How is diet quality linked to death risk?

Data regarding the dietary habits of tens of thousands of adults in the United States suggest that those who follow healthful low fat and low carb diets have a lower overall death risk.

 “Diet plays an important role in […] public health, and suboptimal diet is estimated as the first leading cause of death and the third leading cause of disability-adjusted life-years lost in the [U.S.],” write Dr. Zhilei Shan — from the Harvard T. H. Chan School of Public Health in Boston, MA — and colleagues in their new study paper.

Their findings now appear in the journal JAMA Internal Medicine.

In their research, Dr. Shan and team analyzed the data of more than 37,000 people to determine whether or not there were any associations between different diet types and mortality.

More specifically, the investigators wanted to find out if different types of low fat and low carb diet are associated with total mortality.

Although there have been several studies into the links between diet and death risk, the researchers note that — to their knowledge — none have looked specifically at how low carb and low fat diets of different qualities may fit into the equation.

“Consumption of carbohydrates from refined grains and added sugars has been adversely associated with health outcomes, whereas consumption of carbohydrates from whole grains, nonstarchy vegetables, and whole fruits appears to be beneficial,” explain the study authors.

“Likewise,” they say, “replacing saturated fat with unsaturated fat was associated with lower risk of heart disease and mortality.”

For these reasons, the investigators thought it was important to identify and emphasize any associations between different diet types, different quality diets, and mortality risk.

Low fat, low carb, and mortality

For their study, the researchers analyzed the data of 37,233 U.S. adults with a mean age of 49.7 years. The data came from eight cycles of the National Health and Nutrition Examination Survey (NHANES), from 1999 to 2014.

In total, the follow-up period accounted for 297,768 person years. This refers to the amount of follow-up time for all the participants included in the NHANES surveys.

During this time, the researchers recorded a total of 4,866 deaths, of which 849 were related to heart disease and 1,068 were related to cancer.

Using the NHANES reports regarding people’s macronutrient consumption, the researchers were able to infer different diet quality types.

The team found no association between overall low carb and low fat diet scores and total mortality risk.

However, they did find an association between unhealthful low carb and low fat diet scores — indicating adherence to poor quality low fat and low carb diets — and a higher total mortality risk.

On the other hand, better quality low fat and low carb diets were associated with a lower total mortality risk.

The researchers also report that “participants with a higher overall [low carb dirt score] score” — indicative of a poorer quality diet — “were more likely to be older and non-Hispanic white, to have higher [body mass index], educational level, income level, and cholesterol intake, and to have lower total energy intake.”

As for those with higher low fat diet scores, the investigators point out that they tended to be part of an ethnic minority group, to not smoke, to have lower weights, and to have lower cholesterol levels.

When trying to find an explanation for the association between different diet quality types and mortality risk, Dr. Shan and colleagues point out that many biological mechanisms could play a role.

They write, “Fat provides more than twice as much energy as carbohydrates and protein by weight. A high saturated fat diet is highly palatable and may […] [lead] to overconsumption and obesity.”

“Low quality carbohydrates, such as refined grains and added sugars, provide limited nutritional value, and their high glycemic load could be associated with high postprandial glucose and insulin, inflammation, insulin resistance, and dyslipidemia.”

Although the researchers emphasize that the main strength of their study was the sheer size of the population sample — as well as the lengthy follow-up time for data collection — they also caution that the research had a number of limitations.

These include the fact that they could not identify which specific versions of the various low carb and low fat diets each participant had followed.

This means, in the study authors’ words, that “the results could not be directly translated to the assessment of health benefit or risk associated with the popular versions of the diets.”

They also note that the participants self-reported the data regarding their diets, which means that they may not be entirely accurate. The team was also unable to verify whether or not the relationship between diet quality and mortality risk was of a causal nature.

The funding for this study came from the Young Scientists Fund of the National Natural Science Foundation of China, the Major International (Regional) Joint Research Project of the National Natural Science Foundation of China, and the National Institutes of Health (NIH).

