Medical Myths: All about COPD

 COPD is an umbrella term for a collection of progressive respiratory conditions, all of which cause breathing difficulties.

Two of the most common forms of COPD are chronic bronchitis and emphysema.

The most prevalent symptoms of COPD are shortness of breath and a cough. Over time, even everyday activities, such as getting dressed, can become challenging.

In this article, we cover some of the most common myths associated with COPD. To ensure we provide accurate information, we have recruited two experts.

Dr. Neil Schachter is a professor of medicine — pulmonary, critical care, environmental medicine, and public health — at the Icahn School of Medicine at Mount Sinai in New York. He is also medical director of pulmonary rehabilitation at the Mount Sinai Health System.

Dr. Shahryar Yadegar is a critical care medicine specialist, pulmonologist, and medical director of the ICU at Providence Cedars-Sinai Tarzana Medical Center, CA.

1. COPD is rare

According to the World Health Organization (WHO), COPD caused 3.23 millionTrusted Source deaths in 2019, making it the third leading cause of death worldwide.

Dr. Schachter explained that in the United States, COPD “is the fourth leading causeTrusted Source of death. More than 16 million Americans are diagnosed.”

Additionally, as Dr. Yadegar told Medical News Today, “millionsTrusted Source more people may be undiagnosed.”

The American Lung Association (ALA) recommends that anyone who is “experiencing COPD symptoms — chronic cough, shortness of breath, frequent respiratory infections, significant mucus production (also called phlegm or sputum), and/or wheezing — speak with [a] doctor about obtaining a breathing test called ‘spirometry,’ which can help diagnose COPD.”

2. Only smokers develop COPD

It is true that smoking tobacco is the leading cause of COPD, but as Dr. Schachter told MNT, “There are many other risk factors that contribute to the development of the disease, including air pollution, work-related pollution, infection, and some forms of asthma.”

Alpha-1 antitrypsin is an enzyme that protects the body from an immune attack. Some people have a mutation in the gene that codes for this enzyme; this causes alpha-1 antitrypsin deficiency.

Deficiency of alpha-1 antitrypsin increases the risk of developing COPD and other conditions that affect a range of bodily systems.

3. Only older adults develop COPD

COPD is certainly more common in older adults than in younger people, but younger people are not immune to the condition.

For instance, in the U.S., between 2007 and 2009, COPD affected 2%Trusted Source of males and 4.1% of females aged 24–44 years. Similarly, the condition affected 2% of males and 3% of females aged 18–24 years.

Dr. Schachter told us that a “significant proportion of those individuals diagnosed before the age of 50” have a hereditary form of the disease that causes a deficiency of alpha-1 antitrypsin.

4. COPD only affects the lungs

“False,” said Dr. Schachter. “COPD coexists with many comorbidities, including heart disease, lung cancer, hypertension, osteoporosis, and diabetes. The association may be due to common causative factors, as well as ‘systemic inflammation.’”

In other words, some of these conditions share risk factors, which makes them more likely to occur with COPD. For instance, smoking is a risk factor for both COPD and heart disease.

At the same time, health experts associate COPD with systemic inflammation, which can also independently increase the risk of other conditions.

5. People with COPD cannot exercise

According to Dr. Yadegar, “Without proper guidance, patients with COPD may have difficulty completing physical exercises.”

However, he also explained that doctors recommend people with COPD do exercise, as it can help “increase their breathing capacity and improve their daily symptoms.”

“Pulmonary rehabilitation programs typically offer guided breathing techniques in conjunction with physical exercise in order to maximize better patient outcomes,” he continued.

In a nutshell, Dr. Schachter told us that “exercise is therapeutic for COPD, reducing the number of exacerbations and improving quality of life.”

6. There are no treatments for COPD

This, thankfully, is a myth. “There are numerous therapies and strategies that improve the course of the disease,” Dr. Schachter told MNT, “including medications, rehabilitation, diet, and vaccines that protect against respiratory infections that accelerate the course of the disease.”

Dr. Yadegar said, “With a spectrum of presentations, patients may benefit from inhaled bronchodilators, anticholinergics, corticosteroids, and supplemental oxygen.” These, he said, can be tailored uniquely to each person.

“Certain patients may also benefit from alpha-1 antitrypsin augmentation or even lung transplants,” he added.

7. COPD is the same as asthma

“While both diseases are considered obstructive lung diseases, there are several differences between COPD and asthma,” Dr. Yadegar explained.

