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Navigating Election Anxiety: How Worry Affects the Brain
Once again, America is deeply divided before a national election, with people on each side convinced of the horrors that will be visited upon us if the other side wins.
’Tis the season — and regrettably, not to be jolly but to be worried.
As a neuroscientist, I am especially aware of the deleterious mental and physical impact of chronic worry on our citizenry. That’s because worry is not “all in your head.” We modern humans live in a world of worry which appears to be progressively growing.
Flight or Fight
Worry stems from the brain’s rather remarkable ability to foresee and reflexively respond to threat. Our “fight or flight” brain machinery probably arose in our vertebrate ancestors more than 300 million years ago. The fact that we have machinery akin to that possessed by lizards or tigers or shrews is testimony to its crucial contribution to our species’ survival.
As the phrase “fight or flight” suggests, a brain that senses trouble immediately biases certain body and brain functions. As it shifts into a higher-alert mode, it increases the energy supplies in our blood and supports other changes that facilitate faster and stronger reactions, while it shuts down less essential processes which do not contribute to hiding, fighting, or running like hell.
This hyperreactive response is initiated in the amygdala in the anterior brain, which identifies “what’s happening” as immediately or potentially threatening. The now-activated amygdala generates a response in the hypothalamus that provokes an immediate increase of adrenaline and cortisol in the body, and cortisol and noradrenaline in the brain. Both sharply speed up our physical and neurologic reactivity. In the brain, that is achieved by increasing the level of excitability of neurons across the forebrain. Depending on the perceived level of threat, an excitable brain will be just a little or a lot more “on alert,” just a little or a lot faster to respond, and just a little or a lot better at remembering the specific “warning” events that trigger this lizard-brain response.
Alas, this machinery was designed to be engaged every so often when a potentially dangerous surprise arises in life. When the worry and stress are persistent, the brain experiences a kind of neurologic “burn-out” of its fight versus flight machinery.
Dangers of Nonstop Anxiety and Stress
A consistently stressed-out brain turns down its production and release of noradrenaline, and the brain becomes less attentive, less engaged. This sets the brain on the path to an anxiety (and then a depressive) disorder, and, in the longer term, to cognitive losses in memory and executive control systems, and to emotional distortions that can lead to substance abuse or other addictions.
Our political distress is but one source of persistent worry and stress. Worry is a modern plague. The head counts of individuals seeking psychiatric or psychological health are at an all-time high in the United States. Near-universal low-level stressors, such as 2 years of COVID, insecurities about the changing demands of our professional and private lives, and a deeply divided body politic are unequivocally affecting American brain health.
The brain also collaborates in our body’s response to stress. Its regulation of hormonal responses and its autonomic nervous system’s mediated responses contribute to elevated blood sugar levels, to craving high-sugar foods, to elevated blood pressure, and to weaker immune responses. This all contributes to higher risks for cardiovascular and other dietary- and immune system–related disease. And ultimately, to shorter lifespans.
Strategies to Address Neurologic Changes Arising From Chronic Stress
There are many things you can try to bring your worry back to a manageable (and even productive) level.
- Engage in a “reset” strategy several times a day to bring your amygdala and locus coeruleus back under control. It takes a minute (or five) of calm, positive meditation to take your brain to a happy, optimistic place. Or use a mindfulness exercise to quiet down that overactive amygdala.
- Talk to people. Keeping your worries to yourself can compound them. Hashing through your concerns with a family member, friend, professional coach, or therapist can help put them in perspective and may allow you to come up with strategies to identify and neurologically respond to your sources of stress.
- Exercise, both physically and mentally. Do what works for you, whether it’s a run, a long walk, pumping iron, playing racquetball — anything that promotes physical release. Exercise your brain too. Engage in a project or activity that is mentally demanding. Personally, I like to garden and do online brain exercises. There’s nothing quite like yanking out weeds or hitting a new personal best at a cognitive exercise for me to notch a sense of accomplishment to counterbalance the unresolved issues driving my worry.
- Accept the uncertainty. Life is full of uncertainty. To paraphrase from Yale theologian Reinhold Niebuhr’s “Serenity Prayer”: Have the serenity to accept what you cannot help, the courage to change what you can, and the wisdom to recognize one from the other.
And, please, be assured that you’ll make it through this election season.
Dr. Merzenich, professor emeritus, Department of Neuroscience, University of California San Francisco, disclosed ties with Posit Science. He is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is BrainHQ, a brain exercise app.
A version of this article appeared on Medscape.com.
Once again, America is deeply divided before a national election, with people on each side convinced of the horrors that will be visited upon us if the other side wins.
’Tis the season — and regrettably, not to be jolly but to be worried.
As a neuroscientist, I am especially aware of the deleterious mental and physical impact of chronic worry on our citizenry. That’s because worry is not “all in your head.” We modern humans live in a world of worry which appears to be progressively growing.
Flight or Fight
Worry stems from the brain’s rather remarkable ability to foresee and reflexively respond to threat. Our “fight or flight” brain machinery probably arose in our vertebrate ancestors more than 300 million years ago. The fact that we have machinery akin to that possessed by lizards or tigers or shrews is testimony to its crucial contribution to our species’ survival.
As the phrase “fight or flight” suggests, a brain that senses trouble immediately biases certain body and brain functions. As it shifts into a higher-alert mode, it increases the energy supplies in our blood and supports other changes that facilitate faster and stronger reactions, while it shuts down less essential processes which do not contribute to hiding, fighting, or running like hell.
This hyperreactive response is initiated in the amygdala in the anterior brain, which identifies “what’s happening” as immediately or potentially threatening. The now-activated amygdala generates a response in the hypothalamus that provokes an immediate increase of adrenaline and cortisol in the body, and cortisol and noradrenaline in the brain. Both sharply speed up our physical and neurologic reactivity. In the brain, that is achieved by increasing the level of excitability of neurons across the forebrain. Depending on the perceived level of threat, an excitable brain will be just a little or a lot more “on alert,” just a little or a lot faster to respond, and just a little or a lot better at remembering the specific “warning” events that trigger this lizard-brain response.
Alas, this machinery was designed to be engaged every so often when a potentially dangerous surprise arises in life. When the worry and stress are persistent, the brain experiences a kind of neurologic “burn-out” of its fight versus flight machinery.
Dangers of Nonstop Anxiety and Stress
A consistently stressed-out brain turns down its production and release of noradrenaline, and the brain becomes less attentive, less engaged. This sets the brain on the path to an anxiety (and then a depressive) disorder, and, in the longer term, to cognitive losses in memory and executive control systems, and to emotional distortions that can lead to substance abuse or other addictions.
Our political distress is but one source of persistent worry and stress. Worry is a modern plague. The head counts of individuals seeking psychiatric or psychological health are at an all-time high in the United States. Near-universal low-level stressors, such as 2 years of COVID, insecurities about the changing demands of our professional and private lives, and a deeply divided body politic are unequivocally affecting American brain health.
The brain also collaborates in our body’s response to stress. Its regulation of hormonal responses and its autonomic nervous system’s mediated responses contribute to elevated blood sugar levels, to craving high-sugar foods, to elevated blood pressure, and to weaker immune responses. This all contributes to higher risks for cardiovascular and other dietary- and immune system–related disease. And ultimately, to shorter lifespans.
Strategies to Address Neurologic Changes Arising From Chronic Stress
There are many things you can try to bring your worry back to a manageable (and even productive) level.
- Engage in a “reset” strategy several times a day to bring your amygdala and locus coeruleus back under control. It takes a minute (or five) of calm, positive meditation to take your brain to a happy, optimistic place. Or use a mindfulness exercise to quiet down that overactive amygdala.
- Talk to people. Keeping your worries to yourself can compound them. Hashing through your concerns with a family member, friend, professional coach, or therapist can help put them in perspective and may allow you to come up with strategies to identify and neurologically respond to your sources of stress.
- Exercise, both physically and mentally. Do what works for you, whether it’s a run, a long walk, pumping iron, playing racquetball — anything that promotes physical release. Exercise your brain too. Engage in a project or activity that is mentally demanding. Personally, I like to garden and do online brain exercises. There’s nothing quite like yanking out weeds or hitting a new personal best at a cognitive exercise for me to notch a sense of accomplishment to counterbalance the unresolved issues driving my worry.
- Accept the uncertainty. Life is full of uncertainty. To paraphrase from Yale theologian Reinhold Niebuhr’s “Serenity Prayer”: Have the serenity to accept what you cannot help, the courage to change what you can, and the wisdom to recognize one from the other.