It is also worth noting that some of the researchers disclosed possible conflicts of interests, as some received personal fees and grants — for separate work — from private sponsors including the California Walnut Commission and the Standard Process, Metagenics, and Diet Quality Photo Navigation program.

Source: Medical News Today

Blue light may aid recovery after concussion

A study that the United States military funded concludes that blue light can help heal mild traumatic brain injury simply by helping the person sleep better.

Mild traumatic brain injury (mTBI), or concussion, can result from a range of causes, from a car accident to fights, falls, or sports.

Following such an injury, people might see stars, become disoriented, or even lose consciousness briefly, but many come round without realizing that they have been concussed at all.

However, for some, mTBI can result in weeks or months of symptoms, including headaches, mental fogginess, dizziness, memory loss, fatigue, and disturbed sleep. According to the researchers behind the current study, some 50% of people with mTBI complain of chronic sleep problems after the injury, which affects their ability to think and recover.

And 15% of those with mTBI have symptoms that last for at least 1 year.

Scientists believe that these symptoms occur due to the stretches and tears that the impact inflicts on microscopic brain cells.

“Your brain is about the consistency of thick Jell-O,” explains lead author William D. “Scott” Killgore, a psychiatry professor at the University of Arizona in Tucson. “Imagine a bowl of Jell-O getting hit from a punch or slamming against the steering wheel in a car accident. What’s it doing? It’s absorbing that shock and bouncing around. During that impact, microscopic brain cells thinner than a strand of hair can easily stretch and tear and rip from the force.”

Such injury can also occur during explosive blasts, when shock waves hitting the soft tissue of the gut push a surge of pressure into the brain, damaging blood vessels and brain tissue.

“Mild traumatic brain injury (mTBI), which is commonly known as concussion, is one of the most common injuries experienced by military personnel and is a major health concern worldwide,” Killgore told Medical News Today.

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Sleep as a healer

“At present, there are virtually no effective treatments for concussion,” said Killgore. “We sought a nonpharmacologic (or nondrug) method to help people.”

Killgore and his research team received funding from the U.S. Army Medical Research and Development Command to conduct the study, which features in the journal Neurobiology of Disease.

The solution that they set out to prove effective was sleep.

“Because sleep is so important for brain health and recovery, we reasoned that improving sleep timing and duration could lead to a more rapid recovery from mTBI,” said Killgore. “Considerable evidence suggests that sleep is important for brain repair processes,” he added.

Killgore explained that scientists have shown that following an injury, sleep facilitates the production of new insulating brain cells called oligodendrocytes.

“Without sufficient restorative sleep, the repair of brain tissue will likely be slowed or incomplete,” Killgore said.

Blue light in the morning

The recent clinical trial, which involved 32 adults with mTBI, focused on solidifying the participants’ circadian rhythm — the natural process that dictates our 24 hour sleep-wake cycle.

The researchers achieved this by exposing the participants to blue light from a cube-like device for 30 minutes early each morning for 6 weeks. The participants in the control group used amber lights instead of blue.

Source: Medical News Today

Could AI replace the finger prick blood sugar test?

New research shows that artificial intelligence (AI) could someday replace invasive glucose testing. If the technology works, the switch would be particularly significant for individuals with diabetes.

Some recent reports in the media suggest that the pace of AI development is slowing down.

Despite this, AI developers continue to design cutting-edge technology that promises to, someday, make daily life easier for everyone.

Certain AI technologies are being tailored to improve treatments for specific health issues. For example, scientists recently developed an AI system that can detect low blood sugar, or hypoglycemia.

The researchers hope that this system will enable patients to measure their blood glucose levels without the need for an invasive method called a finger prick test.

The team recently published the results of a pilot study in the journal Scientific Reports.

