scientificamerican--2020-08-20--Why Some People Get Terribly Sick from COVID-19

You might have a sniffle and be done .
You might run a fever with a cough and unshakable fatigue for five days—or 10 .
Or you might end up in a hospital , gasping air into congested lungs , an immunological storm raging in your body .
And you might not make it through COVID-19 alive .
What determines if someone gets desperately ill from the disease that is ripping its way across the planet ?
You are likely familiar with the broad categories of people who face greater risk : older individuals , men , those who have @ @ @ @ @ @ @ U.S. and England—people of color .
But researchers are looking deeper into these groups to determine the underlying roots , both biological and social , for their vulnerability .
Investigators are relating age-related risk to the ways that the immune system changes over the years , for example , and examining male-female differences in immune responses .
Some scientists are probing for genetic variations that might raise susceptibility .
Others are highlighting the social , environmental and economic factors that elevate risk , including racism .
For a given individual , the elements @ @ @ @ @ @ @ of a Russian nesting doll .
The innermost core includes genes , biological sex and age .
Cellular and hormonal factors that accompany these characteristics affect vulnerability to infectious microbes , including SARS-CoV-2 , the coronavirus causing the pandemic .
The second layer consists of diseases and chronic conditions acquired over time , many of which make it easier for the virus to enter cells or harder for the body to fight it effectively .
The outermost layer reflects the accumulated nicks and gouges of external circumstance : housing and work conditions , @ @ @ @ @ @ @ status , and exposure to toxins and pollution .
For people of color , these social and economic aspects include the cumulative stresses of systemic racism and discrimination .
These layers are not independent .
With aging , for example , comes more chronic disease and , too frequently , a decline in living conditions such as housing , social support and food security .
Nor are all the contributing risk factors known for an infection that emerged little more than eight months ago .
Still , by applying existing science to emerging @ @ @ @ @ @ @ these layers , researchers say , one can begin to make sense of COVID-19 ’ s dramatic range of severity .
Age is probably the single biggest determinant of how sick someone gets from the coronavirus .
In China , where the pandemic began , the average person with a confirmed infection had a 2.3 percent chance of dying .
But for people between 70 and 79 , it was 8 percent , and for those older than 80 , it was 14.8 percent .
In New York City , nearly half of @ @ @ @ @ @ @ aged 75 and older , and another quarter were among those aged 65 to 74 .
An analysis of 17 million people in England , published in Nature in July , concluded that patients older than 80 were at least 20 times more likely to die of the infection than those in their 50s .
“ Age was our biggest predictor of outcome , ” says Mangala Narasimhan , regional director of critical care at Northwell Health , the largest health care provider in the New York City area , and a co-author @ @ @ @ @ @ @ characteristics of 5,700 hospitalized COVID-19 patients .
The dense concentration of elderly people in nursing homes , where infections can spread quickly and prevention is often inadequate , is clearly one reason for this correlation .
But biology is another factor , particularly the aging of the immune system .
As the decades roll by , the human body becomes less effective at fighting infections .
This decline is one reason why roughly 90 percent of U.S. deaths from influenza are among people aged 65 and older and why vaccines are less protective @ @ @ @ @ @ @ defensive cells become thinned out in number and variety .
And like old warriors , they become more geared toward fighting yesterday ’ s battles with familiar enemies than tackling something new , such as the latest flu strain or the novel coronavirus .
[ A visual guide shows what scientists have learned about the workings of SARS-CoV-2 and how it causes devastating disease . ]
With age , B cells , which make antibodies , and T cells , some of which directly kill infected cells and some of which alert the @ @ @ @ @ @ @ in large quantities in the bone marrow and thymus gland , respectively .
Eventually , production nearly grinds to a halt .
“ It goes from a fire hose at eight years old to a leaky , dripping faucet when you are 80 , ” explains immunologist Kenneth Dorshkind , a professor of pathology and laboratory medicine at the University of California , Los Angeles .
Older adults maintain populations of these essential immune cells in the lymph nodes and spleen , but “ they develop defects with age , so they don @ @ @ @ @ @ @ he says .
For example , as people age , both the stem and arms of the Y-shaped antibody molecule become less flexible .
This limits the body ’ s ability to modify them to match an unfamiliar invader .
As a result , antibodies may not lock on as effectively .
T cells , meanwhile , lose a lot of the variety of receptors that allow them to respond to diverse pathogens , and they may lack the vigor to rapidly multiply in response to infection , says Jörg Goronzy , an @ @ @ @ @ @ @ Stanford University .
“ Healthy old people have lost at least 75 percent of their T cell receptor repertoire , ” he estimates .
“ At one point , we may lack the receptors that have an optimal fit ” for the invading microbe .
Older people are also far more prone to chronic diseases that involve low-grade inflammation , which seems to further compromise the immune system .
Goronzy says it is unclear whether a geriatric immune system resorts to more inflammation to protect the body or whether the inflammation comes first @ @ @ @ @ @ @ is a combination of the two .
Both he and Dorshkind predict that if a coronavirus vaccine becomes available , it will probably be less protective for aged people .
As with the flu shot , an extra strong dose or some kind of booster may be needed .
Sex also contributes to COVID-19 severity : men are roughly twice as likely to die of the infection as women , although the gender gap varies somewhat from place to place .
In Italy , for example , 70 percent of those who died @ @ @ @ @ @ @ the U.S , the figure was 59 percent .
Whether men are also more likely to acquire the infection is unclear because of biases and country-by-country discrepancies in who gets tested for the virus .
But globally , “ the death rate data is more robust and consistent , ” says molecular biologist Sabra Klein , co-director of the Johns Hopkins Center for Women ’ s Health , Sex and Gender Research .
Klein sees three plausible biological factors in women ’ s relative survival .
First , the female immune system is @ @ @ @ @ @ @ , partly because female estrogen hormones tend to amp up the immune system , whereas male androgen hormones tend to dial it back .
( A hypervigilant system is a double-edged sword for women , who pay a price by having a greater risk of autoimmune diseases . )
“ When the female immune system sees a virus , we tend to mount a much more rapid response , and the magnitude is often greater , ” Klein says .
This advantage , which includes antibody response , has been shown with other @ @ @ @ @ @ @ mouse models of the earlier SARS coronavirus , which also killed more men than women .
Women may have evolved a stronger immune system to allow for antibodies , intercell signals called cytokines and other defense mechanisms to be passed to their babies in utero and through breast milk .
A second factor in the sex gap , Klein says , is that “ as they start to hit their 50s and 60s , men have more of the underlying conditions—heart disease , hypertension , diabetes ” —that worsen coronavirus outcomes .
Women @ @ @ @ @ @ @ , which could help explain why the discrepancy between male and female mortality in the U.S. appears largest in the 45-to-64 age range .
A third possible contributor is differences between genes on the female X and male Y sex chromosomes .
“ It turns out that there are over 60 genes associated with immune function on the X chromosome , ” Klein says .
Some are involved in the production of interferons , key modulators of the body ’ s response to viruses .
“ My group and others have shown that @ @ @ @ @ @ @ these genes than do males , ” Klein adds , “ and this can have functional significance.
” Behavior may also factor into the higher male death rate .
In many cultures , men are more likely to smoke—a habit linked to a worse prognosis .
Women , in contrast , are inclined toward more protective conduct .
They were about 50 percent more likely than men to wear a face mask , wash their hands and avoid public transit during earlier respiratory disease epidemics such as bird flu and SARS , according @ @ @ @ @ @ @ and Sara Del Valle , both at Los Alamos National Laboratory .
Such gender differences in attitude and behavior have continued in the current pandemic , according to a survey conducted in March and April by the National Bureau of Economic Research .
Responses from 21,649 people in eight developed nations indicated that women are more likely to take COVID-19 seriously and agree to comply with public safety measures .
Other genes besides those on the sex chromosomes might influence vulnerability to COVID-19 .
Andrea Ganna and Mark Daly , both at the @ @ @ @ @ @ @ Molecular Medicine Finland , have organized a global consortium called the COVID-19 Host Genetics Initiative to search for genetic variations that might put people at a higher or lower risk of becoming seriously ill. ( Most variants affect the genes in subtle ways without interfering with their main functions . )
Some of the more intriguing findings so far come from a study of 1,980 patients in Italy and Spain that was published in the New England Journal of Medicine .
The researchers identified a cluster of variants on chromosome 3 that are @ @ @ @ @ @ @ in COVID-19 patients .
A few of the genes encode key immune system molecules called cytokines .
An additional one codes for a protein that interacts with the molecular doorway that the virus uses to enter cells : a surface enzyme called angiotensin-converting enzyme 2 , or ACE2 .
More tentatively , the investigators found that genes on chromosome 9 that determine blood type could be linked to risk , putting people with type A blood in slightly greater danger of severe illness .
“ The jury is still out ” on that @ @ @ @ @ @ @ larger analysis did not confirm it .
“ But the signal on chromosome 3 is real and has been replicated robustly .
It is associated with COVID severity.
” [ How DNA changes tied to immune reactions , a viral doorway and possibly blood type could influence COVID-19 severity . ]
A second genetics initiative , led by Jean-Laurent Casanova of the Rockefeller University and Helen Su of the National Institute of Allergy and Infectious Diseases , is searching for genes that might help account for two types of pandemic outliers .
The @ @ @ @ @ @ @ , otherwise healthy individuals who develop severe COVID-19 , or , as Casanova puts it , “ the guy who runs a marathon in 2019 and then he is in the ICU , intubated.
” The second group comprises people who remain uninfected despite extreme exposure , such as the virus-negative spouse of an ill patient .
“ We will test the hypothesis that some of them carry single-gene variations that make them naturally resistant to the entry of the virus , ” Casanova says .
