Scientific Research Into Happiness

I am unsure how much I agree with the conclusions of this happiness research, but it is interesting to read nonetheless.

Over the past two decades, the positive psychology movement has brightened up psychological research with its science of happiness, human potential and flourishing.

It argues that psychologists should not only investigate mental illness but also what makes life worth living.

The founding father of positive psychology, Martin Seligman, describes happiness as experiencing frequent positive emotions, such as joy, excitement and contentment, combined with deeper feelings of meaning and purpose.

It implies a positive mindset in the present and an optimistic outlook for the future.

Importantly, happiness experts have argued that happiness is not a stable, unchangeable trait but something flexible that we can work on and ultimately strive towards.

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Recent research indicates that psychological flexibility is the key to greater happiness and well-being.

For example, being open to emotional experiences and the ability to tolerate periods of discomfort can allow us to move towards a richer, more meaningful existence.

Studies have demonstrated that the way we respond to the circumstances of our lives has more influence on our happiness than the events themselves.

Experiencing stress, sadness and anxiety in the short term doesn’t mean we can’t be happy in the long term.

Two paths to happiness

Philosophically speaking there are two paths to feeling happy, the hedonistic and the eudaimonic.

Hedonists take the view that in order to live a happy life we must maximise pleasure and avoid pain. This view is about satisfying human appetites and desires, but it is often short lived.

In contrast, the eudaimonic approach takes the long view. It argues that we should live authentically and for the greater good. We should pursue meaning and potential through kindness, justice, honesty and courage.

If we see happiness in the hedonistic sense, then we have to continue to seek out new pleasures and experiences in order to “top up” our happiness.

We will also try to minimise unpleasant and painful feelings in order to keep our mood high.

If we take the eudaimonic approach, however, we strive for meaning, using our strengths to contribute to something greater than ourselves. This may involve unpleasant experiences and emotions at times, but often leads to deeper levels of joy and contentment.

So leading a happy life is not about avoiding hard times; it is about being able to respond to adversity in a way that allows you to grow from the experience.

Growing from adversity

Research shows that experiencing adversity can actually be good for us, depending on how we respond to it. Tolerating distress can make us more resilient and lead us to take action in our lives, such as changing jobs or overcoming hardship.

In studies of people facing trauma, many describe their experience as a catalyst for profound change and transformation, leading to a phenomenon known as “post-traumatic growth”.

Often when people have faced difficulty, illness or loss, they describe their lives as happier and more meaningful as a result.

The ConversationUnlike feeling happy, which is a transient state, leading a happier life is about individual growth through finding meaning.

It is about accepting our humanity with all its ups and downs, enjoying the positive emotions, and harnessing painful feelings in order to reach our full potential.

Scientists Find Where Nicotine Addiction Can be Blocked in the Mouse Brain, Providing an Advance to Blocking It in the Human Brain

Humans and mice have some similar enough brain structures that make this a relevant advance in giving people increased control to stop the scourge of nicotine addiction.

Brain researchers have pinpointed a small group of brain cells that are especially responsive to nicotine, and which might be the main culprits in driving addiction to the substance.

By tweaking these neurons in mouse brains, scientists were able to curb nicotine addiction in the animals. Not only have their results solved an important piece of the nicotine addiction puzzle, but they could also lead us towards new treatments for the problem.

Nicotine is one of humanity’s most popular drugs – it’s considered to be the third most addictive substance we know. And because it holds such a sway on our brains, it’s extremely difficult to quit.

According to the US Centres for Disease Control and Prevention, smoking is a leading cause of preventable death, with about 1,300 people in the US dying every day due to cigarette smoking or smoke exposure.

Which is why a team led by researchers from The Rockefeller University has been digging around brain chemistry to identify potential new drug targets that could help curb the addiction.

They focussed on two small brain regions located in the midbrain – the evolutionary older part of vertebrate brains, and one of the many brain features we share with mice.

These two interconnected regions – the medial habenula and the interpeduncular nucleus (IPN) – are known to be involved in drug dependence, and also contain the receptors that nicotine binds to once it enters the bloodstream and crosses into the brain.