And, please, be assured that you’ll make it through this election season.
Dr. Merzenich, professor emeritus, Department of Neuroscience, University of California San Francisco, disclosed ties with Posit Science. He is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is BrainHQ, a brain exercise app.
A version of this article appeared on Medscape.com.
Once again, America is deeply divided before a national election, with people on each side convinced of the horrors that will be visited upon us if the other side wins.
’Tis the season — and regrettably, not to be jolly but to be worried.
As a neuroscientist, I am especially aware of the deleterious mental and physical impact of chronic worry on our citizenry. That’s because worry is not “all in your head.” We modern humans live in a world of worry which appears to be progressively growing.
Flight or Fight
Worry stems from the brain’s rather remarkable ability to foresee and reflexively respond to threat. Our “fight or flight” brain machinery probably arose in our vertebrate ancestors more than 300 million years ago. The fact that we have machinery akin to that possessed by lizards or tigers or shrews is testimony to its crucial contribution to our species’ survival.
As the phrase “fight or flight” suggests, a brain that senses trouble immediately biases certain body and brain functions. As it shifts into a higher-alert mode, it increases the energy supplies in our blood and supports other changes that facilitate faster and stronger reactions, while it shuts down less essential processes which do not contribute to hiding, fighting, or running like hell.
This hyperreactive response is initiated in the amygdala in the anterior brain, which identifies “what’s happening” as immediately or potentially threatening. The now-activated amygdala generates a response in the hypothalamus that provokes an immediate increase of adrenaline and cortisol in the body, and cortisol and noradrenaline in the brain. Both sharply speed up our physical and neurologic reactivity. In the brain, that is achieved by increasing the level of excitability of neurons across the forebrain. Depending on the perceived level of threat, an excitable brain will be just a little or a lot more “on alert,” just a little or a lot faster to respond, and just a little or a lot better at remembering the specific “warning” events that trigger this lizard-brain response.
Alas, this machinery was designed to be engaged every so often when a potentially dangerous surprise arises in life. When the worry and stress are persistent, the brain experiences a kind of neurologic “burn-out” of its fight versus flight machinery.
Dangers of Nonstop Anxiety and Stress
A consistently stressed-out brain turns down its production and release of noradrenaline, and the brain becomes less attentive, less engaged. This sets the brain on the path to an anxiety (and then a depressive) disorder, and, in the longer term, to cognitive losses in memory and executive control systems, and to emotional distortions that can lead to substance abuse or other addictions.
Our political distress is but one source of persistent worry and stress. Worry is a modern plague. The head counts of individuals seeking psychiatric or psychological health are at an all-time high in the United States. Near-universal low-level stressors, such as 2 years of COVID, insecurities about the changing demands of our professional and private lives, and a deeply divided body politic are unequivocally affecting American brain health.
The brain also collaborates in our body’s response to stress. Its regulation of hormonal responses and its autonomic nervous system’s mediated responses contribute to elevated blood sugar levels, to craving high-sugar foods, to elevated blood pressure, and to weaker immune responses. This all contributes to higher risks for cardiovascular and other dietary- and immune system–related disease. And ultimately, to shorter lifespans.
Strategies to Address Neurologic Changes Arising From Chronic Stress
There are many things you can try to bring your worry back to a manageable (and even productive) level.
- Engage in a “reset” strategy several times a day to bring your amygdala and locus coeruleus back under control. It takes a minute (or five) of calm, positive meditation to take your brain to a happy, optimistic place. Or use a mindfulness exercise to quiet down that overactive amygdala.
- Talk to people. Keeping your worries to yourself can compound them. Hashing through your concerns with a family member, friend, professional coach, or therapist can help put them in perspective and may allow you to come up with strategies to identify and neurologically respond to your sources of stress.
- Exercise, both physically and mentally. Do what works for you, whether it’s a run, a long walk, pumping iron, playing racquetball — anything that promotes physical release. Exercise your brain too. Engage in a project or activity that is mentally demanding. Personally, I like to garden and do online brain exercises. There’s nothing quite like yanking out weeds or hitting a new personal best at a cognitive exercise for me to notch a sense of accomplishment to counterbalance the unresolved issues driving my worry.
- Accept the uncertainty. Life is full of uncertainty. To paraphrase from Yale theologian Reinhold Niebuhr’s “Serenity Prayer”: Have the serenity to accept what you cannot help, the courage to change what you can, and the wisdom to recognize one from the other.
And, please, be assured that you’ll make it through this election season.
Dr. Merzenich, professor emeritus, Department of Neuroscience, University of California San Francisco, disclosed ties with Posit Science. He is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is BrainHQ, a brain exercise app.
A version of this article appeared on Medscape.com.
Do new Alzheimer’s drugs get us closer to solving the Alzheimer’s disease riddle?
Two antiamyloid drugs were recently approved by the Food and Drug Administration for treating early-stage Alzheimer’s disease (AD). In trials of both lecanemab (Leqembi) and donanemab, a long-held neuropharmacologic dream was realized: Most amyloid plaques – the primary pathologic marker for AD – were eliminated from the brains of patients with late pre-AD or early AD.
Implications for the amyloid hypothesis
The reduction of amyloid plaques has been argued by many scientists and clinical authorities to be the likely pharmacologic solution for AD. These trials are appropriately viewed as a test of the hypothesis that amyloid bodies are a primary cause of the neurobehavioral symptoms we call AD.
In parallel with that striking reduction in amyloid bodies, drug-treated patients had an initially slower progression of neurobehavioral decline than did placebo-treated control patients. That slowing in symptom progression was accompanied by a modest but statistically significant difference in neurobehavioral ability. After several months in treatment, the rate of decline again paralleled that recorded in the control group. The sustained difference of about a half point on cognitive assessment scores separating treatment and control participants was well short of the 1.5-point difference typically considered clinically significant.
A small number of unexpected and unexplained deaths occurred in the treatment groups. Brain swelling and/or micro-hemorrhages were seen in 20%-30% of treated individuals. Significant brain shrinkage was recorded. These adverse findings are indicative of drug-induced trauma in the target organ for these drugs (i.e., the brain) and were the basis for a boxed warning label for drug usage. Antiamyloid drug treatment was not effective in patients who had higher initial numbers of amyloid plaques, indicating that these drugs would not measurably help the majority of AD patients, who are at more advanced disease stages.
These drugs do not appear to be an “answer” for AD. A modest delay in progression does not mean that we’re on a path to a “cure.” Treatment cost estimates are high – more than $80,000 per year. With requisite PET exams and high copays, patient accessibility issues will be daunting.
Of note, To the contrary, they add strong support for the counterargument that the emergence of amyloid plaques is an effect and not a fundamental cause of that progressive loss of neurologic function that we ultimately define as “Alzheimer’s disease.”
Time to switch gears
The more obvious path to winning the battle against this human scourge is prevention. A recent analysis published in The Lancet argued that about 40% of AD and other dementias are potentially preventable. I disagree. I believe that 80%-90% of prospective cases can be substantially delayed or prevented. Studies have shown that progression to AD or other dementias is driven primarily by the progressive deterioration of organic brain health, expressed by the loss of what psychologists have termed “cognitive reserve.” Cognitive reserve is resilience arising from active brain usage, akin to physical resilience attributable to a physically active life. Scientific studies have shown us that an individual’s cognitive resilience (reserve) is a greater predictor of risk for dementia than are amyloid plaques – indeed, greater than any combination of pathologic markers in dementia patients.
Building up cognitive reserve
It’s increasingly clear to this observer that cognitive reserve is synonymous with organic brain health. The primary factors that underlie cognitive reserve are processing speed in the brain, executive control, response withholding, memory acquisition, reasoning, and attention abilities. Faster, more accurate brains are necessarily more physically optimized. They necessarily sustain brain system connectivity. They are necessarily healthier. Such brains bear a relatively low risk of developing AD or other dementias, just as physically healthier bodies bear a lower risk of being prematurely banished to semi-permanent residence in an easy chair or a bed.
Brain health can be sustained by deploying inexpensive, self-administered, app-based assessments of neurologic performance limits, which inform patients and their medical teams about general brain health status. These assessments can help doctors guide their patients to adopt more intelligent brain-healthy lifestyles, or direct them to the “brain gym” to progressively exercise their brains in ways that contribute to rapid, potentially large-scale, rejuvenating improvements in physical and functional brain health.