Such a gene , if it exists @ @ @ @ @ @ @ in 1996 called CCR5 delta 32 , which confers resistance to HIV .
The identification of genes providing immunity or raising vulnerability , even if their effects are small , could offer useful clues for developing drugs for COVID-19 , Ganna and Casanova say .
From the earliest days of the pandemic , it has been clear that patients with certain chronic diseases are especially endangered by SARS-CoV-2 .
The JAMA report on 5,700 patients who were hospitalized for COVID-19 in and around New York City found that 94 percent had at least @ @ @ @ @ @ @ more than one .
In mid-June , the U.S. Centers for Disease Control and Prevention published an analysis of 287,320 confirmed cases for which accompanying conditions were reported .
It showed that the most common ones were cardiovascular disease ( in 32 percent of patients ) , diabetes ( 30 percent ) and chronic lung disease ( 18 percent ) .
People with COVID-19 who had chronic ailments such as these were six times as likely to be hospitalized and 12 times as likely to die as those who did not have them @ @ @ @ @ @ @ of things .
First , most are associated with chronic low-grade inflammation , which compromises immune system function .
Although the precise mechanisms by which inflammation does so are unclear , there are several leading suspects .
One of them , at least in people who are significantly overweight , is the activity of fat cells , which churn out a variety of inflammatory substances such as interleukin-6 .
“ People with excess fat tissue may have a dysregulated immune response and not be able to counterbalance a severe infection , ” says @ @ @ @ @ @ @ epidemiologist at the Johns Hopkins University School of Medicine .
Diabetes , hypertension , cardiovascular disease and obesity have something else in common , Narasimhan observes : “ All have upregulation of ACE2.
” Heightened expression of the protein in these conditions may possibly give the virus more entry points throughout the body .
Doctors already know that SARS-CoV-2 breezes into a host via the respiratory tract and attacks the lungs .
But additional evidence suggests that it may move into other ACE2-rich tissues such as the heart and kidneys .
When it @ @ @ @ @ @ @ the virus itself or the body ’ s battle to contain it—can include blood clots and strokes , kidney injury , heart attacks , heart failure and arrhythmias .
Michos says that preexisting chronic conditions endanger COVID-19 patients in multiple ways .
At the most elemental level , people with these ailments have less “ cardiopulmonary reserve ” to call on when the body is fighting a massive respiratory infection .
Lack of oxygen from overwhelmed lungs forces the heart to work so hard that it can fail—especially if its capacity is already @ @ @ @ @ @ @ .
“ It ’ s like a tremendous stress test , ” Michos says .
Another route to danger are the now infamous immune-system freak-outs known as cytokine storms , which can further damage organs that are already fragile .
The Hazards of Inequality and Racism Beyond the inner layers , a wide range of external stressors also shape vulnerability to a virus such as SARS-CoV-2 .
As the pandemic has torn through the population of the U.S. , it has taken an uneven toll .
The CDC ’ s mid-June analysis looked @ @ @ @ @ @ @ ethnicity were reported .
It found that 33 percent occurred in people of Latinx origin and 22 percent in Black people , even though these groups form , respectively , just 18 percent and 13 percent of the U.S. population .
Some Native American groups , such as the Navajo , are also being hit tremendously hard .
Mortality is disproportionate as well : Overall , Black Americans are dying at more than twice the rate of white people .
In some states , their deaths occur at four or five times that @ @ @ @ @ @ @ excessive toll , but they stem from the biased attitudes and actions of American society , not from Black American biology , says epidemiologist and family physician Camara Phyllis Jones of the Morehouse School of Medicine .
“ Race doesn ’ t put you at higher risk .
Racism puts you at higher risk , ” says Jones , who is a past president of the American Public Health Association .
“ Racism puts you at higher risk through the two mechanisms of being more infected because we are more exposed and less @ @ @ @ @ @ @ , we are more likely to have a very severe course and die.
” [ Physician Camara Phyllis Jones explains the multiple ways that racial injustice and racism increase Black people ’ s vulnerability to the virus . ]
The higher risk of catching the virus comes both on the job and at home .
An analysis conducted for Bloomberg found , for example , that only 19.7 percent of Black workers were in a position to work remotely during lockdowns , as opposed to 29.9 percent of white workers .
A larger @ @ @ @ @ @ @ of color are essential but low-paid ones .
These are positions such as home health aide , grocery store worker , meatpacker , delivery worker and hospital orderly—roles that require constant contact with the public or crowded conditions with co-workers , both of which lead to high exposure to the coronavirus .
The jobs do not come with the protections , such as telecommuting , afforded to those in higher-paid positions .
For such workers , Jones says , “ the personal protective equipment has been very slow in coming.
” On top @ @ @ @ @ @ @ people of color live in high-density , lower-income neighborhoods .
“ You ’ re in a one-bedroom apartment with five people living there , and one is your grandmother , ” Jones relates .
“ You can ’ t safely isolate , so people are more exposed by family members who are frontline workers that have gone out and then bring the infection home.
” In addition , compared with white Americans , a higher proportion of minority group members are held in prisons and sleep in homeless shelters , where infections spread @ @ @ @ @ @ @ the coronavirus , they are more at risk of becoming severely ill because they shoulder a greater burden of the chronic illnesses that can make COVID-19 more deadly .
Black Americans , for example , suffer a 40 percent higher rate of hypertension and a 60 percent higher rate of diabetes than white Americans .
Native Americans , meanwhile , are twice as likely to have diabetes as white Americans .
Structural inequities—such as neighborhoods that lack high-quality food options , the absence of safe places and leisure time to exercise , and @ @ @ @ @ @ @ of illness , noted Sherita Hill Golden , an endocrinologist at Johns Hopkins Medicine , at a May seminar on racial disparities and COVID-19 .
Poorer access to medical care and discrimination within the health care system add to these burdens .
As the pandemic got worse in early spring , many people of color had a hard time getting tested for COVID-19 .
“ Testing sites were often located in more affluent neighborhoods , ” Jones says .
“ Or there was drive-through testing .
And what if you don ’ t @ @ @ @ @ @ @ out that fear of immigration authorities and concerns about the Trump administration ’ s new public charge rule—which makes it difficult for people who use Medicaid to gain legal immigration status—might be leading undocumented individuals to “ avoid using [ health ] services they might otherwise have used.
” Epidemiologists who study health inequities have found that lifelong stressors related to racial and ethnic discrimination take a direct toll on health .
Ongoing elevated levels of stress hormones , such as cortisol and catecholamines , are thought to mediate this wear and tear @ @ @ @ @ @ @ result , Black Americans tend to develop hypertension , glaucoma and some other aging-associated disorders earlier than white people do .
The phenomenon has been termed “ weathering ” by Arline Geronimus , a professor of public health at the University of Michigan .
Her research indicates that this premature aging can not be explained by poverty and posits that it is the direct result of race-based injustice and bias .
[ The stress of racism , which accompanies the growing gap between poor and rich , inflicts biological harm through several pathways @ @ @ @ @ @ @ risk factors become clearer , physicians and scientists say , health authorities need to shift resources and intensify protections for communities , groups and individuals who are most vulnerable .
That effort has begun to happen in nursing homes , for example— though only after tremendous losses of life .
Diagnostic testing for the virus is one such resource .
“ We know that there are communities at higher risk , and we need to be doing more testing there , ” Jones says .
And that means examining people without symptoms who @ @ @ @ @ @ @ knowing they are infected .
“ If we restrict ourselves to only testing people who are symptomatic , ” she warns , “ we will just be documenting the course of the pandemic , but we will lose the opportunity to change the course of the pandemic.
” On an individual level , people need to take stock of every layer of their own vulnerability , from the biological to the societal , and do what they can to mitigate hazards through pandemic-specific practices such as social distancing , mask wearing and avoiding @ @ @ @ @ @ @ to try to maintain healthy habits , such as a good diet and regular exercise , although current circumstance can make doing so difficult . )
At the same time , it is wise to remember that risk-group analyses reflect averages .
An individual might have no obvious risk factors and still wind up desperately sick or dead .
“ The only job of this virus is to replicate itself , ” Jones points out .
“ It will make its way through all the susceptibles that it can find.
” Read more @ @ @ @ @ @ @ here .
And read coverage from our international network of magazines here .

You might have a sniffle and be done. You might run a fever with a cough and unshakable fatigue for five days—or 10. Or you might end up in a hospital, gasping air into congested lungs, an immunological storm raging in your body. And you might not make it through COVID-19 alive.
What determines if someone gets desperately ill from the disease that is ripping its way across the planet? You are likely familiar with the broad categories of people who face greater risk: older individuals, men, those who have certain chronic conditions, and—notably in the U.S. and England—people of color. But researchers are looking deeper into these groups to determine the underlying roots, both biological and social, for their vulnerability. Investigators are relating age-related risk to the ways that the immune system changes over the years, for example, and examining male-female differences in immune responses. Some scientists are probing for genetic variations that might raise susceptibility. Others are highlighting the social, environmental and economic factors that elevate risk, including racism.
For a given individual, the elements of risk stack up like the layers of a Russian nesting doll. The innermost core includes genes, biological sex and age. Cellular and hormonal factors that accompany these characteristics affect vulnerability to infectious microbes, including SARS-CoV-2, the coronavirus causing the pandemic. The second layer consists of diseases and chronic conditions acquired over time, many of which make it easier for the virus to enter cells or harder for the body to fight it effectively. The outermost layer reflects the accumulated nicks and gouges of external circumstance: housing and work conditions, poor access to health care, nutritional status, and exposure to toxins and pollution. For people of color, these social and economic aspects include the cumulative stresses of systemic racism and discrimination.
