Climate change is already killing people, but countries don’t have an easy way to count those deaths. A new project might change that.
Climate change can kill people in all kinds of ways. There are the obvious ones—wildfires, storms, and floods—yet rising temperatures may also lead to the increased spread of deadly diseases, make food harder to come by, and increase the risk of conflict.
Although we know about these wide-ranging but equally terrifying risks, attempts to pinpoint the number of deaths caused by climate change have been piecemeal. One recent study estimated that climate change was to blame for 37 percent of heat-related deaths over the past three decades. In 2021, Daniel Bressler, a PhD student at Columbia University in New York, estimated that every additional 4,400 metric tons of carbon dioxide emitted will cause one heat-related death later this century. He called this number the “mortality cost of carbon.”
Putting a number on climate deaths isn’t just an academic exercise. People are already dying because of extreme temperature and weather events, and we can expect this to become more common as the planet continues to heat up. If governments want to put in place policies to prevent these deaths, they need a way of accurately measuring the deaths and ill health linked to warming. The search is on for the true mortality cost of carbon.
As part of this search, the UK government has made its first attempt at putting a number on climate change deaths. The UK Office for National Statistics (ONS)—an independent government agency responsible for producing official data—has for the first time reported climate-related deaths and hospital admissions in England and Wales. The report covers the years 2001 to 2020, but future reports will be released annually, revealing for the first time detailed information about the impact that climate change is having on health in the two nations. (Statistics for Scotland and Northern Ireland are recorded separately.)
The main finding from this investigation is counterintuitive. The report found that the number of deaths associated with warm or cold temperatures actually decreased between 2001 and 2020. On average, 27,755 fewer people were dying each year due to unusually warm or cold temperatures. In other words, climate change might have actually prevented over half a million deaths in England and Wales over this period. In 2001 there were 993 climate-related deaths per 100,000 people in England and Wales. By 2019 that figure had fallen to 771.
But let’s not get ahead of ourselves. There are a number of reasons why the net number of temperature-related deaths appeared to decline over this period, says Myer Glickman, head of the epidemiological, climate, and global health team at the ONS. For a start, statisticians took a relatively narrow definition of climate-related deaths. They only included deaths from conditions where scientists had previously found a clear link between temperature and disease outcome, and they also excluded any health condition where their own analysis showed no link between temperature and outcome. This means that the mortality data doesn’t include deaths from violence or natural forces (such as storms, landslides, or flooding).
The analysis also excluded deaths from air pollution, which Public Health England estimates is equivalent to between 28,000 and 36,000 deaths each year in the UK. Glickman says that there is no accepted way to separate out the effect that temperature increases have on air pollution. Add all these caveats together and it’s likely that the ONS analysis is a little on the conservative side.
Then there is the big reason why climate change has not led to more deaths in England and Wales: the very mild climate. Although average temperatures in the UK have increased by 0.9 degrees compared to the period from 1961 to 1990, its residents are not some of the 3 billion people who face unlivable conditions if greenhouse gas emissions increase rapidly. And while deaths linked to cold weather were down in England and Wales, on warmer days there was a net increase in hospital admissions linked to warmer weather. This was particularly true when it comes to injuries, which may be because more people do outdoor activities when it’s warmer or might be linked to the increases in violence and mental health problems that are associated with warmer temperatures.
The lower rate of deaths might also be a sign that our attempts to fight back against cold weather are working. Widespread flu vaccinations, support for people to pay their heating bills, and increases in home insulation mean that the coldest days didn’t hit as hard as they might have without these mitigations in place, Glickman says. And warmer homes might be a good thing now, but as summers in the UK get hotter and air-conditioning remains rare, it may start to become a problem.
The ONS will now release this data on a yearly basis, but Glickman’s next project is to look more closely at how temperature changes affected different areas. “We’re going to drill down to a local level temperature,” he says. “That’s going to give us a lot more resolution on what’s happening and who it’s happening to.” The impact of climate change might depend on how wealthy an area is, for example, or whether its residents have easy access to health care or community support.
Glickman also wants to explore indirect impacts of climate on health. “What will be a big interest in the coming years is the lower-level health impacts of things like flooding,” he says. If someone’s home is flooded, it might increase their vulnerability to respiratory disease or worsen their mental health. Researchers from the UK have already found that people with mental illnesses are more at risk of death during hot weather. We don’t know why that is exactly, but researchers think it might be because people with mental illnesses are more likely to be socially isolated or already have poorer health, which makes them more vulnerable when temperatures rise.
The team behind the ONS report are also part of a wider effort to create a global system to count climate-related health impacts. “What we don’t have is a robust set of statistics to categorize the impact of climate on health,” says Bilal Mateen, a senior manager of digital technology at Wellcome Trust, the health charity funding the new climate change health impact initiative.
The first year of the project will be spent identifying countries to partner with before developing and testing different ways of measuring climate change deaths that work for specific countries, says Mateen. The idea is to use this data to help countries devise policies that lessen the health impact of climate change. “We can begin to tease out what works, what doesn’t, and what adaptation and mitigation interventions we should be supporting,” Mateen says.
If it’s true that warmer homes and flu vaccines helped reduce climate change deaths in England and Wales, it’s a sign that populations that are healthier on the whole might be better at surviving the ravages of a heating world. Other countries may want to take note. “All policies are health policies,” says Mateen. “There is a clear need to support job stability, to address fuel poverty and every other policy that’s outside of the mandate of the health minister, because we know that those social determinants of health have downstream impact.”