Randomized controlled trials incorporating different combinations of physical exercise, diet, and cognitive training have recorded significant improvements in physical and functional neurologic status, indicating substantially advanced brain health. Consistent moderate-to-intense physical exercise, brain- and heart-healthy eating habits, and, particularly, computerized brain training have repeatedly been shown to improve cognitive function and physically rejuvenate the brain. With cognitive training in the right forms, improvements in processing speed and other measures manifest improving brain health and greater safety.
In the National Institutes of Health–funded ACTIVE study with more than 2,800 older adults, just 10-18 hours of a specific speed of processing training (now part of BrainHQ, a program that I was involved in developing) reduced the probability of a progression to dementia over the following 10 years by 29%, and by 48% in those who did the most training.
This approach is several orders of magnitude less expensive than the pricey new AD drugs. It presents less serious issues of accessibility and has no side effects. It delivers far more powerful therapeutic benefits in older normal and at-risk populations.
Sustained wellness supporting prevention is the far more sensible medical way forward to save people from AD and other dementias – at a far lower medical and societal cost.
Dr. Merzenich is professor emeritus, department of neuroscience, University of California, San Francisco. He reported conflicts of interest with Posit Science, Stronger Brains, and the National Institutes of Health.
A version of this article first appeared on Medscape.com.
Two antiamyloid drugs were recently approved by the Food and Drug Administration for treating early-stage Alzheimer’s disease (AD). In trials of both lecanemab (Leqembi) and donanemab, a long-held neuropharmacologic dream was realized: Most amyloid plaques – the primary pathologic marker for AD – were eliminated from the brains of patients with late pre-AD or early AD.
Implications for the amyloid hypothesis
The reduction of amyloid plaques has been argued by many scientists and clinical authorities to be the likely pharmacologic solution for AD. These trials are appropriately viewed as a test of the hypothesis that amyloid bodies are a primary cause of the neurobehavioral symptoms we call AD.
In parallel with that striking reduction in amyloid bodies, drug-treated patients had an initially slower progression of neurobehavioral decline than did placebo-treated control patients. That slowing in symptom progression was accompanied by a modest but statistically significant difference in neurobehavioral ability. After several months in treatment, the rate of decline again paralleled that recorded in the control group. The sustained difference of about a half point on cognitive assessment scores separating treatment and control participants was well short of the 1.5-point difference typically considered clinically significant.
A small number of unexpected and unexplained deaths occurred in the treatment groups. Brain swelling and/or micro-hemorrhages were seen in 20%-30% of treated individuals. Significant brain shrinkage was recorded. These adverse findings are indicative of drug-induced trauma in the target organ for these drugs (i.e., the brain) and were the basis for a boxed warning label for drug usage. Antiamyloid drug treatment was not effective in patients who had higher initial numbers of amyloid plaques, indicating that these drugs would not measurably help the majority of AD patients, who are at more advanced disease stages.
These drugs do not appear to be an “answer” for AD. A modest delay in progression does not mean that we’re on a path to a “cure.” Treatment cost estimates are high – more than $80,000 per year. With requisite PET exams and high copays, patient accessibility issues will be daunting.
Of note, To the contrary, they add strong support for the counterargument that the emergence of amyloid plaques is an effect and not a fundamental cause of that progressive loss of neurologic function that we ultimately define as “Alzheimer’s disease.”
Time to switch gears
The more obvious path to winning the battle against this human scourge is prevention. A recent analysis published in The Lancet argued that about 40% of AD and other dementias are potentially preventable. I disagree. I believe that 80%-90% of prospective cases can be substantially delayed or prevented. Studies have shown that progression to AD or other dementias is driven primarily by the progressive deterioration of organic brain health, expressed by the loss of what psychologists have termed “cognitive reserve.” Cognitive reserve is resilience arising from active brain usage, akin to physical resilience attributable to a physically active life. Scientific studies have shown us that an individual’s cognitive resilience (reserve) is a greater predictor of risk for dementia than are amyloid plaques – indeed, greater than any combination of pathologic markers in dementia patients.
Building up cognitive reserve
It’s increasingly clear to this observer that cognitive reserve is synonymous with organic brain health. The primary factors that underlie cognitive reserve are processing speed in the brain, executive control, response withholding, memory acquisition, reasoning, and attention abilities. Faster, more accurate brains are necessarily more physically optimized. They necessarily sustain brain system connectivity. They are necessarily healthier. Such brains bear a relatively low risk of developing AD or other dementias, just as physically healthier bodies bear a lower risk of being prematurely banished to semi-permanent residence in an easy chair or a bed.
Brain health can be sustained by deploying inexpensive, self-administered, app-based assessments of neurologic performance limits, which inform patients and their medical teams about general brain health status. These assessments can help doctors guide their patients to adopt more intelligent brain-healthy lifestyles, or direct them to the “brain gym” to progressively exercise their brains in ways that contribute to rapid, potentially large-scale, rejuvenating improvements in physical and functional brain health.
Randomized controlled trials incorporating different combinations of physical exercise, diet, and cognitive training have recorded significant improvements in physical and functional neurologic status, indicating substantially advanced brain health. Consistent moderate-to-intense physical exercise, brain- and heart-healthy eating habits, and, particularly, computerized brain training have repeatedly been shown to improve cognitive function and physically rejuvenate the brain. With cognitive training in the right forms, improvements in processing speed and other measures manifest improving brain health and greater safety.
In the National Institutes of Health–funded ACTIVE study with more than 2,800 older adults, just 10-18 hours of a specific speed of processing training (now part of BrainHQ, a program that I was involved in developing) reduced the probability of a progression to dementia over the following 10 years by 29%, and by 48% in those who did the most training.
This approach is several orders of magnitude less expensive than the pricey new AD drugs. It presents less serious issues of accessibility and has no side effects. It delivers far more powerful therapeutic benefits in older normal and at-risk populations.
Sustained wellness supporting prevention is the far more sensible medical way forward to save people from AD and other dementias – at a far lower medical and societal cost.
Dr. Merzenich is professor emeritus, department of neuroscience, University of California, San Francisco. He reported conflicts of interest with Posit Science, Stronger Brains, and the National Institutes of Health.
A version of this article first appeared on Medscape.com.
Two antiamyloid drugs were recently approved by the Food and Drug Administration for treating early-stage Alzheimer’s disease (AD). In trials of both lecanemab (Leqembi) and donanemab, a long-held neuropharmacologic dream was realized: Most amyloid plaques – the primary pathologic marker for AD – were eliminated from the brains of patients with late pre-AD or early AD.
Implications for the amyloid hypothesis
The reduction of amyloid plaques has been argued by many scientists and clinical authorities to be the likely pharmacologic solution for AD. These trials are appropriately viewed as a test of the hypothesis that amyloid bodies are a primary cause of the neurobehavioral symptoms we call AD.
In parallel with that striking reduction in amyloid bodies, drug-treated patients had an initially slower progression of neurobehavioral decline than did placebo-treated control patients. That slowing in symptom progression was accompanied by a modest but statistically significant difference in neurobehavioral ability. After several months in treatment, the rate of decline again paralleled that recorded in the control group. The sustained difference of about a half point on cognitive assessment scores separating treatment and control participants was well short of the 1.5-point difference typically considered clinically significant.
A small number of unexpected and unexplained deaths occurred in the treatment groups. Brain swelling and/or micro-hemorrhages were seen in 20%-30% of treated individuals. Significant brain shrinkage was recorded. These adverse findings are indicative of drug-induced trauma in the target organ for these drugs (i.e., the brain) and were the basis for a boxed warning label for drug usage. Antiamyloid drug treatment was not effective in patients who had higher initial numbers of amyloid plaques, indicating that these drugs would not measurably help the majority of AD patients, who are at more advanced disease stages.
These drugs do not appear to be an “answer” for AD. A modest delay in progression does not mean that we’re on a path to a “cure.” Treatment cost estimates are high – more than $80,000 per year. With requisite PET exams and high copays, patient accessibility issues will be daunting.
Of note, To the contrary, they add strong support for the counterargument that the emergence of amyloid plaques is an effect and not a fundamental cause of that progressive loss of neurologic function that we ultimately define as “Alzheimer’s disease.”
Time to switch gears
The more obvious path to winning the battle against this human scourge is prevention. A recent analysis published in The Lancet argued that about 40% of AD and other dementias are potentially preventable. I disagree. I believe that 80%-90% of prospective cases can be substantially delayed or prevented. Studies have shown that progression to AD or other dementias is driven primarily by the progressive deterioration of organic brain health, expressed by the loss of what psychologists have termed “cognitive reserve.” Cognitive reserve is resilience arising from active brain usage, akin to physical resilience attributable to a physically active life. Scientific studies have shown us that an individual’s cognitive resilience (reserve) is a greater predictor of risk for dementia than are amyloid plaques – indeed, greater than any combination of pathologic markers in dementia patients.