These layers are not independent. With aging, for example, comes more chronic disease and, too frequently, a decline in living conditions such as housing, social support and food security. Nor are all the contributing risk factors known for an infection that emerged little more than eight months ago. Still, by applying existing science to emerging data about the features that make up these layers, researchers say, one can begin to make sense of COVID-19’s dramatic range of severity.
How Age Impacts Immunity
Age is probably the single biggest determinant of how sick someone gets from the coronavirus. In China, where the pandemic began, the average person with a confirmed infection had a 2.3 percent chance of dying. But for people between 70 and 79, it was 8 percent, and for those older than 80, it was 14.8 percent. In New York City, nearly half of confirmed deaths were among the elderly, aged 75 and older, and another quarter were among those aged 65 to 74. An analysis of 17 million people in England, published in Nature in July, concluded that patients older than 80 were at least 20 times more likely to die of the infection than those in their 50s.
“Age was our biggest predictor of outcome,” says Mangala Narasimhan, regional director of critical care at Northwell Health, the largest health care provider in the New York City area, and a co-author of a report in JAMA on the characteristics of 5,700 hospitalized COVID-19 patients. The dense concentration of elderly people in nursing homes, where infections can spread quickly and prevention is often inadequate, is clearly one reason for this correlation. But biology is another factor, particularly the aging of the immune system.
As the decades roll by, the human body becomes less effective at fighting infections. This decline is one reason why roughly 90 percent of U.S. deaths from influenza are among people aged 65 and older and why vaccines are less protective in the elderly. Basically, our defensive cells become thinned out in number and variety. And like old warriors, they become more geared toward fighting yesterday’s battles with familiar enemies than tackling something new, such as the latest flu strain or the novel coronavirus.
[A visual guide shows what scientists have learned about the workings of SARS-CoV-2 and how it causes devastating disease.]
With age, B cells, which make antibodies, and T cells, some of which directly kill infected cells and some of which alert the B cells, are no longer produced in large quantities in the bone marrow and thymus gland, respectively. Eventually, production nearly grinds to a halt. “It goes from a fire hose at eight years old to a leaky, dripping faucet when you are 80,” explains immunologist Kenneth Dorshkind, a professor of pathology and laboratory medicine at the University of California, Los Angeles. Older adults maintain populations of these essential immune cells in the lymph nodes and spleen, but “they develop defects with age, so they don’t function as well,” he says.
For example, as people age, both the stem and arms of the Y-shaped antibody molecule become less flexible. This limits the body’s ability to modify them to match an unfamiliar invader. As a result, antibodies may not lock on as effectively. T cells, meanwhile, lose a lot of the variety of receptors that allow them to respond to diverse pathogens, and they may lack the vigor to rapidly multiply in response to infection, says Jörg Goronzy, an immunologist who studies T cell aging at Stanford University. “Healthy old people have lost at least 75 percent of their T cell receptor repertoire,” he estimates. “At one point, we may lack the receptors that have an optimal fit” for the invading microbe.
Older people are also far more prone to chronic diseases that involve low-grade inflammation, which seems to further compromise the immune system. Goronzy says it is unclear whether a geriatric immune system resorts to more inflammation to protect the body or whether the inflammation comes first and impairs defenses. He suspects it is a combination of the two. Both he and Dorshkind predict that if a coronavirus vaccine becomes available, it will probably be less protective for aged people. As with the flu shot, an extra strong dose or some kind of booster may be needed.
Why Men Fare Worse
Sex also contributes to COVID-19 severity: men are roughly twice as likely to die of the infection as women, although the gender gap varies somewhat from place to place. In Italy, for example, 70 percent of those who died by this spring were men; in the U.S, the figure was 59 percent. Whether men are also more likely to acquire the infection is unclear because of biases and country-by-country discrepancies in who gets tested for the virus. But globally, “the death rate data is more robust and consistent,” says molecular biologist Sabra Klein, co-director of the Johns Hopkins Center for Women’s Health, Sex and Gender Research.
Klein sees three plausible biological factors in women’s relative survival. First, the female immune system is simply stronger at just about every level, partly because female estrogen hormones tend to amp up the immune system, whereas male androgen hormones tend to dial it back. (A hypervigilant system is a double-edged sword for women, who pay a price by having a greater risk of autoimmune diseases.)
“When the female immune system sees a virus, we tend to mount a much more rapid response, and the magnitude is often greater,” Klein says. This advantage, which includes antibody response, has been shown with other infections and reactions to vaccines and in mouse models of the earlier SARS coronavirus, which also killed more men than women. Women may have evolved a stronger immune system to allow for antibodies, intercell signals called cytokines and other defense mechanisms to be passed to their babies in utero and through breast milk.
A second factor in the sex gap, Klein says, is that “as they start to hit their 50s and 60s, men have more of the underlying conditions—heart disease, hypertension, diabetes”—that worsen coronavirus outcomes. Women tend to develop these ailments somewhat later, which could help explain why the discrepancy between male and female mortality in the U.S. appears largest in the 45-to-64 age range.
A third possible contributor is differences between genes on the female X and male Y sex chromosomes. “It turns out that there are over 60 genes associated with immune function on the X chromosome,” Klein says. Some are involved in the production of interferons, key modulators of the body’s response to viruses. “My group and others have shown that females show greater expression of some of these genes than do males,” Klein adds, “and this can have functional significance.”
Behavior may also factor into the higher male death rate. In many cultures, men are more likely to smoke—a habit linked to a worse prognosis. Women, in contrast, are inclined toward more protective conduct. They were about 50 percent more likely than men to wear a face mask, wash their hands and avoid public transit during earlier respiratory disease epidemics such as bird flu and SARS, according to a 2016 meta-analysis by Kelly Moran and Sara Del Valle, both at Los Alamos National Laboratory. Such gender differences in attitude and behavior have continued in the current pandemic, according to a survey conducted in March and April by the National Bureau of Economic Research. Responses from 21,649 people in eight developed nations indicated that women are more likely to take COVID-19 seriously and agree to comply with public safety measures.
Genetic Vulnerability
Other genes besides those on the sex chromosomes might influence vulnerability to COVID-19. Andrea Ganna and Mark Daly, both at the University of Helsinki’s Institute of Molecular Medicine Finland, have organized a global consortium called the COVID-19 Host Genetics Initiative to search for genetic variations that might put people at a higher or lower risk of becoming seriously ill. (Most variants affect the genes in subtle ways without interfering with their main functions.) Some of the more intriguing findings so far come from a study of 1,980 patients in Italy and Spain that was published in the New England Journal of Medicine. The researchers identified a cluster of variants on chromosome 3 that are associated with severe illness and respiratory failure in COVID-19 patients. A few of the genes encode key immune system molecules called cytokines. An additional one codes for a protein that interacts with the molecular doorway that the virus uses to enter cells: a surface enzyme called angiotensin-converting enzyme 2, or ACE2.
More tentatively, the investigators found that genes on chromosome 9 that determine blood type could be linked to risk, putting people with type A blood in slightly greater danger of severe illness. “The jury is still out” on that finding, Ganna says, because a larger analysis did not confirm it. “But the signal on chromosome 3 is real and has been replicated robustly. It is associated with COVID severity.”
[How DNA changes tied to immune reactions, a viral doorway and possibly blood type could influence COVID-19 severity.]
A second genetics initiative, led by Jean-Laurent Casanova of the Rockefeller University and Helen Su of the National Institute of Allergy and Infectious Diseases, is searching for genes that might help account for two types of pandemic outliers. The first group is made up of young, otherwise healthy individuals who develop severe COVID-19, or, as Casanova puts it, “the guy who runs a marathon in 2019 and then he is in the ICU, intubated.” The second group comprises people who remain uninfected despite extreme exposure, such as the virus-negative spouse of an ill patient. “We will test the hypothesis that some of them carry single-gene variations that make them naturally resistant to the entry of the virus,” Casanova says. Such a gene, if it exists, would be analogous to one discovered in 1996 called CCR5 delta 32, which confers resistance to HIV.
The identification of genes providing immunity or raising vulnerability, even if their effects are small, could offer useful clues for developing drugs for COVID-19, Ganna and Casanova say.
How Underlying Disorders Raise Risks
From the earliest days of the pandemic, it has been clear that patients with certain chronic diseases are especially endangered by SARS-CoV-2. The JAMA report on 5,700 patients who were hospitalized for COVID-19 in and around New York City found that 94 percent had at least one chronic condition and 88 percent had more than one.
In mid-June, the U.S. Centers for Disease Control and Prevention published an analysis of 287,320 confirmed cases for which accompanying conditions were reported. It showed that the most common ones were cardiovascular disease (in 32 percent of patients), diabetes (30 percent) and chronic lung disease (18 percent). People with COVID-19 who had chronic ailments such as these were six times as likely to be hospitalized and 12 times as likely to die as those who did not have them.
The high-risk conditions share a couple of things. First, most are associated with chronic low-grade inflammation, which compromises immune system function. Although the precise mechanisms by which inflammation does so are unclear, there are several leading suspects. One of them, at least in people who are significantly overweight, is the activity of fat cells, which churn out a variety of inflammatory substances such as interleukin-6. “People with excess fat tissue may have a dysregulated immune response and not be able to counterbalance a severe infection,” says Erin D. Michos, a cardiologist and epidemiologist at the Johns Hopkins University School of Medicine.
Diabetes, hypertension, cardiovascular disease and obesity have something else in common, Narasimhan observes: “All have upregulation of ACE2.” Heightened expression of the protein in these conditions may possibly give the virus more entry points throughout the body. Doctors already know that SARS-CoV-2 breezes into a host via the respiratory tract and attacks the lungs. But additional evidence suggests that it may move into other ACE2-rich tissues such as the heart and kidneys. When it hits those organs, the damage—whether from the virus itself or the body’s battle to contain it—can include blood clots and strokes, kidney injury, heart attacks, heart failure and arrhythmias.