Dr. Yadegar dove into the details: “COPD is a disease of the alveoli, mostly […] a result of elasticity loss induced primarily by smoking. Asthma is a disease of the airways, primarily […] a result of chronic airway inflammation.”

“While clinical symptoms may overlap between the two diseases,” he continued, “treatments vary in order to best help patients in the short and long term.”

8. Body weight does not affect COPD

This is not true. Dr. Schachter told us that carrying excess body weight can increase the disability associated with COPD.

Conversely, if people have a body weight that is below moderate, it can be “a sign of emphysema and also indicates a poor prognosis.”

9. If you have COPD, there is no point quitting smoking

This is another myth. As Dr. Schachter told MNT, “It is never too late to quit.”

He explained that “smoking accelerates the loss of lung function that accompanies COPD.” He also said that smoking tobacco can promote exacerbations of the symptoms.

10. Shortness of breath is the only symptom of COPD

“Shortness of breath is a major presenting symptom but hardly the only one,” according to Dr. Schachter.

“Cough, excess phlegm production, respiratory infections, and all the symptoms of the comorbidities are often signs of progressing COPD.”

Other symptoms can include sleep problems, anxiety, depression, pain, and cognitive decline.

11. A healthy diet cannot help with COPD

As a matter of fact, a healthy diet can make a difference for people living with COPD. Dr. Schachter told MNT that a healthy diet promotes “general health and can protect against exacerbations of COPD itself and its comorbidities.”

For example, a 2020 meta-analysis of eight observational studies investigated the role of diet in COPD. The authors conclude that “healthy dietary patterns are associated with a lower prevalence of COPD, while unhealthy dietary patterns are not.”

Similarly, the data generated in another reviewTrusted Source suggest that “a higher intake of fruits, probably dietary fiber, and fish reduce the risk of COPD.”

In summary, although there is no cure for COPD, treatments are available, and lifestyle changes can reduce symptom severity.

Source: Medical News Today

Plant-based diets produce less greenhouse gas

 

• A new study, led by researchers at the University of Leeds in the United Kingdom, found that healthy eating may produce lower greenhouse gas (GHG) emissions.
• The researchers say that diets low in red meat, certain beverages, and sweet snacks have a smaller environmental impact.
• They conclude that governmental policies should encourage plant-based diets for personal and planetary health.

Food production, processing, and packaging are responsible for more than one-third of global GHG emissions.

However, research on the environmental effect of food behaviors has mostly focused on a limited number of broad food categories. A recent study set out to provide more granular information to how food production affects the environment.

As the authors write in the new paper, “To move beyond general advice at the population level to specific advice tailored to the individual requires measures of environmental sustainability applied to a comprehensive range of specific food items at a more granular level.”

Lead author Dr. Holly Rippin, Ph.D., and her colleagues analyzed GHG emissions of over 3,000 food items. Tying these data to a diet survey, the researchers concluded that healthier diets tend to be more Earth-friendly.

Their findings appear in the journal PLOS One.

Choosing parameters

Dr. Rippin and her team added GHG emissions of individual foods to the U.K. Composition of Foods Integrated Dataset. From this, they generated an estimate of GHG emissions for individual diets.

The researchers looked at emissions by dietary pattern, demographics, and the World Health Organization (WHO) recommended nutrient intakes (RNIs).

The team “chose to report on GHG emissions, rather than land and water use, or acidifying and eutrophying emissions, as this is where associations between health and environmental gains have previously appeared strongest.”

Linking dietary data

Nutritools myfood24 is an online food diary for tracking and analyzing nutritional intake.

The current study involved a validation cohort of 212 participants using the myfood24 tool and an interviewer-based 24-hour recall.

The researchers compared the participants’ results against reference measures from biomarkers and RNIs on one to three occasions roughly 2 weeks apart.

Largest dietary GHG sources

According to the analysis, meat contributed an estimated 32% of total diet-related GHG emissions.

Beverages including coffee, tea, and alcoholic drinks were associated with 15% of emissions, and dairy contributed 14%. Cake, cookies, and candies may have been responsible for 8% of GHG emissions.

The study also found that the diets followed by the men were associated with 41% higher GHG emissions than the diets followed by the women. As the authors explain, this disparity was “driven by differences in meat intake and, to a lesser extent, by GHG emissions from drinks.”