Building up cognitive reserve
It’s increasingly clear to this observer that cognitive reserve is synonymous with organic brain health. The primary factors that underlie cognitive reserve are processing speed in the brain, executive control, response withholding, memory acquisition, reasoning, and attention abilities. Faster, more accurate brains are necessarily more physically optimized. They necessarily sustain brain system connectivity. They are necessarily healthier. Such brains bear a relatively low risk of developing AD or other dementias, just as physically healthier bodies bear a lower risk of being prematurely banished to semi-permanent residence in an easy chair or a bed.
Brain health can be sustained by deploying inexpensive, self-administered, app-based assessments of neurologic performance limits, which inform patients and their medical teams about general brain health status. These assessments can help doctors guide their patients to adopt more intelligent brain-healthy lifestyles, or direct them to the “brain gym” to progressively exercise their brains in ways that contribute to rapid, potentially large-scale, rejuvenating improvements in physical and functional brain health.
Randomized controlled trials incorporating different combinations of physical exercise, diet, and cognitive training have recorded significant improvements in physical and functional neurologic status, indicating substantially advanced brain health. Consistent moderate-to-intense physical exercise, brain- and heart-healthy eating habits, and, particularly, computerized brain training have repeatedly been shown to improve cognitive function and physically rejuvenate the brain. With cognitive training in the right forms, improvements in processing speed and other measures manifest improving brain health and greater safety.
In the National Institutes of Health–funded ACTIVE study with more than 2,800 older adults, just 10-18 hours of a specific speed of processing training (now part of BrainHQ, a program that I was involved in developing) reduced the probability of a progression to dementia over the following 10 years by 29%, and by 48% in those who did the most training.
This approach is several orders of magnitude less expensive than the pricey new AD drugs. It presents less serious issues of accessibility and has no side effects. It delivers far more powerful therapeutic benefits in older normal and at-risk populations.
Sustained wellness supporting prevention is the far more sensible medical way forward to save people from AD and other dementias – at a far lower medical and societal cost.
Dr. Merzenich is professor emeritus, department of neuroscience, University of California, San Francisco. He reported conflicts of interest with Posit Science, Stronger Brains, and the National Institutes of Health.
A version of this article first appeared on Medscape.com.
Bruce Willis’ frontotemporal dementia is not your grandpa’s dementia
What is remarkable about the swamp that we call FTD is that it’s a somewhat rare and unusual type of dementia. We tend to characterize dementia as the erosion of memory, but FTD is more characterized by the loss of control over emotions and other cognitive functions. What›s especially tragic for performers like Mr. Willis is the loss of the verbal fluency required for delivering one’s lines.
Frontotemporal dementia
To this casual observer, Bruce Willis was an almost invincible force, vigorous, vital, one of the “immortals.” Alas, with his FTD diagnosis, we know that even a die-hard like Mr. Willis, now only 67 years of age, may have to endure years of progressive decline. If the disease follows its typical path, that will probably include slowly disconnecting and progressively losing emotional judgment and control as well as losing a reasonable understanding of what or why any of it is happening. He may also experience a progressive deterioration of the control of bodily functions and general health.
Most people with dementia lose their neurocognitive abilities through a number of different pathways, all of which result in brain shrinkage, disconnection, evident neuropathology, neurobehavioral expressions of loss, and forms of befuddlement. Alzheimer’s disease leads the list as the most common form of dementia, but vascular dementias; dementia with Lewy bodies; “mixed” dementias; dementias associated with Parkinson’s, Huntington’s, or other diseases; dementia rising from alcoholic or other brain poisoning, HIV, Lyme disease, or a host of other brain infections; or from traumatic encephalopathy (chronic or more current) may present at any active neurology clinic. These are what you might think of as your “grandpa’s dementia” – the common types often associated with old age.
FTD is a particularly interesting variant for several reasons. First, it usually arises in relatively young individuals, with initial symptoms emerging in one’s 50s or 60s. In most cases, there is no genetic and, with rare exception, any other explanation of origin – except that old medical standby, bad luck.
Second, FTD has little initial impact on a patient’s broader memory and associated cognitive abilities. The patient will stumble to come up with that next word and ultimately slow down their speech as their brain struggles with verbal fluency; they will struggle with translating their feelings and emotions into fast and appropriate actions expressed in their mind and their physical body while their memory will appear intact.
In all other dementias, cognitive losses can be profound, whereas social and emotional control and voluble speech production are generally better sustained. Imagine the impact that these struggles in verbal fluency and in emotional calibration and response must have for an established actor. By all reports, Mr. Willis vigorously pursued the work that he loved right up until the time of his dementia diagnosis, even as his colleagues would almost certainly have seen that he was struggling. Sadly, a lack of that type of self-awareness is an expected consequence of FTD.
The salience network and von Economo neurons
Third and most intriguing to a neuroscientific nerd like me is that patients with FTD experience an initial loss of a special population of cortical neurons located within the salience network in our brains, called the von Economo neurons. That salience network is designed to quickly read and evaluate our complex thoughts and emotions and via those Economo neurons, initiate appropriate neurologic and physical responses.
We share this special von Economo machinery with great apes, whales, elephants, and a handful of other especially social mammalian species.
When we see or hear or otherwise sense something that induces fear, alarm, or a potential reward, the salience network in our brain acts as a kind of gatekeeper. First, it assesses the emergent or changing situation, then it rapidly initiates an emotional and physical response. As I sit with a patient in obvious distress in my office, my salience network turns on an empathetic alarm. My brain and body immediately adjust to initiate appropriately sympathetic reactions. The von Economo neurons – those very neurons that have substantially died off in a brain with FTD – are the linchpins in this fast-response emotion and complex body signal-informed system.
Controlled emotional response is at the heart of our humanity. It’s a sad day when we lose it.
In other neurologic clinical conditions marked by the loss of specific brain cells, different forms of “disuse atrophy” are partly the cause. We don’t know whether that’s the case for FTD. Scientists have shown that specific forms of computerized brain exercises can sharply increase activity levels in the salience network which is linked to improvements in the regulatory control of the autonomic nervous system – one of the key response-mediating targets of the network’s von Economo neurons.
Interestingly, superagers who sustain body and brain health into their 90s (and beyond) die with a full complement of von Economo neurons operating happily in a still-vigorous salience network.
This neuroscientist can foresee a day when we routinely assess the integrity of this important brain system and more reliably maintain its good health. Keeping those very special neurons alive would have probably allowed Mr. Willis to sustain himself on the soundstage and on the grander stage of life for a long time to come. Alas, like so many things in medicine, there is promise. But at this moment for this famous patient, our current medical science appears to be a day late, and a dollar short.
Dr. Merzenichis is professor emeritus at the University of California, San Francisco, and a Kavli Laureate in Neuroscience. He reported conflicts of interest with the National Institutes of Health, Stronger Brains, and Posit Science.
A version of this article first appeared on Medscape.com.
What is remarkable about the swamp that we call FTD is that it’s a somewhat rare and unusual type of dementia. We tend to characterize dementia as the erosion of memory, but FTD is more characterized by the loss of control over emotions and other cognitive functions. What›s especially tragic for performers like Mr. Willis is the loss of the verbal fluency required for delivering one’s lines.
Frontotemporal dementia
To this casual observer, Bruce Willis was an almost invincible force, vigorous, vital, one of the “immortals.” Alas, with his FTD diagnosis, we know that even a die-hard like Mr. Willis, now only 67 years of age, may have to endure years of progressive decline. If the disease follows its typical path, that will probably include slowly disconnecting and progressively losing emotional judgment and control as well as losing a reasonable understanding of what or why any of it is happening. He may also experience a progressive deterioration of the control of bodily functions and general health.
Most people with dementia lose their neurocognitive abilities through a number of different pathways, all of which result in brain shrinkage, disconnection, evident neuropathology, neurobehavioral expressions of loss, and forms of befuddlement. Alzheimer’s disease leads the list as the most common form of dementia, but vascular dementias; dementia with Lewy bodies; “mixed” dementias; dementias associated with Parkinson’s, Huntington’s, or other diseases; dementia rising from alcoholic or other brain poisoning, HIV, Lyme disease, or a host of other brain infections; or from traumatic encephalopathy (chronic or more current) may present at any active neurology clinic. These are what you might think of as your “grandpa’s dementia” – the common types often associated with old age.