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Even though so far we only have seen these results in mice, we do share similar brain structures with these animals, so the researchers are confident we can learn something about human addiction here.

“What all of this tells us is that the habenula-IPN pathway is important for smoking in humans,” says Ibanez-Tallon.

Now that the researchers know where to look, they’ll be further investigating how to manipulate the Amigo1 neurons in order to discover new ways to target nicotine addiction.

The study has been published in PNAS.

Bacteria Can Acquire Antibiotic Resistance from Rival Bacteria, New Research Proves

It seems as though this is really important research into antibiotic resistance, as new metrics based on this research will need to be used to evaluate the dangerousness of antibiotic resistant bacteria in the future. The World Health Organization has said that “antimicrobial resistance is a global health emergency,” and reports for years have warned of the trillions of dollars and millions of lives that could be lost if this antibiotic resistance problem isn’t addressed.

Bacteria not only develop resistance to antibiotics, they also can pick it up from their rivals. Researchers have demonstrated that some bacteria inject a toxic cocktail into their competitors causing cell lysis and death. Then, by integrating the released genetic material, which may also carry drug resistance genes, the predator cell can acquire antibiotic resistance.

The frequent and sometimes careless use of antibiotics leads to an increasingly rapid spread of resistance. Hospitals are a particular hot spot for this. Patients not only introduce a wide variety of pathogens, which may already be resistant but also, due to the use of antibiotics to combat infections, hospitals may be a place where anti-microbial resistance can develop and be transferred from pathogen to pathogen. One of these typical hospital germs is the bacterium Acinetobacter baumannii. It is also known as the “Iraq bug” because multidrug-resistant bacteria of this species caused severe wound infections in American soldiers during the Iraq war.

Multidrug-resistant bacteria due to gene exchange

The emergence and spread of multidrug resistance could be attributed, among other things, to the special skills of certain bacteria: Firstly, they combat their competitors by injecting them with a cocktail of toxic proteins, so-called effectors, using the type VI secretion system (T6SS), a poison syringe. And secondly, they are able to uptake and reuse the released genetic material. In the model organism Acinetobacter baylyi, a close relative of the Iraq bug, Prof. Marek Basler’s team at the Biozentrum of the University of Basel, has now identified five differently acting effectors. “Some of these toxic proteins kill the bacterial competition very effectively, but do not destroy the cells,” explains Basler. “Others severely damage the cell envelope, which leads to lysis of the attacked bacterium and hence the release of its genetic material.”

The predator bacteria take up the released DNA fragments. If these fragments carry certain drug resistance genes, the specific resistance can be conferred upon the new owner. As a result, the antibiotic is no longer effective and the bacterium can reproduce largely undisturbed.

Pathogens with such abilities are a major problem in hospitals, as through contact with other resistant bacteria they may accumulate resistance to many antibiotics — the bacteria become multidrug-resistant. In the worst case, antibiotic treatments are no longer effective, thus nosocomial infections with multidrug-resistant pathogens become a deadly threat to patients.

Toxic proteins and antitoxins

“The T6SS, as well as a set of different effectors, can also be found in other pathogens such as those which cause pneumonia or cholera,” says Basler. Interestingly, not all effectors are sufficient to kill the target cell, as many bacteria have developed or acquired antitoxins — so-called immunity proteins. “We have also been able to identify the corresponding immunity proteins of the five toxic effectors in the predator cells. For the bacteria it makes absolute sense to produce not only a single toxin, but a cocktail of various toxins with different effects,” says Basler. “This increases the likelihood that the rivals can be successfully eliminated and in some cases also lysed to release their DNA.”

Conquest of new environmental niches

Antibiotics and anti-microbial resistance have existed for a long time. They developed through the coexistence of microorganisms and enabled bacteria to defend themselves against enemies or to eliminate competitors. This is one of the ways in which bacteria can conquer and colonize new environmental niches. With the use of antibiotics in medicine, however, the natural ability to develop resistance has become a problem. This faces researchers with the challenge of continually developing new antibiotics and slowing down the spread of drug resistance.

Research: Viruses Can Transfer Genes to Organisms They Don’t Typically Infect

It’s a little surprising that this wasn’t found before now considering what a significant role viruses have played in the development of humans.

