5 Ways Positive Thinking Can Transform Your Health

Our emotional world has a remarkable power to determine not only our mental health, but also how our physical well-being.

"Positive characteristics, such as optimism, vitality, meaning, and subjective life satisfaction are immensely important in their own right," psychologist Dr. Scott Barry Kaufman wrote in a recent Scientific American blog on optimism and heart health. "The related fields of positive psychology and health psychology focus on rigorous scientific investigations of how people adapt to life’s inevitable challenges, and how that is related (or even leads to) a better quality of life." 

And a growing body of research in psychology, medicine and public health is demonstrating the health benefit of positive emotions and their effect on physical health. When past studies have looked at the effect of emotions on physical health, it has tended to focus on the deleterious effect of negative emotions like anger and mental health conditions such as anxiety and depression. 

Here are five positive emotions that have been shown to improve physical health and prevent disease. 

Optimism may protect the heart. 
While we usually define optimism as a sunny outlook towards the future, it also encompasses much more than that. The hopeful emotion acts as a coping mechanism that can help individuals to prevail through life's challenges by maintaining a conviction that things will work out in life.
A growing body of research has suggested that cultivating this quality can have a protective effect on the heart. According to a 2012 review of literature , a number of studies have shown that people with optimistic personalities are at a reduced risk of cardiovascular events. More recently, a fascinating study found that language used on Twitter could predict mortality from heart disease -- specifically, language related to optimism and resiliency ("overcome," "stronger," "faith") was associated with a lower risk of mortality within a particular community.
Optimism's benefits for physical health also extend beyond heart health. Here are a few other ways that a sunny disposition may improve health outcomes, including improved immune system function and increased longevity.

Experiencing awe reduces inflammatory markers associated with autoimmune disease.
Hiking through a beautiful natural landscape, listening to moving classical music, or participating in a religious or spiritual ritual are some of the experiences in life that make us feel most joyful and alive. Research has shown that experiences of art, religion and philosophy are the most common experiences that evoke a sense of awe -- that sense of wonder and connection to something larger than ourselves. 

According to new research from the University of California at Berkeley, awe is not only pleasurable but also enormously beneficial for one's physical and mental health. The Berkeley study found that those who had recently experienced awe had lower levels of cytokines, inflammatory markers that, in chronically high levels, have been implicated in the development of autoimmune diseases, as well as other health problems including including heart disease, Alzheimer's and depression. This suggests that awe promotes healthier levels of cytokines and may prevent disease.

"Rather than seeing a walk through the park or a trip to the museum as an indulgence, we hope people will view these kind of experiences as important ways to promote a healthy body in addition to a healthy mind," one of the study's authors, Dr. Jennifer Stellar, told the Huffington Post. "Folding these kinds of positive experiences into your daily routine may be more important for health than we previously realized. 

Compassion and care for others can improve vagus nerve function.
Compassion -- a loving concern for the well-being of others -- can make us feel positively towards both ourselves and other people, and may improve our physical health in at least one important way. 

Positive psychologist Barbara Frederickson has conducted research on the effects of lovingkindness meditation (LKM), a traditional Buddhist practice that involves meditating on love and extending compassion to oneself and a progressively large group of others. Frederickson found just six weeks of LKM training to have a positive impact on the vagus nerve, which extends from the brain stem to the heart, helping to regulate emotions as well as bodily systems including the cardiovascular and digestive systems. 

In boosting feelings of compassion, the meditation led to improvements in resting vagal tone (which can be used to assess the degree of activity in the automatic nervous system). In an interview with Emory University, Frederickson explained that the vagus nerve plays an important role in both a person's physical health and their feeling of love and connection to others. 

“In a way, our bodies are designed for love, because the more we love, the more healthy we become,” she said. 

Gratitude may also benefit heart health and immune system function.
Like optimism, an "attitude of gratitude" -- an appreciation and feeling of thankfulness for the blessings one has in life -- carries significant mental and physical health benefits. Gratefulness, like optimism, has been linked with improved immune health, and has also been shown to improve sleep quality. 

