Sunday, 31 December 2017
Saturday, 30 December 2017
Amidst the rising tensions in the world around us, people are finding themselves in the unique position of having to make hard decisions about choosing passive observation or active participation, causing some to toss their opinions into the fray of the multitude of voices speaking out within society today.
In contrast to what we have been accustomed to living and being for several decades, the pendulum of Change has begun its swing towards the opposite direction. The social tension created from this shift in direction has many of us unsettled. Enough so that many of us have turned inward in order to make sense of our external reality.
The need to seek balance and stability is inherent within us as human beings. We are meant to understand the other person’s point of view and seek the middle ground in between our two views in order to create perspective. Out of that informed perspective, we make decisions on how to act, our behavior evolves from those decisions, and consequently, our lives come into being from those personal thoughts and actions. This is how human beings are naturally designed to grow, evolve, and become within a constantly ever-changing world. If we are in the right place (along the spectrum of choices), at the right time (to make a decision), then right action (behavior and action) is effortless as we pivot our way into a greater life. This is one of the key tenets of my book, How Me Found I: Mastering the Art of Pivoting Gracefully Through Life.
Compassionate Neutrality vs. “My Way or the Highway”
The word “Dual” means two or something composed of two parts – harmony and balance is achieved in the coming together. The word “Duality” is when the two parts are in opposition to each other – competitive adversaries moving away from each other towards extreme polarization.
In that context, we are naturally hardwired to seek balance, “true inner balance”. Yet our external world is filled with ego-driven polarization ? “duality” ? the corrupted version of what “dual” really means. Because we are naturally designed to always seek balance (whether we are aware of it or not) and because the only constant we can expect in life is “Change”, then balance in an environment of dynamic change is achieved through a “two-party system”, a dual-system structure of compensating complimentary counterparts. As humans, psychologically our dual-system structure is the Ego-Heart handshake. This uniquely human complimentary relationship is inherent within what I call a “Natural Person”. To strive for continual balance is our natural state of mind in dealing with changing realities.
Unfortunately, our society, in its current presence of mind, does not recognize that the ego and the heart has a dual-system relationship, meant to counter balance each other so that we humans can continue to evolve within an ever-changing dynamic environment. For many of us, as we age and grow, the individual personalities that we exhibit outwardly are the reflections of our egos maturing as we learn how to adhere to the conditional social norms set forth for us to survive and operate within society. In contrast to the “natural person”, this ego-developed persona is what I call our “Conditioned Personality”.
Today, the word “dual” has become synonymous with the word “duality”, “It’s my way or the highway,” or “I’m right, you’re wrong”. Absent of the true meaning of a two-party system of balance, we have disintegrated into a mindset of where everything is now seen from the corrupted filters of polarized duality. Collaborative and communal dialogue has given way to personalized monologues based on absolute judgment and opinion.
This need to convince people that one way, and only one way, “my way”, is the cause for the rising tensions in the world today, as evidenced in the political, socio-economic, and ethno-diverse arenas of discussion. Unaware that balance is inherently a desire that we are hardwired for and ignorant that it is a partner to the heart, the ego interprets that innate desire as a need to convince others that its viewpoint is the right way to go and disregards, seeks to dominate, even eliminate the natural role the heart is meant to play. For the ego, all roads must lead to Rome and it is all about me, only me. There can be no other.
We all have individual egos; each convinced that its way is the correct way to go. Our own heartfelt knowing and the innate need for natural equilibrium have been mutated into a need to strive for a dominant view, absent of room for another view to exist. We have left the middle field in the center to take up position at either end of the playing field. As it meets resistance from other egos, our ego’s need for superiority can only lead to an outcome of aggressive force, more domination, and ultimately violence. We will kill to be right. We must be right at all costs. The end justifies the means.
And yet, the heart does exist and is very much a part of our physical and psychological makeup. It cannot be ignored, subjugated, or disregarded. Without the heart, we physically cease to exist. Without the heart, we have no conscience. It is through the heart that we connect to the greater wholeness of life in accordance to God, Nature, and the Universe, whichever you choose to refer to the larger part of who we are. The heart inherently knows that balance is necessary for our very own existence as a species. It defines our humanness, guides our humanitarian endeavors, and nourishes our humanity. It knows that it is the counterpart to the ego in a dual-system structure designed to move towards compassionate neutrality, thus bringing well-being into our lives. It is what allows us to respond to the environment in a nonjudgmental and loving way. It doesn’t need to be justified; it just needs us to be aware so that it can guide the ego towards creating a better life. Together, this heart-ego handshake is what allows us to make sense of what is happening in our extrinsic environment and make the right intrinsic decisions that can mutually benefit ourselves and others, not only ourselves. It is this communal awareness that we are both individually a person, and yet connected to each other as part of an overall human community, that gives us comfort that we are truly ever alone, unprotected, isolated, or abandoned. This awareness is the umbilical existence of our personality within the nesting doll collective of the human species. If we take care and look out for the welfare of others, then in turn we also receive benefit for our own self. Vice versa, if we look for balance within, then our external society also receives the benefit of that internal balance because we will emanate that behavior out into our external world.
In order for us to de-escalate the rising tension and violence in the external world of our society today, we, as members of humanity, need to look within and seek balance the way a natural person would. We need to reestablish the dual-system structure of the ego-heart handshake through intention, voice, and action. Because we are human and inherently designed for balance, we will naturally always seek to return to a state of compassionate neutrality; regardless of how long it takes to do so and despite what our ego thinks. The pendulum will eventually swing from any extreme edge to the center fulcrum.
So when we are at the extreme edge of a pendulum swing (the ego’s viewpoint), the pull from the other extreme edge (the heart’s viewpoint) will become intense enough to cause the pendulum to begin swinging back to the center where the heart’s communal compassion and a neutral ego’s informed judgment jointly resides. It is Mother Nature’s way of ensuring survival in a dynamically changing way.
The fallacy of our egos not understanding this natural fundamental principle of life will cause us to resist that innate impulse of allowing the other viewpoint to change our mind. Instead, we will literally fight to enforce our viewpoint to maintain our position. We don’t want the pendulum to swing at all. We want to remain in status quo, defiant to the extreme, and will react violently, determined to maintain our current position, against all natural forces of movement. This is the cause of the rising tensions in our world today.
We All Have a Choice
As an alternative, may I suggest that it is compassionate neutrality that we all seek, an aligned response to the natural forces of constant change occurring within our environment. It is what Buddhism calls, “the middle way”. It is operating from the center fulcrum of the pendulum swing, the vesica piscis of creation, the ability to see both sides and optimally benefit from the combined viewpoints. It is living life from both the macro and micro views of both the mountain peak and the valley below. This is how we survive, evolve, and grow as humans being humans, citizens of humankind, and as members of the human species.via Brain Blogger Read More Here..
The large mouth of largemouth bass is of interest to scientists trying to understand how joints work
Read more here: https://www.nytimes.com/2017/12/26/science/largemouth-bass-jaw.html?smid=tw-share
“More than 1,000 days of families driven from their homes by brutal violence. 1,000 days without enough food to eat and safe water to drink. 1,000 days of bombed hospitals and damaged schools. 1,000 days of children recruited to fight. 1,000 days of disease and death … of unimaginable human suffering. via WHO news Read More Here..
Friday, 29 December 2017
There’s so much out there that beckons—family, friends, ethnic textiles, and, more recently, the writers’ world. I am compelled to answer the call—all the calls! I reject the invalid role that my bloody brain repeatedly tries to thrust on me.
In order to live a full life, I’ve had to learn to set up safety nets wherever I go.
Before the brain injury, I had no difficulty living a fast-paced life. I combined a full-time job with a variety of extra curricular activities including time-consuming hobbies, such as weaving and dragon boating. Travel was an integral part of my life, with trips to conferences, workshops, and with family and friends at home and abroad.