New research shows that viruses can transfer genes to organisms that they aren’t known to infect — including organisms in different superkingdoms, or domains. The study, published in open-access journal Frontiers in Microbiology, also finds that viruses and cellular organisms share a large group of genes that help cells to function, suggesting that viruses may have an ancient cell-like origin.

Viruses can sometimes infect very different organisms during their lifecycle, such as mosquitoes and humans in the case of Zika virus. Viruses can also jump between different species, such as from birds to humans in the case of avian flu. However, no virus has been discovered that can infect organisms from different superkingdoms — the highest-level divisions of life, also known as domains.

“Normally, we associate viruses with very specific host organisms, and we do not know of any virus that, for example, can infect both bacteria and humans,” explains Arshan Nasir from COMSATS Institute of Information Technology, Pakistan, and University of Illinois, USA, and one of the study’s authors. “Virus-host boundaries make sense since organisms that are separated by large evolutionary distances differ starkly in their cellular biology. This makes it hard for a virus to successfully replicate inside two very diverse environments.”

Nevertheless, Nasir and his colleagues suspected leaps between such distant species could occur, not necessarily involving virus infection. “In addition to infecting and killing cells, viruses can also insert their genes into a cell’s DNA,” says Nasir. “We therefore hypothesized that viruses might interact in non-harmful ways to exchange genes between distantly related organisms.”

To investigate such viral gene exchange, Nasir and colleagues looked at protein structures found in all known viruses and cellular organisms. By looking for protein structures that are specifically associated with viruses or cells, the researchers could detect virus-derived genes in cellular organisms and cell-derived genes in viruses.

Strikingly, viral hallmark genes weren’t just found in the expected host organisms, but in all sorts of species — including those from different superkingdoms. For example, the research team found examples where viruses thought to only infect bacteria had likely transferred genes to complex organisms, such as plants and animals. This suggests that viruses can transfer genes to organisms that are dramatically different from their usual host, and that they can influence and interact with a much wider range of organisms than previously thought.

The team also found evidence that viruses and cellular organisms share a large group of protein structures that help cells to function. This is a little surprising in the case of viruses, as they aren’t cells and have no obvious need for these proteins. One intriguing possibility is that viruses may have originally evolved from primitive cells, and these proteins were once useful during their ancient origins.

Nasir believes the results could change the way we think about virus-host relationships. “The study shows that the concept of a ‘virus host’ is rather blurry, since viruses do not necessarily need to kill a cell in order to interact with it,” he says. “We should consider viruses to be a source of new genes that cellular organisms can acquire, and not necessarily just as a source of disease.”

Fracking Endangers Localized Infant Health

The results of fracking are in actuality worse than the study details. The practice of fracking should be banned for a variety of reasons — including the contamination of drinking water reserves — and the dangers posed to infant health provide another example of why.

Health risks increase for infants born to mothers living within 2 miles of a hydraulic fracturing site, according to a study published Dec. 13 in Science Advances. The research team found that infants born within a half a mile from a fracking site were 25 percent more likely to be born at low birth weights, leaving them at greater risk of infant mortality, ADHD, asthma, lower test scores, lower schooling attainment and lower lifetime earnings.

“Given the growing evidence that pollution affects babies in utero, it should not be surprising that fracking, which is a heavy industrial activity, has negative effects on infants,” said co-author Janet M. Currie, the Henry Putnam Professor of Economics and Public Affairs at Princeton University.

“As local and state policymakers decide whether to allow hydraulic fracturing in their communities, it is crucial that they carefully examine the costs and benefits, including the potential impacts from pollution,” said study co-author Michael Greenstone, the Milton Friedman Professor in Economics and director of the Energy Policy Institute at the University of Chicago. “This study provides the strongest large-scale evidence of a link between the pollution that stems from hydraulic fracturing activities and our health, specifically the health of babies.”

Positively Transforming Greenhouse Gases — Catalyst to Recycle Carbon Dioxide and Methane for Valuable Chemicals Developed

This new research looks to be quite important, as it could provide an added incentive to address the immense threat of climate change. Methane may be only about 11 percent of greenhouse gas emissions, but it traps about 85 times more heat in the atmosphere than carbon dioxide does, so it too is definitely part of the environmental threat.

