers have already replaced the BVO in their products, and "today, few beverages in the U.S. contain BVO," according to the FDA. 

Related: PFAS 'forever chemicals' to officially be removed from food packaging, FDA says

Manufacturers started using BVO in food in the 1920s, prior to the FDA's establishment. The agency initially added the modified oil to its list of foods that are "generally recognized as safe" (GRAS). However, in the 1960s and 1970s, the oil's safety came into question as animal studies suggested that consuming the product might harm the heart. 

These early studies, however, fed the animals doses far beyond what humans would be exposed to, and later studies overturned the idea that BVO hurts the heart. But nonetheless, at the time, the FDA moved to limit the use of BVO. In the late 1960s, the oil lost its place on the GRAS list and was restricted to being used as an additive in very small amounts — 15 parts per million. 

In recent years, technologies improved and enabled the FDA to undertake better studies of the concentration of BVO in drinks and of the effects of the oil on lab animals. The animals were fed amounts of BVO that mimicked the real-life exposure a human might realistically experience.

A study published in 2022 showed that rats fed BVO accumulated high amounts of bromine in their blood and tissues, and breakdown products of the oil accumulated in various organs and in fat. The particularly concerning finding was that high doses led to enlargement of cells in the thyroid, a hormone-making gland in the throat. These effects on the thyroid can lead to conditions such as goiter, which is sometimes accompanied by the thyroid making too much or too little hormone. 

Following studies such as this, the FDA proposed that BVO should no longer be allowed in food. "Animal and human data, including new information from recent FDA-led studies on BVO, no longer provide a basis to conclude the use of BVO in food is safe," the agency stated.

The newly finalized rule will take effect Aug. 2, after which companies will have one year to reformulate, relabel and deplete their inventory of BVO-containing products. Many companies have already phased out BVO in their products, and some — such as Keurig Dr Pepper, the maker of Sun Drop soda — told news outlets last year that they were moving to drop the additive.   

"The removal of the only authorized use of BVO from the food supply was based on a thorough review of current science and research findings that raised safety concerns," Jim Jones, the FDA's deputy commissioner for human foods, said in a statement. 

"We will continue to monitor emerging evidence on the chemicals we have targeted for reassessment," he said, "and in cases such as this, where the science no longer supports continued authorized use, we will take action to protect public health."

When used in products, BVO must be listed as an ingredient on the label, either as "brominated vegetable oil" or as the specific oil that has been brominated, such as "brominated soybean oil."

You might hear bromine poisoning mentioned in relation to BVO. However, this type of poisoning most often happens when people inhale too much bromine — for example, when they're working in an environment with a lot of the element. Bromism, another bromine-related condition, is caused by chronic exposure to the element. This condition was more common when people used bromine as a sedative. There is only one known case in which a person seemingly got bromism from excessive soda consumption, so this is an extremely slim risk.

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

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The new hybrid creations, which researchers have dubbed "chimeroids," are a variation of brain organoids — tiny 3D models made of tissue that mimic the structure and function of a full-size brain. These models are more accurate to human biology than 2D cellular models or animals like lab mice. Because of this, scientists hope that the models will accelerate drug research and development. 

Typically, brain organoids are grown from cells that are collected from just one donor. This means they can't capture the genetic variability that exists between people, which can impact individuals' brain development and their responses to drugs. 

Creating chimeroids could overcome this hurdle, according to the scientists behind a new study, published June 26 in the journal Nature. Such a "village in a dish" could be particularly useful in the early stages of drug testing, they said. 

Researchers have previously grown sheets of brain cells from the stem cells of different people, but this is the first time that 3D models of the brain have been grown this way. 

Related: Lab-grown 'minibrains' may have just confirmed a leading theory about autism

"Chimeroids are an exciting tool that will be widely adopted in the field of neurodevelopment, probably with diverse applications," Aparna Bhaduri, an assistant professor of biological chemistry at the University of California, Los Angeles who was not involved in the research, wrote in a commentary of the study. 

To make the chimeroids, researchers collected stem cells from five people and then in the lab used growth-inducing chemicals to coax them into growing into brain organoids — each of which had cells from just one person. The scientists then tore the resulting organoids apart and recombined the cells within them to form chimeroids. This ensured that each chimeroid contained an equal number of cells derived from each person. 