Michos says that preexisting chronic conditions endanger COVID-19 patients in multiple ways. At the most elemental level, people with these ailments have less “cardiopulmonary reserve” to call on when the body is fighting a massive respiratory infection. Lack of oxygen from overwhelmed lungs forces the heart to work so hard that it can fail—especially if its capacity is already limited by narrowed arteries or heart disease. “It’s like a tremendous stress test,” Michos says. Another route to danger are the now infamous immune-system freak-outs known as cytokine storms, which can further damage organs that are already fragile.
The Hazards of Inequality and Racism
Beyond the inner layers, a wide range of external stressors also shape vulnerability to a virus such as SARS-CoV-2. As the pandemic has torn through the population of the U.S., it has taken an uneven toll. The CDC’s mid-June analysis looked at 599,636 U.S. cases where race and ethnicity were reported. It found that 33 percent occurred in people of Latinx origin and 22 percent in Black people, even though these groups form, respectively, just 18 percent and 13 percent of the U.S. population. Some Native American groups, such as the Navajo, are also being hit tremendously hard. Mortality is disproportionate as well: Overall, Black Americans are dying at more than twice the rate of white people. In some states, their deaths occur at four or five times that rate.
Many factors contribute to this excessive toll, but they stem from the biased attitudes and actions of American society, not from Black American biology, says epidemiologist and family physician Camara Phyllis Jones of the Morehouse School of Medicine. “Race doesn’t put you at higher risk. Racism puts you at higher risk,” says Jones, who is a past president of the American Public Health Association. “Racism puts you at higher risk through the two mechanisms of being more infected because we are more exposed and less protected, and then, once infected, we are more likely to have a very severe course and die.”
[Physician Camara Phyllis Jones explains the multiple ways that racial injustice and racism increase Black people’s vulnerability to the virus.]
The higher risk of catching the virus comes both on the job and at home. An analysis conducted for Bloomberg found, for example, that only 19.7 percent of Black workers were in a position to work remotely during lockdowns, as opposed to 29.9 percent of white workers. A larger proportion of the jobs held by people of color are essential but low-paid ones. These are positions such as home health aide, grocery store worker, meatpacker, delivery worker and hospital orderly—roles that require constant contact with the public or crowded conditions with co-workers, both of which lead to high exposure to the coronavirus. The jobs do not come with the protections, such as telecommuting, afforded to those in higher-paid positions. For such workers, Jones says, “the personal protective equipment has been very slow in coming.”
On top of that, she says, many people of color live in high-density, lower-income neighborhoods. “You’re in a one-bedroom apartment with five people living there, and one is your grandmother,” Jones relates. “You can’t safely isolate, so people are more exposed by family members who are frontline workers that have gone out and then bring the infection home.” In addition, compared with white Americans, a higher proportion of minority group members are held in prisons and sleep in homeless shelters, where infections spread quickly.
When people of color get the coronavirus, they are more at risk of becoming severely ill because they shoulder a greater burden of the chronic illnesses that can make COVID-19 more deadly. Black Americans, for example, suffer a 40 percent higher rate of hypertension and a 60 percent higher rate of diabetes than white Americans. Native Americans, meanwhile, are twice as likely to have diabetes as white Americans. Structural inequities—such as neighborhoods that lack high-quality food options, the absence of safe places and leisure time to exercise, and poor air quality—contribute to these elevated levels of illness, noted Sherita Hill Golden, an endocrinologist at Johns Hopkins Medicine, at a May seminar on racial disparities and COVID-19.
Poorer access to medical care and discrimination within the health care system add to these burdens. As the pandemic got worse in early spring, many people of color had a hard time getting tested for COVID-19. “Testing sites were often located in more affluent neighborhoods,” Jones says. “Or there was drive-through testing. And what if you don’t have a car?”
Golden points out that fear of immigration authorities and concerns about the Trump administration’s new public charge rule—which makes it difficult for people who use Medicaid to gain legal immigration status—might be leading undocumented individuals to “avoid using [health] services they might otherwise have used.”
Epidemiologists who study health inequities have found that lifelong stressors related to racial and ethnic discrimination take a direct toll on health. Ongoing elevated levels of stress hormones, such as cortisol and catecholamines, are thought to mediate this wear and tear and aggravate tissue damage. As a result, Black Americans tend to develop hypertension, glaucoma and some other aging-associated disorders earlier than white people do. The phenomenon has been termed “weathering” by Arline Geronimus, a professor of public health at the University of Michigan. Her research indicates that this premature aging cannot be explained by poverty and posits that it is the direct result of race-based injustice and bias.
[The stress of racism, which accompanies the growing gap between poor and rich, inflicts biological harm through several pathways.]
As these and other COVID-19 risk factors become clearer, physicians and scientists say, health authorities need to shift resources and intensify protections for communities, groups and individuals who are most vulnerable. That effort has begun to happen in nursing homes, for example— though only after tremendous losses of life. Diagnostic testing for the virus is one such resource. “We know that there are communities at higher risk, and we need to be doing more testing there,” Jones says. And that means examining people without symptoms who are able to spread the virus without knowing they are infected. “If we restrict ourselves to only testing people who are symptomatic,” she warns, “we will just be documenting the course of the pandemic, but we will lose the opportunity to change the course of the pandemic.”
On an individual level, people need to take stock of every layer of their own vulnerability, from the biological to the societal, and do what they can to mitigate hazards through pandemic-specific practices such as social distancing, mask wearing and avoiding crowds. (It is also important to try to maintain healthy habits, such as a good diet and regular exercise, although current circumstance can make doing so difficult.) At the same time, it is wise to remember that risk-group analyses reflect averages. An individual might have no obvious risk factors and still wind up desperately sick or dead. “The only job of this virus is to replicate itself,” Jones points out. “It will make its way through all the susceptibles that it can find.”
Read more about the coronavirus outbreak from Scientific American here. And read coverage from our international network of magazines here.


scientificamerican--2020-08-20--Mounting Climate Impacts Threaten U.S. Nuclear Reactors

Soaring temperatures , intensified flood risks and heightened water stress will threaten 57 U.S. nuclear plants over the next 20 years , forcing operators to take additional resiliency measures , according to a new report .
“ The consequences of climate change can affect every aspect of nuclear plant operations—from fuel handling and power and steam generation to maintenance , safety systems and waste processing , ” said the analysis , which was published yesterday by Moody ’ s Investors Service .
Analysts used data from Four Twenty Seven , a Moody ’ s affiliate that provides climate risk intelligence @ @ @ @ @ @ @ plants .
“ It looks like almost all plants see some kind of climate risk worsening over the next 20 years , ” said David Kamran , the report ’ s author .
The study also underscored that the nuclear sector ’ s vulnerability to regional climate risks in large part depends on plants ’ proximity to water .
Because nuclear generation facilities rely on external water sources for cooling , the vast majority are situated near rivers , lakes and oceans .
That exposes them to flooding and storm surges , which @ @ @ @ @ @ @ Twenty Seven data show 37 gigawatts of U.S. nuclear capacity is overly exposed to flood risk .
That includes plants along the East and Gulf coasts , which are likely to grapple with rising sea levels and intensifying hurricanes in the decades to come .
Storm-related rainfall , the reports adds , could “ inundate ” nuclear facilities and “ damage transmission lines or substations , hindering a plant ’ s ability to deliver power.
” Facilities in the Midwest and South Florida , meanwhile , are more likely to suffer from higher @ @ @ @ @ @ @ plants ’ ability to generate power .
The generation process involves creating steam , which is then cooled and condensed into liquid for reuse .
“ If the temperature of incoming water to cool and condense steam is too high , or if the temperature of the discharge water is too high , power plants can be forced to curtail production or shut down temporarily , ” the report says .
Facilities in the Rocky Mountain region , near the Colorado River and in California , on the other hand , are projected @ @ @ @ @ @ @ about having long-term access to necessary water supplies .
Kamran emphasized that despite these risks , the majority of nuclear plants are “ some of the most hardened industrial assets in the U.S. ” That ’ s in large part , he said , because they ’ ve already made major investments in resiliency measures to ensure nuclear safety and protection in the case of environmental impacts .
Even still , he noted , some of the plants are 30 , 40 and 50 years old and may soon be approved by the @ @ @ @ @ @ @ licenses decades longer .
“ Don ’ t get me wrong , they have obviously updated their [ climate ] assumptions over the last two decades several times .
They ’ re not living in the world of the 1950s , ” he added .
“ With that being said , the point is that these plants are aging , and they ’ re going to need improvements in certain cases.
” Reprinted from Climatewire with permission from E & E News .
E & E provides daily coverage of essential energy and @ @ @ @ @

Soaring temperatures, intensified flood risks and heightened water stress will threaten 57 U.S. nuclear plants over the next 20 years, forcing operators to take additional resiliency measures, according to a new report.
“The consequences of climate change can affect every aspect of nuclear plant operations—from fuel handling and power and steam generation to maintenance, safety systems and waste processing,” said the analysis, which was published yesterday by Moody’s Investors Service.
Analysts used data from Four Twenty Seven, a Moody’s affiliate that provides climate risk intelligence, to examine threats to operating nuclear plants.
“It looks like almost all plants see some kind of climate risk worsening over the next 20 years,” said David Kamran, the report’s author.
The study also underscored that the nuclear sector’s vulnerability to regional climate risks in large part depends on plants’ proximity to water.
Because nuclear generation facilities rely on external water sources for cooling, the vast majority are situated near rivers, lakes and oceans. That exposes them to flooding and storm surges, which can damage critical equipment.
