Because sleep often becomes increasingly lighter and more disrupted as we get older, the study reinforces and potentially explains the links among aging, sleep deprivation, and heightened risk for Alzheimer’s disease.
“Sleep is critical to the function of the brain’s waste removal system and this study shows that the deeper the sleep the better,” says Maiken Nedergaard, codirector of the Center for Translational Neuromedicine at the University of Rochester Medical Center (URMC) and lead author of the study.
“These findings also add to the increasingly clear evidence that quality of sleep or sleep deprivation can predict the onset of Alzheimer’s and dementia.”
The study, which appears in the journal Science Advances, indicates that the slow and steady brain and cardiopulmonary activity associated with deep non-REM sleep are optimal for the function of the glymphatic system, the brain’s unique process of removing waste. The findings may also explain why some forms of anesthesia can lead to cognitive impairment in older adults.
WASHING AWAY WASTE
Nedergaard and her colleagues first described the previously unknown glymphatic system in 2012. Prior to that point, scientists didn’t fully understand how the brain, which maintains its own closed ecosystem, removed waste. The study revealed a system of plumbing which piggybacks on blood vessels and pumps cerebral spinal fluid (CSF) through brain tissue to wash away waste. A subsequent study showed that this system primarily works while we sleep.
Because the accumulation of toxic proteins such as beta amyloid and tau in the brain are associated with Alzheimer’s disease, researchers have speculated that impairment of the glymphatic system due to disrupted sleep could be a driver of the disease. This squares with clinical observations which show an association between sleep deprivation and heightened risk for Alzheimer’s.
In the current study, researchers conducted experiments with mice anesthetized with six different anesthetic regimens. While the animals were under anesthesia, the researchers tracked brain electrical activity, cardiovascular activity, and the cleansing flow of CSF through the brain.
The team observed that a combination of the drugs ketamine and xylazine (K/X) most closely replicated the slow and steady electrical activity in the brain and slow heart rate associated with deep non-REM sleep. Furthermore, the electrical activity in the brains of mice administered K/X appeared to be optimal for function of the glymphatic system.
“The synchronized waves of neural activity during deep slow-wave sleep, specifically firing patterns that move from front of the brain to the back, coincide with what we know about the flow of CSF in the glymphatic system,” says Lauren Hablitz, a postdoctoral associate in Nedergaard’s lab and first author of the study.
“It appears that the chemicals involved in the firing of neurons, namely ions, drive a process of osmosis which helps pull the fluid through brain tissue.”
The study raises several important clinical questions. It further bolsters the link between sleep, aging, and Alzheimer’s disease. Researchers have known that as we age it becomes more difficult to consistently achieve deep non-REM sleep, and this study reinforces the importance of deep sleep to the proper function of the glymphatic system.
The study also demonstrates that enhancing sleep can manipulate the glymphatic system, a finding that may point to potential clinical approaches, such as sleep therapy or other methods to boost the quality of sleep, for at-risk populations.
Furthermore, because several of the compounds used in the study were analogous to anesthetics used in clinical settings, the study also sheds light on the cognitive difficulties that older patients often experience after surgery and suggests classes of drugs that could help avoid this phenomenon. Mice in the study that researchers exposed to anesthetics that did not induce slow brain activity saw diminished glymphatic activity.
“Cognitive impairment after anesthesia and surgery is a major problem,” says coauthor Tuomas Lilius with the Center for Translational Neuromedicine at the University of Copenhagen in Denmark. “A significant percentage of elderly patients that undergo surgery experience a postoperative period of delirium or have a new or worsened cognitive impairment at discharge.”
Additional researchers from the University of Rochester and the University of Copenhagen contributed to the study. The National Institute of Neurological Disorders and Stroke, the National Institute on Aging, the Adelson Foundation, the Sigrid Juselius Foundation, the Novo Nordisk Foundation, and the Lundbeck Foundation supported the research.