FTD is a particularly interesting variant for several reasons. First, it usually arises in relatively young individuals, with initial symptoms emerging in one’s 50s or 60s. In most cases, there is no genetic and, with rare exception, any other explanation of origin – except that old medical standby, bad luck.
Second, FTD has little initial impact on a patient’s broader memory and associated cognitive abilities. The patient will stumble to come up with that next word and ultimately slow down their speech as their brain struggles with verbal fluency; they will struggle with translating their feelings and emotions into fast and appropriate actions expressed in their mind and their physical body while their memory will appear intact.
In all other dementias, cognitive losses can be profound, whereas social and emotional control and voluble speech production are generally better sustained. Imagine the impact that these struggles in verbal fluency and in emotional calibration and response must have for an established actor. By all reports, Mr. Willis vigorously pursued the work that he loved right up until the time of his dementia diagnosis, even as his colleagues would almost certainly have seen that he was struggling. Sadly, a lack of that type of self-awareness is an expected consequence of FTD.
The salience network and von Economo neurons
Third and most intriguing to a neuroscientific nerd like me is that patients with FTD experience an initial loss of a special population of cortical neurons located within the salience network in our brains, called the von Economo neurons. That salience network is designed to quickly read and evaluate our complex thoughts and emotions and via those Economo neurons, initiate appropriate neurologic and physical responses.
We share this special von Economo machinery with great apes, whales, elephants, and a handful of other especially social mammalian species.
When we see or hear or otherwise sense something that induces fear, alarm, or a potential reward, the salience network in our brain acts as a kind of gatekeeper. First, it assesses the emergent or changing situation, then it rapidly initiates an emotional and physical response. As I sit with a patient in obvious distress in my office, my salience network turns on an empathetic alarm. My brain and body immediately adjust to initiate appropriately sympathetic reactions. The von Economo neurons – those very neurons that have substantially died off in a brain with FTD – are the linchpins in this fast-response emotion and complex body signal-informed system.
Controlled emotional response is at the heart of our humanity. It’s a sad day when we lose it.
In other neurologic clinical conditions marked by the loss of specific brain cells, different forms of “disuse atrophy” are partly the cause. We don’t know whether that’s the case for FTD. Scientists have shown that specific forms of computerized brain exercises can sharply increase activity levels in the salience network which is linked to improvements in the regulatory control of the autonomic nervous system – one of the key response-mediating targets of the network’s von Economo neurons.
Interestingly, superagers who sustain body and brain health into their 90s (and beyond) die with a full complement of von Economo neurons operating happily in a still-vigorous salience network.
This neuroscientist can foresee a day when we routinely assess the integrity of this important brain system and more reliably maintain its good health. Keeping those very special neurons alive would have probably allowed Mr. Willis to sustain himself on the soundstage and on the grander stage of life for a long time to come. Alas, like so many things in medicine, there is promise. But at this moment for this famous patient, our current medical science appears to be a day late, and a dollar short.
Dr. Merzenichis is professor emeritus at the University of California, San Francisco, and a Kavli Laureate in Neuroscience. He reported conflicts of interest with the National Institutes of Health, Stronger Brains, and Posit Science.
A version of this article first appeared on Medscape.com.
What is remarkable about the swamp that we call FTD is that it’s a somewhat rare and unusual type of dementia. We tend to characterize dementia as the erosion of memory, but FTD is more characterized by the loss of control over emotions and other cognitive functions. What›s especially tragic for performers like Mr. Willis is the loss of the verbal fluency required for delivering one’s lines.
Frontotemporal dementia
To this casual observer, Bruce Willis was an almost invincible force, vigorous, vital, one of the “immortals.” Alas, with his FTD diagnosis, we know that even a die-hard like Mr. Willis, now only 67 years of age, may have to endure years of progressive decline. If the disease follows its typical path, that will probably include slowly disconnecting and progressively losing emotional judgment and control as well as losing a reasonable understanding of what or why any of it is happening. He may also experience a progressive deterioration of the control of bodily functions and general health.
Most people with dementia lose their neurocognitive abilities through a number of different pathways, all of which result in brain shrinkage, disconnection, evident neuropathology, neurobehavioral expressions of loss, and forms of befuddlement. Alzheimer’s disease leads the list as the most common form of dementia, but vascular dementias; dementia with Lewy bodies; “mixed” dementias; dementias associated with Parkinson’s, Huntington’s, or other diseases; dementia rising from alcoholic or other brain poisoning, HIV, Lyme disease, or a host of other brain infections; or from traumatic encephalopathy (chronic or more current) may present at any active neurology clinic. These are what you might think of as your “grandpa’s dementia” – the common types often associated with old age.
FTD is a particularly interesting variant for several reasons. First, it usually arises in relatively young individuals, with initial symptoms emerging in one’s 50s or 60s. In most cases, there is no genetic and, with rare exception, any other explanation of origin – except that old medical standby, bad luck.
Second, FTD has little initial impact on a patient’s broader memory and associated cognitive abilities. The patient will stumble to come up with that next word and ultimately slow down their speech as their brain struggles with verbal fluency; they will struggle with translating their feelings and emotions into fast and appropriate actions expressed in their mind and their physical body while their memory will appear intact.
In all other dementias, cognitive losses can be profound, whereas social and emotional control and voluble speech production are generally better sustained. Imagine the impact that these struggles in verbal fluency and in emotional calibration and response must have for an established actor. By all reports, Mr. Willis vigorously pursued the work that he loved right up until the time of his dementia diagnosis, even as his colleagues would almost certainly have seen that he was struggling. Sadly, a lack of that type of self-awareness is an expected consequence of FTD.
The salience network and von Economo neurons
Third and most intriguing to a neuroscientific nerd like me is that patients with FTD experience an initial loss of a special population of cortical neurons located within the salience network in our brains, called the von Economo neurons. That salience network is designed to quickly read and evaluate our complex thoughts and emotions and via those Economo neurons, initiate appropriate neurologic and physical responses.
We share this special von Economo machinery with great apes, whales, elephants, and a handful of other especially social mammalian species.
When we see or hear or otherwise sense something that induces fear, alarm, or a potential reward, the salience network in our brain acts as a kind of gatekeeper. First, it assesses the emergent or changing situation, then it rapidly initiates an emotional and physical response. As I sit with a patient in obvious distress in my office, my salience network turns on an empathetic alarm. My brain and body immediately adjust to initiate appropriately sympathetic reactions. The von Economo neurons – those very neurons that have substantially died off in a brain with FTD – are the linchpins in this fast-response emotion and complex body signal-informed system.
Controlled emotional response is at the heart of our humanity. It’s a sad day when we lose it.
In other neurologic clinical conditions marked by the loss of specific brain cells, different forms of “disuse atrophy” are partly the cause. We don’t know whether that’s the case for FTD. Scientists have shown that specific forms of computerized brain exercises can sharply increase activity levels in the salience network which is linked to improvements in the regulatory control of the autonomic nervous system – one of the key response-mediating targets of the network’s von Economo neurons.
Interestingly, superagers who sustain body and brain health into their 90s (and beyond) die with a full complement of von Economo neurons operating happily in a still-vigorous salience network.
This neuroscientist can foresee a day when we routinely assess the integrity of this important brain system and more reliably maintain its good health. Keeping those very special neurons alive would have probably allowed Mr. Willis to sustain himself on the soundstage and on the grander stage of life for a long time to come. Alas, like so many things in medicine, there is promise. But at this moment for this famous patient, our current medical science appears to be a day late, and a dollar short.
Dr. Merzenichis is professor emeritus at the University of California, San Francisco, and a Kavli Laureate in Neuroscience. He reported conflicts of interest with the National Institutes of Health, Stronger Brains, and Posit Science.
A version of this article first appeared on Medscape.com.
For the Fourth of July, a neuroscientist reflects on patriotism
This week, we celebrate our nation’s birth in a national and individual display of our patriotic attachment to this country. — which includes our self-definition as Americans.
For each of us, personhood is an almost miraculous product of our brain’s plasticity — the brain’s ability to change chemically, structurally, and functionally, based on our life experiences — arising from near countless moments of change in the wiring of our brain.
The incredibly complex remodeling that created “you” is a product, of course, of your very complicated, unique passage in life. You have a repertoire of skills and ability; you have stories and understanding and a history of sensing and acting and thinking in the world that is, in detail, unique only to you and your experiences.