The Four Twenty Seven data show 37 gigawatts of U.S. nuclear capacity is overly exposed to flood risk.
That includes plants along the East and Gulf coasts, which are likely to grapple with rising sea levels and intensifying hurricanes in the decades to come. Storm-related rainfall, the reports adds, could “inundate” nuclear facilities and “damage transmission lines or substations, hindering a plant’s ability to deliver power.”
Facilities in the Midwest and South Florida, meanwhile, are more likely to suffer from higher temperatures that have the potential to reduce plants’ ability to generate power. The generation process involves creating steam, which is then cooled and condensed into liquid for reuse.
“If the temperature of incoming water to cool and condense steam is too high, or if the temperature of the discharge water is too high, power plants can be forced to curtail production or shut down temporarily,” the report says.
Facilities in the Rocky Mountain region, near the Colorado River and in California, on the other hand, are projected to face water scarcity, spiking uncertainty about having long-term access to necessary water supplies.
Kamran emphasized that despite these risks, the majority of nuclear plants are “some of the most hardened industrial assets in the U.S.”
That’s in large part, he said, because they’ve already made major investments in resiliency measures to ensure nuclear safety and protection in the case of environmental impacts.
Even still, he noted, some of the plants are 30, 40 and 50 years old and may soon be approved by the Nuclear Regulatory Commission to extend their operating licenses decades longer.
“Don’t get me wrong, they have obviously updated their [climate] assumptions over the last two decades several times. They’re not living in the world of the 1950s,” he added. “With that being said, the point is that these plants are aging, and they’re going to need improvements in certain cases.”
Reprinted from Climatewire with permission from E&E News. E&E provides daily coverage of essential energy and environmental news at www.eenews.net.


scientificamerican--2020-08-20--California Looks to Battle Mega Wildfires with Fire

Kyburz , Calif.—Near the top of a 7,000-foot ridge in California ’ s Sierra Nevada , crews wielding gasoline-dripping torches began igniting piles of small logs and branches on an unusually cold morning late last September .
Ignoring snow flurries and light rain , they trudged from one pile to another , nursing the flames that licked into pine needles and twigs on the surrounding ground and monitoring small trees that flared up like bonfires .
The fire starters worked their way down the mountain north of Caples Creek over the next week , their blazes efficiently controlled with the @ @ @ @ @ @ @ been cleared of forest debris .
They supervised flames racing across meadows that , remarkably , had not burned since at least 1916 .
Crews paid particular attention to the largest Jeffrey and ponderosa pines , some of them 300 years old .
These trees had been protected in advance by volunteers , who had removed shrubs and raked fuels away from trunks that were more than 30 inches in diameter .
By the time the flames were out , the Caples Ecological Restoration Project had burned 3,435 acres in the mountainous watershed @ @ @ @ @ @ @ east of Sacramento—part of an area that provides the primary water supply for more than 110,000 people .
It was the largest intentional fire ever set in the Sierra Nevada and one of the largest on federal land in the state .
The effort marks a milestone in California ’ s pivot away from a century of suppressing fire at all costs and toward working with it instead—using controlled flames to restore ecosystems that evolved to burn in frequent , mostly low-intensity blazes .
Suppression has left forests throughout the West unnaturally crowded @ @ @ @ @ @ @ larger , far more damaging conflagrations .
California ’ s forests are even more vulnerable because more than 147 million drought-weakened trees have died statewide since 2010 , leaving them primed to burn .
Because of these and other factors , such as poor management practices and warmer temperatures from climate change , the extent of fires that escape even the most aggressive suppression has increased fivefold over the past five decades .
Scientists say tangled masses of ultradry fuel represent a fire hazard of unprecedented size and intensity if left alone .
@ @ @ @ @ @ @ Fire in the mountains north of Los Angeles and the L.N.U .
Lightning Complex west of Sacramento , have already burned 30 percent more than the acreage flames blackened across California last year , stretching firefighting crews thin and prompting Governor Gavin Newsom to declare a state of emergency .
U.S. Forest Service officials had been planning the Caples prescribed burn for five years—nervously hoping the forest would not go up in flames sparked by lightning or a careless camper before they could implement their meticulously designed , scientific burn strategy .
“ @ @ @ @ @ @ @ into the landscape : restoring that vital natural ecosystem process , which will ultimately slow the spread of wildfire , ” says Jeff Marsolais , Eldorado ’ s forest supervisor .
In 2011 Eldorado forest officials identified the steep , granite-strewn slopes of the Caples Creek area as a priority for restoration efforts that would gradually reintroduce fire and restore the meadows dotting the pine and fir forests .
Funded by a $ 477,000 Sierra Nevada Conservancy grant , the plan scientists developed involves 8,800 acres of prescribed burning over 15 years to @ @ @ @ @ @ @ vegetation .
Along with preventing huge and uncontrollable wildfires , they aim to reestablish forests healthy enough to allow small fires to burn unimpeded .
The path of the Caples prescribed burn was designed to promote a mixture of species in a mosaic , with large openings between tree stands where fire could occasionally burn undergrowth without damaging large trees .
“ We wanted to reintroduce fire where it would bring the greatest benefits and inflict the least harm , ” says Forest Service ecologist Becky Estes , who designed the monitoring plots @ @ @ @ @ @ @ in the project went as envisioned .
Unexpected high winds roared through the area 10 days into the carefully calculated plan , blowing the intentional fire out of the 1,080-acre designated zone and into forests that had not been prepared for burning .
Eldorado forest officials brought in suppression crews , halting the escaped fire after it burned through 2,355 acres .
Such glitches are part of the learning process as forest managers try bringing fire back to the Sierra Nevada after 100 years of fighting it off , says Tony Scardina , @ @ @ @ @ @ @ .
“ We understand that when we ’ re managing fire , whether it ’ s a wildland or a planned fire , there ’ s always risk , ” he says .
But Scardina is undaunted .
“ We remain committed to bringing those ecosystems back to a resilient state in a planned , careful and controlled manner , ” he says .
“ And we are committed to applying what we learned from this situation to continuously improve our prescribed fire program.
” Scardina and others had to wait for winter @ @ @ @ @ @ @ to come up with COVID-19 pandemic protocols that made it safe for a group of scientists to inspect the burned area to see what was growing come spring .
Nine months after the fire , the trail along Caples Creek climbs through gray granite boulders and purple lupines blooming among charred logs .
Blackened tree trunks rise out of thick grass carpets , and the sun filters through a canopy of conifer needles , half of them green , half of them scorched rust-red .
Helen Payne , a botanist in Estes ’ @ @ @ @ @ @ @ her hands and knees just off the trail on a hot July morning , examining a spindly cedar tree with black burn streaks on its trunk .
Behind her , fire-felled pines the size of utility poles are toppled against trees that are still standing but weakened by fire , likely to fall in the next big storm .
The ground is littered with dry needles sprinkled across the ashes of last year ’ s burn .
Payne is taking inventory of every detail within an area about the size of a home @ @ @ @ @ @ @ , flowering plants and fungi , as well as the size and number of trees and whether they are healthy , scorched or fire-killed .
This plot is one of 105 that Estes established before the burn to monitor its effects on as much of the vegetation as possible—every five years for the foreseeable future .
Payne points to a tiny seedling , its trunk no thicker than darning thread but somehow supporting the fragile fronds of new life .
“ We found two , ” she says , clearly excited by the @ @ @ @ @ @ @ 46 monitoring plots in a November assessment have provided information about the immediate effects of the fire .
Despite intense burning in some places and an extra 2,355 acres catching fire , the experiment generally produced healthier forests , says Scott Dailey , one of the Forest Service ecologists who conducted the assessment .
Before the burn , eight-inch-diameter saplings were nearly triple the density scientists believe a resilient forest should harbor .
These small trees ignite easily , providing a ladder for fire to climb into the tops of large ones .
@ @ @ @ @ @ @ away actually cut their number to a more sustainable density—and the intentional fire did not reduce them as much as officials would have liked , Dailey says .
The prescribed burn did not kill any trees greater than 30 inches in diameter , but these centuries-old survivors did not fare so well in the escaped wildfire .
Among the plots he surveyed in that area , Dailey found nearly 25 percent fewer large trees after the fire .
The prescribed burn effectively reduced the ground litter under trees , where wildfires generally start @ @ @ @ @ @ @ from around two inches to less than half an inch .
The wildfire was even more effective : nearly two and a half inches of duff were reduced to around one third of an inch .
Overall , the combined Caples planned burn and inadvertent wildfire produced forests much closer to natural conditions , Dailey says .
Still , there was some damage : The bulldozers brought in to control the escaped flames left scars on the forest floor .
And trees were haphazardly strewn about some areas , because firefighters had to @ @ @ @ @ @ @ One of the lessons Caples taught managers is the crucial role of meteorology , Marsolais says .
No one predicted the winds that blew the fire beyond the planned area .
“ Our forecasting has only so much capability .
We ’ re focusing now on how good predictions can be , ” he says .
The burn also made clear that many forests in the Sierra Nevada are simply too crowded for fire to return without the extraordinary effort that went into preparing the Caples area .
“ You can ’ t @ @ @ @ @ @ @ , ” Marsolais says .
The Caples prescribed burn is an important first step—but a small one—in a long march toward restoring forest resilience , says Malcolm North , a U.S. Forest Service scientist at the Pacific Southwest Research Station .
He studies Sierra Nevada forests but was not involved in the Caples burn .
To return forests to their original state ( in which they survive and benefit from natural fire ) , he says crews would have to burn 500,000 acres a year on the five million acres the Forest Service @ @ @ @ @ @ @ agency ’ s “ fuels reduction ” goal for this year is 230,000 acres , including just 60,000 acres of prescribed burning .
For the rest , chain saws and other mechanical equipment will be used to thin trees .