Getting too little sleep can sometimes feel like torture. It can also lead to more serious health consequences than one can imagine. According to a recent study published in the journal Anaesthesia, sleep deprivation can affect our genes and even damage our DNA, something that can lead to cancer.
The Case of Night Shift Doctors
In the study, a team of researchers from University of Hong Kong looked at 49 healthy full-time doctors, 24 of whom had to work overnight onsite shifts, which meant they were required to work from late afternoon until the next morning.
The study set out to examine the effects of acute sleep deprivation on DNA damage.
After three night shifts for the on-call group and three days of adequate sleep for the control group, blood samples were taken from all participants. Upon analyzing the blood samples of the participants, the researchers found that the on-call doctors had lower DNA repair gene expression and more DNA breaks than those who didn’t take night shifts. To put it simply, their DNA was more damaged.
However, more research is needed to determine the significance of DNA damage in the relationship between sleep deprivation and disease, as the study’s sample size was small.
The team also noted that many other factors could explain why shift workers seem to have a greater predisposition to suffering from chronic illnesses. These range from changes to activity and eating patterns to disruption to the body’s circadian rhythms and sex hormone balances.
The researchers pointed out that a discrepancy that may have affected the study’s results, since their night shift participants were younger than their control group, as junior doctors are more likely to work the night shift than their senior counterparts. In addition, all of the participants were Chinese, so the findings might not apply to a wider population.
DNA Damage: How Bad Can it Be?
DNA damage has been associated with numerous serious health issues, ranging from heart attacks and diabetes to certain types of cancer. In their paper, researchers stated that a meta-analysis of 2 million participants confirmed a link between working night shifts and incidence of breast tumors, although studies on other kinds of cancers have given mixed results.
Just as our body shows signs of aging, such as grey hair and wrinkles, so does our genome. Damage comes from chemical reactions that alter the structure of our DNA, and from errors introduced when it is copied. Our cells protect against these ravages, but these mechanisms usually don’t have everything fixed perfectly.
As a result, cells gradually accumulate DNA damage over a lifetime. This means as you age, your genome is no longer the same in every cell. When a cell divides it will pass on these changes, and as these mutations accumulate, there is more and more likelihood that cancer will emerge.
Common Dangers of Sleep Deprivation
Lack of sleep doesn’t just make you tired; it can have dangerous unseen effects. Our brains simply stop functioning properly without getting enough sleep. This means we have to struggle with memory, learning, planning and reasoning.
A lack of sleep can have severe effects on our performance, ranging from irritability and low mood, to an increased risk of heart disease. Here are some common dangers of sleep deprivation:
Sleep deprivation has a negative impact on your visual working memory, making it difficult to tell the difference between relevant and irrelevant stimuli in your environment. It also affects your emotional intelligence, behavior, and ability to manage stress.
Mental health problems are linked to sleep disorders, and sleep deprivation can play havoc with neurotransmitters in the brain, mimicking the symptoms of depression, anxiety and mania.
Raised Blood Pressure
Poor sleep can raise blood pressure and in the long term is associated with an increased risk of diseases such as coronary heart disease and stroke. This danger is increased in people with sleep apnea.
Sleep deprivation affects the levels of hormones involved in regulating appetite. Levels of leptin, the hormone that tells you how much stored fat you have, decreases, and levels of ghrelin, the hormone that tells your body that you’re hungry, increases. As a result, you eat more.
It doesn’t really take a long time, or a lot of sleep deprivation, to bring the weight on. A study from researchers of University of Colorado reported that one week of sleeping about five hours a night led participants to gain an average of two pounds.
Severe sleep deprivation can lead to delusions and hallucinations, seeing or sensing things that aren’t really there. In extreme cases, it can lead to temporary psychosis or symptoms that resemble paranoid schizophrenia.