Moreover, nonvegetarian diets contributed 59% higher GHG emissions than vegetarian ones.

The researchers also found that the participants exceeding the RNI for saturated fat and sodium but not achieving the RNI for carbohydrates ate higher GHG emission diets.

Diets meeting the RNIs, such as those with lower saturated fat and sodium intake, were also lower in meat and produced lower GHG emissions.

Efforts to optimize diets

Dr. Rippin and her co-authors believe that nutritionally optimized diets can have a reduced carbon footprint. They do recognize, however, that trade-offs are inevitable.

For instance, the U.K. Eatwell Guide could lower GHG emissions, but water use could increase.

Medical News Today discussed this research with Dr. Diego Rose, Ph.D., MPH, a professor and director of Nutrition at Tulane University School of Public Health & Tropical Medicine in New Orleans.

MNT asked Dr. Rose if the U.K.’s target of reducing GHG emissions by 80% by 2050 is achievable. He answered:

“We need major changes across all sectors to address our climate problem, and that includes the food sector. As for the possibility of accomplishing this, well, I’m an optimist, so, yes, I do think this is possible. It’s not just about the production side, though. Changes in consumer practices are needed, both in terms of the types of food chosen and in terms of the amount of food wasted.”

However, Dr. Rose is not certain whether taxing foods is the optimal route to curbing red meat consumption, as the study authors suggest. He remarked:

“Instituting consumer food taxes can be challenging because of the political environment, so it will depend on the context. Many people don’t understand the connection between dietary choice and environmental impact, so before thinking about taxes, it makes more sense to think about consumer education, dietary guidance, or food labeling.”

A different view

Nicolette Hahn Niman, the author of Defending Beef, is a rancher and former environmental lawyer. She argues that industrialization, not red meat, poses the biggest threat to individual and planetary health.

In a September 2021 podcast, Niman suggested that the Earth itself holds the answers for achieving sustainable agriculture and diets:

“We need […] to look at nature to get the solutions. That doesn’t mean that we throw out technology. We also need to look at all the emerging science around these things, dietary issues and soil health, and carbon sequestration. There’s a great deal of benefit to a lot of research that’s happening around the world. But we also have to look at and learn the wisdom that humans and animals have had for forever.”

“We need to understand the landscape function,” she continued. “What was this Earth meant to do whatever area we are in? How was it meant to function, and how will it ecologically function optimally? […] When we do that, we will be creating healthy diets and also a healthy planet.”

Study limitations

Dr. Rippin and her team recognize several limitations to their study. For instance, the cohort included only 212 participants reporting food consumption during a maximum of 3 days.

Also, this research only measured GHG emissions, but “multiple environmental impacts need consideration to ensure cohesion within the food production system. For example, although nuts and olive oil have a relatively low GHG emissions impact, water use is high.”

Understanding the links between the food that we eat and its impact on the environment is dizzyingly complex. Understanding it requires analyzing everything, including land usage, the manufacture of packaging, the distance the food travels to reach our dinner plates, and everything in between.

This study helps build up a clearer picture, but much more research is needed to fill the gaps and assess how all the moving parts work together.

Source: Medical News Today

Crohn’s: How stress may increase disease-associated bacteria, causing flare-ups

 

• Researchers investigated the impact of psychological stress on Crohn’s disease in a mouse model.
• Psychological stress in mice caused an increase of adherent-invasive E. coli (AIEC) in the gut.
• Stress also eliminated cells that make IL-22, a protein that protects the gut’s lining and may prevent Crohn’s flare-ups.
• The researchers believe their study may lead to the development of new treatments, including an IL-22 treatment, narrow-spectrum antibiotic, or both.

Over the past few years, there has been much research surrounding stress and its effects on human health. Scientists have found that stress increases the risk for stroke, Alzheimer’s disease, and diabetes. It can also adversely affect the gut, causing problems such as constipation.

Now, a team of researchers from McMaster University in Ontario, Canada, has found a connection between psychological stress and Crohn’s disease.

Using a rodent model, the team observed how stress increased bacteria, such as E. coli, in the gut and also negatively affected a cytokine that helps protect the gut lining from invading bacteria.

Bacteria, such as E. coli, entering the gut can cause Crohn’s flare-ups.

The study appears in the journal Nature CommunicationsTrusted Source.

What is Crohn’s disease?