Now, in the wake of my injury, I can’t do nearly as much. Tasks that in my past life were a matter of course, such as grocery shopping and driving, deplete my resources. Travel now drains me, especially when it involves flying. Contending with the high volumes of sensory input streaming in at airports and in flight wears me out.
I’ve had to learn to apply coping mechanisms and compensation techniques to function with my damaged brain. Though pacing myself to prevent debilitating fatigue would seem easy to apply, for me, it is one of the hardest adjustments I’ve had to implement. When I travel, it’s especially difficult.
When I’m outside my home territory, having less control over the agenda hampers any attempts to slow down. Also, I don’t want people to worry. I don’t want to call attention to myself. I don’t want to miss out, and I don’t want to slow others down.
Another obstacle in my way is that future events, including possible sources of trouble, now mean less to me. As far as I’m concerned, much of the future is abstract. It’s as if the wiring between cause and effect, between my notion of past and future, is faulty.
Trips often don’t seem real until I actually land at the destination. As a result, planning and preparations don’t make sense. I usually pack for an upcoming trip at the last moment, and when I finally get to it, I have to force myself to do it. In my mind, there’s no good reason for me to undertake a task that now feels so overwhelming in its complexity. Since the injury, poor organizational skills and the difficulties in managing high volumes of data—figuring out what I need to pack, how to arrange it in my luggage, what bags should I take—are daunting.
In time, as I healed, I became better able to manage my bloody brain. I learned to set myself a list of unbreakable rules that help me prepare for trips. A side effect of my brain injury, a strong OCD (obsessive-compulsive disorder) streak, has a surprising benefit: I have a list of basics I need to pack that I follow religiously, plus a set way to organize items in my suitcase.
My rules also include arranging for safety nets.
I knew the trip to visit my family in Israel would be grueling. I knew better than to trust my own judgment. If I hoped to convince my bloody brain to cooperate, I needed someone to watch out for me, to keep me out of trouble.
Before the trip to Israel, I spoke to my sister about my anxiety. She understood and empathized—she’s walked in my shoes. She too has cavernous angiomas that have bled. Like me, she is often tempted to outpace herself. But unlike me she is assertive, and when all hell breaks loose with her bloody brain, she knows to take it easy and to rest despite outside pressure. I, on the other hand, have trouble protecting myself, no matter how bad shape I’m in.
During the trip, she shielded me from ambitious plans from well-meaning family and friends who wanted me to participate in activities that would drain my resources. And she also shielded me from myself; I was excited to spend time with my family, not wanting to cause concern, reluctant to disappoint, and too willing to go along with the crowd.
Unfortunately, the safety nets don’t always work. Some of the changes that the bloody brain brought about get in the way. I am more emotionally volatile now, and often, my emotions drive me instead of reason. In addition, my impaired memory and poor grasp of the connection between cause and effect often results in me downplaying potential difficulties.
During my first couple of days in Israel, I didn’t listen to my sister’s advice. I was sure I knew better and that I would be fine. Even after the bloody brain lashed out at me with a crippling headache, I felt that she was being overprotective. I did finally listen to her—not because I fully agreed with her, but because I didn’t want to upset her.
As my brain rewired post-injury, my memory and my ability to make connections improved. As my self-awareness grew and I became more in-tune with myself and the bloody brain, planning ahead was easier.
But even now, more than a decade since the surgeries, when I realize that common sense says, “wait a bit, take a break, don’t do so much,” there is still a niggling little voice inside me telling me that it’s not really necessary. I still overstretch myself, though nowhere near as much as I used to. I’m doing better now, I’ll be fine.
Now, where did I put that safety net?Read More Here..
In this NEJM study, fremanezumab was effective as a preventive treatment for chronic migraine: http://www.nejm.org/doi/full/10.1056/NEJMoa1709038
Thursday, 28 December 2017
Wednesday, 27 December 2017
Too much of anything can be dangerous, and social media is no exception. Today many of us spend more time on internet-enabled devices than even sleeping. Due to this overindulgence in social media and the internet, we may become socially reclusive rather than inclusive. This, in turn, may lead to various physical and mental health problems.
Nowadays, around two billion residents of our planet are online. Hundreds of millions of emails and social messages are exchanged each day. Perhaps, this online over-engagement is becoming more of a problem. The amount of time we spend online and on social media is increasing each year. It is estimated that most people spend more than two hours each day on social media in the US.
Although social media anxiety and addiction are still not recognized as individual disorders, most investigations support the view that mental issues related to internet overuse are on the rise. Moreover, it seems to be a particularly big problem in younger people. Most individuals nowadays have their first exposure to the internet while in school. Overuse of the internet may lead to problems with concentration, sleep deprivation, failure to exercise, anxiety, and even depression. Although studying the prevalence of internet addiction or social media addiction is challenging, it could be affecting as many as 10% of people in certain sections of society.
Is social media engagement a disorder?
Is social media engagement itself a disorder? Perhaps the answer is both yes and no. It is no secret that some people get too submerged in the internet and social media. They feel bad if they do not get likes or see negative comments on their posts, and may even get depressed. Many others, however, think that social media is helpful in overcoming loneliness and depression, having a positive effect on self-esteem. The supporters of social media are saying that the compulsion to go online is not associated with the kind of harm done by substance abuse.
Most scientific review studies have provided mixed results, with only one thing certain: not all users gets depressed or feel anxiety with social media, but some do. For mental disorders related to internet abuse, as with any other psychological issues, there have to be predisposing factors like genetics, personality, lifestyle, other diseases, or a recent history of trauma.
Risk factors and identification of social media disorder
With all of the contradicting findings, there is still no doubt that social media disorder exists, and some people are at higher risk of developing it than others. Some individuals are more prone to get dependent on the internet, cultivate impulsive behavior, and are inclined towards risky internet use, as well as being more susceptible to social and emotional impairment, and even physical harm.
In recent years, some tools and measures have been developed to qualify and quantify the disorders related to social media and internet overuse. One of the scales that can be used to measure social media disorder assesses several items over the period of one year—preoccupation, tolerance, withdrawal, persistence, displacement (neglecting other hobbies), problems (arguments on social media), deception, escape, and conflict.
Social media addiction and neural changes
Some anatomical brain structures are well known to be associated with mood, emotion, and learning. Hence in one investigation, specific attention was given to the structures involved in the limbic system and reward pathway.
In the study, 20 subjects known to be addicted to social media were examined for any morphological changes in the brain, with the help of MRI. The study identified changes characteristic of impulsive behavior, with a bilateral decrease in grey matter in the amygdala without any changes in the nucleus accumbens. In contrast to other types of addiction, the anterior and mid-cingulate cortex was not found to be impaired in social media addiction, indicating that the inhibitor function of these structures is well-preserved in this condition. The study demonstrated both similarities and differences between the structural changes in the brain in social media addiction and in addiction related to substance abuse or gambling.
Other health aspects
Social media is a powerful tool that affects multiple facets of life. It has an additive effect on our already increasing sedentary lifestyle. Hence it is not stretch of the imagination that is is related to increased risk of obesity, insulin resistance, cardiovascular ailments, and other non-communicable diseases.
People who use social media too often are also more prone to bullying. They may get involved in risky behavior more frequently. In some people, social media addiction may also lead to disturbed sleep patterns. Moreover, adolescents are considered to be at higher risk of developing an addiction to social media.
Management of social media or internet addiction
Treatment of social media addiction-related pathologies depends on the nature of the problem. Although there is a lack of trials and evidence for treatment of social media-related mental issues, treatment is often a combination of pharmacological drugs and cognitive-behavioral therapy (CBT)—the kind of treatment that has already shown efficacy in other types of addictions, anxiety, and depression.
Although at present there are very few clinical studies on the topic, one can surmise that social media-related addiction, anxiety, depression, and other mental issues are going to become more common. It would be unwise to think that of social media disorder as merely a habit, we should keep in mind the related structural changes in the brain, imparting serious problems for an affected person.