“ Whatever we can do to change the pace and scale of prescribed burning , that ’ s the 99.9 percent priority , ” North says .
Forest resilience has implications for most of California ’ s residents .
The effects of unhealthy forests have proliferated , particularly following the devastating wildfires of @ @ @ @ @ @ @ and tripled for those lucky enough to get policies at all .
Too many people have experienced the terror of wildfires bearing down on them , forcing last-minute evacuations and taking dozens of lives .
Most pervasive , however , are the effects of the smoke that smothers cities , small towns and rural areas alike , increasing the risk of asthma and other respiratory problems .
Public acceptance of smoke is one of the greatest challenges facing the drive to return natural fire to the Sierra Nevada ’ s forests .
Prescribed @ @ @ @ @ @ @ wildfires carries far more toxic ingredients from burned homes and vehicles , Marsolais says .
Craig Thomas , former executive director of Sierra Forest Legacy , a nonprofit conservation group , calls smoke a trade-off .
He has engaged air resource officials through a multiparty collaboration to improve coordination between the management of fire and public health .
Because California ’ s Sierra Nevada forests have a natural propensity to ignite , whether as wildfires or controlled burns , Thomas says , “ we either work with fire , or it eats our @ @ @ @ @ @ @ to study the effects of the Caples burn as they prepare for the next prescribed fire , likely in an adjacent area in 2021 .
Restoring forest health and ecosystem values at a meaningful scale is a long-term process , Marsolais says .
“ We can not let up , ” he adds .
“ Uncontrolled wildfire is knocking on the doors of these communities .
”

Kyburz, Calif.—Near the top of a 7,000-foot ridge in California’s Sierra Nevada, crews wielding gasoline-dripping torches began igniting piles of small logs and branches on an unusually cold morning late last September. Ignoring snow flurries and light rain, they trudged from one pile to another, nursing the flames that licked into pine needles and twigs on the surrounding ground and monitoring small trees that flared up like bonfires.
The fire starters worked their way down the mountain north of Caples Creek over the next week, their blazes efficiently controlled with the help of “lanes” that had been cleared of forest debris. They supervised flames racing across meadows that, remarkably, had not burned since at least 1916. Crews paid particular attention to the largest Jeffrey and ponderosa pines, some of them 300 years old. These trees had been protected in advance by volunteers, who had removed shrubs and raked fuels away from trunks that were more than 30 inches in diameter. By the time the flames were out, the Caples Ecological Restoration Project had burned 3,435 acres in the mountainous watershed of Eldorado National Forest, 70 miles east of Sacramento—part of an area that provides the primary water supply for more than 110,000 people. It was the largest intentional fire ever set in the Sierra Nevada and one of the largest on federal land in the state.
The effort marks a milestone in California’s pivot away from a century of suppressing fire at all costs and toward working with it instead—using controlled flames to restore ecosystems that evolved to burn in frequent, mostly low-intensity blazes. Suppression has left forests throughout the West unnaturally crowded with small trees and shrubs—ready tinder for larger, far more damaging conflagrations. California’s forests are even more vulnerable because more than 147 million drought-weakened trees have died statewide since 2010, leaving them primed to burn. Because of these and other factors, such as poor management practices and warmer temperatures from climate change, the extent of fires that escape even the most aggressive suppression has increased fivefold over the past five decades. Scientists say tangled masses of ultradry fuel represent a fire hazard of unprecedented size and intensity if left alone. Blazes this year, including the Lake Fire in the mountains north of Los Angeles and the L.N.U. Lightning Complex west of Sacramento, have already burned 30 percent more than the acreage flames blackened across California last year, stretching firefighting crews thin and prompting Governor Gavin Newsom to declare a state of emergency.
U.S. Forest Service officials had been planning the Caples prescribed burn for five years—nervously hoping the forest would not go up in flames sparked by lightning or a careless camper before they could implement their meticulously designed, scientific burn strategy. “This is all about reintroducing fire back into the landscape: restoring that vital natural ecosystem process, which will ultimately slow the spread of wildfire,” says Jeff Marsolais, Eldorado’s forest supervisor.
Nine months after this meadow burned, purple lupines line the edges and sheer-white bistort fill the open expanse between burned trees. Credit: Jane Braxton Little
Planned and Unplanned
In 2011 Eldorado forest officials identified the steep, granite-strewn slopes of the Caples Creek area as a priority for restoration efforts that would gradually reintroduce fire and restore the meadows dotting the pine and fir forests. Funded by a $477,000 Sierra Nevada Conservancy grant, the plan scientists developed involves 8,800 acres of prescribed burning over 15 years to reduce the heavy load of flammable low-lying vegetation. Along with preventing huge and uncontrollable wildfires, they aim to reestablish forests healthy enough to allow small fires to burn unimpeded. The path of the Caples prescribed burn was designed to promote a mixture of species in a mosaic, with large openings between tree stands where fire could occasionally burn undergrowth without damaging large trees. “We wanted to reintroduce fire where it would bring the greatest benefits and inflict the least harm,” says Forest Service ecologist Becky Estes, who designed the monitoring plots in the Caples burn.
Not everything in the project went as envisioned. Unexpected high winds roared through the area 10 days into the carefully calculated plan, blowing the intentional fire out of the 1,080-acre designated zone and into forests that had not been prepared for burning. Eldorado forest officials brought in suppression crews, halting the escaped fire after it burned through 2,355 acres.
Such glitches are part of the learning process as forest managers try bringing fire back to the Sierra Nevada after 100 years of fighting it off, says Tony Scardina, deputy forester of national forests in California. “We understand that when we’re managing fire, whether it’s a wildland or a planned fire, there’s always risk,” he says. But Scardina is undaunted. “We remain committed to bringing those ecosystems back to a resilient state in a planned, careful and controlled manner,” he says. “And we are committed to applying what we learned from this situation to continuously improve our prescribed fire program.”
Checking In
Scardina and others had to wait for winter snows to melt—and for Forest Service officials to come up with COVID-19 pandemic protocols that made it safe for a group of scientists to inspect the burned area to see what was growing come spring. Nine months after the fire, the trail along Caples Creek climbs through gray granite boulders and purple lupines blooming among charred logs. Blackened tree trunks rise out of thick grass carpets, and the sun filters through a canopy of conifer needles, half of them green, half of them scorched rust-red. Helen Payne, a botanist in Estes’s ecological field-monitoring crew, is on her hands and knees just off the trail on a hot July morning, examining a spindly cedar tree with black burn streaks on its trunk. Behind her, fire-felled pines the size of utility poles are toppled against trees that are still standing but weakened by fire, likely to fall in the next big storm. The ground is littered with dry needles sprinkled across the ashes of last year’s burn.
Payne is taking inventory of every detail within an area about the size of a home swimming pool: the presence of seedlings, flowering plants and fungi, as well as the size and number of trees and whether they are healthy, scorched or fire-killed. This plot is one of 105 that Estes established before the burn to monitor its effects on as much of the vegetation as possible—every five years for the foreseeable future. Payne points to a tiny seedling, its trunk no thicker than darning thread but somehow supporting the fragile fronds of new life. “We found two,” she says, clearly excited by the speed of rejuvenation.
Data collected at 46 monitoring plots in a November assessment have provided information about the immediate effects of the fire. Despite intense burning in some places and an extra 2,355 acres catching fire, the experiment generally produced healthier forests, says Scott Dailey, one of the Forest Service ecologists who conducted the assessment. Before the burn, eight-inch-diameter saplings were nearly triple the density scientists believe a resilient forest should harbor. These small trees ignite easily, providing a ladder for fire to climb into the tops of large ones. The part of the blaze that got away actually cut their number to a more sustainable density—and the intentional fire did not reduce them as much as officials would have liked, Dailey says. The prescribed burn did not kill any trees greater than 30 inches in diameter, but these centuries-old survivors did not fare so well in the escaped wildfire. Among the plots he surveyed in that area, Dailey found nearly 25 percent fewer large trees after the fire.
The prescribed burn effectively reduced the ground litter under trees, where wildfires generally start, knocking the average litter depth down from around two inches to less than half an inch. The wildfire was even more effective: nearly two and a half inches of duff were reduced to around one third of an inch. Overall, the combined Caples planned burn and inadvertent wildfire produced forests much closer to natural conditions, Dailey says. Still, there was some damage: The bulldozers brought in to control the escaped flames left scars on the forest floor. And trees were haphazardly strewn about some areas, because firefighters had to fell them to suppress the blaze.
One of the lessons Caples taught managers is the crucial role of meteorology, Marsolais says. No one predicted the winds that blew the fire beyond the planned area. “Our forecasting has only so much capability. We’re focusing now on how good predictions can be,” he says. The burn also made clear that many forests in the Sierra Nevada are simply too crowded for fire to return without the extraordinary effort that went into preparing the Caples area. “You can’t just put fire back on the landscape,” Marsolais says.
Fire, absent in this pine stand for over a century, rejuvenates the grasses and other plants, which thrive on the surge of nutrients it provides. Pine needles were scorched rust-red by the prescribed burn. Credit: Jane Braxton Little
Small but Important Step
The Caples prescribed burn is an important first step—but a small one—in a long march toward restoring forest resilience, says Malcolm North, a U.S. Forest Service scientist at the Pacific Southwest Research Station. He studies Sierra Nevada forests but was not involved in the Caples burn. To return forests to their original state (in which they survive and benefit from natural fire), he says crews would have to burn 500,000 acres a year on the five million acres the Forest Service manages in the Sierra Nevada. The agency’s “fuels reduction” goal for this year is 230,000 acres, including just 60,000 acres of prescribed burning. For the rest, chain saws and other mechanical equipment will be used to thin trees. “Whatever we can do to change the pace and scale of prescribed burning, that’s the 99.9 percent priority,” North says.