Crohn’s disease is an autoimmune disease that causes inflammation of the gastrointestinal tract. The gastrointestinal tract includes everything a person’s body requires for eating, digesting, and expelling food and waste. It comprises the mouth, stomach, intestines, and rectum.

Crohn’s disease is one of two types of inflammatory bowel disease (IBD)Trusted Source. It is a chronic condition most common in North America and western Europe, affecting about 100–300 for every 100,000 people.

Symptoms of Crohn’s disease include:

• diarrhea
• constipation
• loss of appetite
• weight loss
• swollen joints
• tiredness
• skin complications

Treatments for Crohn’s include medications, diet modifications, and possible surgery to fix any damaged sections of the gastrointestinal tract.

Examining Crohn’s disease and stress

Causes for Crohn’s disease are not completely known. Researchers believe genetic, hereditary, and environmental components may play a part in the condition. And while stress does not cause Crohn’s, past research shows it can affect IBD and Crohn’s disease.

According to Dr. Brian Coombes, senior author, professor, and chair of biochemistry and biomedical sciences at McMaster University, many individuals with Crohn’s disease report feeling episodes of psychological stress that precede inflammatory flares or increased disease activity.

Examples of psychological stress include relationship issues, the death of a loved one, financial problems, moving, or work troubles.

“We were interested to better understand the connection between brain and gut that might be driving this connection between stress and poor health outcomes in the gut,” he explained to Medical News Today.

For the study, Dr. Coombes’ team used a preclinical mouse model. Researchers utilized “overnight restraint” as a psychological stress stimulant in one group of mice and deprived a matched control group of the animals of food and water for 16 hours.

The mice in the physiological stress group showed an increase of Enterobacteriaceae — a large family of bacteria, including E. coli, that previous research has linked to IBD.

From there, researchers gave the mice AIECTrusted Source, and they once again either deprived them of food and water or administered overnight restraint stress. The team found the amount of AIEC in the rodents subjected to overnight restraint stress increased significantly, while that of the food deprivation group did not change.

The researchers continued their experiment for 1 month. They applied weekly applications of psychological stress to the mice, finding that the continued psychological stress led to a “marked expansion” of AIEC throughout the gut of the rodents.

And within the study of the AIEC rodent model, the research team also found stress hormones killed off CD45+CD90+ cells that help make IL-22Trusted Source — a cytokine that helps ensure the cells of the gut wall function normally.

If IL-22 production halts, then bacteria, such as AIEC, can get into the gut, causing a Crohn’s flare-up.

Dr. Coombes and his team found that giving mice in their model an external IL-22 treatment helped correct the damage that stress hormones caused to gut tissues and keep AIEC from expanding.

Research for new potential treatments

Dr. Coombes believes the outcomes of this study may help lead to the development of new treatments for Crohn’s disease. For example, IL-22 treatment might be one avenue that researchers further explore through clinical trials, which he said other groups are already conducting.

“We also found that stress allows Crohn’s disease-associated bacteria to expand in the gut,” he added.

“Knowing this, if one could find a narrow-spectrum antibiotic that selectively inhibits these disease-associated bacteria, that might have benefit for patients as well.”

Dr. Gerard Honig, director of research innovation for the Crohn’s & Colitis Foundation, told MNT this study has allowed researchers to establish a novel mechanistic link between psychological stress, nutritional state, and the growth of AIEC — a well-studied type of bacteria thought to contribute to inflammation in many people with Crohn’s.

“While the link between AIEC and stress-induced colitis will need to be validated in patients prior to drawing clinically relevant conclusions, there are numerous potential implications, which merit further study,” Dr. Honig explained.

“Second, there are numerous clinical-stage investigational therapies already under development targeting the factors studied here, including IL-22 and AIEC colonization, which could be particularly beneficial in patients at high risk of stress-related disease exacerbation.”

For his research’s next steps, Dr. Coombes said they plan to explore how quickly the gut’s microbiota recovers after stress and if there are any long-term consequences. “We also would like to explore the corrective therapies, such as IL-22 and narrow-spectrum antibiotics, (alone) or in combination, to see how this helps to resolve the disease activity in the gut.”

Source: Medical News Today

How meditation can help you make fewer mistakes

 If you are forgetful or make mistakes when in a hurry, a new study from Michigan State University -- the largest of its kind to-date -- found that meditation could help you to become less error prone.