ACOG (2016, February). Concerns Regarding Social Media and Health Issues in Adolescents and Young Adults – ACOG. Access here.
Cash, H., Rae, C. D., Steel, A. H., & Winkler, A. (2012). Internet Addiction: A Brief Summary of Research and Practice. Current Psychiatry Reviews, 8(4), 292–298. https://doi.org/10.2174/157340012803520513
He, Q., Turel, O., & Bechara, A. (2017). Brain anatomy alterations associated with Social Networking Site (SNS) addiction. Scientific Reports, 7, 45064. https://doi.org/10.1038/srep45064
Li, W., O’Brien, J. E., Snyder, S. M., & Howard, M. O. (2015). Characteristics of Internet Addiction/Pathological Internet Use in U.S. University Students: A Qualitative-Method Investigation. PLoS ONE, 10(2). https://doi.org/10.1371/journal.pone.0117372
Moreno, M. A., Jelenchick, L. A., & Christakis, D. A. (2013). Problematic internet use among older adolescents: A conceptual framework. Computers in Human Behavior, 29(4), 1879–1887. https://doi.org/10.1016/j.chb.2013.01.053
Seabrook, E. M., Kern, M. L., & Rickard, N. S. (2016). Social Networking Sites, Depression, and Anxiety: A Systematic Review. JMIR Mental Health, 3(4). https://doi.org/10.2196/mental.5842
Spada, M. M. (2014). An overview of problematic Internet use. Addictive Behaviors, 39(1), 3–6. https://doi.org/10.1016/j.addbeh.2013.09.007
Statista (2017). Global time spent on social media daily 2017. Access here.
van den Eijnden, R. J. J. M., Lemmens, J. S., & Valkenburg, P. M. (2016). The Social Media Disorder Scale. Computers in Human Behavior, 61(Supplement C), 478–487. https://doi.org/10.1016/j.chb.2016.03.038Read More Here..
The founders say: "Genetic-based human attraction has to do with pheromones. And when we smell pheromones, what we're actually smelling is how diverse someone's immune system is compared to our own."
"Evolution is very strong. So we're smelling each other, trying to figure out who is the best person to mate with. And that's what love at first sight actually is. It's smelling someone's pheromones from across the room, and your brain says, "That's the most perfect pheromone profile I've ever smelled in my entire life. I love them."
Human chromosomes (grey) capped by telomeres (white). Image source: Wikipedia, public domain.
When someone swabs their cheek with a Pheramor kit, the lab scans for 11 genes, which scientists have linked to attraction.
Read more here: Genetic-based dating app works to find true love using your DNA http://bit.ly/2lgiT2x
Monday, 25 December 2017
Sunday, 24 December 2017
Saturday, 23 December 2017
The Director-General of the World Health Organization welcomes the appointment of Henrietta H Fore as Executive Director of UNICEF.
Friday, 22 December 2017
A fortunate knock of luck is always welcomed by scientists and researchers, yet any treatment modalities should be novel by design rather than by serendipity. Antidepressants were discovered by chance in the 1950s, and it seems that they suffer from specific deficiencies when it comes to their clinical effectiveness and safety profile. It is something that very few in the medical field negate, although the degree of disagreement may vary.
Depression—a poorly understood disorder
Depression is a heterogeneous disorder that may be characterized by a group of common symptoms, but the underlying cause may vary from person to person. Despite considerable research about the structural and neurochemical changes caused in the brain of a person suffering from depression, there is no specific brain-based test for the condition. Two of the most widely accepted diagnostic systems, ICD-10 and DSM-IV, have similar but not identical criteria. This means that they have a different threshold for various depression symptoms.
Some of the universally accepted symptoms of depression are depressed mood, fatigue, loss of interest, worthlessness, recurrent thoughts of suicide, insomnia, and alternation in appetite.
The rise of antidepressants
Both the US- and European-based statistics show a sharp increase in the prescription of antidepressants since the 1990s. Although statistics also indicate that no more than 8% of the population suffers from depression, 13% are taking antidepressants. Moreover, these drugs are much more commonly used in people above 60 years of age, with almost one-fourth of them taking antidepressants and many older adults using them for more than a decade.
Such a rise in the use of antidepressants is also explained by the fact that these drugs are given not only to treat depression. They have become a kind of all-purpose drugs that are considered useful to treat various mood disorders, painful conditions, inflammatory bowel syndrome, anxiety, panic disorders, and many more.
How antidepressants work?
Antidepressants are drugs belonging to various groups. Almost all of them work by changing the level of monoamine neurotransmitters in the brain. There are some additional effects too, as not all drugs capable of altering monoaminergic functioning may work as antidepressants.
Antidepressants change the presynaptic and postsynaptic concentration of dopamine, serotonin, and norepinephrine in the neurons, with most modern antidepressants targeting serotonin and to some extent norepinephrine. Dopamine, serotonin, and norepinephrine are vital neurotransmitters, playing an essential role in the limbic system and reward system. The drugs help to reset these systems, consequently contributing to the regain of mood and emotional balance.
Antidepressants have been shown to increase the activation of the prefrontal cortex but decrease the activation of the hippocampus, parahippocampal region, amygdala, ventral anterior cingulate cortex, and orbitofrontal cortex. These areas of the brain play an important role in shaping mood and emotions and are part of limbic and reward systems.
Apart from modifying the transmission of monoaminergic neuromediators, antidepressant drugs also have a complex effect on various receptors and the hypothalamic–pituitary–adrenal (HPA) axis. The impact of some of the novel antidepressants on different serotonin receptors (e.g., 5-hydroxytryptamine receptors) has been well-studied.
Some of the most commonly used antidepressants these days are tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), and selective serotonin noradrenaline reuptake inhibitors (SSNRIs).
What are the safety issues?
When we talk about drug safety, it is not just about the adverse effect but also about the clinical efficacy. Too many side effects and little clinical effectiveness as compared to placebo could put the utility of any drug therapy under doubt.
When it comes to side effects, anticholinergic side effects like dryness of mouth, blurring of vision, and dizziness are common with most antidepressants. Most of them may also alter appetite and sexual function, and cause an upset stomach, joint and muscular pains, problems with drug interactions, irritability, mood changes, movement disorders and the risk of falling in the elderly, and much more. Moreover, these side effects continue to persist when the drugs are used long term.
The development of tolerance and withdrawal symptoms are widespread. Discontinuation syndrome can be really bad in many cases.
Perhaps the most worrisome of all the adverse effects is the higher occurrence of suicide and violence in those on antidepressants. Although there are many studies with contradicting conclusions, the majority seem to show that suicide and violence are much higher in those taking antidepressants. Moreover, abnormal behavior is equally common with the newer SSRIs and SSNRIs.
There is an abundance of literature mentioning the risk of suicide in depression. However, the efficacy of antidepressants in the prevention of depression-related suicide remains inconclusive.
Clinical studies have demonstrated that the newer non-tricyclic antidepressants are not any better in their safety profile in the elderly population.
Finally, a considerable number of studies seems to put doubt on the effectiveness of antidepressants. Some medical specialists believe that antidepressants do not help at all, and many studies support their view. Thus in one of the studies published in the JAMA, it was concluded that the therapeutic benefit with antidepressants may actually be non-existent or minimal for mild to moderate depression, with more substantial benefits in severe cases of depression.
Although the diversity of depression is well-recognized, almost all the drugs made to treat depression inhibit reuptake of one or another monoamine neuromediator, and very little has changed in our approach towards treatment since the advent of the first antidepressant drug. In order to overcome the dangers and limitations of therapy with antidepressants, there is an urgent need to create antidepressants that have a novel mechanism of action and better tolerance. More caution should be exercised by medical professionals when prescribing anti-depressants, as the ability to promote positive effects in many patients is questionable.