The University of Surrey has developed a new and cost-effective catalyst to recycle two of the main causes behind climate change — carbon dioxide (CO2) and methane (CH4).

In a study published by the Applied Catalysis B: Environmental, scientists have described how they created an advanced nickel-based catalyst strengthened with tin and ceria, and used it to transform CO2 and CH4 into a synthesis gas that can be used to produce fuels and a range of valuable chemicals.

The project is part of the Engineering and Physical Sciences Research Council’s Global Research Project, which is looking into ways to lessen the impact of global warming in Latin America. The study has led the University of Surrey to file a patent for a family of new “supercatalysts” for chemical CO2 recycling.

According to the Global Carbon Project, global CO2 emissions are set to rise in 2017 for the first time in four years — with carbon output growing on average three per cent every year since 2006.

While carbon capture technology is common, it can be expensive and, in most cases, requires extreme and precise conditions for the process to be successful. It is hoped the new catalyst will help make the technology more widely available across industry, and both easier and cheaper for it to be extracted from the atmosphere.

Dr Tomas R. Reina from the University of Surrey said: “This is an extremely exciting project and we believe we have achieved something here that can make a real impact on CO2 emissions.

“The goal we’re all chasing as climate scientists is a way of reversing the impacts of harmful gases on our atmosphere — this technology, which could see those harmful gases not only removed but converted into renewable fuels for use in poorer countries is the Holy Grail of climate science.”

Professor Harvey Arellano-Garcia, Head of Research in the Chemical Engineering Department at the University of Surrey, said: “Utilising CO2 in this way is a viable alternative to traditional carbon capture methods, which could make a sizable impact to the health of our planet.

“We’re now seeking the right partners from industry to take this technology and turn it into a world-changing process.”

Research Finds Where the Earliest Signs of Alzheimer’s Occur in the Brain

This discovery has considerable potential for stopping the devastation Alzheimer’s often induces in those who develop the disease.

Researchers at Lund University in Sweden have for the first time convincingly shown where in the brain the earliest signs of Alzheimer’s occur. The discovery could potentially become significant to future Alzheimer’s research while contributing to improved diagnostics.

In Alzheimer’s, the initial changes in the brain occur through retention of the protein, ?-amyloid (beta-amyloid). The process begins 10-20 years before the first symptoms become noticeable in the patient.

In Nature Communications, a research team headed by Professor Oskar Hansson at Lund University has now presented results showing where in the brain the initial accumulation of ?-amyloid occurs. It is in the inner parts of the brain, within one of the brain’s most important functional networks — known as the default mode network.

“A big piece of the puzzle in Alzheimer’s research is now falling into place. We previously did not know where in the brain the earliest stages of the disease could be detected. We now know which parts of the brain are to be studied to eventually explain why the disease occurs,” says Sebastian Palmqvist, associate professor at Lund University and physician at Skåne University Hospital.

The default mode network is one of several networks, each of which has a different function in the brain. It is most active when we are in an awake quiescent state without interacting with the outside world, for example, when daydreaming. The network belongs to the more advanced part of the brain. Among other things, it processes and links information from lower systems.

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The difficulty of determining which individuals are at risk of developing dementia later in life, in order to subsequently monitor them in research studies, has been an obstacle in the research world. The research team at Lund University has therefore developed a unique method to identify, at an early stage, which individuals begin to accumulate ?-amyloid and are at risk.

The method combines cerebrospinal fluid test results with PET scan brain imaging. This provides valuable information about the brain’s tendency to accumulate ?-amyloid.

In addition to serving as a roadmap for future research studies of Alzheimer’s disease, the new results also have a clinical benefit:

“Now that we know where Alzheimer’s disease begins, we can improve the diagnostics by focusing more clearly on these parts of the brain, for example in medical imaging examinations with a PET camera,” says Oskar Hansson, professor at Lund University, and medical consultant at Skåne University Hospital.

Although the first symptoms of Alzheimer’s become noticeable to others much later, the current study shows that the brain’s communication activity changes in connection with the early retention of ?-amyloid. How, and with what consequences, will be examined by the research team in further studies.