The research, published in Brain Sciences, tested how open monitoring meditation -- or, meditation that focuses awareness on feelings, thoughts or sensations as they unfold in one's mind and body -- altered brain activity in a way that suggests increased error recognition.

"People's interest in meditation and mindfulness is outpacing what science can prove in terms of effects and benefits," said Jeff Lin, MSU psychology doctoral candidate and study co-author. "But it's amazing to me that we were able to see how one session of a guided meditation can produce changes to brain activity in non-meditators."

The findings suggest that different forms of meditation can have different neurocognitive effects and Lin explained that there is little research about how open monitoring meditation impacts error recognition.

"Some forms of meditation have you focus on a single object, commonly your breath, but open monitoring meditation is a bit different," Lin said. "It has you tune inward and pay attention to everything going on in your mind and body. The goal is to sit quietly and pay close attention to where the mind travels without getting too caught up in the scenery."

Lin and his MSU co-authors -- William Eckerle, Ling Peng and Jason Moser -- recruited more than 200 participants to test how open monitoring meditation affected how people detect and respond to errors.

The participants, who had never meditated before, were taken through a 20-minute open monitoring meditation exercise while the researchers measured brain activity through electroencephalography, or EEG. Then, they completed a computerized distraction test.

"The EEG can measure brain activity at the millisecond level, so we got precise measures of neural activity right after mistakes compared to correct responses," Lin said. "A certain neural signal occurs about half a second after an error called the error positivity, which is linked to conscious error recognition. We found that the strength of this signal is increased in the meditators relative to controls."

While the meditators didn't have immediate improvements to actual task performance, the researchers' findings offer a promising window into the potential of sustained meditation.

"These findings are a strong demonstration of what just 20 minutes of meditation can do to enhance the brain's ability to detect and pay attention to mistakes," Moser said. "It makes us feel more confident in what mindfulness meditation might really be capable of for performance and daily functioning right there in the moment."

While meditation and mindfulness have gained mainstream interest in recent years, Lin is among a relatively small group of researchers that take a neuroscientific approach to assessing their psychological and performance effects.

Looking ahead, Lin said that the next phase of research will be to include a broader group of participants, test different forms of meditation and determine whether changes in brain activity can translate to behavioral changes with more long-term practice.

"It's great to see the public's enthusiasm for mindfulness, but there's still plenty of work from a scientific perspective to be done to understand the benefits it can have, and equally importantly, how it actually works," Lin said. "It's time we start looking at it through a more rigorous lens."

Source: ScienceDaily

Sense of smell is our most rapid warning system

 The ability to detect and react to the smell of a potential threat is a precondition of our and other mammals' survival. Using a novel technique, researchers at Karolinska Institutet in Sweden have been able to study what happens in the brain when the central nervous system judges a smell to represent danger. The study, which is published in PNAS, indicates that negative smells associated with unpleasantness or unease are processed earlier than positive smells and trigger a physical avoidance response.

"The human avoidance response to unpleasant smells associated with danger has long been seen as a conscious cognitive process, but our study shows for the first time that it's unconscious and extremely rapid," says the study's first author Behzad Iravani, researcher at the Department of Clinical Neuroscience, Karolinska Institutet.

The olfactory organ takes up about five per cent of the human brain and enables us to distinguish between many million different smells. A large proportion of these smells are associated with a threat to our health and survival, such as that of chemicals and rotten food. Odour signals reach the brain within 100 to 150 milliseconds after being inhaled through the nose.

The survival of all living organisms depends on their ability to avoid danger and seek rewards. In humans, the olfactory sense seems particularly important for detecting and reacting to potentially harmful stimuli.

It has long been a mystery just which neural mechanisms are involved in the conversion of an unpleasant smell into avoidance behaviour in humans. One reason for this is the lack of non-invasive methods of measuring signals from the olfactory bulb, the first part of the rhinencephalon (literally "nose brain") with direct (monosynaptic) connections to the important central parts of the nervous system that helps us detect and remember threatening and dangerous situations and substances.

Researchers at Karolinska Institutet have now developed a method that for the first time has made it possible to measure signals from the human olfactory bulb, which processes smells and in turn can transmits signals to parts of the brain that control movement and avoidance behaviour.

Their results are based on three experiments in which participants were asked to rate their experience of six different smells, some positive, some negative, while the electrophysiological activity of the olfactory bulb when responding to each of the smells was measured.