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Issues with current methods

For many people, measuring blood glucose currently involves pricking a finger with a needle attached to a device. The blood sample is then analyzed by a continuous glucose monitor (CGM), which often needs to be calibrated at least twice a day.

The process can be difficult, uncomfortable, and inconvenient, especially for children and people who need to test their blood in the middle of the night. As a result, some people are unable to measure their levels as often or as accurately as necessary.

The researchers behind the current study hope that a noninvasive method will help improve compliance rates, particularly among those who need to monitor their glucose levels closely, such as people with diabetes.

The new AI technology was developed at the University of Warwick, in the United Kingdom, and it can detect hypoglycemia using electrocardiogram (ECG) signals from the heart.

In their study, the scientists demonstrated that this new technology is accurate 82% of the time, a rate similar to that of current CGM systems. Senior study author Leandro Pecchia, Ph.D., an associate professor of biomedical engineering at the university, commented:

“Our innovation consisted in using [AI] for automatic detecting [of] hypoglycemia via few ECG beats. This is relevant because ECG can be detected in any circumstance, including sleeping.”

How does it work?

Hypoglycemia affects the electrophysiology of the heart, and because it has slightly different effects on each individual’s heart, an AI system makes it possible to monitor glucose levels in a highly personalized way.

In the recent pilot study, the team used AI to automatically detect nocturnal hypoglycemia from just a few heartbeat signals recorded by a wearable device. The study included healthy individuals, whom the scientists monitored for 24 hours a day for 14 consecutive days.

This study was unique because the scientists monitored the participants’ glucose levels individually, whereas previous trials had analyzed results from the participants as a group.

The authors believe that their new approach captures the considerable diversity in ECG signals among individuals, which previous trials could not accurately incorporate.

Real-time alarm system

The wave-shaped readouts from an ECG machine give a detailed picture of how the heart is behaving; each section of the wave provides information about specific cardiac events, such as heartbeats.

The authors behind the current study developed a way to visualize precisely which part of the ECG wave is associated with a hypoglycemic event.

This could result in a real-time alarm system that alerts individuals if their blood sugar levels change dramatically. Having such an early warning could drastically shorten the amount of time that a person experiences hypoglycemia, which can be very dangerous, especially for people with diabetes.

The team’s new method is one example of precision medicine that could vastly improve the way that people manage diabetes. While there is still some way to go before this technology becomes available, the initial results are promising.

AI has been controversial since its conception. However, while certain technologies may evoke visions reminiscent of George Orwell’s 1984, they could alternately hold the promise of a world in which technological innovation complements medicine to improve the lives of millions of people.

If successful, the technology tested in the present study could pave the way for many more uses of AI and electrophysiology of the heart. It could also possibly be used to manage a variety of disorders that result from changes in the blood, with highly personalized precision.

Source: Medical News Today

Leukemia’s unexpected link to vitamin B6

Researchers have discovered a new target for leukemia treatment after their study revealed that cancerous cells utilize vitamin B6. The development of a new drug that could prove to be more effective than current treatments is underway.

Leukemia — a form of blood cancer that typically affects children and older adults — is the tenth most common cancer in the United States, representing 3.5% of all new cancer cases in the country.

According to the National Cancer Institute, the disease is also the fifth- highest cause of U.S. cancer deaths. Figures show an estimated 22,840 people died as a result of leukemia in 2019.

Acute myeloid leukemia (AML) is the second most common form of the disease. AML spreads quickly, leading to a comparatively low survival rate. Less than one-third of people with AML survive for 5 years after being diagnosed.

AML’s cancerous cells divide faster than the current treatment can kill them. Finding a new therapy that better targets these cells is crucial for long-term survival.

Cancer cells use metabolism changes — where chemical reactions result in various cell functions being switched on or sped up — to grow and spread at an abnormal rate.

