Addiction is now understood to be a brain disease. Whether it’s alcohol, prescription pain pills, nicotine, gambling, or something else, overcoming an addiction isn’t as simple as just stopping or exercising greater control over impulses.
That’s because addiction develops when the pleasure circuits in the brain get overwhelmed, in a way that can become chronic and sometimes even permanent. This is what’s at play when you hear about reward “systems” or “pathways” and the role of dopamine when it comes to addiction.
But what does any of that really mean?
This video explainer from Yale Medicine shows how addiction takes hold of the brain.
Ever wonder how ballet dancers can spin and spin and spin, but never seem to get dizzy? Neuroplasticity, that’s how. This short video explains how it works, and how you can use your brain in the same way.
Today has been designated International Day of Happiness. I’d like to take the opportunity to share again a video that I shared several years ago on some simple but profound changes we can make to create a happier brain.
Twenty years ago, Dr. Amit Sood, a Professor of Medicine at Mayo Clinic, came to the U.S. thinking he was coming to the Disneyland of the world.
He expected everyone here to be very happy.
What he saw surprised and shocked him.
In this funny, fast-moving, and deeply insightful talk, Dr. Sood shares his journey over two decades and across two continents, finding a way to help us outsmart our neural predispositions to suffering. I
n the process, he takes us on a back-stage tour of the human brain and outlines the gist of a structured program he is taking globally to decrease stress and improve focus, resilience, and happiness.
I was delighted to join Migraine Ireland this week to discuss recent neuroscience findings on how our brain responds to worry and stress, and provides various strategies to overcome them.
Adults who played Pokémon video games extensively as children have a brain region that responds preferentially to images of Pikachu and other characters from the series.
The findings, published in the journal Nature Human Behavior, help shed light on mysteries about our visual system.
The first Pokémon game was released in 1996 and played by children as young as 5 years old, many of whom continued to play later versions of the game well into their teens and even early adulthood.
The games not only exposed these children to the same characters over and over again, it rewarded them when they won a Pokémon battle or added a new character to the in-game encyclopedia called the Pokédex.
Furthermore, every child played the games on the same handheld device – the Nintendo Game Boy – which had the same small square screen and required them to hold the devices at roughly the same arm’s length. Playing Pokémon on a tiny screen means that the Pokémon characters only take up a very small part of the player’s center of view. The eccentricity bias theory thus predicts that preferential brain activations for Pokémon should be found in the part of the visual cortex that processes objects in our central, or foveal, vision.
The occipitotemporal sulcus (OTS) of adults who played Pokémon extensively as children activated more (right) upon seeing images of Pokémon characters from their childhood videogames compared to adults who did not (left). (Image credit: Jesse Gomez)
The new findings are just the latest evidence that our brains are capable of changing in response to experiential learning from a very early age, but that there are underlying constraints hardwired into the brain that shape and guide how those changes unfold.
Decades of scientific research into Alzheimer’s have failed to find a cure. Little is known about the degenerative brain disease—but this may be about to change.
As populations have aged, dementia has soared to become the fifth leading cause of death worldwide. Alzheimer’s disease, a form of dementia, accounts for most of these cases. All attempts to halt the progression of the disease have failed. Now many major drug companies have pulled out of research altogether.
So why is Alzheimer’s disease still such a medical mystery?
One of the signs of Alzheimer’s in the brain is damage of connections and the loss of large numbers of neurons over time. It affects the hippocampus and its connected structures making it harder to form new memories or learn new information. As damage spreads through the brain the cortex becomes thinner and more memories are lost. Although emotional responses can often remain. As the brain shrinks further it slowly alters personality and behaviour and eventually the ability to live and function independently.
For 35 years there has been scientific disagreement about the origins of the disease. The main area of debate has focused on the abnormal build up of clumps of protein called amyloid plaques often found in brains of those affected by Alzheimer’s. But all attempts to target this protein with drugs have failed. A new study is now challenging the way science thinks about the disease. The study suggests that the bacterium Porphyromonas gingivalis, which is involved in gum disease, may contribute to Alzheimer’s.