Bet, P. M., Hugtenburg, J. G., Penninx, B. W. J. H., & Hoogendijk, W. J. G. (2013). Side effects of antidepressants during long-term use in a naturalistic setting. European Neuropsychopharmacology, 23(11), 1443–1451. https://doi.org/10.1016/j.euroneuro.2013.05.001
Bielefeldt, A. Ø., Danborg, P. B., & Gøtzsche, P. C. (2016). Precursors to suicidality and violence on antidepressants: systematic review of trials in adult healthy volunteers. Journal of the Royal Society of Medicine, 109(10), 381–392. https://doi.org/10.1177/0141076816666805
Delaveau, P., Jabourian, M., Lemogne, C., Guionnet, S., Bergouignan, L., & Fossati, P. (2011). Brain effects of antidepressants in major depression: A meta-analysis of emotional processing studies. Journal of Affective Disorders, 130(1), 66–74. https://doi.org/10.1016/j.jad.2010.09.032
Fournier, J. C., DeRubeis, R. J., Hollon, S. D., Dimidjian, S., Amsterdam, J. D., Shelton, R. C., & Fawcett, J. (2010). Antidepressant Drug Effects and Depression Severity: A Patient-Level Meta-analysis. JAMA, 303(1), 47. https://doi.org/10.1001/jama.2009.1943
Hollinghurst, S., Kessler, D., Peters, T. J., & Gunnell, D. (2005). Opportunity cost of antidepressant prescribing in England: analysis of routine data. BMJ, 330(7498), 999–1000. https://doi.org/10.1136/bmj.38377.715799.F7
Köhler, S., Cierpinsky, K., Kronenberg, G., & Adli, M. (2016). The serotonergic system in the neurobiology of depression: Relevance for novel antidepressants. Journal of Psychopharmacology, 30(1), 13–22. https://doi.org/10.1177/0269881115609072
Mahar, I., Bambico, F. R., Mechawar, N., & Nobrega, J. N. (2014). Stress, serotonin, and hippocampal neurogenesis in relation to depression and antidepressant effects. Neuroscience & Biobehavioral Reviews, 38(Supplement C), 173–192. https://doi.org/10.1016/j.neubiorev.2013.11.009
National Collaborating Centre for Mental Health (UK). (2010). THE CLASSIFICATION OF DEPRESSION AND DEPRESSION RATING SCALES/QUESTIONNAIRES. British Psychological Society. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK63740/
Pratt, L. A., Brody, D. J., & Gu, Q. (2017). Antidepressant Use Among Persons Aged 12 and Over: United States, 2011–2014. https://www.cdc.gov/nchs/products/databriefs/db283.htmRead More Here..
Thursday, 21 December 2017
Wednesday, 20 December 2017
A person suffering from an anxiety disorder experiences neurology-based changes in mood and bodily functions that are discussed in more detail in this article.
As with anxiety, various personality traits and emotional responses are by-products of the interaction between our genetic coding and environmental influences. Our genes make us more receptive to some specific stimuli and play a role in developing the resilience to some other stimuli. Our brain is a plastic organ. Thus, the role of environmental factors in its development and casting cannot be negated.
Fear and stress are normal defensive reactions to threats that help our body to deal with challenges more efficiently. Anxiety is different from fear in that it is a set of emotional and somatic reactions to a future threat that may or may not be realistic. To some extent, having anxiety is a normal human reaction. However, if it continues for a prolonged period, it may have an adverse effect on our daily life and health.
In the state of anxiety, worrying about the future makes it difficult to concentrate and leads to irritability. Somatic symptoms like palpation, sweating, and gastrointestinal changes are also common in this state. Anxiety is considered as a disorder if such symptoms persist over a period of six or more months.
Anxiety disorders are most prevalent among people with psychiatric disorders, affecting around 10% of the population at any given time. Nonetheless, only a small number of those suffering from anxiety disorders seek treatment. This can be partially explained by the difficulties in identifying the condition. General anxiety disorder, panic disorder, specific phobias, and social anxiety are some of the most common types of anxiety disorders.
What makes a person vulnerable to anxiety disorders?
The hereditary nature of various forms of anxiety disorders has been established through clinical and observational studies. Multiple studies have demonstrated that a person is at 3–5 times greater risk of developing anxiety disorders if such a condition is found among first-degree relatives. The importance of familial clustering in anxiety has been demonstrated by a number of twin studies. Other internal factors like certain personality traits also make a person more vulnerable to developing anxiety disorders.
Apart from internal factors, environmental factors may also make some people more anxious. These factors include exposure to stressful condition, drug or alcohol use, parenting style, and stressful life events.
Neuroanatomy of stress and anxiety
Higher cognitive centers in our brain are located in the prefrontal cortex. They are involved in thinking, planning, and social behavior. From an evolutionary perspective, the prefrontal cortex is the “newer” part of the brain that helps us to keep our emotional responses in check.
Most of the emotion processing takes place in more ancient parts of the cortex. These anatomical brain structures are collectively called the “limbic system”. One fundamental structure in the limbic system is the hippocampus that plays a vital role in the stress response and regulation of the hypothalamic–pituitary–adrenal (HPA) axis. Both hippocampal growth and neurogenesis play an essential role in the development of resiliency towards stress and anxiety.
But perhaps the most crucial part of the limbic system that plays a central role in the regulation of emotions is the amygdala. The amygdala is central to the formation of fear and anxiety-related memory and has been shown to be hyperactive in anxiety disorders. It is well connected with other brain structures like the hippocampus, thalamus, and hypothalamus.
Apart from anatomical changes, it is essential to understand that brain functionality or communication between various brain centers and networks takes place through neurotransmitters. In the case of emotional responses, gamma-aminobutyric acid (GABA) is known to have an inhibitory effect on emotions, while glutamate has an excitatory effect. The roles of serotonin, dopamine, and norepinephrine are also well documented in the pathogenesis of various emotional states. Other neurotransmitters that may play a role in the pathogenesis of anxiety disorders are cholecystokinin (CCK), galanin (Gal), neuropeptide Y (NPY), oxytocin (OT), vasopressin (AVP), and corticotrophin-releasing factor.
Neuroanatomical changes in stress
Most anxiety disorder cases develop in childhood, where the long-term and repetitive experience of anxiety leads to changes in specific brain structures that can be observed using neuroimaging. fMRI studies on generalized anxiety disorder (GAD) have shown a higher level of activity in the ventrolateral prefrontal cortex. Furthermore, a significant level of activity is seen in the amygdala, especially when a person is told to focus on his or her stress, as well changes in the cingular cortex and insular cortex.
During adolescence, there is an acceleration in the physical growth, along with changes in behavior, cognition, and emotional control. The development of the body during this period may result in permanent changes in various brain areas that can be implicated in the development of psychiatric disorders in adult life.
During adolescence, it might be easier to remodel various brain structures with the help of cognitive behavioral therapy or other modalities than in adults. Meanwhile, in adults, various therapeutic agents can be used to alter the biochemical structure of the brain.
For patients with anxiety disorders, selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) are often prescribed as the first line treatment. Other drugs that can be used to treat various anxiety disorders include monoamine oxidase inhibitors, tricyclic antidepressants, and benzodiazepines.
Despite the immense progress in our understanding of neuroanatomy and neuroendocrinology, not all cases of anxiety can currently be treated. However, the latest research on the subject has improved the selection of drugs available for various anxiety disorders. For instance, benzodiazepines are known to be more efficient in the treatment of panic disorders than GAD.
As neuroimaging technologies continue to evolve, a better understanding of the neurobiology of anxiety is bound to influence the way we treat anxiety and other related disorders.