As Lingbo Zhang, a fellow at the Cold Spring Harbor Laboratory (CSHL), NY, explains in a video: “One central feature of [a] leukemic cell is that its metabolic processes have been reprogrammed to support abnormal cell growth.”

A vitamin’s role 

Zhang and a team from both CSHL and Memorial Sloan Kettering Cancer Center (MSK), NY, have now discovered how AML cell division happens so speedily. Surprisingly, it revolves around a particular vitamin.

Vitamin B6 is essential for the body to function normally. Derived solely from a person’s diet, it helps with cell growth and metabolism, as well as producing neurotransmitters and red blood cells.

Taking genes from AML’s cancerous white blood cells, Zhang studied them to find more than 230 separate genes that were “very active in leukemic cells.”

The team tested each one using CRISPR gene-editing technology to block the activity of each gene. The authors published their findings in the Cancer Celljournal.

Used and abused by cancer 

The scientists aimed to find a gene that halted the spread of the cancerous cells, and they did: a gene that produces a metabolic enzyme called pyridoxal kinase (PDXK).

PDXK controls the usage of vitamin B6 by making proteins that, in turn, produce the active form of the vitamin.

When cells are healthy, they do not need vitamin B6 all the time. The enzyme activates it when the time is right for cells to divide.

However, the researchers found that in rapidly dividing cancerous cells, the enzyme promoted this vitamin.

This led to the proliferation of the AML cells, which could potentially lead to further growth and spread of the disease.

“We have shown that this enzyme is essential for leukemic cell growth,” Zhang says, explaining: “Leukemic cells are addicted to vitamin B6. You can call it a vulnerability of the cancer.”

Scott Lowe, co-author and chair of the Cancer Biology and Genetics Program at MSK, adds: “We already knew that vitamin B6 served as a regulator for a whole series of enzymes that are needed to make the building blocks required for cell growth and proliferation.”

But, he says, “this research suggested for the first time that the vitamin B6 pathway might be important for sustaining cancer.”

The path to a more effective treatment 

Most importantly, this enzyme and vitamin combination could be a target for a new, more effective form of therapy.

It would not be as simple as reducing patients’ vitamin B6 intake because this may affect vital functions throughout the body, including the brain and the rest of the central nervous system.

Instead, Zhang and his colleagues are working with medicinal chemists to develop a drug that influences the PDXK enzyme.

By doing this, leukemic cells would not be able to use vitamin B6 to their advantage.

The method might not only slow or halt the spread of leukemia, but it could also avoid harming healthy cells that require vitamin B6 for survival.

Source: Medical News Today

Could sunlight combat metabolic syndrome?

A new study in mice concludes that light-sensitive proteins on fat cells can detect sunlight. It also finds that too little natural light can alter how fat cells behave and may increase the risk of metabolic syndrome.

Throughout the evolution of life on Earth, much has changed. One notable constant, however, is the light from our sun. We cannot overstate our reliance on this huge ball of plasma 93 million miles away.

Because life in all its forms evolved under the glow of our nearest star, animals have evolved to utilize its emissions. Most obviously, the eyes contain photoreceptors that detect light and share the information with the brain, which then generates an image of a person’s surroundings.

The light from the sun also trains us into a roughly 24 hour circadian sleep–wake cycle. Virtually every land animal on Earth uses the sun to maintain their daily rhythms.

A new study that now appears in the journal Cell Reports describes a new way that sunlight might influence the lives of mammals.

Light beyond the eyes

Animals can detect light using proteins called opsins. Two of the most well-known in humans are melanopsin and neuropsin, which are expressed in some retinal cells.

In other animals, light-detecting compounds are present outside of the visual system. For example, frogs can detect light through cells in their skin called chromatophores.

Until quite recently, scientists believed that mammals only detected light through their eyes. However, several studies have now overturned this notion.

For instance, one study from 2019 found that neuropsin in the skin of rats can detect light and help them maintain their circadian rhythms. Still, evidence of so-called extraocular photoreception in mammals is scarce.