According to some scientific studies, the ability to see life on the right or wrong side is linked to the gene of happiness. This gene regulates in particular the circulation of serotonin the hormone of good humour. Why should you embrace your emotions?People with the long form of this gene are more predisposed to happiness…
Over the last decade, the prevalence of opioid addiction has increased to epidemic levels, but unfortunately therapeutic interventions for the treatment of addiction remain limited. We need to better understand the triggers for the development of addiction in order to develop more targeted prevention and treatments. One of the key questions that researchers in the field of neuropsychiatry are trying to answer is why some people are more vulnerable to addiction. As in most cases of psychiatric disorders, genetic and environmental factors interact to determine how vulnerable, or likely, you are to developing a substance use disorder.
Drugs of abuse, including opioids, act on the brain’s reward system, a system that transfers signals primarily via a molecule (neurotransmitter) called dopamine. The function of this system is affected by genetic and environmental factors. For example, a recent study published in the scientific journal PNAS revealed one of those genetic factors. Researchers demonstrated that a type of small infectious agent (a type of RNA virus called human endogenous retrovirus-K HML-2, or HK2) integrates within a gene that regulates activity of dopamine. This integration is more frequently found in people with substance use disorders, and is associated with drug addiction.
How does stress induce epigenetic changes?
Accumulating evidence suggests that environmental factors, such as stress, induce epigenetic changes that can trigger the development of psychiatric disorders and drug addiction. Epigenetic changes refer to regulations of gene expression that do not involve alterations in the sequence of the genetic material (DNA) itself. Practically, epigenetic changes are information that is added on to already existing genetic material, but can affect the expression of genes.
A stressful situation, such as the death of a significant other or the loss of a job, triggers the release of steroid hormones called glucocorticoids. Those stress hormones trigger alterations in many systems throughout the body, induce epigenetic changes, and regulate the expression of other genes in the brain. One of the systems that is affected by stress hormones is the brain’s reward circuitry. The interaction between stress hormones and the reward system can trigger the development of addiction, as well as a stress-induced relapse in drug or alcohol recovery.
Stress reduction can help reduce the risk of developing an addiction and prevent relapse
Fortunately, the negative effects of stress can be alleviated by other factors, such as physical activity or social support. These behaviors produce epigenetic changes that prevent the development of addiction and can have a beneficial role in treatment when used in combination with other interventions, such as cognitive behavioral therapy and, for some people, medications. One of the ways that physical activity could be effective is by reducing negative feelings, including stress and the accompanied stress-induced epigenetic changes. In the example of a stressful situation such as the death of a significant other or loss of a job, if a person engages in physical activity this can reduce their stress-induced epigenetic changes, which will decrease the risk of developing addiction or stress-induced relapse.
Hope for targeted addiction treatments
We now know that the function and dysfunction of the brain’s reward system is complicated, plastic (undergoes changes based on negative and positive factors), and involves complex interactions of genetic and environmental factors. Alterations in gene expression can lead to changes in the function of the brain’s reward system, so a person is more or less likely to self-administer drugs. Together this knowledge can ultimately lead to the development of multilevel and more efficient prevention and therapeutic approaches to address the ongoing opioid epidemic.
One morning in July, here’s the scene outside a neighborhood train station: While an ambulance winds its way through traffic nearby, people sit on the stairs with their heads buried in their arms. Others hustle for spare change or hawk “works” — street slang for a syringe. Several of the drug users stand stooped, their bodies droop then jerk back up again in the rhythm of a heroin nod.
At this spot, less than a week earlier, six people overdosed in the span of 15 minutes.
“It’s like watching TV,” said local resident Cano Gomez. “You stand here and it’s like watching a whole reality show, a one-hour reality show, to stand out here. I’m telling you man, it’s crazy.”
For people addicted on the streets, overdosing is just one worry on a long list of hardships. Many have lost their homes, jobs and families. They’ve seen friends die and get locked up. And when they try to explain how all of this happened, many say they are sick.
No matter who is talking about addiction these days, chances are they are using that term: “disease.”
From former President Barack Obama, to former New Jersey Governor Chris Christie, to President Donald Trump, politicians on both sides of the aisle now talk about addiction as a public health issue.