Andrews, G., Stewart, G., Allen, R., & Henderson, A. S. (1990). The genetics of six neurotic disorders: a twin study. Journal of Affective Disorders, 19(1), 23–29. doi:10.1016/0165-0327(90)90005-S
Bandelow, B., & Michaelis, S. (2015). Epidemiology of anxiety disorders in the 21st century. Dialogues in Clinical Neuroscience, 17(3), 327–335. PMCID: PMC4610617
Bystritsky, A., Khalsa, S. S., Cameron, M. E., & Schiffman, J. (2013). Current diagnosis and treatment of anxiety disorders. Pharmacy and Therapeutics, 38(1), 30–57. PMCID: PMC3628173
Martin, E. I., Ressler, K. J., Binder, E., & Nemeroff, C. B. (2009). The neurobiology of anxiety disorders: brain imaging, genetics, and psychoneuroendocrinology. The Psychiatric Clinics of North America, 32(3), 549–575. doi:10.1016/j.psc.2009.05.004
Miguel-Hidalgo, J. J. (2013). Brain structural and functional changes in adolescents with psychiatric disorders. International Journal of Adolescent Medicine and Health, 25(3), 245–256. doi:10.1515/ijamh-2013-0058
Morris-Rosendahl, D. J. (2002). Are there anxious genes? Dialogues in Clinical Neuroscience, 4(3), 251–260. PMCID: PMC3181683
Ravindran, L. N., & Stein, M. B. (2010). The pharmacologic treatment of anxiety disorders: a review of progress. The Journal of Clinical Psychiatry, 71(7), 839–854. doi:10.4088/JCP.10r06218bluRead More Here..
Tuesday, 19 December 2017
Monday, 18 December 2017
A lot of public back-and-forth banter has been going on lately between two giant tech personalities: Elon Musk and Mark Zuckerberg. Their public debate centers on whether or not artificial intelligence (AI) represents an existential threat to humanity.
For example, Elon Musk, when speaking at the National Governors Association in July said:
AI is a fundamental existential risk for human civilization, and I don’t think people fully appreciate that…It’s the greatest risk we face as a civilization [that will cause World War III]
Mark Zuckerberg on the other hand, touts the benefits of AI and says that Elon Musk’s doomsday predictions about AI are “pretty irresponsible.”
This prompted Elon Musk to fire back that Mark Zuckerberg’s understanding of AI is “pretty limited.”
So who is right? Only time will tell of course, but by my science-based speculation, I would say the evidence favors Musk. And greater brains than my own are telling us that artificial intelligence could be the end of Homo sapiens or any other Homo that follows, including Bill Joy, Stephen Hawking, Vernor Vinge, Shane Legg, Stuart Russell, Max Tegmark, Nick Bostrom, James Barrat, Michael Anissimov, and Irving Good. Brilliant minds, Nobel Prize winners, renowned inventors, and IT pioneers are all on record giving us warnings.
Of course other existential threats to Homo sapiens are possible and could come in the form of another bolide impact like the one that doomed the dinosaurs 66 million years ago or a supervolcano leading to extreme global weather events, a phenomena that also affected early species. Unlike the relentless human pursuit of technologies that could alter, if not eliminate, our species, these threats are essentially out of our control.
Genetic engineering, especially if aided by AI, could lead to the future speciation of Homo sapiens and pose yet another existential threat. Lee Silvers, in his book Remaking Eden, envisions a future society practicing an extreme form of behavioral isolation based on genetic engineering. In this society, only a small portion of the population, which he calls the GenRich, have the financial means to genetically enhance their children.
Over decades, the GenRich use genetic engineering techniques to optimize a variety of human traits—such as intelligence, athletic skill, physical appearance, and creativity—that give them a controlling position in society. Over time, cultural disparity between this GenRich minority population and the remaining “naturals” becomes so great that there’s little interbreeding between the two groups. Such a scenario could lead to the genetic development of a postzygotic reproductive barrier.
In other words, genetic engineering could eventually lead to a new species of humans. Once this occurs, the long-term results are unpredictable. This new species—I call it Homo nouveau—like the GenRich, may not be an existential threat, at least in the early centuries or millennia.
It’s uncertain what could happen when two human species try to coexist. We know things didn’t work out very well for the Neanderthals after Homo sapiens arrived. In fact, the same is true for Homo heidelbergensis, Homo erectus, Homo denisova, and every other Homo species that may have coexisted with Homo sapiens.
In considering all the possible existential threats to us humans, genetic engineering is a possibility in the not too distant future—say in the next two to four centuries. However, if Elon Musk is right AI could supersede that in one or two centuries if we’re unsuccessful in controlling it. Then again, at any time we could be hit by a bolide. None of this bodes well for us.
L. Grossman, “2045: The Year Man Becomes Immortal”, Time Magazine, February 10, 2011. Access here.
Hawking, S., Tegmark, T., Russell, S. (2017). Transcending Complacency on Superintelligent Machines. Huffington Post. Access here.
Bostrom, N. Superintelligence: Paths, Danger, Strategies, Oxford: Oxford University Press, 2014.
F. Heylighen, “Return to Eden? Promises and Perils on the Road to Global Superintelligence,” in The End of the Beginning: Life, Society and Economy on the Brink of the Singularity, Ben and Ted Goerzel, eds., Humanity + Press, 2015.Read More Here..
Source: HealthDay via Exercise and Physical Fitness New Links: MedlinePlus RSS Feed Read More Here..
Sunday, 17 December 2017
Saturday, 16 December 2017
For years as a hard-nosed neuroscientist, I’ve been baffled by the success of clinical techniques that my wife, Chris Gilbert M.D. Ph.D., has pioneered to diagnose and cure illnesses such as back pain, chronic fatigue, stomach ailments, and recurring respiratory infections.
The reason for my head-scratching is that many of Dr. Chris’s diagnostic tests and therapies involve no technology at all, and are brain-dead simple. The bench scientist and geek in me (sensory physiology/chrono-neurobiology) instinctively rebels against a no-tech approach to anything, let alone medicine.
In an age of biotech marvels such as MRI, gene therapies, and targeted immunotherapies, my inner scientist is certain that no-tech approaches can’t be nearly as effective as modern medical science.
But the maddening fact is, my wife’s techniques do often work—so well in fact—that the bulk of her patients come to her because visits to other doctors who employ the latest drugs, tests, and procedures have failed to yield lasting results.
A cornerstone of Dr. Chris’s approach is a belief that patients’ bodies know more about what is ailing them and how to achieve lasting cures than do the patients’ conscious minds. So although she will start by asking questions of a patient’s mind, such as “What is going on in your life?” she quickly transitions to a dialogue with a patient’s body.
What’s the difference between talking to the mind and talking to the body?
When she addresses a patient’s mind, Dr. Chris simply asks the patient a question, but when she addresses the patient’s body she will first coach the patient to “become” the body part that is suffering, such the lower back, then to respond in the first person as the lower back.
I once witnessed (with the patient’s permission) a dialogue between Dr. Chris and an ailing back that went like this:
Dr. Chris: Welcome to my office, Back, tell me how you feel.
Back: I am stiff all the time, with shooting pains. After the drive home from work, I get horrible spasms.
Dr. Chris. Thank you, Back. Do your spasms usually come after sitting for a long time?
Back: Yes!! I hate, hate, hate sitting.
Dr. Chris: Is there anything else you hate?
Back: I can’t stand my owner’s mother. When we go over for dinner she picks at him endlessly and I get really tense and tight. I want to stay away from that woman!!! I never want to see her again!!
Dr. Chris: Ok, now that I know what you hate, what do you like?
Back: Swimming! I love it when my owner does laps in the pool. I get warm and loose.
After observing such sessions and having been Dr. Chris’s patient myself (for stomach troubles), I have been shocked by how much patient’s bodies “know” what their minds don’t know, and how quickly a dialogue with the body can relieve symptoms.
For example, the patient in the Back-to-Dr.Chris dialogue professed ignorance about what was triggering his back spasms, only to immediately pinpoint specific triggers for his pain (such as sitting and a nagging mother) when he was queried as his back.