For the first time, a new study has investigated whether or not certain proteins on fat cells that lie beneath the skin might also detect light.

Senior study author Richard Lang, Ph.D. — from Cincinnati Children’s Hospital Medical Center in Ohio — explains, “This idea of light penetration into deep tissue is very new, even to many of my scientific colleagues. But we and others have been finding opsins located in a variety of tissue types. This is still just the beginning of this work.”

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Opsin 3 in fat cells

The researchers focused on opsin 3 (OPN3). This protein is present throughout the body, including in the brain, testis, liver, and kidneys.

They demonstrated that OPN3 is also present in both human and mouse fat cells, or adipocytes. Also, importantly, they showed that light can travel deep enough through a rat’s skin to trigger OPN3 in adipocytes.

A specific wavelength of blue light (480 nanometers) stimulates OPN3. This occurs in sunlight but not artificial light.

In their experiments, the scientists used genetically engineered mice that lack the gene coding for OPN3, called Opn3, in their adipocytes.

In the refrigerator

When mammals, including humans, are in a cold environment, the body adapts. Aside from shivering, the body burns fat to create heat. White adipose tissue is the primary energy store, and brown adipose tissue is mainly responsible for generating heat (without shivering) when we are cold.

In a process called lipolysis, white adipose tissue releases free fatty acids and glycerol into the bloodstream. Brown adipose fat then takes these fatty acids and uses them to generate heat.

There is a growing body of evidence supporting the idea that activating brown adipose fat might protect against metabolic syndrome. Metabolic syndrome is a collection of conditions, including hypertension, high blood sugar, abnormal blood lipids, and excess body fat around the waist.

When the researchers exposed mice lacking Opn3 in their adipocytes to cold temperatures of 39.2ºF (4ºC), their response to the cold was impaired. Their core body temperatures were lower than those of control mice with intact Opn3 genes.

Brown fat in the modified mice did not generate as much heat. Interestingly, when the researchers deprived these mice of food, they did not burn off as much fat under cold conditions as normal mice.

Testing the refrigerator light

In another experiment, the researchers placed normal adult mice in a cold environment with full-spectrum lighting and monitored their core body temperatures.

After 3 hours, they switched off the blue light of the wavelength that triggers OPN3 but left the rest of the spectrum. Without the blue wavelength, the animals’ core temperatures dropped, providing further evidence that natural, full-spectrum light influences metabolism.

In another set of experiments, the researchers raised mice with intact Opn3 genes under lights that lacked the specific blue light wavelengths that normally stimulate OPN3. The study authors refer to this as “minus blue” lighting conditions.

Like the mice that lacked Opn3, the mice raised in minus blue lighting conditions did not respond efficiently to cold temperatures and had lower core temperatures when in cold conditions. They also had larger adipocytes and did not lose weight when fasting.

Overall, animals without Opn3 used less energy and consumed less food and water. Despite being just as active as normal mice, they expended less energy and carried higher levels of fat.

In short, the study authors conclude that sunlight is essential for healthy energy metabolism.

Looking forward

Although the scientists conducted this study in mice, they believe that a similar mechanism probably exists in humans. Of course, they will need to carry out more research to explore whether or not this is the case. They write:

“If the light-OPN3 adipocyte pathway exists in humans, there are potentially broad implications for human health. Our modern lifestyle subjects us to unnatural lighting spectra, exposure to light at night, shift work, and jet lag, all of which result in metabolic disruption.”

Although scientists are at the very start of this line of investigation, the study authors theorize that “insufficient stimulation of the light-OPN3 adipocyte pathway is part of an explanation for the prevalence of metabolic deregulation in industrialized nations where unnatural lighting has become the norm.”

Looking even further into the future — and assuming that other researchers can replicate these findings — doctors might one day prescribe “light therapy” to people at risk of developing metabolic syndrome.