"It was clear that the bulb reacts specifically and rapidly to negative smells and sends a direct signal to the motor cortex within about 300 ms," says the study's last author Johan Lundström, associate professor at the Department of Clinical Neuroscience, Karolinska Institutet. "The signal causes the person to unconsciously lean back and away from the source of the smell."

He continues:

"The results suggest that our sense of smell is important to our ability to detect dangers in our vicinity, and much of this ability is more unconscious than our response to danger mediated by our senses of vision and hearing."

The study was financed by the Knut and Alice Wallenberg Foundation, the National Institute on Deafness and Other Communication Disorders and the Swedish Research Council. There are no reported conflicts of interest.

Source: ScienceDaily

Baby seals can change their tone of voice

 Hoover the seal was initially kept in a family home and could imitate human speech, barking catch phrases in a gruff accent ("Come over here"). But vocal learning -- the ability to imitate sounds -- is a rare trait among mammals. Only a few species may be capable of changing the pitch of their voice to sound higher or lower, which is a crucial element of human speech. "By looking at one of the few other mammals who may be capable of learning sounds, we can better understand how we, humans, acquire speech, and ultimately why we are such chatty animals," explains MPI's Andrea Ravignani, senior investigator of the study. Are seal pups already capable of changing the pitch (or 'tone height') of their voices?

Wadden Sea noises

The researchers studied eight harbour seal pups -- 1 to 3 weeks old -- that were being held in a rehabilitation centre (the Dutch Sealcentre Pieterburen) before being released back into the wild. To investigate whether the pups could adapt their voices to noises in the environment, the team first recorded noises from the nearby Wadden Sea. For several days, the sea noises were then played back to the pups, in three degrees of loudness (varying from no sound to 65 decibel), but with a similar tone height to that of the seal pups' calls. The team also recorded the pups' spontaneous calls. Would the pups change their tone of voice to adapt to the sea noises?

When the seal pups heard louder sea noises, they lowered their tone of voice. The pups also kept a more steady pitch with the more intense noise levels. One seal clearly showed the so-called Lombard effect, producing louder calls when the noise got louder. The Lombard effect is typical for human speech, as people raise their voices in noise to be better understood. The pups did not produce more or longer calls when they heard different levels of sea noise.

Direct neural connections

Apparently, young seals adapt to the noises in their environment by lowering the tone of their voice, an ability they seem to share with humans and bats. Other animals in similar experiments only raise their voice (i.e. make louder calls) in response to louder noise.

"Seal pups have a more advanced control over their vocalisations than assumed up until now," says Ravignani. "This control seems to be already present at only few weeks of age. This is astonishing, as few other mammals seem capable of that. To date, humans seem to be the only mammals with direct neural connections between the cortex ('the outer layer of the brain') and the larynx ('what we use to produce tone of voice')," he concludes. "These results show that seals may be the most promising species to find these direct connections, and unravel the mystery of speech."

Source: ScienceDaily

Brain cell differences could be key to learning in humans and AI

 Imperial researchers have found that variability between brain cells might speed up learning and improve the performance of the brain and future artificial intelligence (AI).

The new study found that by tweaking the electrical properties of individual cells in simulations of brain networks, the networks learned faster than simulations with identical cells.

They also found that the networks needed fewer of the tweaked cells to get the same results, and that the method is less energy intensive than models with identical cells.

The authors say that their findings could teach us about why our brains are so good at learning, and might also help us to build better artificially intelligent systems, such as digital assistants that can recognise voices and faces, or self-driving car technology.

First author Nicolas Perez, a PhD student at Imperial College London's Department of Electrical and Electronic Engineering, said: "The brain needs to be energy efficient while still being able to excel at solving complex tasks. Our work suggests that having a diversity of neurons in both brains and AI systems fulfils both these requirements and could boost learning."

The research is published in Nature Communications.

Why is a neuron like a snowflake?

The brain is made up of billions of cells called neurons, which are connected by vast 'neural networks' that allow us to learn about the world. Neurons are like snowflakes: they look the same from a distance but on further inspection it's clear that no two are exactly alike.

By contrast, each cell in an artificial neural network -- the technology on which AI is based -- is identical, with only their connectivity varying. Despite the speed at which AI technology is advancing, their neural networks do not learn as accurately or quickly as the human brain -- and the researchers wondered if their lack of cell variability might be a culprit.

