Not Getting Enough Sleep? It Can Damage Your DNA, Study Says

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Not Getting Enough Sleep? It Can Damage Your DNA, Study Says

BY GQ PAN

February 19, 2019 Updated: February 20, 2019

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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.

hospital doctor
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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.

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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?

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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

(Marcos Mesa Sam Wordley/Shutterstock)

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:

Impaired Judgement

angry boss
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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.

Mood Disorders

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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

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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.

Weight Gain

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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.

Delusions

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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.

Your Genes and Addiction

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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.

Resources

Human Endogenous Retrovirus-K HML-2 integration within RASGRF2 is associated with intravenous drug abuse and modulates transcription in a cell-line modelProceedings of the National Academy of Sciences, September 24, 2018.

The Biological Basis Of Mental Illness

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By Adrian Woolfson

A vaguely indistinct floating face made of white spots on a black background.

No. 348. Candid Portrait of a Woman on a Street Corner by Trent Parke (2013).Credit: Trent Parke/Magnum

Good Reasons for Bad Feelings: Insights From the Frontier of Evolutionary Psychiatry Randolph 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 alProc. R. Soc. Lond. B 205, 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.

Genetic trade-offs

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 Evolution 11, 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.