And that same patient, who walked into the office with a lower back so stiff that he couldn’t bend at the waist, loosened up almost immediately after the Back-to-Dr.Chris dialogue, as if venting of the true source of back pain (sitting too long and being with his mother too long) in and of itself was therapeutic.
Once I overcame my skepticism that such simple, direct techniques could actually work a lot of the time (although not always), I started asking myself:
How can neuroscience explain the success of Dr. Chris’s brand of mind-body medicine?
I confess that I didn’t have a good answer until recently when I stumbled upon two unrelated sets of research findings more or less at the same time.
The first body of research described implicit memory. It turns out that we are constantly learning things and storing them away in our unconscious without any conscious awareness that we are learning, or indeed, any overt knowledge of what we have learned.
Ken Paller and Joel Voss of Northwestern University, for example, have shown that unconscious learning occurs when test subjects passively observed kaleidoscope images while paying attention to something else. Moreover, those same subjects were able to make correct “intuitive” guesses based upon what they have learned, without having any conscious awareness that they had learned anything in the first place.
This finding, along with a host of similar results from other labs, implies that much of what we ascribe to gut feelings, hunches, or intuition are actually products of unconscious or implicit learning from past experiences. For example, Dr. Chris’s patient with lower back pain probably learned unconsciously that his back tightened up every time he went over to his mother’s house for dinner.
The second body of research that offered clues to the success of Dr. Chris’s methods, concerned the storage of long-term memories in the sensory cortex. These studies suggest that sensory experiences leave lasting memory traces in the very parts of the cerebral cortex that initially activate when the experiences originally occurred.
Putting the implicit learning and sensory memory research together (admittedly something of an intuitive leap) one could conclude that unconscious memories relating to sensations in a particular body part, might be stored in the region of the sensory cortex that activates when that body part experiences sensations.
Below is a brain map that shows the how areas of the body stimulate different areas of somatosensory cerebral cortex responsible that are responsible for processing touch, vibration, pain, and other sensations from different body parts. The somatosensory cortex occupies a gyrus (i.e., ridge) of the brain just behind the central sulcus (i.e, central fold/groove) called the post-central gyrus. Referring to this map, unconscious sensory memories from the back region (as designated by the blue arrow in the diagram below) would be stored near the top of the post-central gyrus, next to the hemispheric fissure that divides the left and right half of the brain.
So, what might be happening when Dr. Chris addresses a patient’s back (vs. the patient themselves) is that she is focusing the patient’s attention on somatosensory memories and associations stored in a particular region of the cerebral cortex and that the local activation in the somatosensory cortex occurs that when she does this helps release memories stored in the “back cortex” that would otherwise have remained unconscious.
True, I have no experimental data (such as fMRI brain scans showing somatosensory activation during Dr. Chris’s dialogues) to support this theory, so for the moment, it remains just a theory.
But at least the scientist in me is less baffled knowing that a plausible explanation for Dr. Chris’s successes in mind-body medicine is out there.
Based on lots of implicit learning accumulated watching Dr. Chris work, my gut intuition is that neuroscience has as much to learn from the success of her methods as she does from neuroscience.
Learn more about Dr. Chris’s methods and my neuro-scientific explanations of them in The listening cure: healing secrets of an unconventional doctor
Gandhi, S. (2001). Memory retrieval: Reactivating sensory cortex. Current Biology, 11(1), R32-R34. doi:10.1016/s0960-9822(00)00040-3
Gilbert, C. (2017). Listening Cure : Healing Secrets of an Unconventional Doctor. SelectBooks, Incorporated. ISBN:1590794370
Hasan, M., Hernández-González, S., Dogbevia, G., Treviño, M., Bertocchi, I., Gruart, A., & Delgado-García, J. (2013). Role of motor cortex NMDA receptors in learning-dependent synaptic plasticity of behaving mice. Nature Communications, 4. doi:10.1038/ncomms3258
Voss, J., & Paller, K. (2009). An electrophysiological signature of unconscious recognition memory. Nature Neuroscience, 12(3), 349-355. doi:10.1038/nn.2260Read More Here..
Friday, 15 December 2017
Is gambling an addictive pathology that causes changes in the brain and requires treatment? Or is it merely a compulsive behaviour? This question has long kept the medical world confused.
Traditionally, it was thought that addiction could happen only when a person is dependent on some physically existing substance. However, now this traditional way of thinking is changing. The brain seems to have a weakness of getting trapped by either a substance or experience that brings a reward, be it drugs, sex, eating, or gambling. Like addiction to substances, addiction to gambling can affect a person of any background, education level, and level of income. Many celebrities are known to be overindulging in gambling. The list includes Tiger Woods, Ben Affleck, and Pamela Anderson, to name just a few.
Once researchers agreed that pathological gambling exists, the question as to whether it is more like drug addiction or similar to other obsessive-compulsive disorders remained unanswered. Modern research seems to support the idea of higher similarity with substance addiction than with obsessive-compulsive disorder. However, it is entirely possible that pathological gambling is a heterogeneous disorder and thus shares the components of both conditions. Hence, in some people it may be more like an obsessive-compulsion, while in others it is similar to substance dependence.
Functional MRI studies seem to support the view that gambling addiction is more like a substance-abuse disorder. Therefore, in the Diagnostic and Statistical Manual of Mental Disorders (5th edition; DSM-5) is has been classified as a behavioral addiction. It does not necessarily mean that other types of this disorder do not exist, as this condition is still not fully understood from a medical point of view.
Why should gambling be considered an addiction?
Perhaps due to the absence of any physical substance, addition to experiences like gambling is more challenging to recognize until considerable harm is done. A large number of people addicted to gambling fail to accept this fact. Yet, it is no secret that gambling addiction can ruin life as effectively as substance addiction.
The person involved in gambling gets ‘high’ and finds it difficult to control or limit gambling, which is also characteristic of drugs addiction. Moreover, there are negative emotions similar to withdrawal syndrome when a person is deprived of the gambling activity. And finally, even the medications used to treat substance addiction have shown to be efficient in the management of gambling disorder.
Neural changes in gambling addiction
Any addiction is caused by the combination of several factors such as genetic causes, environmental issues, and social influences and problems.
Mesolimbic and mesocortical dopaminergic pathways are central to motivation, desire, and perception of pleasure. Dysregulation in the mesolimbic pathway (often referred to as reward pathway) is known to play a vital role in the development of addiction.
Research on pathological gambling is still ongoing; this phenomenon is still not fully understood from a neurobiological point of view. It is clear that in pathological gambling multiple neurotransmitter systems (including dopamine, serotonin, norepinephrine, opioid, and glutamate) and various brain regions are implicated (including the amygdala, nucleus accumbens, prefrontal cortex, and insula).
Addiction to gambling is the result of a pathological importance being attached to the activity. High level gambling and substance addicts give excessive motivational significance to the addictive activity. Glutamatergic projections from the prefrontal cortex to the accumbens is thought to be the neural pathway involved in provoking gambling seeking behavior. This anatomical path is found to play a role in most forms of behavior dysregulation and addiction. The prefrontal accumbens pathway is vital to providing motivational or reward salience and goal-directed behavior.
A few years ago, fMRI was used to compare the brain activity of people occasionally involved in gambling against those known to be suffering from pathological gambling. The scans demonstrated a significant difference in blood-oxygen-level dependent (BOLD) signals between the two groups in the superior temporal regions, inferior frontal, and thalamic region. Those pathologically addicted to gambling showed a distinct frontoparietal activation pattern triggered by gambling-related cues, which is known to play a role in the addiction memory network.
Treatment of pathological gambling
Though the prevalence of pathological gambling is much higher than many psychiatric disorders like schizophrenia, there is a lack of studies and trials aimed at finding the appropriate treatment for this problem. Still, there is a small number of studies that seem to favor the effectiveness of pharmacological treatment.