After three months, the chimeroids were around 0.12 to 0.2 inches (3 to -5 millimeters) in diameter and contained all the same types of cells that are normally found within the cortex — the outermost layer of the brain — of a fetus. 

Separately, the team exposed the chimeroids to two neurotoxic chemicals: ethanol, which is associated with fetal alcohol spectrum disorders, and the antiepileptic drug valproic acid, which can increase the risk of birth defects. The team found that cells that came from different donors responded differently to these drugs, in terms of how extensively the chemicals hindered their growth, for example. 

If scaled up to contain cells from even more people, chimeroids could theoretically help determine how patients will respond to drugs before they are tested in a clinical trial, the team said. They could then be segregated into specific treatment response groups. 

"I'm excited about what the future holds in terms of using organoids, such as the chimeroids, to develop brand new ways to achieve therapeutic innovation for neurological disease," Paola Arlotta, co-senior study author and a professor of stem cell and regenerative biology at Harvard University, told Live Science in an email. 

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Evidence suggests that, in adults, the abundance of certain microbes in the gut fluctuates daily. In other words, this flux follows a circadian rhythm, similar to the bodily processes that dictate when we sleep and wake up. 

Recently, a study revealed that bacteria living in the guts of babies as young as 2 weeks old also have a circadian rhythm. The report, published in April in the journal Cell Host and Microbe, showed that this rhythmicity increases with age. 

The researchers found that the microbes maintain these day-night rhythms even when they're extracted from the body and grown in the lab, suggesting that their rhythm is intrinsically regulated and thus not dictated solely by factors in the gut itself. 

Related: Scientists may have found the missing link between heart disease and sleep problems

It's unknown why gut microbes behave this way, but their cyclical behavior may somehow help them colonize the human intestine, the study authors theorize. 

"Everything in biology has a reason," which often relates to whether a given trait would help an organism survive, Dirk Haller, co-senior study author and a professor of nutrition and immunology at the Technical University of Munich, told Live Science. In regard to the gut microbiome, the microbial community has evolved alongside the human body, becoming a core feature of our physiology.

The microbiome is beneficial to humans in many ways. For example, it helps protect us against infections by regulating the immune system and metabolizes parts of our food that we can't readily digest. The gut, in turn, provides microbes with a safe, warm place to live. There is therefore "extremely strong competition" between microbes for space in the gut, Haller said, and this competition drives the microbes to evolve. 

Following this logic, microbes within the gut likely have a circadian rhythm because there was an evolutionary benefit to doing so, both for the microbes and for their human hosts. Haller and his colleagues' recent study sheds some light on when these bacterial rhythms might start to appear in a given person's body — but how might that circadian rhythm affect our health?

"This is the most open question," Vincent Cassone, a professor of biology at the University of Kentucky who was not involved in the new study, told Live Science. 

Sleep, disease and drugs

Some past research has probed the circadian clocks of human gut bacteria, such as Klebsiella aerogenes and Bacillus subtilis. However, so far, most work in this field has focused on rodents' gut microbiomes. About 20% of microbes in the mouse gut are known to have a circadian rhythm, showing consistent fluctuations in their abundance at various points in the day. These microbes include bacteria in the orders Clostridiales, Lactobacillales and Bacteroidales, which are all also found in the human gut. 

These bacteria are called "oscillators," said Dr. Eugene Chang, a professor of medicine at the University of Chicago who was not involved in the new research. Most produce byproduct molecules, called metabolites, that are absorbed into the bloodstream and are taken to other organs, including the brain, he told Live Science. 

Once released into the blood, the metabolites can feed into the host's circadian networks and alter their function — for instance, they might influence the pattern and strength of activation of so-called circadian clock genes, Chang said. Scientists have tried disrupting this circadian cross talk in lab mice and have found that it affects physiological processes, including metabolism and inflammation. 

Some findings in mice hint that byproducts made by bacteria in our own guts may influence our sleep-wake cycles. One called butyric acid is produced when bacteria digest dietary fiber and has been shown to promote sleep in mice. However, more evidence is needed to see if the findings actually translate to humans.  