Source: Medical News Today

Are gut bacteria the key to healthy aging?

A

n increasing number of recent studies are asking an important question: Do gut bacteria hold the key to healthy aging? New research, recently presented at the London Microbiome Meeting, brings us closer to the answer.

In the ancient myth of Tithonus, the eponymous protagonist asks the gods to live forever but forgets to demand eternal youth.

Although he gained immortality, the diseases of old age eventually defeat Tithonus, and he bitterly regrets his immortality.

While achieving longevity is a goal worth pursuing and an ambition that humankind has harbored since the times of Ancient Greece, the myth of Tithonus reminds us that a long life has little value if riddled with disease.

As human life expectancy increases, the world population is aging at much higher rates. In fact, the United Nations estimate that the senior population — that is, the number of people aged 60 and above — is increasing at a rate of approximately 3 percent per year.

Currently, there are 962 million people aged 60 and above across the globe, according to the most recent estimates. By the year 2050, this number is projected to more than double, and the number of people aged 80 and above is expected to triple.

A range of chronic diseases accompanies aging. By the year 2060, for example, the Alzheimer's disease burden in the United States will have doubled, say the Centers for Disease Control and Prevention (CDC).

They predict that almost 14 million people will have Alzheimer's and other forms of dementia by then, and researchers are hard at work trying to prevent this and other age-related diseases.

So, the question "How can we live longer and healthier lives?" is slowly replacing that of "How can we live longer?" As scientists embark on the quest for a longer healthspan, it is becoming clearer that aging is not just an inevitable process that simply "happens," but that there are precise molecular mechanisms that regulate it.

Marina Ezcurra, Ph.D. — a lecturer in neuroscience at the School of Biological & Chemical Sciences at Queen Mary University of London in the United Kingdom — dedicates her time to understanding these mechanisms.

Her research focuses on how aging and its related diseases occur in a worm called Caenorhabditis elegans. More recently, Ezcurra and her team have been examining gastrointestinal aging and the role of the microbiome in this process.

On 24 October, 2018, Ezcurra presented her research at the London Microbiome Meeting in the U.K. In this Spotlight feature, we report on the key takeaways from her presentation.

Using a 'worm-bug' to study human aging

In her presentation — entitled "The worm-bug: a combined model system to study host-microbiome interactions" — Ezcurra introduced C. elegans as a viable model for studying aging. C. elegans has a lifespan of only 2–3 weeks, but as it ages, it develops several pathologies — just like the human organism.

However, in the case of C. elegans, all the pathologies come down to a single one: gastrointestinal aging.

As Ezcurra explained in her talk, all the lifespan-increasing treatments that scientists have applied to C. elegans work by suppressing intestinal aging.

Using C. elegans, researchers can examine a host of age-related processes, such as resistance to stress, growth, fecundity, and lifespan. Experts have also used C. elegans as a model for several human diseases, such as Alzheimer's.

Ezcurra quotes existing research that saw C. elegans fed with Escherichia coli. As the worm feeds on bacteria, the researchers created about 4,000 mutant strains of E. coli, each with a specific gene deleted. Then, the team fed C. elegans each of these strains and examined the effects.

Senior study author Meng Wang — who is an associate professor of molecular and human genetics at the Baylor College of Medicine in Houston, TX — reported on the findings, saying, "We fed C. elegans each individual mutant bacteria and then looked at the worms' lifespan."

"Of the nearly 4,000 bacterial genes we tested, 29, when deleted, increased the worms' lifespan. Twelve of these bacterial mutants also protected the worms from tumor growth and accumulation of amyloid-beta, a characteristic of Alzheimer's disease in humans."

Meng Wang

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Also, the researchers found that one bacterial mutant overproduced a substance called colanic acid; this compound increased longevity by stimulating activity in the mitochondria, the so-called powerhouses of the cell, which are responsible for turning nutrients into energy.