Drugs that have shown the ability to modulate dopaminergic transmission in the mesolimbic pathways, like opioid-receptor antagonists (e.g., naltrexone) have demonstrated effectiveness in trials. Antidepressants and mood stabilizers are the groups of drugs that may prove to be effective in overcoming gambling addiction.
Various clinical investigations have also examined the effectiveness of non-pharmacological treatments. It has been demonstrated that cognitive-behavioural therapy (CBT) could be one such option. Some studies have also investigated the usefulness of video conferencing for ongoing supervision, and the use of congruence couple therapy and therapies that have a holistic approach to the problem.
To sum up, the latest neurobiology studies confirm that gambling addiction is similar to substance addictions. It may also have serious implications for the person involved, yet little is known regarding how to effectively treat this problem.
Blanco, C., Moreyra, P., Nunes, E. V., Sáiz-Ruiz, J., & Ibáñez, A. (2001). Pathological gambling: addiction or compulsion? Seminars in Clinical Neuropsychiatry, 6(3), 167–176. doi:10.1053/scnp.2001.22921
Grant, J. E., & Kim, S. W. (2006). Medication Management of Pathological Gambling. Minnesota Medicine, 89(9), 44–48.
Holden, C. (2001). “Behavioral” Addictions: Do They Exist? Science, 294(5544), 980–982. doi:10.1126/science.294.5544.980
Kalivas, P. W., & Volkow, N. D. (2005). The Neural Basis of Addiction: A Pathology of Motivation and Choice. American Journal of Psychiatry, 162(8), 1403–1413. doi:10.1176/appi.ajp.162.8.1403
Leung, K. S., & Cottler, L. B. (2009). Treatment of pathological gambling. Current Opinion in Psychiatry, 22(1). doi:10.1097/YCO.0b013e32831575d9
Miedl, S. F., Fehr, T., Meyer, G., & Herrmann, M. (2010). Neurobiological correlates of problem gambling in a quasi-realistic blackjack scenario as revealed by fMRI. Psychiatry Research: Neuroimaging, 181(3), 165–173. doi:10.1016/j.pscychresns.2009.11.008
Potenza, M. N. (2013). Neurobiology of gambling behaviors. Current Opinion in Neurobiology, 23(4), 660–667. doi:10.1016/j.conb.2013.03.004
Potenza, M. N. (2014). The neural bases of cognitive processes in gambling disorder. Trends in Cognitive Sciences, 18(8), 429–438. doi:10.1016/j.tics.2014.03.007Read More Here..
Thursday, 14 December 2017
This marks an increase on the previous global estimate of 250 000-500 000, which dates from over ten years ago and covered all influenza-related deaths, including cardiovascular disease or diabetes. The new figures of 290 000-650 000 deaths are based on more recent data from a larger, more diverse group of countries, including lower middle-income countries, and exclude deaths from non-respiratory diseases. via WHO news Read More Here..
Wednesday, 13 December 2017
BMJ study: Patients treated by older physicians (60 and older) had higher mortality vs. younger physicians (39 and younger)
The researchers evaluated a 20% random sample of Medicare fee-for-service beneficiaries aged 65 and older admitted to hospital with a medical condition in 2011-14 and treated by hospitalist physicians.
Main outcome measures 30 day mortality and readmissions and costs of care.
The study included 700,000 admissions managed by 18,800 hospitalist physicians (median age 41).
Patients’ adjusted 30 day mortality rates were:
- 10.8% for physicians younger than 40
- 11.1% for physicians aged 40-49
- 11.3% for physicians aged 50-59
- 12.1% for physicians aged 60 and older
See the figure here: http://www.bmj.com/content/bmj/357/bmj.j1797/F1.large.jpg
Note: Among physicians with a high volume of patients, however, there was no association between physician age and patient mortality.
Within the same hospital, patients treated by older physicians had higher mortality than patients cared for by younger physicians, except those physicians treating high volumes of patients. The calculated "number need to harm (NNH)" was 77.
Patients treated by physicians aged younger than 40 had 0.85 times the odds of dying or an 11% lower probability of dying compared with patients cared for by physicians aged 60 and older. This difference in mortality is comparable with the impact of statins for the primary prevention of cardiovascular mortality on all cause mortality (odds ratio of 0.86) or the impact of β blockers on mortality among patients with myocardial infarction (incidence rate ratio of 0.86), thus indicating that the observed difference in mortality is not only statistically significant but arguably clinically significant.
The adjusted risk difference of 1.3 percentage points suggests that for every 77 patients treated by doctors aged 60 and older, one fewer patient would die within 30 days of admission if those patients were cared for by physicians aged 39 and younger.
Though clinical skills and knowledge accumulated by more experienced physicians could lead to improved quality of care, physicians’ skills might become outdated as scientific knowledge, technology, and clinical guidelines change.
Older physicians might have decreased clinical knowledge, adhere less often to standards of appropriate treatment, and perform worse on process measures of quality with respect to diagnosis, screening, and preventive care.
Physician age and outcomes in elderly patients in hospital in the US: observational study. BMJ 2017; 357 doi: https://doi.org/10.1136/bmj.j1797 (Published 16 May 2017)
Cite this as: BMJ 2017;357:j1797
Image source: OpenClipArt, https://openclipart.org/detail/284296/instructor
World Bank and WHO: Half the world lacks access to essential health services, 100 million still pushed into extreme poverty because of health expenses
A singular cutoff point for school entry results in age differences between children of the same grade. In many school systems, September-born children, begin compulsory education in September of the year in which they turn five, making them relatively older than summer born children who begin school aged four.
Research on these annually age-grouped cohorts reveal relative age effects (RAEs) that convey the greater achievements accrued by the relatively old (RO) students compared to the relatively young (RY) students. RAEs are pervasive. Across OECD countries, in fourth grade, RY students scored 4–12% lower than RO students, while in eight grade the difference was 2–9% lower. RAEs are most evident in early formal education and can diminish as children mature. In 2016 for instance, Thoren, Heinig, and Brunner published a study on three grades attending public school in Berlin, Germany, and showed that the RAE in disappeared for reading by grade 8 and was reversed for math in favor of RY students.
Investigating the mechanisms involved is important because RAEs can remain evident in high-stakes exams taken at the end of compulsory education. RAEs may impact educational attainment, which is defined as an individual’s highest educational qualification (i.e., compulsory schooling, apprenticeship, or university education). For example, research by Sykes, Bell, and Rodeiro found that 5% less August-born GCSE students than September-born GCSE students chose at least one A level. Likewise, August-born students were 20% less likely to progress to university than September-born students. RO students also outperformed RY students on college admission tests to a university in Brazil, which significantly impacted the probability of being accepted to that university. Moreover, in Japan the percentage of graduates (aged 19–22 and 23–25) was two points greater for those born in April than those born in March. Collectively, these findings indicate that RAEs impact educational attainment because of their direct link to students’ acceptance to higher education. Since much of children’s development occurs within compulsory education, a natural question is whether educators act to alleviate or exacerbate RAE.
RAEs emerge primarily because of within-group maturity differences among RO and RY children (age-at-school-entry effect). RO children, have a one-year developmental advantage over RY children when they sit exams (age-at-test effect). Based on these advantaged test scores and maturation, RO children receive special opportunities from educators to excel in school. Using attainment, program participation, and attendance data from 657 students aged 11–14 from a secondary school in North England, a study by Cobley, McKenna, Baker and Wattie found that RO students were more likely than RY students achieve high scores across various subjects and be admitted to gifted programs. Even if RO students accepted to gifted programs are not actually gifted, the prestige of attending such programs would help them to foster strong positive self-esteem, which can persist over time. In turn, RO students may experience enhanced learning and praise long after small age differences are important in and of themselves.