Forest resilience has implications for most of California’s residents. The effects of unhealthy forests have proliferated, particularly following the devastating wildfires of 2018. Homeowners’ insurance rates doubled and tripled for those lucky enough to get policies at all. Too many people have experienced the terror of wildfires bearing down on them, forcing last-minute evacuations and taking dozens of lives. Most pervasive, however, are the effects of the smoke that smothers cities, small towns and rural areas alike, increasing the risk of asthma and other respiratory problems.
Public acceptance of smoke is one of the greatest challenges facing the drive to return natural fire to the Sierra Nevada’s forests. Prescribed burns do emit smoke—but the smoke from wildfires carries far more toxic ingredients from burned homes and vehicles, Marsolais says. Craig Thomas, former executive director of Sierra Forest Legacy, a nonprofit conservation group, calls smoke a trade-off. He has engaged air resource officials through a multiparty collaboration to improve coordination between the management of fire and public health. Because California’s Sierra Nevada forests have a natural propensity to ignite, whether as wildfires or controlled burns, Thomas says, “we either work with fire, or it eats our lunch.”
Eldorado forest officials will continue to study the effects of the Caples burn as they prepare for the next prescribed fire, likely in an adjacent area in 2021. Restoring forest health and ecosystem values at a meaningful scale is a long-term process, Marsolais says. “We cannot let up,” he adds. “Uncontrolled wildfire is knocking on the doors of these communities.”


scientificamerican--2020-08-20--COVID-19 Spit Tests Used by NBA Are Now Authorized by FDA

A shortage in U.S. testing capacity has been a major bottleneck in containment efforts throughout the COVID-19 pandemic .
At first , the Centers for Disease Control and Prevention developed its own test kits and distributed them nationwide .
But problems with their chemical reagents and overly strict testing criteria caused major setbacks .
The Food and Drug Administration later gave companies the green light to make their own assays , and testing capacity increased significantly .
But the numbers of tests has declined worryingly in recent weeks , possibly because fewer people are seeking them as a result of @ @ @ @ @ @ @ Yale University researchers have developed a saliva-based assay that is easier to administer and analyze than the standard nasal swabs and can be manufactured using a range of chemical suppliers .
The FDA granted the COVID-19 diagnostic test , called SalivaDirect , an emergency use authorization last week .
Unlike the typical test for the disease—which infamously involves inserting a long swab up the nose to what has been described as a “ brain-tickling ” depth—SalivaDirect only requires a subject to spit into any sterile container .
It also skips the lengthy extraction @ @ @ @ @ @ @ ’ s genetic material , or RNA , before amplifying it to a detectable amount using a technique called polymerase chain reaction ( PCR ) .
And while it is not the first saliva test the FDA has authorized , SalivaDirect has been shown to work with chemical reagents from a variety of companies , so it reduces the risk of the supply-chain issues that have plagued other methods .
The assay can run 92 samples in about three hours , although the turnaround time depends on the lab conducting the test .
@ @ @ @ @ @ @ , so labs could charge about $ 10 .
SalivaDirect was evaluated in a seemingly unlikely population—the National Basketball Association—which hopes to use it to detect players who have the virus but show no symptoms .
Scientific American spoke with Chantal Vogels , a medical entomologist at the Yale School of Public Health , who helped develop the saliva test , about how accurate it is , how it compares with nasal swab assays and how easily it could be scaled up for use by other laboratories .
[ An edited transcript of @ @ @ @ @ @ @ the saliva test differ from a standard nasal swab assay for COVID-19 ?
Our SalivaDirect method has three main differences : the first one is we use saliva instead of a nasopharyngeal , [ or nasal ] , swab .
And that is mainly because the nasopharyngeal swab is very uncomfortable , and you need a very skilled person to take a swab .
If you do n't get deep enough and get enough virus , then you might not detect it .
When you take the swab , there ’ s a @ @ @ @ @ @ @ , which puts the person who takes the swab at risk .
That ’ s why we figured if we can use saliva—which you can essentially just gently expel into a couple of tubes—that ’ s more comfortable , and it ’ s safer to collect .
And we found that it actually works really well for detection of SARS-CoV-2 .
The second major difference is that many of the other methods that are out there use an RNA extraction step in the sample processing .
That is a step where you try @ @ @ @ @ @ @ virus : you break down the virus particles and everything that ’ s in the sample , you purify that , and that then goes into your final testing step ( for instance , PCR ) .
What we found is that you can actually skip , or at least simplify , that [ extraction ] step .
Instead of needing this whole extraction with special equipment , if we simply treat the saliva with an enzyme called proteinase K and heat it , we can successfully break open the virus .
We @ @ @ @ @ @ @ but still , it ’ s very good for virus detection .
It ’ s important to note that our method still uses PCR , and that means you do need to perform the test in a CLIA [ Clinical Laboratory Improvement Amendments ] –certified lab—a clinical lab that is equipped to run these tests .
So it ’ s not a test that you can run at home .
It ’ s not a point-of-care test .
The third thing—and I think it ’ s kind of the most unique part about @ @ @ @ @ @ @ flexible .
Normally , most of the methods that are out there are based on a [ specific test ] kit .
But if this kit is running into supply-chain issues , then that ’ s really going to negatively affect that testing .
So we validated saliva directly with reagents and instruments from different vendors .
Therefore , if one vendor is running into supply-chain issues , at least there are still other options out there that you can use .
And this flexibility really minimizes the risk for supply-chain bottlenecks .
@ @ @ @ @ @ @ part of our FDA application for emergency use authorization , we had a couple of components that we had to perform in the lab .
One is a “ limit of detection ” experiment , [ which determines ] the lowest concentration of virus that you can detect in a sample .
What we found is that we can detect six to 12 copies of virus in a sample , which is pretty sensitive .
The other component was a clinical evaluation .
In that part , we had a selection of paired @ @ @ @ @ @ @ individuals , and we tested the swabs with an already authorized assay .
Then , in parallel , we tested saliva with SalivaDirect just to show that both [ were in ] agreement in testing results .
What we found there is that if you compare those nasopharyngeal swabs with saliva , there ’ s a 94 percent positive agreement .
It ’ s important to note , though , that we had a couple of nasopharyngeal swabs that were testing positive with SalivaDirect but that were negative for the nasopharyngeal swabs .
@ @ @ @ @ @ @ point that if you compare these two different sample types , there ’ s always some variation .
If saliva works , why do we use nasal swabs at all ?
Before the pandemic , the nasopharyngeal swab was used for detection of many other pathogens .
So it has always been the gold standard .
Early on in the pandemic , you had to rely on information that was previously known .
And because the swab is used a lot on these respiratory pathogens , that ’ s the sort of the @ @ @ @ @ @ @ Along the way , we just started developing this more and looking into alternatives .
Now it seems like saliva is indeed a good alternative .
It doesn ’ t rule out the swab totally , but at least for certain contacts and certain scenarios , [ saliva samples ] may prove to be better .
Do you see SalivaDirect as replacing existing COVID-19 tests or complementing them ?
I think it ’ s never like “ One test is going to solve the whole problem.
” I mean , we 're dealing @ @ @ @ @ @ @ we just need options .
There are many [ other ] saliva tests out there , and that ’ s really what we need .
It ’ s not that our test is going to be , like , the answer .
I think we have to be realistic .
We still need that PCR test that needs to be performed in a highly complex laboratory .
And for certain settings in certain contexts , it might be better to have an in-home test .
But if you need to do lots of @ @ @ @ @ @ @ might be better .
So I think we just need a lot of different tests out there that can be used to tailor what is best in a certain context .
Also , for instance , in low-resource settings , if you don ’ t have a constant supply of electricity or if you do n't have access to one of those PCR machines , then you do need an alternative .
I think having multiple options for testing out there is great .
How did the NBA come to work with your @ @ @ @ @ @ @ was not involved in how that all got set up .
That was my principal investigator , who the NBA reached out to .
But essentially , to [ authorize the test for ] asymptomatic individuals , you would need a population of asymptomatic individuals who are still being tested regularly .
Then the type of study that you need to do is , again , to compare results from the nasopharyngeal swab [ with those from ] saliva .
It ’ s quite hard to set up a study with an asymptomatic @ @ @ @ @ @ @ tested with both the swab and saliva .
The NBA has been great because the players and the staff were going to be tested regularly with the swab : by also taking the saliva sample , we could just really nicely use them as our testing population to set up the study , to actually collect the data .
What are the next steps in scaling up this type of testing ?
Even though now SalivaDirect has received emergency use authorization , so far it ’ s just for suspected COVID-19 cases .
@ @ @ @ @ @ @ with the NBA to also get asymptomatic individuals authorized .
We ’ re also looking into pooling : Can you pool multiple saliva [ samples ] together and still be able to detect the virus so that you can find ways to scale up testing ?
We ’ re looking into ways of automation , because now it ’ s all manual processing of the sample .
But if you could use robots , that can be a way to really scale up the testing .
We ’ re trying to team up @ @ @ @ @ @ @ well to really help people push out their tests , because it ’ s not like our test is going to be the answer to everything .
I think it ’ s a very good first step , but there ’ s still a lot more to do .
Read more about the coronavirus outbreak from Scientific American here .
And read coverage from our international network of magazines here .

A shortage in U.S. testing capacity has been a major bottleneck in containment efforts throughout the COVID-19 pandemic. At first, the Centers for Disease Control and Prevention developed its own test kits and distributed them nationwide. But problems with their chemical reagents and overly strict testing criteria caused major setbacks. The Food and Drug Administration later gave companies the green light to make their own assays, and testing capacity increased significantly. But the numbers of tests has declined worryingly in recent weeks, possibly because fewer people are seeking them as a result of long lines and wait times.