“This epidemic is a national health emergency,” Trump declared less than a year into his presidency.
There’s a growing consensus that addiction is a disease of the brain that requires medical treatment. Among consensus are people in recovery, their advocates, and police.
It feels like a far cry from the days when conventional wisdom viewed addiction as a moral failing that called for criminal punishment.
But calling addiction a brain disease, and not a bad life choice, is still a fairly new concept — one that has been built up over the past few decades by researchers toiling to understand how addiction affects the brain. As that view gains wider acceptance, some critics are challenging whether it’s really appropriate to call addiction a “brain disease.”
A rewired reward system
Charles O’Brien, a professor of psychiatry at the University of Pennsylvania, has been doing research on addiction since the 1960s. He says back then, psychiatrists tended to view drug addicts as, essentially, psychopaths.
“It was related to antisocial personality, and that’s not really true,” O’Brien said.
Researchers did know that the body could become dependent on a drug over time. And with new technologies, O’Brien and his colleagues were able to see the impact drugs had on the brain.
“Beginning in the 1980s, we started doing brain imaging, and we developed cues that were associated with drug use,” he said.
The cues were pictures of things like drug paraphernalia, or a syringe jabbed into a forearm. When O’Brien showed these pictures to people who had a history of addiction and scanned their brains, the effects were astounding.
“People thought that I was giving drugs to my patients in the laboratory, and I wasn’t,” O’Brien said.
The pictures were enough to activate parts of the brain that form what’s known as the “reward system.” They were the same areas that would light up if the person had, say, snorted a line of cocaine.
“Drugs like heroin or alcohol can take over that system,” O’Brien said. “People use the term ‘hijack.’ ”
The reward system is the brain circuitry that gives us a motivating hit of pleasure when we get the things that we need to survive, such as food, sex, and social connection. But drugs deliver a reward that’s much more powerful than those so-called “natural” rewards. When someone becomes addicted, the drug rewards begin to drown out the natural rewards, and the brain gets wired to seek the drug above anything else.
O’Brien’s brain imaging research revealed one very important way the brain gets rewired: people developed a conditioned response to things they associated with their drug use that mimicked the effects of getting high. So even just the sight of a needle or a bottle could trigger powerful cravings that could make it almost irresistible to start using again, even long after someone’s gotten clean.
“They relapse because it’s still in their brain,” O’Brien said.
His finding helped explain the hallmarks of addiction: how people almost always relapse, and keep using drugs despite the often devastating personal costs. The work provided a scientific basis for calling addiction a brain disease.
Scientists continue to build on this discovery to better understand the complicated — and sometimes unexpected — ways that addiction affects the brain.
What cute babies can tell us
In a basement laboratory at the University of Pennsylvania, psychiatrist Daniel Langleben uses a giant fMRI machine to see inside the brains of people recovering from addiction.
As a 25-year-old mother — who’s in treatment for opioid addiction — lies inside, researchers show her a series of baby photos while the machine scans the woman’s brain.
“The task involves you being asked to either rate how cute is the baby, or to what extent you would like to take care of it,” said Langleben, a research professor at the university.
As it turns out, these cute babies can activate the same part of the brain’s reward system that lights up when people use drugs.
“Specifically it’s called nucleus accumbens,” Langleben said. “It’s a very, very small area, deep inside the brain.”
He’s done other research showing that the nucleus accumbens responds to the unique features of an infant’s face, which are called “baby schema.”
“Big eyes relative to the face for example, large forehead, small chin — all these things that will tell you this is a baby,” Langleben said.
Research suggests that our brains are wired to get a motivating hit of pleasure just from seeing baby schema, he says.
“The hypothesis is that it is made to be rewarding exactly because nature needs us to take care of the young,” Langleben said.
But opioid addiction could make people less sensitive to baby schema. So he’s testing whether a participant’s response to those cute babies changes as they progress through addiction treatment, and whether that correlates with better parenting.
