Video Game Addiction

If you don't think kids get hooked on video games, think again. If you Google "video game addiction," you will find more than a dozen pages of Web sites dealing with this issue. There are also many pages of formal research papers found via search on Google Scholar.

The point at which gaming becomes an actual addiction is hard to define, but some 7-21 criteria can measure the addiction. These criteria include modification of mood, conflict, behavioral problems, and, more tellingly, the same phenomena seen in drug addiction (tolerance and withdrawal symptoms).

So many kids spend nearly every possible moment glued to a game screen that an addiction recovery program known as ReSTART was developed eight years ago in which addicts receive individual and group therapy in a resident campus. The ReSTART therapy program requires patients to take a 45-90 abstention from computer screens. Part of the reason that addiction develops in the first place is the strong positive reinforcement provided by developing game prowess. The young person's self-esteem becomes entangled with gaming.  The therapy program aims at finding other substitute reinforcers for self-identity and self-esteem. Training is provided in the basic life skills that have been neglected from the years of immersion in gaming.

The organization's guiding principle is "Connect with life, not your device." Children who become addicted to video games withdraw from daily living. They are most likely to be male, poorly developed physically, and socially awkward. They often suffer from ill-defined anxiety.

Just how widespread is video game use? Apparently 155 million Americans play video games at least three times a week. Particular concern is the violent nature of many video games, and it is clear that playing such games stimulates the players to be more aggressive.

The Dana Foundation and the American Association for the Advancement of Science recently sponsored a conference on internet gaming. The speaker from ReSTART, co-founder Hilarie Cash, predicted that internet gaming is so addictive that it will probably become listed in newer editions of the Diagnostic and Statistical Manual of mental Disorders.

Another speaker, psychology professor Craig Anderson, summarized the evidence that violent video games promote aggressive behavior in the player. Increases occur in hitting, kicking, punching, biting, fights at school, and juvenile delinquency. Anderson points out that longitudinal studies rule out the possibility that children who are already violent are the ones who become addicted to violent video games. Playing violent games actually makes children more violent.

Video games that are not violent may help develop mental quickness and other cognitive skills. But like much in life, too much of a good thing is a bad thing.

Sources:

Lemmens, Jeroen S. et al. (2009). Development and validation of a game addiction scale for adolescents. Media Psychology. 12(1), 77-95. http://dx.doi.org/10.1080/15213260802669458

https://netaddictionrecovery.com/

Jarvis, Michaela. 2014. Video games: the bad, the ugly, and the (potentially) good. Science. 355, 1385. 

Forever Now. Living Life Without a Past

Imagine living every day where you don't remember what happened an hour ago, nor anything that happened to you for all the time before that. Imagine that you can't remember your old friends, even relatives. Imagine that you can't remember what you decided to do anytime in the future.

Lonnie Sue Johnson, a former pilot, commercial artist, and musician, knows what that is like. As told in Michael Lemonick's new arresting new book about her life story, The Perpetual Now, Lonnie Sue experienced a catastrophic herpes simplex viral infection that spread into her brain, almost killed her, and left her with crippling memory failures after she survived. Normally, this virus just causes cold sores, but in a few cases the virus inflames and damages the brain. In Lonnie Sue's case, brain scans revealed that the virus destroyed the part of brain, the hippocampus, that forms past experiences (episodic memory) and general world knowledge (facts, ideas, meaning and concepts—semantic memory).

As she recovered from near death, which took many months, Lonnie Sue gradually recovered some old, well-established memories, like the ability to speak and understand English. She regained her ability to read sheet music and play the viola.

Her memory loss was similar to that of an epilepsy patient, Henry Molaison, known in the brain research literature as "H.M." before he recently died of old age.  The seat of his severe epilepsy was the hippocampus, and surgeons removed it to cure the epilepsy before they knew about the devastating memory loss such surgery would cause. H.M. gladly volunteered for research on his memory loss for many years. Much of what we thought we knew about memory was learned from Henry. The standard model is that there are two kinds of memory, declarative (episodic and semantic) and procedural (motor memories like how to ride a bicycle, play a piano, and the like). The hippocampus is crucial for declarative memories but not procedural ones. At least that is what we thought. Lonnie Sue has revealed that the boundaries between declarative and procedural memories are fuzzy and maybe we don't understand memory as well as we thought.

The comparison with H.M. is not completely parallel. His memory limitations came from an otherwise healthy brain that no longer had a hippocampus. Lonnie Sue may well have had other brain damage than just the hippocampus.

Lonnie Sue, for example, lost many of her procedural memories, such as how to draw and fly a plane. But some of this ability gradually returned. All along she recognized herself in the mirror, and she recognized some old friends even though she couldn't recall anything about them.

Author Lemonick worked with Lonnie Sue and family for some three years as she recovered. His story paints a vivid picture of what life was like for Lonnie Sue and those who cared for her, particularly her devoted sister, Aline, who spent part of every day helping Lonnie Sue take care of herself and cope with the memory problems that never went away.