As your brain created its model of your world by recording “what goes with what” at each brief moment of time, your brain — that most complicated and wonderful of “machines” on planet Earth — also associated billions of moments of feeling and action and thought with their source, your Self.
Because we primarily construct our model of the world through our eyes and ears, it’s not surprising that the emergent Self that is located somewhere in the center of your head behind your eyes and between your ears. Through billions of contacts with the surfaces of your hide and sensory organs, you have embodied yourself.
Your sense of ‘us’
These same neurologic processes extend beyond our physical beings to incorporate other contributors to our well-being into our personhoods. Loving parents, siblings, friends — and others in your clans and tribes and nations — literally grow into your personhood by these same self-associating processes. These relationships are supported in mutual identity by all of the tokens and icons and charms and customs that collectively define you and enable a sense of “us.”
Put another way, Mother Nature (or, in another cultural perspective, our Creator) has designed our brains to incorporate all of those who are close to us — and more broadly, other individuals in our clan or tribe or nation — to be a part of each of us.
Humans are highly social creatures. When we rise up and risk our lives to defend our friends, family, or cultural “in-groups,” we are literally fighting to defend ourselves — because those other individuals have grown into our very being. In defending them, we are literally defending a part of ourselves.
From one human perspective, this attachment to family and clan and tribe and nation is obviously key for our survival. We are an individually vulnerable but collectively powerful species, and attachment and mutual support are a key to our personal and collective successes in life.
From another perspective, there is also a dark side to this “gift of nature.”
We draw lines in substantially arbitrary locations across the surface of planet Earth, or we may define our self as belonging to a group in a political or social or religious context, or sect. Our tribalism can support a generally strong level of support and succor for fellow humans on our side of that line, while we regard those just across the line as undeserving of our support. If they offend us, they may become targets of our capacity for cruelty.
Our allegiances can be both wonderful and harmful.
The individuality of us
As we celebrate this holiday — a favorite day on my personal calendar — I am compelled to reflect on the fact that America was designed to be fractious. We Americans are not required to all operate like “peas in the pod.”
While we, as a nation, often fail to live up to our ideals, when we pursue the highest standards of liberty, we celebrate diversity, difference, and the ability of each member of our tribe to find their own path.
In a very real sense, the great American “invention” was to create a nation in which we could all find a wonderful place of our own, with the sympathy and protection of fellow citizens, and with liberty and justice for all.
Happy Independence Day to my American tribe!
Michael Merzenich, PhD, is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is professor emeritus at UCSF and a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is BrainHQ, a brain exercise app. He has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Posit Science Corporation; Stronger Brains Inc. Serve(d) as a speaker or a member of a speakers bureau for: Posit Science Corporation; Stronger Brains Inc. Received research grant from: National Institutes of Health Have a 5% or greater equity interest in: Posit Science Corporation; Stronger Brains Inc. Received income in an amount equal to or greater than $250 from: Posit Science Corporation; Stronger Brains Inc.; National Institutes of Health.
A version of this article first appeared on Medscape.com.
This week, we celebrate our nation’s birth in a national and individual display of our patriotic attachment to this country. — which includes our self-definition as Americans.
For each of us, personhood is an almost miraculous product of our brain’s plasticity — the brain’s ability to change chemically, structurally, and functionally, based on our life experiences — arising from near countless moments of change in the wiring of our brain.
The incredibly complex remodeling that created “you” is a product, of course, of your very complicated, unique passage in life. You have a repertoire of skills and ability; you have stories and understanding and a history of sensing and acting and thinking in the world that is, in detail, unique only to you and your experiences.
As your brain created its model of your world by recording “what goes with what” at each brief moment of time, your brain — that most complicated and wonderful of “machines” on planet Earth — also associated billions of moments of feeling and action and thought with their source, your Self.
Because we primarily construct our model of the world through our eyes and ears, it’s not surprising that the emergent Self that is located somewhere in the center of your head behind your eyes and between your ears. Through billions of contacts with the surfaces of your hide and sensory organs, you have embodied yourself.
Your sense of ‘us’
These same neurologic processes extend beyond our physical beings to incorporate other contributors to our well-being into our personhoods. Loving parents, siblings, friends — and others in your clans and tribes and nations — literally grow into your personhood by these same self-associating processes. These relationships are supported in mutual identity by all of the tokens and icons and charms and customs that collectively define you and enable a sense of “us.”
Put another way, Mother Nature (or, in another cultural perspective, our Creator) has designed our brains to incorporate all of those who are close to us — and more broadly, other individuals in our clan or tribe or nation — to be a part of each of us.
Humans are highly social creatures. When we rise up and risk our lives to defend our friends, family, or cultural “in-groups,” we are literally fighting to defend ourselves — because those other individuals have grown into our very being. In defending them, we are literally defending a part of ourselves.
From one human perspective, this attachment to family and clan and tribe and nation is obviously key for our survival. We are an individually vulnerable but collectively powerful species, and attachment and mutual support are a key to our personal and collective successes in life.
From another perspective, there is also a dark side to this “gift of nature.”
We draw lines in substantially arbitrary locations across the surface of planet Earth, or we may define our self as belonging to a group in a political or social or religious context, or sect. Our tribalism can support a generally strong level of support and succor for fellow humans on our side of that line, while we regard those just across the line as undeserving of our support. If they offend us, they may become targets of our capacity for cruelty.
Our allegiances can be both wonderful and harmful.
The individuality of us
As we celebrate this holiday — a favorite day on my personal calendar — I am compelled to reflect on the fact that America was designed to be fractious. We Americans are not required to all operate like “peas in the pod.”
While we, as a nation, often fail to live up to our ideals, when we pursue the highest standards of liberty, we celebrate diversity, difference, and the ability of each member of our tribe to find their own path.
In a very real sense, the great American “invention” was to create a nation in which we could all find a wonderful place of our own, with the sympathy and protection of fellow citizens, and with liberty and justice for all.
Happy Independence Day to my American tribe!
Michael Merzenich, PhD, is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is professor emeritus at UCSF and a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is BrainHQ, a brain exercise app. He has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Posit Science Corporation; Stronger Brains Inc. Serve(d) as a speaker or a member of a speakers bureau for: Posit Science Corporation; Stronger Brains Inc. Received research grant from: National Institutes of Health Have a 5% or greater equity interest in: Posit Science Corporation; Stronger Brains Inc. Received income in an amount equal to or greater than $250 from: Posit Science Corporation; Stronger Brains Inc.; National Institutes of Health.
A version of this article first appeared on Medscape.com.
This week, we celebrate our nation’s birth in a national and individual display of our patriotic attachment to this country. — which includes our self-definition as Americans.
For each of us, personhood is an almost miraculous product of our brain’s plasticity — the brain’s ability to change chemically, structurally, and functionally, based on our life experiences — arising from near countless moments of change in the wiring of our brain.
The incredibly complex remodeling that created “you” is a product, of course, of your very complicated, unique passage in life. You have a repertoire of skills and ability; you have stories and understanding and a history of sensing and acting and thinking in the world that is, in detail, unique only to you and your experiences.
As your brain created its model of your world by recording “what goes with what” at each brief moment of time, your brain — that most complicated and wonderful of “machines” on planet Earth — also associated billions of moments of feeling and action and thought with their source, your Self.
Because we primarily construct our model of the world through our eyes and ears, it’s not surprising that the emergent Self that is located somewhere in the center of your head behind your eyes and between your ears. Through billions of contacts with the surfaces of your hide and sensory organs, you have embodied yourself.
Your sense of ‘us’
These same neurologic processes extend beyond our physical beings to incorporate other contributors to our well-being into our personhoods. Loving parents, siblings, friends — and others in your clans and tribes and nations — literally grow into your personhood by these same self-associating processes. These relationships are supported in mutual identity by all of the tokens and icons and charms and customs that collectively define you and enable a sense of “us.”
Put another way, Mother Nature (or, in another cultural perspective, our Creator) has designed our brains to incorporate all of those who are close to us — and more broadly, other individuals in our clan or tribe or nation — to be a part of each of us.
Humans are highly social creatures. When we rise up and risk our lives to defend our friends, family, or cultural “in-groups,” we are literally fighting to defend ourselves — because those other individuals have grown into our very being. In defending them, we are literally defending a part of ourselves.
From one human perspective, this attachment to family and clan and tribe and nation is obviously key for our survival. We are an individually vulnerable but collectively powerful species, and attachment and mutual support are a key to our personal and collective successes in life.