Fighting aging with a diabetes drug

In her talk, Ezcurra mentioned another example of successful research into C. elegans that showed the effects of the microbiome on the aging process. This study involved the common diabetes drug metformin.

Metformin is currently the world's most widely prescribed diabetes drug. Previous research has found that the oral medication does not only reduce blood sugar levels, but that it also reduces the risk of cancer.

Scientists found that the drug can delay aging in mice and C. elegans. Metformin is currently being tested in clinical trials as a potential treatment against aging and aging-related diseases.

As the researcher explained in her talk, this means that metformin could potentially target several age-related chronic diseases at once. Metformin may be able to target not just diabetes, but also cancer and Alzheimer's pathologies.

The interesting thing about metformin's effects is that they delay aging through bacteria. Studies in C. elegans that Ezcurra cited have shown that the longevity effects of metformin do not work in the absence of bacteria.

Specifically, metformin affects the folate bacterial metabolism, Ezcurra explained, which, in turn, triggers a chain reaction that ends with the activation of a molecular pathway known to regulate aging.

Combining E.coli with C. elegans

Ezcurra's own research seeks to combine two model organisms — E. coli and C. elegans — to study how bacteria mediate the aging process.

Previous studies have teased out the microbiome of C. elegans, and others have colonized the gut of C. elegans with E. coli OP50 and noticed some interesting effects. The bacterial strain had positive effects on reproduction, immunity, and the organism's response to stress.

So, Ezcurra and her colleagues wondered whether there are any other additional effects that OP50 has on the aging process. Experiments carried out in her laboratory revealed that adding antibiotics to worms colonized with E. coli OP50 improves intestinal aging. Wiping out bacterial growth delayed the atrophy of the intestine that tends to happen with age in C. elegans.

Also, the researchers found two strains of bacteria from the C. elegans microbiome that reduce intestinal aging. Therefore, the research found, anti-aging effects can also be achieved without wiping out bacterial growth, but by doing quite the opposite: colonizing the gut with specific strains of bacteria.

Another experiment carried out in Ezcurra's laboratory used a previously established human disease model that used C. elegans to recreate age-related muscle paralysis. The researchers analyzed the effects of a "cocktail" of 14 different bacterial strains that make up the experimental microbiome.

They found that this experimental cocktail strongly suppressed age-induced paralysis. Also, the media extracted from the experimental microbiome had the same positive effect.

Gut bacteria and human aging: What's next?

In the future, Ezcurra's team aims to see if it can colonize C. elegans with human bacterial strains to study the effects on aging and healthspan.

Share on PinterestPrebiotic and probiotic therapies may help seniors age more healthily.

The researcher recently received funding from the Wellcome Trust to use simple human microbiomes — such as bacteria that have a beneficial effect on health and bacteria that impact health negatively — and study their effects in C. elegans.

Using real-time imaging, the scientists hope to unravel the molecular mechanisms that underpin the interactions between the host and the microbiome, as well as their effects on the aging process.

"The next step for my research," Ezcurra told Medical News Today, "is to use C. elegans to ask specific questions about the role of the microbiome in human health."

"There are many, many studies showing that there are links between the microbiome and diseases, such as psychiatric diseases, neurodegenerative diseases, obesity, diabetes etc., but we don't understand what is cause and [what is] effect."

"There is a real need to figure out the exact relationship between the microbiome composition and disease," she went on. "Which microbial strains contribute to health and disease, and more importantly, how do these strains contribute to health?"

"It is becoming clear that microbiome diversity is important for human health," Ezcurra added. "Many factors contribute to microbiome diversity, such as diet and lifestyle, and as we become old we typically experience a loss in diversity."

"By better understanding the links between nutrition, microbiome, and health, we can understand how the elderly can maintain their microbiome, and also help them directly by using pre- and probiotic strategies. This would help us age in [a] better way, maintaining health and quality of life in old age without drugs or surgery."

Source: MedicalNewsToday