I admire Lemoncik's ability to explain complex issues of neuroscience in ways that are interesting and easy to understand. Readers will learn quite a bit about brain function from his user-friendly explanations. He even tells of recent studies under way of a very small group of apparently healthy people who have extraordinarily good memory. These people can tell you what happened on every day of their life. But they don't remember everything that happened. Their problem seems to be that certain events every day cannot be forgotten, even decades later. But the real message of the book is the power of love from those who care for Lonnie Sue and her own courage and cheerful spirit in the way she copes with her profound disability.

Lonnie Sue's story compels us to reflect thankfully on our own memory ability that we too often take for granted, with no thought of what life would be like without it. Her story reminds us that the memory of who we have been is an inevitable part of who we are now and who we strive to become. Our memories are not all pleasant, but life without memory of the past would surely be empty.

Lemonick, Michael D. (2016). The Perpetual Now. A Story of Amnesia, Memory, and Love. New York: Doubleday.

Genes Change in Your Brain. Do They Change You?

A startling discovery of enormous implication has just been reported in the premier research journal, Science. Despite the accepted dogma that all of a person's cells have the same genetic coding, it turns out that this is not true, especially in neurons. The DNA in each nerve cell (we don't know about sex cells) has hundreds of mutations of the A-T, C-G nucleotides that constitute the genetic code for the neuron. Thus, no two neurons are alike. The study was conducted by 18 research teams at 15 U.S. institutions, formed as a consortium by the National Institute of Mental Health to examine neural genetic coding, using repositories of postmortem brain tissue taken from both healthy people and those with various mental diseases.

The scientists have no explanation at present for what is causing so many mutations and why each neuron has a different genetic profile. The most obvious possibility might seem to be that the mutations occurred as transcription errors during cell division. But there is a major problem with this explanation. We don't know when these mutations occurred. Except for granule cells in the hippocampus and cerebellum, neurons generally do not divide after the first few days after birth. So, if cell division is the cause of mutations, it must be due to what happens during the early post-natal period.

If the mutations occurred sporadically throughout a lifetime, a likely cause for mutation might be DNA damage caused by the free radicals that are generated in ordinary metabolism. Environmental toxins are another possible cause. The point is that the DNA changes are likely to affect how a neuron functions, and that change can last a lifetime.

We know that mutations can cause brain cancer and even certain other brain diseases. The research consortium was commissioned to see if the genetic variants predisposed to neuropsychiatric disease. Obviously, the vast majority of people have these diverse genetic codes in their neurons that do not cause disease. What do they cause? Can the mutations affect which neurons participate in which circuits? Can mutations affect how well you reason, or memorize, or your emotional responsivity? Nobody knows.

A whole new field of research has now been opened. Scientists need to examine different neuronal cell types to see if they are equally affected by mutation. Obvious comparisons needed are between granule cells and all the other neuron types that do not divide.

There is a related aspect that is not considered in this context. That is the likelihood that each neuron differs not only in its genetic code, but also in which genes are expressed. The new field of "epigenetics" has revealed that environmental influences, ranging from drugs, toxins, metabolites, and perhaps even lifestyles can affect the expression of genes, even when there is no mutation. In the case of brain, there is the distinct possibility that one's mental life can affect gene expression. This needs to be studied.

So far, what I have said about gene change and expression refers to single individuals. But what if some of these gene mutations or epigenetic effects that occur in neurons also occur in sex cells? That would mean that traits acquired during one's lifetime could be passed on to future generations. I would hope that the research consortium that has made this monumental discovery about brain cells will extend its charter to also examine sperm and ova.

Recent research on the genetics of the classic animal model of brain function, C. elegans, reveals that epigenetic inheritance of neuronal traits does occur. Gene expression was modified by exposing the animals to high temperatures, and the genetic change was conveyed via both ova and sperm to offspring that had no exposure to high temperature. The epigenetic change was still present some 5-14 generations later.

To the extent that the findings of both of these studies can be extrapolated to humans, we must now consider the possibility that personal lifestyle, environmental, and cultural influences on people may be propagated to successive generations of their children. Bad environments and lifestyle choices may extend well into the future, magnifying the deleterious consequences through multiple generations. We now have to consider that medical and behavioral problems, poverty, and degenerate cultures can arise not only when people make poor choices but that the effects can be genetically propagated to subsequent generations.

These issues may seem to present a challenge to the notion that humans have free will. We are programmed by things that happen to us. But do we not have a choice in deciding much of what we expose ourselves to? The issues are explored in my recent book, Making a Scientific Case for Conscious Agency and Free Will (Academic Press).

Sources:

McConnell, M. J. et al. (2017).Intersection of diverse neuronal genomes and neuropsychiatric diseases: The brain somatic mosaicism network. Science.  356(6336), 395. doi: 10.1126/scienceaa1641.

Klosin, Adam et al. (2017). Transgenerational transmission of environmental information in C. elegans. Science. 356 (6335), 320-323.