They set out to study whether emulating the brain by varying neural network cell properties could boost learning in AI. They found that the variability in the cells improved their learning and reduced energy consumption.

Lead author Dr Dan Goodman, of Imperial's Department of Electrical and Electronic Engineering, said: "Evolution has given us incredible brain functions -- most of which we are only just beginning to understand. Our research suggests that we can learn vital lessons from our own biology to make AI work better for us."

Tweaked timing

To carry out the study, the researchers focused on tweaking the "time constant" -- that is, how quickly each cell decides what it wants to do based on what the cells connected to it are doing. Some cells will decide very quickly, looking only at what the connected cells have just done. Other cells will be slower to react, basing their decision on what other cells have been doing for a while.

After varying the cells' time constants, they tasked the network with performing some benchmark machine learning tasks: to classify images of clothing and handwritten digits; to recognise human gestures; and to identify spoken digits and commands.

The results show that by allowing the network to combine slow and fast information, it was better able to solve tasks in more complicated, real-world settings.

When they changed the amount of variability in the simulated networks, they found that the ones that performed best matched the amount of variability seen in the brain, suggesting that the brain may have evolved to have just the right amount of variability for optimal learning.

Nicolas added: "We demonstrated that AI can be brought closer to how our brains work by emulating certain brain properties. However, current AI systems are far from achieving the level of energy efficiency that we find in biological systems.

"Next, we will look at how to reduce the energy consumption of these networks to get AI networks closer to performing as efficiently as the brain."

This research was funded by the Engineering and Physical Sciences Research Council and Imperial College President's PhD Scholarship.

Source: ScienceDaily

Neuroscientists roll out first comprehensive atlas of brain cells

 When you clicked to read this story, a band of cells across the top of your brain sent signals down your spine and out to your hand to tell the muscles in your index finger to press down with just the right amount of pressure to activate your mouse or track pad.

A slew of new studies now shows that the area of the brain responsible for initiating this action -- the primary motor cortex, which controls movement -- has as many as 116 different types of cells that work together to make this happen.

The 17 studies, appearing online Oct. 6 in the journal Nature, are the result of five years of work by a huge consortium of researchers supported by the National Institutes of Health's Brain Research Through Advancing Innovative Neurotechnologies (BRAIN) Initiative to identify the myriad of different cell types in one portion of the brain. It is the first step in a long-term project to generate an atlas of the entire brain to help understand how the neural networks in our head control our body and mind and how they are disrupted in cases of mental and physical problems.

"If you think of the brain as an extremely complex machine, how could we understand it without first breaking it down and knowing the parts?" asked cellular neuroscientist Helen Bateup, a University of California, Berkeley, associate professor of molecular and cell biology and co-author of the flagship paper that synthesizes the results of the other papers. "The first page of any manual of how the brain works should read: Here are all the cellular components, this is how many of them there are, here is where they are located and who they connect to."

Individual researchers have previously identified dozens of cell types based on their shape, size, electrical properties and which genes are expressed in them. The new studies identify about five times more cell types, though many are subtypes of well-known cell types. For example, cells that release specific neurotransmitters, like gamma-aminobutyric acid (GABA) or glutamate, each have more than a dozen subtypes distinguishable from one another by their gene expression and electrical firing patterns.

While the current papers address only the motor cortex, the BRAIN Initiative Cell Census Network (BICCN) -- created in 2017 -- endeavors to map all the different cell types throughout the brain, which consists of more than 160 billion individual cells, both neurons and support cells called glia. The BRAIN Initiative was launched in 2013 by then-President Barack Obama.

"Once we have all those parts defined, we can then go up a level and start to understand how those parts work together, how they form a functional circuit, how that ultimately gives rise to perceptions and behavior and much more complex things," Bateup said.

Together with former UC Berkeley professor John Ngai, Bateup and UC Berkeley colleague Dirk Hockemeyer have already used CRISPR-Cas9 to create mice in which a specific cell type is labeled with a fluorescent marker, allowing them to track the connections these cells make throughout the brain. For the flagship journal paper, the Berkeley team created two strains of "knock-in" reporter mice that provided novel tools for illuminating the connections of the newly identified cell types, she said.

"One of our many limitations in developing effective therapies for human brain disorders is that we just don't know enough about which cells and connections are being affected by a particular disease and therefore can't pinpoint with precision what and where we need to target," said Ngai, who led UC Berkeley's Brain Initiative efforts before being tapped last year to direct the entire national initiative. "Detailed information about the types of cells that make up the brain and their properties will ultimately enable the development of new therapies for neurologic and neuropsychiatric diseases."