Gratitude may also improve health and well-being in a variety of ways insofar as it lowers stress levels -- stress being one of the main contributing factors to many chronic diseases. Research has shown that among older adults, feeling a sense of gratitude towards God acts as a buffer against the negative health effects of stress. 

Self-compassion improves health-related behaviors.
People who cultivate kindness towards themselves are also kinder to their bodies, potentially helping them to prevent or manage a range of negative physical and mental health outcomes. 

A 2013 study published in the Personality and Social Psychology Bulletin examined the relationship between self-compassion, reactions to illness, and a range of health-related behaviors, finding that self-compassionate people sought medical attention sooner for symptoms that they were experiencing than people who were lacking in self-compassion. Self-compassionate people also tended to be less depressed about health problems they were experiencing, and also to take a more proactive approach towards their own health. 

"It is fine to experience the pain of a negative event," cognitive scientist Dr. Art Markman wrote in Psychology Today. "But, after acknowledging the pain, it is also important to get up and try again -- to remember that failures and illnesses and bad relationships are not a verdict on your worth as a person, but just another hurdle to be overcome."


 http://www.huffingtonpost.com/2015/03/16/optimism-heart-health_n_6744052.html

Conformity Starts Young

Nobody likes a show-off. So someone with a singular skill will often hide that fact to fit in with a group.

 A recent study reported for the first time that this behavior begins as early as two years old.

In the study, led by a team at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, and published in Psychological Science, two-year-old children, chimpanzees and orangutans dropped a ball into a box divided into three sections, one of which consistently resulted in a reward (chocolate for the children; a peanut for the apes). After the participants figured out how to get the treat on the first try, they watched as untrained peers did the same activity but without any reward. Then the roles were flipped, and the participants took another turn while being watched by the others. More than half the time the children mimicked their novice peers and dropped the ball into the sections that did not produce chocolate. The apes, on the other hand, stuck to their prizewinning behaviors. The children did not simply forget the right answer—if no one watched them, they were far less likely to abandon the winning choice.

The results suggest that the human desire to conform is inborn or at least develops at a very young age. This urge to conform probably evolved to be stronger than that of our ape cousins because group harmony was extremely important in growing hominin communities dependent on the exchange of cultural information, according to the authors. “We all like others who are similar to us,” explains psychologist and lead author Daniel Haun. Conforming boosts these feelings of sameness.

Of course, conformity is not always the best choice, nor is it always the norm—plenty of people prefer to lead, not follow. Yet in the absence of all other information about a group, “following the majority is usually a very good first choice,” Haun says.


http://www.scientificamerican.com/article/conformity-starts-young/

How Genetic Changes Lead to Familial Alzheimer’s Disease

Mutations in the presenilin-1 gene are the most common cause of inherited, early-onset forms of Alzheimer’s disease. In a new study, published in Neuron, scientists replaced the normal mouse presenilin-1 gene with Alzheimer’s-causing forms of the human gene to discover how these genetic changes may lead to the disorder. Their surprising results may transform the way scientists design drugs that target these mutations to treat inherited or familial Alzheimer’s, a rare form of the disease that affects approximately 1 percent of people with the disorder. The study was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health.

For decades, it has been unclear exactly how the presenilin mutations cause Alzheimer’s disease. Presenilin is a component of an important enzyme, gamma secretase, which cuts up amyloid precursor protein into two protein fragments, Abeta40 and Abeta42. Abeta42 is found in plaques, the abnormal accumulations of protein in the brain which are a hallmark of Alzheimer’s. Numerous studies suggested that presenilin-1 mutations increased activity of gamma-secretase. Investigators have developed drugs that block gamma-secretase, but they have so far failed in clinical trials to halt the disease.