Related: 8 common sleep myths debunked

In a 2020 study of more than 4,000 people, Haller and his colleagues discovered that individuals with type 2 diabetes and obesity don't have the same daily variations in their gut microbiome as those without the conditions. This implies that there is a potential link between circadian rhythms and the microbiome in metabolic disease, but the reason why is still unknown, Haller said. 

The internal clocks that govern gut microbes, as well as those of the host's cells, all interact in a complex manner and are also affected by external factors, such as when we eat, said Dr. Garret A. FitzGerald, a professor in translational medicine and therapeutics at the University of Pennsylvania who was not involved in the research. Theoretically, this "complex interplay" might be disturbed by diseases that affect the gut, he told Live Science in an email. 

For instance, if cells that line the gut are damaged for some reason, this could influence how much of the breakdown products of drug metabolism end up in the bloodstream and affect other organs, such as the lungs, liver or brain, FitzGerald said. Our gut bugs play a role in how drugs are broken down and thus have a hand in this chain reaction.

There's an emerging scientific discipline called chronopharmacology in which scientists are investigating whether the time you take a drug can affect its safety and effectiveness. In addition to influencing people's sleep-wake cycles, bacterial circadian rhythms might partly dictate how the body reacts to a given drug. 

Furthermore, bacterial circadian rhythms may affect the bugs' resistance to antibiotics. For example, research has shown that the concentration of antibiotics needed to kill certain bacteria, such as Staphylococcus aureus, changes at specific times of the day. 

"Everybody tells us that we should take our drugs at certain times a day, Cassone said. "Maybe the gut microbiome and the human host have already known this — that certain times of the day are the best at which to get your vitamin B12, or your butyric acid for sleep or the like," he said. 

Whether this is true or not is "probably one of the great mysteries that I think will be solved pretty soon," Cassone said. 

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A pioneering surgical procedure provides amputees with bionic limbs that are directly controlled by the nervous system, enabling patients to sense the limb's position in space. 

Scientists demonstrated the success of this technique in a new study of seven people who received bionic legs, which was published Monday (July 1) in the journal Nature Medicine. Including these seven, about 60 people worldwide have undergone this type of procedure, which can be used to install either bionic legs or arms. 

"This is the first prosthetic study in history that shows a leg prosthesis under full neural modulation, where a biomimetic gait emerges," Hugh Herr, co-senior study author and a professor of media arts and sciences at MIT, said in a statement. In other words, the synthetic prosthesis is able to fill in for the lost function of the missing limb and thus produce a natural gait.

"No one has been able to show this level of brain control that produces a natural gait, where the human's nervous system is controlling the movement, not a robotic control algorithm," Herr said.

Related: 'You can get the feeling that you are touching another human': New prosthetic device detects temperature

The surgery itself, known as agonist-antagonist myoneural interface (AMI), involves reconnecting muscles in a patient's residual limb after a below-the-knee amputation, in the case that the patient is getting a bionic leg. 

Electrical signals from the central nervous system, which relay instructions for movement, can then pass between these muscles, and be detected by electrodes in a newly installed prosthetic limb. The signals are picked up by a robotic controller in the prosthesis that enables it to control a patient's gait, or way of walking. Signals about the position and movement of a patient's prosthesis are then fed back to the nervous system. 

In a series of experiments described in the new paper, the seven patients who received AMI surgery were able to walk faster than people who received the same type of prosthetic limb, but who had traditional amputations. Some of the patients could even walk at the same rate as people without amputations. They could also avoid obstacles and climb stairs more naturally than patients who underwent traditional amputations. 

Current technology for prosthetic limbs already enables amputees to achieve a natural walking gait, according to the team who conducted the surgery. However, these prosthetic limbs rely on robotic sensors and controllers to actually move in a predefined, algorithmic pattern, the team said. AMI, in contrast, enables the limb to dynamically respond to signals from the body.

"The approach we're taking is trying to comprehensively connect the brain of the human to the electromechanics," Herr said.

The patients who underwent AMI also experienced less pain and muscle atrophy, the scientists reported. 

AMI can also be used for people who have arm amputations, the team said, and the surgery can be done either during a patient's original amputation or at a later date. 

"This work represents yet another step in us demonstrating what is possible in terms of restoring function in patients who suffer from severe limb injury," Dr. Matthew Carty, co-senior study author and an associate professor of surgery at Harvard Medical School, said in the statement.

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