Brain research has helped to explain the cravings and relapse people experience in addiction, and this new frontier of research Langleben is involved in may shed light on some of the social consequences, such as neglecting childcare. Science has moved our understanding of addiction out of the realm of morality and into the medical world, as a disease that can be treated.
Nevertheless, the “brain disease” definition of addiction has attracted plenty of critics.
Sally Satel, a psychiatrist in Washington, D.C., and lecturer at Yale School of Medicine, doesn’t contest the science on how addiction affects the brain. But she still takes issue with calling it a “brain disease.”
Satel says addiction isn’t like catching an infection, or a defect that spontaneously appears in the brain. To make her point, she draws a comparison with Alzheimer’s disease. It would be “meaningless,” she said, to ask someone with a brain disease like Alzheimer’s why they have the condition.
“But if I were to ask you why do you drink too much, why are you using heroin everyday, that’s a meaningful question,” Satel said. “And it goes to the fact that people use drugs for reasons.”
That makes her skeptical that interventions such as medication are really enough to help people stay in recovery.
“A lot of people still want to alter their consciousness, they’re in a lot of psychic pain,” Satel said.
Another critic is trying to reconcile addiction’s roots in both biology and behavior. Maia Szalavitz, a journalist who’s been covering addiction for 30 years, was addicted to drugs herself when she was in college.
She’s also a self-described “deadhead,” a devotee of the legendary rock band The Grateful Dead.
In her book, “Unbroken Brain” — a play on the title of one of the band’s songs — she writes about her first time doing cocaine, at age 17, with Jerry Garcia, the front man of the group.
“I sort of had the kind of hippie attitude of like, ‘white powders are bad,’ but you know if Jerry offers you a line you’re gonna do it,” Szalavitz said.
A few years later, she got busted for cocaine possession. It was a wake-up call. Soon she entered treatment and began her recovery.
Szalavitz says you can’t blame Garcia for all of that, though. She’d already experimented with other substances at that point. The druggy music scene she was a part of in the 80s gave her a sense of identity, and the chemicals themselves relieved her social anxiety.
“Generally 90 percent of addictions happen in the teen and young adult [years],” Szalavitz said. “That’s a sensitive period of brain development.”
For Szalavitz, addiction is not a brain disease, exactly. In her book, she takes a deep dive into modern addiction science and makes a case that addiction is fundamentally about learning. She offers the example of what can happen when people are put on opioids in the hospital after surgery.
“There are people who become physically dependent on opioids in the hospital for pain, and they don’t know it,” she said. “And they go home, and they feel like they have the flu […] they never realized that they had a physical dependence on an opioid.”
Eventually, the opioid withdrawal symptoms pass and they go on with their lives, Szalavitz says.
“If you don’t learn that a drug fixes some kind of problem for you, you can’t be addicted to it because you wouldn’t know what to crave,” she said.
Szalavitz says the way that compulsive drug use is learned isn’t given enough weight when we label addiction a brain disease. She thinks it should take center stage. The gist of her argument goes back to those baby photos researcher Daniel Langleben was showing to former opioid users. Szalavitz says the connection between opioid addiction and the way we can become obsessed with a cute baby is key to the story of what addiction really is.
The same holds for other human relationships, she says. A lover’s touch, a friend’s reassuring presence, a happy baby cradled in your arms — all of these moments are rewarded by naturally occurring opioid neurotransmitters in the brain.
“What opioids do in the brain when they’re not relieving pain is they are there to create social bonds,” Szalavitz said.
When we don’t abandon an infant that throws up on us and cries through the night, or continue to chase a love interest after a crushing rejection, Szalavitz points out that these behaviors look a lot like addiction.
“People with addiction are persisting despite negative consequences in a way that’s necessary for human survival,” she said. “We evolved this thing for a reason, because it’s hard to deal with people, and babies are a pain in the butt, and they cry and you have to change them, and you have to persist if you are going to survive and reproduce successfully, right?”
Szalavitz says people have learned to love the wrong rewards.