From another perspective, there is also a dark side to this “gift of nature.”
We draw lines in substantially arbitrary locations across the surface of planet Earth, or we may define our self as belonging to a group in a political or social or religious context, or sect. Our tribalism can support a generally strong level of support and succor for fellow humans on our side of that line, while we regard those just across the line as undeserving of our support. If they offend us, they may become targets of our capacity for cruelty.
Our allegiances can be both wonderful and harmful.
The individuality of us
As we celebrate this holiday — a favorite day on my personal calendar — I am compelled to reflect on the fact that America was designed to be fractious. We Americans are not required to all operate like “peas in the pod.”
While we, as a nation, often fail to live up to our ideals, when we pursue the highest standards of liberty, we celebrate diversity, difference, and the ability of each member of our tribe to find their own path.
In a very real sense, the great American “invention” was to create a nation in which we could all find a wonderful place of our own, with the sympathy and protection of fellow citizens, and with liberty and justice for all.
Happy Independence Day to my American tribe!
Michael Merzenich, PhD, is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is professor emeritus at UCSF and a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is BrainHQ, a brain exercise app. He has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Posit Science Corporation; Stronger Brains Inc. Serve(d) as a speaker or a member of a speakers bureau for: Posit Science Corporation; Stronger Brains Inc. Received research grant from: National Institutes of Health Have a 5% or greater equity interest in: Posit Science Corporation; Stronger Brains Inc. Received income in an amount equal to or greater than $250 from: Posit Science Corporation; Stronger Brains Inc.; National Institutes of Health.
A version of this article first appeared on Medscape.com.
Daylight Savings: How an imposed time change alters your brain, and what you can do
On March 13, most of the United States and Canada will advance the clock an hour to be on Daylight Saving Time. Most other countries in the Northern Hemisphere will do the same within a few weeks; and many countries across the Southern Hemisphere turn the clock back an hour around the same time. A friend of mine, who spent time on Capitol Hill, once told me that whether it’s adjusting to Daylight Saving Time (and losing an hour of sleep) or switching back to Standard Time (and picking up an hour), large numbers of Americans call their member of Congress every season to complain.
Why are so many of us annoyed by the semi-annual resetting of clocks? Those reasons also come into play when we change time zones as we travel, when we work on the night shift, or when we live at higher latitudes, where depressive symptoms from seasonal affective disorder (SAD) can plague us as the period of daylight progressively shortens in winter.
Our internal clock(s)
Each of us has a biological master clock keeping track of where we are in our 24-hour day, making ongoing time-of-day-appropriate physical and neurologic adjustments. We refer to those automatic adjustments as “circadian” rhythms – from the Latin, for “around a day” rhythms.
One of the most important regulated functions that is influenced by this time keeping is our sleep-wake cycle. Our brain’s hypothalamus has a kind of “master clock” that receives inputs directly from our eyes, which is how our brain sets our daily cycle period at about 24 hours.
This master clock turns on a tiny structure in our brains, called the pineal gland, to release more of a sleep-inducing chemical, called melatonin, about the same time every evening. The level of melatonin slowly increases to reach maximum deep sleep in the night, then slowly declines as you advance toward morning awakening. The shift from darkness to daylight in the morning, causing your initial morning awakening, releases the excitatory neuromodulator norepinephrine, which, with other chemicals, “turns on the lights” in your brain.
That works well most of the time – but no one told your brain that you were going to arbitrarily go to bed an hour earlier (or in the fall, later) on Circadian Rhythm Time!
We also obviously shift the time on the mechanical clock – requiring a reset of the brain’s master clock – when we travel across time zones or work the night shift. That type of desynchronization of our master clock from the mechanical clock puts our waking and sleeping behaviors out of sync with the production of brain chemicals that affect our alertness and mood. The result may be that you find yourself tired, but not sleepy, and often grumpy or even depressed. As an example, on average, people who work the night shift are just a little bit more anxious and depressed than people who get up to rise and shine with the sun every morning.
Seasonal affective disorder
An extreme example of this desynchronization of the master clock can manifest as SAD. SAD is a type of depression that’s related to seasonal transitions. The most commonly cited cases of SAD are for the fall-to-winter transition. In North America, its prevalence is significantly influenced by the distance of one’s place of residence from the equator – with about 12 times the impact in Alaska versus Florida. Of note, a weaker effect of latitude has been recorded in Europe, where more settled populations have had thousands of years to biologically and culturally adapt to their seasonal patterns.
What can we do about our clocks being messed with?
The most common treatment for SAD is light therapy, in which patients sit or work under artificial lights in an early-morning period, to try to advance the chemical signaling that controls sleeping and waking. Alas, light therapy doesn’t work for everyone.
Another approach, with or without the lights, is to engage in activities early in the day that produce brain chemicals to contribute to bright and cheerful waking. Those “raring-to-go” brain chemicals include norepinephrine (produced when you encounter novelty and are just having fun), acetylcholine (produced when you are carefully paying attention and are in a learning and remembering mode), serotonin (produced when you are feeling positive and just a little bit euphoric), and dopamine (produced when you feel happy and all is right with the world).
In fact, you would benefit from creating the habit of starting every day with activity that wakes up your brain. I begin my day with computerized brain exercises that are attentionally demanding, filled with novelty, and richly neurologically rewarding. I then take a brisk morning walk in which I vary my path for the sake of novelty (pumping norepinephrine), pay close attention to my surroundings (pumping acetylcholine and serotonin), and delight in all of the wonderful things out there in my world (pumping dopamine). My dog Doug enjoys this process of waking up brain and body almost as much as I do! Of course, there are a thousand other stimulating things that could help you get your day off to a lively start.
If you anticipate feeling altered by a time change, you could also think about preparing for it in advance. If it’s the semi-annual 1-hour change that throws you off kilter, you might adjust your bedtime by 10 minutes a day for the week before. If you are traveling 12 time zones (and flipping night and day), you may need to make larger adjustments over the preceding couple of weeks. Generally, without that preparation, it takes about 1 day per time zone crossed to naturally adjust your circadian rhythms.
If you’re a little lazier, like me, you might also adjust to jet lag by not forgetting to take along your little bottle of melatonin tablets, to give your pineal gland a little help. Still, that pineal gland will work hard to tell you to take a nap every day – just when you’ll probably want to be wide awake.
And if, after reading this column, you find yourself still annoyed by the upcoming 1-hour time change, you might just look around at what’s happening out there in the world and decide that your troubles are very small by comparison, and that you should delight in the “extra” hour of sunshine each evening!
Dr. Merzenich is professor emeritus, department of neuroscience, at the University of California, San Francisco. He reported serving in various positions and speaking for Posit Science and Stronger Brain, and has also received funding from the National Institutes of Health. A version of this article first appeared on Medscape.com.
On March 13, most of the United States and Canada will advance the clock an hour to be on Daylight Saving Time. Most other countries in the Northern Hemisphere will do the same within a few weeks; and many countries across the Southern Hemisphere turn the clock back an hour around the same time. A friend of mine, who spent time on Capitol Hill, once told me that whether it’s adjusting to Daylight Saving Time (and losing an hour of sleep) or switching back to Standard Time (and picking up an hour), large numbers of Americans call their member of Congress every season to complain.
Why are so many of us annoyed by the semi-annual resetting of clocks? Those reasons also come into play when we change time zones as we travel, when we work on the night shift, or when we live at higher latitudes, where depressive symptoms from seasonal affective disorder (SAD) can plague us as the period of daylight progressively shortens in winter.
Our internal clock(s)
Each of us has a biological master clock keeping track of where we are in our 24-hour day, making ongoing time-of-day-appropriate physical and neurologic adjustments. We refer to those automatic adjustments as “circadian” rhythms – from the Latin, for “around a day” rhythms.
One of the most important regulated functions that is influenced by this time keeping is our sleep-wake cycle. Our brain’s hypothalamus has a kind of “master clock” that receives inputs directly from our eyes, which is how our brain sets our daily cycle period at about 24 hours.
This master clock turns on a tiny structure in our brains, called the pineal gland, to release more of a sleep-inducing chemical, called melatonin, about the same time every evening. The level of melatonin slowly increases to reach maximum deep sleep in the night, then slowly declines as you advance toward morning awakening. The shift from darkness to daylight in the morning, causing your initial morning awakening, releases the excitatory neuromodulator norepinephrine, which, with other chemicals, “turns on the lights” in your brain.