Now Yale University researchers have developed a saliva-based assay that is easier to administer and analyze than the standard nasal swabs and can be manufactured using a range of chemical suppliers. The FDA granted the COVID-19 diagnostic test, called SalivaDirect, an emergency use authorization last week.
Unlike the typical test for the disease—which infamously involves inserting a long swab up the nose to what has been described as a “brain-tickling” depth—SalivaDirect only requires a subject to spit into any sterile container. It also skips the lengthy extraction step used to isolate the novel coronavirus’s genetic material, or RNA, before amplifying it to a detectable amount using a technique called polymerase chain reaction (PCR). And while it is not the first saliva test the FDA has authorized, SalivaDirect has been shown to work with chemical reagents from a variety of companies, so it reduces the risk of the supply-chain issues that have plagued other methods. The assay can run 92 samples in about three hours, although the turnaround time depends on the lab conducting the test. Its components cost less than $5, so labs could charge about $10.
SalivaDirect was evaluated in a seemingly unlikely population—the National Basketball Association—which hopes to use it to detect players who have the virus but show no symptoms. Scientific American spoke with Chantal Vogels, a medical entomologist at the Yale School of Public Health, who helped develop the saliva test, about how accurate it is, how it compares with nasal swab assays and how easily it could be scaled up for use by other laboratories.
[An edited transcript of the conversation follows.]
How does the saliva test differ from a standard nasal swab assay for COVID-19?
Our SalivaDirect method has three main differences: the first one is we use saliva instead of a nasopharyngeal, [or nasal], swab. And that is mainly because the nasopharyngeal swab is very uncomfortable, and you need a very skilled person to take a swab. If you don't get deep enough and get enough virus, then you might not detect it. When you take the swab, there’s a chance it will prompt coughing and sneezing, which puts the person who takes the swab at risk. That’s why we figured if we can use saliva—which you can essentially just gently expel into a couple of tubes—that’s more comfortable, and it’s safer to collect. And we found that it actually works really well for detection of SARS-CoV-2.
The second major difference is that many of the other methods that are out there use an RNA extraction step in the sample processing. That is a step where you try to extract the genetic material of the virus: you break down the virus particles and everything that’s in the sample, you purify that, and that then goes into your final testing step (for instance, PCR). What we found is that you can actually skip, or at least simplify, that [extraction] step. Instead of needing this whole extraction with special equipment, if we simply treat the saliva with an enzyme called proteinase K and heat it, we can successfully break open the virus. We lose a little bit of sensitivity, but still, it’s very good for virus detection. It’s important to note that our method still uses PCR, and that means you do need to perform the test in a CLIA [Clinical Laboratory Improvement Amendments]–certified lab—a clinical lab that is equipped to run these tests. So it’s not a test that you can run at home. It’s not a point-of-care test.
Chantal Vogels. Credit: Isabel Ott
The third thing—and I think it’s kind of the most unique part about our method—is that it’s very flexible. Normally, most of the methods that are out there are based on a [specific test] kit. But if this kit is running into supply-chain issues, then that’s really going to negatively affect that testing. So we validated saliva directly with reagents and instruments from different vendors. Therefore, if one vendor is running into supply-chain issues, at least there are still other options out there that you can use. And this flexibility really minimizes the risk for supply-chain bottlenecks.
How accurate is your test?
As part of our FDA application for emergency use authorization, we had a couple of components that we had to perform in the lab. One is a “limit of detection” experiment, [which determines] the lowest concentration of virus that you can detect in a sample. What we found is that we can detect six to 12 copies of virus in a sample, which is pretty sensitive. The other component was a clinical evaluation. In that part, we had a selection of paired nasopharyngeal swabs and saliva from the same individuals, and we tested the swabs with an already authorized assay. Then, in parallel, we tested saliva with SalivaDirect just to show that both [were in] agreement in testing results. What we found there is that if you compare those nasopharyngeal swabs with saliva, there’s a 94 percent positive agreement. It’s important to note, though, that we had a couple of nasopharyngeal swabs that were testing positive with SalivaDirect but that were negative for the nasopharyngeal swabs. And that kind of gets to the point that if you compare these two different sample types, there’s always some variation.
If saliva works, why do we use nasal swabs at all?
Before the pandemic, the nasopharyngeal swab was used for detection of many other pathogens. So it has always been the gold standard. Early on in the pandemic, you had to rely on information that was previously known. And because the swab is used a lot on these respiratory pathogens, that’s the sort of the thing that you go to first. Along the way, we just started developing this more and looking into alternatives. Now it seems like saliva is indeed a good alternative. It doesn’t rule out the swab totally, but at least for certain contacts and certain scenarios, [saliva samples] may prove to be better.
Do you see SalivaDirect as replacing existing COVID-19 tests or complementing them?
I think it’s never like “One test is going to solve the whole problem.” I mean, we're dealing with a pandemic, and I think we just need options. There are many [other] saliva tests out there, and that’s really what we need. It’s not that our test is going to be, like, the answer. I think we have to be realistic. We still need that PCR test that needs to be performed in a highly complex laboratory. And for certain settings in certain contexts, it might be better to have an in-home test. But if you need to do lots of repeated testing, [our assay] might be better. So I think we just need a lot of different tests out there that can be used to tailor what is best in a certain context. Also, for instance, in low-resource settings, if you don’t have a constant supply of electricity or if you don't have access to one of those PCR machines, then you do need an alternative. I think having multiple options for testing out there is great.
How did the NBA come to work with your group to validate the test?
I was not involved in how that all got set up. That was my principal investigator, who the NBA reached out to. But essentially, to [authorize the test for] asymptomatic individuals, you would need a population of asymptomatic individuals who are still being tested regularly. Then the type of study that you need to do is, again, to compare results from the nasopharyngeal swab [with those from] saliva. It’s quite hard to set up a study with an asymptomatic population and then have them get repeatedly tested with both the swab and saliva. The NBA has been great because the players and the staff were going to be tested regularly with the swab: by also taking the saliva sample, we could just really nicely use them as our testing population to set up the study, to actually collect the data.
What are the next steps in scaling up this type of testing?
Even though now SalivaDirect has received emergency use authorization, so far it’s just for suspected COVID-19 cases. We’re now working in collaboration with the NBA to also get asymptomatic individuals authorized. We’re also looking into pooling: Can you pool multiple saliva [samples] together and still be able to detect the virus so that you can find ways to scale up testing? We’re looking into ways of automation, because now it’s all manual processing of the sample. But if you could use robots, that can be a way to really scale up the testing. We’re trying to team up with other universities and other groups as well to really help people push out their tests, because it’s not like our test is going to be the answer to everything. I think it’s a very good first step, but there’s still a lot more to do.
Read more about the coronavirus outbreak from Scientific American here. And read coverage from our international network of magazines here.


scientificamerican--2020-08-20--New Views of Our Mesmerizing, Maddening Minds

It ’ s one of my favorite events in the science world : the annual Art of Neuroscience contest held by the Netherlands Institute for Neuroscience .
Now in its 10th year , the competition looks a lot different than it did even five years ago .
Yes , many entries still show off the vivid and fantastical microscopic images of the brain stained in rainbow colors .
But thanks to more sophisticated technology , more submissions each year use interactive digital features to create immersive experiences for the viewer .
When these types of installations first began appearing in @ @ @ @ @ @ @ ( though I am not now proud to admit it ) .
I love the mesmerizing effect of using fluorescent protein tags that illuminate neural cells , for example , or the cilia of the inner ear , which made up the bulk of entries years ago .
These images are quite like modern art you ’ d see in a museum .
But just as the brain is more than a corporeal lump of flesh , so the art of neurology is more than a static image .
The new generation of @ @ @ @ @ @ @ own brains as part of the experience—and sometimes in a full sensory immersion , as you can see in some of the entries we ’ ve featured in this issue ( see “ The Beautiful Things Inside Your Head : Winners of the 10th Annual Art of Neuroscience Contest ” ) .
In this issue ’ s cover story , social psychologist Scott Barry Kaufman examines some of the debilitating tendencies of those with a victim mindset , and he offers a powerful new paradigm for how to shift into a personal growth @ @ @ @ @ @ @ your life ( see “ Unraveling the Mindset of Victimhood ” ) .
Our heads are filled with beautiful and strange things , whether one or the other depends on how you look at them .

It’s one of my favorite events in the science world: the annual Art of Neuroscience contest held by the Netherlands Institute for Neuroscience. Now in its 10th year, the competition looks a lot different than it did even five years ago. Yes, many entries still show off the vivid and fantastical microscopic images of the brain stained in rainbow colors. But thanks to more sophisticated technology, more submissions each year use interactive digital features to create immersive experiences for the viewer. When these types of installations first began appearing in the contest, I bristled a bit (though I am not now proud to admit it). I love the mesmerizing effect of using fluorescent protein tags that illuminate neural cells, for example, or the cilia of the inner ear, which made up the bulk of entries years ago. These images are quite like modern art you’d see in a museum. But just as the brain is more than a corporeal lump of flesh, so the art of neurology is more than a static image. The new generation of brain science art engages the viewers’ own brains as part of the experience—and sometimes in a full sensory immersion, as you can see in some of the entries we’ve featured in this issue (see “The Beautiful Things Inside Your Head: Winners of the 10th Annual Art of Neuroscience Contest”).
In this issue’s cover story, social psychologist Scott Barry Kaufman examines some of the debilitating tendencies of those with a victim mindset, and he offers a powerful new paradigm for how to shift into a personal growth mode and get the most out of your life (see “Unraveling the Mindset of Victimhood”). Our heads are filled with beautiful and strange things, whether one or the other depends on how you look at them.