The study led by Raymond Kelleher, M.D., Ph.D. and Jie Shen, Ph.D., professors of neurology at Harvard Medical School, Boston, provides a plot twist in the association of presenilin-1 mutations and inherited Alzheimer’s disease. Using mice with altered forms of the presenilin gene, Drs. Kelleher and Shen discovered that the mutations may cause the disease by decreasing, rather than increasing, the activity of gamma-secretase.

One of the presenilin mutations also caused impairment of memory circuits in the mouse brain and age-dependent death of neurons.

“The findings by Drs. Shen and Kelleher are a significant departure from conventional thinking that should open up exciting and creative new possibilities at all levels of research, from basic molecular mechanisms all the way to clinical intervention,” said Roderick Corriveau, Ph.D., program director at NINDS.

“This is a very striking example where we have mutations that inactivate gamma-secretase function and yet they trigger an array of features that resemble Alzheimer’s disease, notably synaptic and cognitive deficits as well as neurodegeneration,” said Dr. Kelleher.

This image compares sections of cortex from a control mouse (left) to a mouse with a presenilin-1 mutation (right). The dashed line indicates the surface of the brain. Presenilin-1 mutations decrease gamma-secretase activity and cause features of neurodegeneration, including shrinkage of the cortex, as shown above. Image credit: Raymond Kelleher and Jie Shen, Harvard Medical School.

Although plaques are the main biological indicator of Alzheimer’s, neurodegenerative changes are also an important feature of the disease. These changes include loss of brain cells, accumulations of a protein called tau inside remaining neurons, cognitive deficits such as problems with memory, changes in the brain’s electrical activity and inflammation. Commonly used mouse models of the disease exhibit excessive plaque deposition, but do not show symptoms of neurodegeneration. According to Dr. Kelleher, this may be one reason that treatments developed in mice have not been successful in patients.

“This study is the first example of a mouse model in which a familial Alzheimer’s mutation is sufficient to cause neurodegeneration. The new model provides an opportunity that we hope will help with the development of therapies focusing on the devastating neurodegenerative changes that occur in the disease,” Dr. Kelleher said.

Dr. Shen’s previous work demonstrated that presenilins and gamma-secretase play an important role in learning and memory, communication between brain cells and neuronal survival, and cautioned against the use of gamma-secretase inhibitors for Alzheimer’s disease therapy. Later, a large phase III trial was stopped because treatment with a gamma-secretase inhibitor worsened the cognitive ability of patients.

Although the majority of cases are not inherited, familial Alzheimer’s disease is associated with early onset of the disorder, with symptoms often appearing before age 60. Drs. Shen and Kelleher hope that the mechanisms uncovered in this study may provide insight into the common forms of the disorder that affect more than five million people in the United States.

The results in this paper suggest a new approach for drug development. “We believe that restoring gamma-secretase would be a better, more effective therapeutic strategy for Alzheimer’s patients,” said Dr. Shen.

 http://neurosciencenews.com/presenilin-1-alzheimers-neurology-1849/

Will Heavy Drinking Really Cause Forgetfulness?