Plus, she says, to understand why people want to alter their experience with chemicals in the first place, you have to look outside the brain.
“Trauma is one of the other big factors,” Szalavitz said. “About two thirds of people with addiction have at least one childhood trauma.”
There’s also socioeconomic factors that contribute.
“Unemployment, poverty, kind of being socially disconnected,” she said. “There are very few people with addiction who have none of those elements.”
Szalavitz says the way we talk about addiction now, as a brain disease, misses the mark. But she says it’s not so much the words that matter, but what exactly we mean when we say them.
“I just want people to understand that this is a learned behavior in which a system that is there for essential survival and reproduction stuff goes in the wrong direction,” Szalavitz said. “It’s not an inhuman behavior, it’s not about evil, manipulative, horrible, lying people.”
This story was made possible in part thanks to a grant from the Scattergood Behavioral Health Foundation.
Good Reasons for Bad Feelings: Insights From the Frontier of Evolutionary PsychiatryRandolph M. Nesse Dutton (2019)
Globally, the burden of depression and other mental-health conditions is on the rise. In North America and Europe alone, mental illness accounts for up to 40% of all years lost to disability. And molecular medicine, which has seen huge success in treating diseases such as cancer, has failed to stem the tide. Into that alarming context enters the thought-provoking Good Reasons for Bad Feelings, in which evolutionary psychiatrist Randolph Nesse offers insights that radically reframe psychiatric conditions.
In his view, the roots of mental illnesses, such as anxiety and depression, lie in essential functions that evolved as building blocks of adaptive behavioural and cognitive function. Furthermore, like the legs of thoroughbred racehorses — selected for length, but tending towards weakness — some dysfunctional aspects of mental function might have originated with selection for unrelated traits, such as cognitive capacity. Intrinsic vulnerabilities in the human mind could be a trade-off for optimizing unrelated features.
Similar ideas have surfaced before, in different contexts. Evolutionary biologists Stephen Jay Gould and Richard Lewontin, for example, critically examined the blind faith of ‘adaptationist’ evolutionary theorizing. Their classic 1979 paper ‘The spandrels of San Marco and the Panglossian paradigm’ challenged the idea that every aspect of an organism has been perfected by natural selection (S. J. Gould et al. Proc. R. Soc. Lond. B205, 581–598; 1979). Instead, like the curved triangles of masonry between arches supporting domes in medieval and Renaissance architecture, some parts are contingent structural by-products. These might have no discernible adaptive advantage, or might even be maladaptive. Gould and Lewontin’s intuition has, to some extent, been vindicated by molecular genetics. Certain versions of the primitive immune-system protein complement 4A, for instance, evolved for reasons unrelated to mental function, and yet are associated with an increased risk of schizophrenia.
Decades earlier, the evolutionary theorist George C. Williams explored perhaps the most perplexing aspect of human biology: our inconvenient tendency to age and die. He suggested in 1957 that some of the genes that cause ageing evolved because they enhanced fitness early in life (G. C. Williams Evolution11, 398–411; 1957). Such ‘antagonistic pleiotropy’ — in which a single gene controls at least one beneficial and one detrimental trait — suggests that the design of biological structures is a complex optimization problem involving multiple trade-offs. Emotions and other aspects of mental function are not like machine components, each with a set function; instead, they are embedded in complex overlapping biochemical pathways.
In 1994, Nesse teamed up with Williams for Why We Get Sick, a manifesto for “Darwinian medicine”. Their insights opened up new perspectives on the origins of diseases, arguing for ‘proximate’ causes (driven by anatomy, biochemistry and physiology) and higher-level ‘ultimate’ (evolutionary) causes. They noted that evolution selects for reproductive success rather than for health and happiness; hence, the existence of human diseases and disorders. They also detailed the contingent and sometimes ‘irrational’ nature of biological legacies, such as the nerves and blood vessels that run across the human eye’s retinal surface. Cephalopod eyes don’t have this ‘flaw’.