Ngai is one of 13 corresponding authors of the flagship paper, which has more than 250 co-authors in all.

Bateup, Hockemeyer and Ngai collaborated on an earlier study to profile all the active genes in single dopamine-producing cells in the mouse's midbrain, which has structures similar to human brains. This same profiling technique, which involves identifying all the specific messenger RNA molecules and their levels in each cell, was employed by other BICCN researchers to profile cells in the motor cortex. This type of analysis, using a technique called single-cell RNA sequencing, or scRNA-seq, is referred to as transcriptomics.

The scRNA-seq technique was one of nearly a dozen separate experimental methods used by the BICCN team to characterize the different cell types in three different mammals: mice, marmosets and humans. Four of these involved different ways of identifying gene expression levels and determining the genome's chromatin architecture and DNA methylation status, which is called the epigenome. Other techniques included classical electrophysiological patch clamp recordings to distinguish cells by how they fire action potentials, categorizing cells by shape, determining their connectivity, and looking at where the cells are spatially located within the brain. Several of these used machine learning or artificial intelligence to distinguish cell types.

"This was the most comprehensive description of these cell types, and with high resolution and different methodologies," Hockemeyer said. "The conclusion of the paper is that there's remarkable overlap and consistency in determining cell types with these different methods."

A team of statisticians combined data from all these experimental methods to determine how best to classify or cluster cells into different types and, presumably, different functions based on the observed differences in expression and epigenetic profiles among these cells. While there are many statistical algorithms for analyzing such data and identifying clusters, the challenge was to determine which clusters were truly different from one another -- truly different cell types -- said Sandrine Dudoit, a UC Berkeley professor and chair of the Department of Statistics. She and biostatistician Elizabeth Purdom, UC Berkeley associate professor of statistics, were key members of the statistical team and co-authors of the flagship paper.

"The idea is not to create yet another new clustering method, but to find ways of leveraging the strengths of different methods and combining methods and to assess the stability of the results, the reproducibility of the clusters you get," Dudoit said. "That's really a key message about all these studies that look for novel cell types or novel categories of cells: No matter what algorithm you try, you'll get clusters, so it is key to really have confidence in your results."

Bateup noted that the number of individual cell types identified in the new study depended on the technique used and ranged from dozens to 116. One finding, for example, was that humans have about twice as many different types of inhibitory neurons as excitatory neurons in this region of the brain, while mice have five times as many.

"Before, we had something like 10 or 20 different cell types that had been defined, but we had no idea if the cells we were defining by their patterns of gene expression were the same ones as those defined based on their electrophysiological properties, or the same as the neuron types defined by their morphology," Bateup said.

"The big advance by the BICCN is that we combined many different ways of defining a cell type and integrated them to come up with a consensus taxonomy that's not just based on gene expression or on physiology or morphology, but takes all of those properties into account," Hockemeyer said. "So, now we can say this particular cell type expresses these genes, has this morphology, has these physiological properties, and is located in this particular region of the cortex. So, you have a much deeper, granular understanding of what that cell type is and its basic properties."

Dudoit cautioned that future studies could show that the number of cell types identified in the motor cortex is an overestimate, but the current studies are a good start in assembling a cell atlas of the whole brain.

"Even among biologists, there are vastly different opinions as to how much resolution you should have for these systems, whether there is this very, very fine clustering structure or whether you really have higher level cell types that are more stable," she said. "Nevertheless, these results show the power of collaboration and pulling together efforts across different groups. We're starting with a biological question, but a biologist alone could not have solved that problem. To address a big challenging problem like that, you want a team of experts in a bunch of different disciplines that are able to communicate well and work well with each other."

Other members of the UC Berkeley team included postdoctoral scientists Rebecca Chance and David Stafford, graduate student Daniel Kramer, research technician Shona Allen of the Department of Molecular and Cell Biology, doctoral student Hector Roux de Bézieux of the School of Public Health and postdoctoral fellow Koen Van den Berge of the Department of Statistics. Bateup is a member of the Helen Wills Neuroscience Institute, Hockemeyer is a member of the Innovative Genomics Institute, and both are investigators funded by the Chan Zuckerberg Biohub.

Source: ScienceDaily