Conversely, teachers lower their expectations of RY students because RY students appear less developed and intelligent than RO students. Interestingly, having RO classmates can prompt a spillover effect that boosts RY students’ grades, but also increases the probability that RY students will to be pathologized. This research suggests that RAEs emerge as a consequence of maturity differences but are maintained by the magnitude and persistence of social factors, such as educator-student interaction. Another study also reported RAEs in the diagnosis and treatment of ADHD in children aged 6–12 in British Columbia. Incorrect diagnosis can unnecessarily limit RY students’ academic performance by diminishing their self-esteem and task involvement, which are school achievement predictors.
If these inequalities decline over time, the influence of RAE on educational attainment is arguably minimal. However, if relative advantages such as skill accumulation persist in favor of RO students throughout formal education, RAEs translate into academic disadvantages for RY students. For instance, RY students’ negative self-perceptions of academic competence and learning disability can mediate the relationship between depressive symptoms and school dropout in adolescence. In turn, lack of formal education or poor academic performance makes entry to higher education arduous. Research illustrates with 16-year-old RY students scoring 0.13 standard deviations lower than RO students. This test score predicted that RY students would have a 5.8% higher potential dropout rate from high school and a consequently 1.5% lower college admission rate than RO students. Initial gains for RO students partly explain why they have a 10% greater probability of attending top-ranking universities and why they are more likely to graduate from university than RY students.
Research on the impact of RAE on educational attainment is not as straightforward as discussed thus far. Cascio and Schanzenbach used experimental variation by randomly assigning students to classrooms. Results showed improved test scores for RY students up to eight years after kindergarten and an increased probability of taking a college-entry exam. These positive spillover effects are evident when RY students, in a relatively mature peer environment, strive to catch up with higher-achieving RO students and end up surpassing them. Since RO students may strain under the expectations placed on them to be top of the class, RY students have an opportunity to catch up. Alternatively, RO students may not have the same incentive as RY students to work hard for academic success because RAEs already work in their favor. To overcome RAEs and succeed academically, RY students need greater persistence and attention than RO students in their schoolwork, which helps them gain a motivated mindset that benefits lifelong learning. For example, RY students in high school are more likely than RO students to study and compensate for poor academic achievement in middle school.
At a university in Italy, RY students obtained better grades than RO students. This reversal effect was also reported at university in the UK. The researchers postulated that due to RAEs, the RY students developed social skills more slowly. Therefore, RY students had less active social lives and more time to concentrate on educational attainment. The impact of RAEs on educational attainment is, subsequently, probabilistic not deterministic. Although research by Abel, Sokol, Kruger, and Yargeau indicated that RAEs do not affect the success of either RO or RY students’ university applications, they reported that more RO than RY students applied to medical school. In addition, Kniffin and Hank’s study did not find RAEs that influence whether a university student obtains a PhD. These two studies suggest that RAEs do not have such an important influence on college acceptance or educational attainment once in college. Instead, RAEs are a salient influence in so far as students in compulsory education obtain the necessary grades to apply to university in the first place.
The acquisition of higher mental functions and schooling over time helps normalize the student population by minimizing the attainment gap between RO and RY students, which helps explain why RAEs lessen in university. In addition, universities are often learning environments with great diversity in age (i.e., mature and repeat students), culture (i.e., international students), and academic achievement (i.e., doctorate/master’s students). Perceived developmental parities are inherently less important in university because classroom composition becomes heterogeneous, mitigating and masking the remaining relative age differences. Given this knowledge, greater classroom heterogeneity could be applied to compulsory education to minimize RAEs. Students in mixed-grade classrooms in Norwegian junior high schools, for example, outperformed students in single-grade classrooms on high-stakes school finishing exams. With this classroom composition, it is not disproportionately skewed in favor of younger/older students, the losses for RO students following class mixing would not outweigh the gains of the RO students. With more heterogenous classes, educational attainment could subsequently become less influenced by RAEs and a more equalized pursuit.
Since mitigating the impact of RAE on educational attainment depends partly on the strength of compensating investments such as classroom environments, streaming remains controversial. Academic streaming involves separating students according to innate ability. In reality, streaming is based on students’ prior academic performance, which is an imperfect measure of ability that can lead to misallocations. Streaming in early education can be particularly unfair because RY students do not get the opportunity to more closely approximate older classmates’ mental and physical development when sitting exams. In Germany for instance, being relatively old increased test scores by 0.40 standard deviations, increasing the probability of attending the highest secondary school track (gymnasium) by 12%. RY students are also at risk of being unfairly streamed into lower-ability classes because they are more likely than RO students to be diagnosed with behavioral problems and learning disabilities. Streaming thereby provides students with unequally differentiated educational experiences of teaching, competition, and opportunity that limit their academic exposure. Therefore, postponing streaming can reduce the impact of RAEs on educational attainment by ensuring that any developmental gaps have time to narrow.
Unequal educational experiences can limit RY students’ educational attainment. In 2015, the average number of 25–64-year-olds with tertiary education was greater for countries who exhibit almost no streaming, such as Ireland (42.8%), compared to the OECD average (35%). Is it the case that streaming at multiple stages can rectify initial misallocations while still enhancing academic achievement? In Austria, children are streamed in grade five (aged ten) and in grade nine (aged fourteen). In one study, RY students in grade five were 40% less likely to be streamed into higher classes, but the second streaming, in grade nine, helped mitigate RAEs by giving students the opportunity to upgrade to a higher stream. In a complex interplay, streaming and RAEs can reinforce and be reinforced by existing socioeconomic inequalities. In this vein, the researchers concluded that RAEs only disappeared for students with favorable parental backgrounds in the second streaming. In contrast, RY students with unfavorable parental backgrounds were 21% less likely than RO students to move to a high-ranking school. As previously mentioned, learning at the wrong academic level can strain academic achievement and reduce the chances of continuing to higher education.
Socioeconomic status is the extent to which learning opportunities are disadvantaged as a result of low-income. Socioeconomic status can exacerbate the impact of RAEs on educational attainment. Huang and Invernizzi’s research examined a cohort of 405 students in a high poverty, low performing school from the beginning of kindergarten until the end of grade two. Results concluded that early-age literacy achievement gaps between RO and RY students narrowed over time but did not fully close by the end of grade two. Similarly, a Madagascar-based study by Galasso, Weber, and Fernald indicated that differences in home stimulation are dependent on the wealth gradient and accounted for 12–18% of the predicted gap in early outcomes between advantaged and disadvantaged children. At least in early education, these findings suggest that diminished academic performance and exacerbated RAEs are in direct proportion to socioeconomic status. Thus, greater flexibility regarding age at entry in compulsory schooling could help lessen the impact of RAE on academic performance.
Suziedelyte and Zhu published a “Longitudinal Study of Australian Children” and reported that starting school early benefits children from low-income families who, compared to children from high-income families, have limited access to learning resources at home and formal pre-school services. However, a three-month postponement of the cutoff enrollment date (increasing grade age) can increase both academic success and the likelihood of repeating a grade. Similarly, a one year delay in school enrollment (redshirting) can produce a 0.303 standard deviation decrease in test scores and lead to significantly lower math scores for students identified with a disability when compared to nonredshirted students with disability. These mixed findings suggest that equalizing educational attainment opportunities among RO and RY students, by implementing a flexible entry cutoff point, varies as a function of individual difference. Therefore, managing and mitigating RAEs requires greater sensitivity to confounds such as socioeconomic status.
The impact of starting school early on educational attainment is mediated by social factors, school policy, and socioeconomic factors, resulting in individual differences in learning outcomes. RAEs fade throughout formal schooling and can even reverse in higher education. The relative age phenomenon, nevertheless, caveats that ascribing merit to students based on relative age can lead to the provision of unequal learning opportunities and harmful pathologies. Unfortunately, the mechanisms that underpin the impact of RAEs on educational attainment are currently quite speculative and inconclusive. In this sense, existing findings warrant further empirical research and reveal the need for more comprehensive methods for determining an appropriate school entry cutoff point.
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