The risk of Alzheimer’s is higher in those who have severe head injuries and also for those with an arterial disease known as atherosclerosis. This suggests there are many causes with one endpoint. And scientists hope that finding an underlying cause that could tie these together will hold the key to better treatments in the future.
Early experiences affect the development of brain architecture, which provides the foundation for all future learning, behaviour, and health.
Brains are built over time, from the bottom up.
The basic architecture of the brain is constructed through a process that begins early in life and continues into adulthood.
Simpler circuits come first and more complex brain circuits build on them later.
Brain architecture is comprised of billions of connections between individual neurons across different areas of the brain.
These connections enable lightning-fast communication among neurons that specialise in different kinds of brain functions. The early years are the most active period for establishing neural connections, but new connections can form throughout life and unused connections continue to be pruned.
The interactions of genes and experience shape the developing brain.
Genes provide the basic blueprint, but experiences influence how or whether genes are expressed. Together, they shape the quality of brain architecture and establish either a sturdy or a fragile foundation for all of the learning, health, and behaviour that follow.
Although genes provide the blueprint for the formation of brain circuits, these circuits are reinforced by repeated use.
A major ingredient in this developmental process is the interaction between children and their parents and other caregivers in the family or community.
In the absence of responsive caregiving—or if responses are unreliable or inappropriate—the brain’s architecture does not form as expected, which can lead to disparities in learning and behavior.
It is easier and less costly to form strong brain circuits during the early years than it is to intervene or “fix” them later.
Cognitive, emotional, and social capacities are inextricably intertwined throughout the life course.
The brain is a highly integrated organ and its multiple functions operate in coordination with one another. Emotional well-being and social competence provide a strong foundation for emerging cognitive abilities, and together they are the bricks and mortar of brain architecture.
A little light relief on Day 4 of #BrainAwarenessWeek. For John Cleese fans, a “serious” discussion on the organization of the brain and its functions to human health.
How do brain cells communicate with one another to produce thoughts, feelings, and behavior?
They signal to one another using a process called neurotransmission.
But the transmission of these important chemical messages could not occur without unique cellular structures called receptors (a molecule in cells that serves as a docking station for another molecule).
Neurotransmission begins when one brain cell releases a neurochemical into the synapse (the space in between neurons.) But for a neighboring cell to “pick up” the message, that neurochemical must bind with one of its receptors.
When an electrical signal reaches the end of a neuron, it triggers the release of tiny sacs that had been inside the cells. Called vesicles, the sacs hold chemical messengers such as dopamine or serotonin.
This drawing shows a synapse — the space between two cells. The chemical messenger dopamine is inside the top cell. Receptors on the bottom cell are waiting to receive it. NATIONAL INSTITUTE ON DRUG ABUSE
As it moves through a nerve cell, an electrical signal will stimulate these sacs. Then, the vesicles move to — and merge with — their cell’s outer membrane. From there, they spill their chemicals into the synapse.
Those freed neurotransmitters then float across the gap and over to a neighboring cell. That new cell has receptors pointing toward the synapse. These receptors contain pockets, where the neurotransmitter needs to fit.
It’s a bit like a game of catch. The first cell releases the neurochemical into the synapse and the receiving cell must catch it before it can read it and respond. The receptor is the
part of the cell that does the catching.
Signals for all of our sensations — including touch, sight and hearing — are relayed this way. So are the nerve signals that control movements, thoughts and emotions.
Each cell-to-cell relay in the brain takes less than a millionth of a second. And that relay will repeat for as far as a message needs to travel.
In recent years, researchers have learned that receptors are just as important as neurotransmitters in maintaining a healthy brain. In fact, studies have demonstrated that receptors play an important role in mood, learning, and social bonds. Receptors also mediate structural plasticity or remodeling of brain circuits that may result in changes to the number and type of synapses.
This short video discusses synaptic transmission in a simple and clear way.