Good Reasons for Bad Feelings builds on these insights. Adopting an “engineers’ point of view” on mental illnesses, Nesse suggests that anxiety, although apparently undesirable, is a design component with utility in certain situations — for instance, as a “smoke detector” for potentially life-threatening events. Depression might also perform adaptive functions. The psychiatrist Aubrey Lewis argued that by signalling distress, depression could prompt others into providing assistance through foraging and other activities. It has even been suggested that depressive behaviour in vervet monkeys (Chlorocebus pygerythrus) evolved to signal loss of status, deflecting attacks from dominant males.
Yet, however functional its components when appropriately regulated, mental illnesses cause suffering, and evidence-based treatments are sparse. Indeed, the field has seen no significant pharmaceutical breakthroughs for many years. Biological causes remain elusive, and biomarkers non-existent.
Psychiatry as a field, meanwhile, quivers with theoretical uncertainty. It has not become a sub-speciality of neurology, as one might have expected if mental illness mapped directly to neural behaviour. And common genetic variations with large effects on mental disorders are elusive. The various incarnations of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders(DSM) have enabled diagnostic consistency and the objectification of mental illnesses. But the DSM has resulted in overlapping diagnoses, and contrived symptom-cluster checklists. At times, it impinges on the territory of healthy mental function. Allen Frances, chair of the task force that wrote the manual’s fourth edition in 1994, revolted against out-of-control mental diagnosis in his 2013 book DSM: Saving Normal.
From adaptive to maladaptive
Nesse argues that evolutionary theory could foster therapeutic breakthroughs by providing a robust theoretical foundation for psychiatry. He posits that it might also help to prevent people from equating psychiatric symptoms with diseases and viewing extremes of emotion such as anxiety as disorders. Nesse also suggests that mental illnesses might result from the disruption of regulators that maintain equilibrium in the body, such as the endocrine system. The normally adaptive function of thoughts and emotions could, in such instances, become maladaptive.
The future success of clinical psychiatry might depend on an evolutionary framework being integrated with whole-genome sequence-data analysis; this could help to identify mutations predisposing people to mental illness. Given the small contributions of individual genes and the diverse mechanisms involved, this will demand analysis of the genomes of hundreds of thousands of people. As a result of the extensive and often paradoxical entanglement of genetic networks, future treatments might, by necessity, require mental circuits to be engineered to release them from hard-wired evolutionary constraints.
In Theodicy (1710), German philosopher Gottfried Leibniz argued that God, being omniscient, must have created the best of all possible worlds. (Fifty years later, in his novel Candide, Voltaire lampooned Leibniz as Doctor Pangloss, who opined that faults in the world are necessary, like contrasting shadows in a painting.)
Ironic readings aside, the philosopher’s optimism might now be shown to have rational echoes in contemporary science. As Good Reasons for Bad Feelings boldly posits, many of the core dysfunctional components of mental illness ultimately help to make us human.
The study participants – 121 women and 84 men, ranging in age from 20 to 82 years – underwent PET scans to measure the flow of oxygen and glucose in their brains.
The findings suggest that gender affects brain aging and could contribute to stronger brain health and the ability to ward off disease later in life.
“It’s not that men’s brains age faster – they start adulthood about three years older than women, and that persists throughout life,” Goyal said. “What we don’t know is what it means.
“I think this could mean that the reason women don’t experience as much cognitive decline in later years is because their brains are effectively younger,” he said, “and we’re currently working on a study to confirm that.”
The finding is “great news for many women,” the University of Arizona’s Roberta Diaz Brinton told NPR. Brinton, who wasn’t connected with the study, said some women’s brains experience a dramatic metabolic decline around menopause, leaving them vulnerable to Alzheimer’s.
Brain aging is one of many differences between the sexes. “It is stronger than many sex differences that have been reported, but it’s nowhere near as big a difference as some sex differences, such as height,” Goyal said.
In a follow-up study, the research team is following a group of adults over time to see whether people with younger-looking brains are less likely to develop cognitive problems.