 Charles F. Zorumski, head of the department of psychiatry at the Washington University School of Medicine in St. Louis, answers:
"It is indeed possible for a person to get intoxicated and not remember what she or he did. This state is called a “blackout” or, more precisely, a “memory blackout.” During a blackout a person is intoxicated but awake and interacting with the environment in seemingly meaningful ways, such as holding a conversation or driving a car. After the period of intoxication, usually the next day, the person has no or, at best, vague recall for events that occurred while inebriated. At times, being in this state can have disastrous consequences, such as waking up in an unknown or unsafe place, losing personal possessions or participating in risky behaviors.
On the neural level, a blackout is a period of anterograde amnesia. That is, a person's ability to form new memories becomes impaired. Although a person does not lose previously learned information, he or she may also find it more difficult to recall certain facts while intoxicated. Yet once a person sobers up, his or her memory and ability to learn new information are not permanently affected.
How alcohol, or ethanol, produces a memory blackout is not completely understood. It is clear, however, that alcohol can impair a process in brain cells called long-term potentiation (LTP), a cellular mechanism thought to underlie memory formation, particularly in the hippocampus.
The amount of alcohol required to impair LTP and learning, and potentially cause a blackout, can vary. Important factors include the type and amount of alcohol consumed—high-potency drinks are worse—and the rate at which alcohol is consumed, with rapid consumption being more problematic. These factors affect how quickly alcohol levels rise in the brain and impair memory formation.
In our studies in rodents, blocking LTP in the hippocampus requires dangerously high concentrations of alcohol, about three times the level necessary to get a person drunk. It is important to note, however, that drugs other than alcohol can affect LTP. And when combined with alcohol, these drugs can cause blackouts at lower concentrations of alcohol. Common sedatives such as the benzodiazepines Xanax and Valium and drugs that act similarly on the brain, including the popular sleeping aid Ambien, can even induce a blackout on their own.
Given the dangers associated with blackouts, the best strategy to avoid having one is to abstain from heavy consumption and from combining alcohol with other neuroactive drugs."
http://www.scientificamerican.com/article/will-heavy-drinking-really-cause-forgetfulness/

Alzheimer's researchers find molecule that delays onset of disease

The onset of Alzheimer’s disease could be delayed by a molecule that occurs naturally in humans, research suggests.
The study in mice showed that the “housekeeping” molecule put the brakes on a runaway process in the brain that leads to the most common form of dementia.

The substance works by slowing the accumulation of sticky clumps of protein in the brain, which typically appear years before symptoms such as memory loss become apparent in patients.

Although the molecule tested would be difficult to convert into a drug for use in humans, the scientists said, the findings prove that the cycle that leads to Alzheimer’s devastating impact on memory and personality can be interrupted.
Samuel Cohen, who led the study at the University of Cambridge, said: “The big advantage is that we haven’t just come up with a drug and not really understood what it is doing. We’ve come up with a general strategy that could work.”

In the earliest stages of Alzheimer’s – long before any outward signs of the disease – proteins in the brain, called amyloid betas start folding into the wrong shape, causing them to stick together in clumps. The clumps slowly grow into long hair-like threads, or fibrils, spreading across the brain. Although the brain has built-in mechanisms to eliminate faulty proteins, this cleanup process quickly falls behind because the fibrils themselves act as a “catalyst” for the formation of further clumps. “Initially the process is really slow, but it becomes a runaway chain reaction,” said Cohen.

Dementia affects around 820,000 people in the UK. Scientists estimate that delaying the onset of Alzheimer’s by five years would halve the number of people who die with the disease.

The latest study, published on Monday in the journal Nature Structural & Molecular Biology, showed that a human molecule, called Brichos, sticks to the amyloid fibrils and, by coating their exterior, stops them from accelerating the formation of more clumps.

“It doesn’t stop the initial formation, but it stops it becoming a chain reaction,” said Cohen.

The scientists tested the molecule in mice that had been given injections of amyloid proteins into the brain to mimic the biology of Alzheimer’s. Normally this reduces the level of electrical activity called “gamma waves” in the brain – an indicator of the toxic effect of the clumpy protein. However, when mice were injected with amyloid proteins together with Brichos, their brains appeared to be protected and their gamma wave activity was indistinguishable from that in healthy control mice.

Brichos is unlikely to be suitable as a drug because it would be absorbed by the body before having the chance to work in the brain. “A good tactic now is to search for other molecules that have this same highly targeted effect and to see if these can be used as the starting point for developing a future therapy,” said Cohen.

Dr Laura Phipps of Alzheimer’s Research UK, said: “This detailed study has revealed a potential way to prevent the build-up of amyloid, and highlights a possible new avenue for research into new treatments for Alzheimer’s disease. Researchers are working hard to identify the molecular process that are most toxic to nerve cells in Alzheimer’s and this technically challenging study has revealed clues to how to block one important chain of events in the disease.”

http://www.theguardian.com/science/2015/feb/16/alzheimers-research-molecule-delay-onset-dementia-found