That works well most of the time – but no one told your brain that you were going to arbitrarily go to bed an hour earlier (or in the fall, later) on Circadian Rhythm Time!
We also obviously shift the time on the mechanical clock – requiring a reset of the brain’s master clock – when we travel across time zones or work the night shift. That type of desynchronization of our master clock from the mechanical clock puts our waking and sleeping behaviors out of sync with the production of brain chemicals that affect our alertness and mood. The result may be that you find yourself tired, but not sleepy, and often grumpy or even depressed. As an example, on average, people who work the night shift are just a little bit more anxious and depressed than people who get up to rise and shine with the sun every morning.
Seasonal affective disorder
An extreme example of this desynchronization of the master clock can manifest as SAD. SAD is a type of depression that’s related to seasonal transitions. The most commonly cited cases of SAD are for the fall-to-winter transition. In North America, its prevalence is significantly influenced by the distance of one’s place of residence from the equator – with about 12 times the impact in Alaska versus Florida. Of note, a weaker effect of latitude has been recorded in Europe, where more settled populations have had thousands of years to biologically and culturally adapt to their seasonal patterns.
What can we do about our clocks being messed with?
The most common treatment for SAD is light therapy, in which patients sit or work under artificial lights in an early-morning period, to try to advance the chemical signaling that controls sleeping and waking. Alas, light therapy doesn’t work for everyone.
Another approach, with or without the lights, is to engage in activities early in the day that produce brain chemicals to contribute to bright and cheerful waking. Those “raring-to-go” brain chemicals include norepinephrine (produced when you encounter novelty and are just having fun), acetylcholine (produced when you are carefully paying attention and are in a learning and remembering mode), serotonin (produced when you are feeling positive and just a little bit euphoric), and dopamine (produced when you feel happy and all is right with the world).
In fact, you would benefit from creating the habit of starting every day with activity that wakes up your brain. I begin my day with computerized brain exercises that are attentionally demanding, filled with novelty, and richly neurologically rewarding. I then take a brisk morning walk in which I vary my path for the sake of novelty (pumping norepinephrine), pay close attention to my surroundings (pumping acetylcholine and serotonin), and delight in all of the wonderful things out there in my world (pumping dopamine). My dog Doug enjoys this process of waking up brain and body almost as much as I do! Of course, there are a thousand other stimulating things that could help you get your day off to a lively start.
If you anticipate feeling altered by a time change, you could also think about preparing for it in advance. If it’s the semi-annual 1-hour change that throws you off kilter, you might adjust your bedtime by 10 minutes a day for the week before. If you are traveling 12 time zones (and flipping night and day), you may need to make larger adjustments over the preceding couple of weeks. Generally, without that preparation, it takes about 1 day per time zone crossed to naturally adjust your circadian rhythms.
If you’re a little lazier, like me, you might also adjust to jet lag by not forgetting to take along your little bottle of melatonin tablets, to give your pineal gland a little help. Still, that pineal gland will work hard to tell you to take a nap every day – just when you’ll probably want to be wide awake.
And if, after reading this column, you find yourself still annoyed by the upcoming 1-hour time change, you might just look around at what’s happening out there in the world and decide that your troubles are very small by comparison, and that you should delight in the “extra” hour of sunshine each evening!
Dr. Merzenich is professor emeritus, department of neuroscience, at the University of California, San Francisco. He reported serving in various positions and speaking for Posit Science and Stronger Brain, and has also received funding from the National Institutes of Health. A version of this article first appeared on Medscape.com.
On March 13, most of the United States and Canada will advance the clock an hour to be on Daylight Saving Time. Most other countries in the Northern Hemisphere will do the same within a few weeks; and many countries across the Southern Hemisphere turn the clock back an hour around the same time. A friend of mine, who spent time on Capitol Hill, once told me that whether it’s adjusting to Daylight Saving Time (and losing an hour of sleep) or switching back to Standard Time (and picking up an hour), large numbers of Americans call their member of Congress every season to complain.
Why are so many of us annoyed by the semi-annual resetting of clocks? Those reasons also come into play when we change time zones as we travel, when we work on the night shift, or when we live at higher latitudes, where depressive symptoms from seasonal affective disorder (SAD) can plague us as the period of daylight progressively shortens in winter.
Our internal clock(s)
Each of us has a biological master clock keeping track of where we are in our 24-hour day, making ongoing time-of-day-appropriate physical and neurologic adjustments. We refer to those automatic adjustments as “circadian” rhythms – from the Latin, for “around a day” rhythms.
One of the most important regulated functions that is influenced by this time keeping is our sleep-wake cycle. Our brain’s hypothalamus has a kind of “master clock” that receives inputs directly from our eyes, which is how our brain sets our daily cycle period at about 24 hours.
This master clock turns on a tiny structure in our brains, called the pineal gland, to release more of a sleep-inducing chemical, called melatonin, about the same time every evening. The level of melatonin slowly increases to reach maximum deep sleep in the night, then slowly declines as you advance toward morning awakening. The shift from darkness to daylight in the morning, causing your initial morning awakening, releases the excitatory neuromodulator norepinephrine, which, with other chemicals, “turns on the lights” in your brain.
That works well most of the time – but no one told your brain that you were going to arbitrarily go to bed an hour earlier (or in the fall, later) on Circadian Rhythm Time!
We also obviously shift the time on the mechanical clock – requiring a reset of the brain’s master clock – when we travel across time zones or work the night shift. That type of desynchronization of our master clock from the mechanical clock puts our waking and sleeping behaviors out of sync with the production of brain chemicals that affect our alertness and mood. The result may be that you find yourself tired, but not sleepy, and often grumpy or even depressed. As an example, on average, people who work the night shift are just a little bit more anxious and depressed than people who get up to rise and shine with the sun every morning.
Seasonal affective disorder
An extreme example of this desynchronization of the master clock can manifest as SAD. SAD is a type of depression that’s related to seasonal transitions. The most commonly cited cases of SAD are for the fall-to-winter transition. In North America, its prevalence is significantly influenced by the distance of one’s place of residence from the equator – with about 12 times the impact in Alaska versus Florida. Of note, a weaker effect of latitude has been recorded in Europe, where more settled populations have had thousands of years to biologically and culturally adapt to their seasonal patterns.
What can we do about our clocks being messed with?
The most common treatment for SAD is light therapy, in which patients sit or work under artificial lights in an early-morning period, to try to advance the chemical signaling that controls sleeping and waking. Alas, light therapy doesn’t work for everyone.
Another approach, with or without the lights, is to engage in activities early in the day that produce brain chemicals to contribute to bright and cheerful waking. Those “raring-to-go” brain chemicals include norepinephrine (produced when you encounter novelty and are just having fun), acetylcholine (produced when you are carefully paying attention and are in a learning and remembering mode), serotonin (produced when you are feeling positive and just a little bit euphoric), and dopamine (produced when you feel happy and all is right with the world).
In fact, you would benefit from creating the habit of starting every day with activity that wakes up your brain. I begin my day with computerized brain exercises that are attentionally demanding, filled with novelty, and richly neurologically rewarding. I then take a brisk morning walk in which I vary my path for the sake of novelty (pumping norepinephrine), pay close attention to my surroundings (pumping acetylcholine and serotonin), and delight in all of the wonderful things out there in my world (pumping dopamine). My dog Doug enjoys this process of waking up brain and body almost as much as I do! Of course, there are a thousand other stimulating things that could help you get your day off to a lively start.
If you anticipate feeling altered by a time change, you could also think about preparing for it in advance. If it’s the semi-annual 1-hour change that throws you off kilter, you might adjust your bedtime by 10 minutes a day for the week before. If you are traveling 12 time zones (and flipping night and day), you may need to make larger adjustments over the preceding couple of weeks. Generally, without that preparation, it takes about 1 day per time zone crossed to naturally adjust your circadian rhythms.
If you’re a little lazier, like me, you might also adjust to jet lag by not forgetting to take along your little bottle of melatonin tablets, to give your pineal gland a little help. Still, that pineal gland will work hard to tell you to take a nap every day – just when you’ll probably want to be wide awake.
And if, after reading this column, you find yourself still annoyed by the upcoming 1-hour time change, you might just look around at what’s happening out there in the world and decide that your troubles are very small by comparison, and that you should delight in the “extra” hour of sunshine each evening!
Dr. Merzenich is professor emeritus, department of neuroscience, at the University of California, San Francisco. He reported serving in various positions and speaking for Posit Science and Stronger Brain, and has also received funding from the National Institutes of Health. A version of this article first appeared on Medscape.com.