And at one rural hospital in Nelson, British Columbia, doctor Kyle Merritt began to feel like there was more he should do than simply treat all the patients coming in with heat stroke and exhaustion. “I was upset with what I was seeing,” he says, “I felt like it should be documented in some way.” So when a 70-year-old woman arrived with heat stroke, he wrote “climate change” in her medical chart as the underlying reason she had to be admitted to the hospital.
It was the first and only time Merritt chose to include “climate change” as an underlying condition in a patient’s chart. “It was the first patient that I felt like it was really clear cut,” he says. Had the conditions outside not been so extreme, he might have been able to discharge her and let her recover at home. When we spoke, Merritt emphasized that it was a decision he made in the heat of the moment. He never expected it to become national news.
Months later, when speaking with the founders of a small organization called Doctors for Planetary Health, Merritt shared the story of his decision to write “climate change” in the patient’s chart. When they asked to use that story in a press release accompanying a planned climate rally, Merritt didn’t think anyone was going to read the press release about this little thing that happened.
But read it they did. Eventually, Merritt’s story was all over the news, often under erroneous headlines claiming he had “diagnosed” a patient with climate change (the phrase appears in her chart as an underlying cause, not a diagnosis). The story was covered by national publications like NBC News, The Hill, The Daily Mail, along with a host of right-wing news sites like GOP USA.
Some praised the decision for bringing necessary awareness to the connection between climate change and health. “When I saw this, I thought, ‘Yes, this is what we need. We need more attention to the social determinants of health,’” says Keisha Ray, an assistant professor at the McGovern Center for Humanities and Ethics at UTHealth. Others claimed this was “the latest example of team-left lunacy.” Some columnists argued, incorrectly, that the patient probably didn’t get proper treatment because her doctor “diagnosed her” with something incurable. (Merritt admitted the patient to the emergency room and she was treated for her condition.)
When I read the story, my question was less about Merritt and more about the patient herself. Did she know she was the center of this news blip? Had he talked to her about climate change, or the fact that he was writing it in her chart? Did she give permission to be in the press release? And what are the ethics of turning a patient into a public point?
Doctors use case studies all the time to communicate with one another, and with the press. And for good reason: People connect with and remember stories far better than generalized facts. But using a patient to explain a concept, or to help educate doctors on how to treat someone more effectively, is different from using a patient’s story to make this broader, public point about climate and health. Even Merritt admitted that writing “climate change” in this woman’s chart didn’t do much to help her or other patients suffering during the heat dome. “It’s not like some other doctor was going to look at it and make sure they were never exposed to climate change,” he says. “Practically speaking, it doesn’t really do that much.”
Medicine has a checkered history when it comes to using patient stories and protecting privacy. For decades, doctors paraded patients in front of the public without their consent. In 1906, for example, a famous doctor named Wilfred Grenfell published the story of a 9-year-old boy who had accidentally shot himself in the knee. Grenfell used the boy’s full name, image, and identity, telling the tale with gusto each time he spoke to the public and his colleagues—even distorting the facts of the case, turning “slight” bleeding in the original chart into “shocking” bleeding and a “heterogeneous mass of bloody rags”—in order to entertain donors, make himself seem more heroic, and maintain his status as a celebrity doctor. Fast forward to today, and issues of patient privacy are still very present. In 2012 the ABC show NY Med, which at the time starred celebrity doctor Mehmet Oz, broadcast the death of a patient without his family’s consent. His widow won $2.2 million in a suit against the hospital.
Given that history, the question of how much to anonymize a patient in these tales is well-trod territory for medical ethicists. “As long as the physician doesn’t give any kind of identifying information, then it would be ethical. You want to always maintain the patient’s privacy,” says Ray. “But you also have to think about how minor information can be pieced together, where someone can figure out who this patient is.”
In Merritt’s case, the details provided to the press go like this: We know the patient’s age, her background medical conditions, the type of home she lives in, and that she was admitted in June. Kootenay Medical Center, where Merritt works, serves less than 4,000 patients. “That’s a lot of identifying information,” Ray said, when I told her the facts that had been publicly confirmed. “Small towns don’t tend to have a lot of physicians, so you could very well be one of three physicians.”
This feels increasingly important when a story is used in a way that might be construed as political —calling for action on something like racism or climate change. In a world where private citizens can be outed and harassed for being associated with a cause or a side, doctors who want to use a patient’s sickness to make an activist point might need to be a little more cautious. “I worry that the sensationalism of this story may encourage people like journalists to go seek this patient out,” says Ray. “And I also worry that because climate change is still very political and it still is considered a left-leaning idea, that it may encourage conservative media to go and find this person and pit them against each other.”
That hasn’t happened in this case. But Merritt says that if he were to do it over, he might have done things differently. As it unfolded, he didn’t tell the patient he was writing “climate change” in her chart. In fact, they didn’t discuss climate change at all. “If I had known when I had written that in the chart that it was something that I was doing to try and tell the story, I don’t know. I may have talked to the patient more about it and asked their permission,” he says. “But of course, at that time when I did it, I had no idea that it would ever become a story of any kind.” To this day, Merritt believes that the patient has no idea she is the one in the story.
Beyond the specifics of Merritt and his patient, the story raises big questions about how medicine can and should handle systemic impacts on health.
Merritt wrote “climate change” in a bout of frustration, wanting to document what he was seeing in real time. Other doctors have taken different approaches. Nyasha Spears, a physician at St. Luke’s Hospital in Duluth, Minnesota, takes nearly the opposite tack that Merritt did—rather than quietly writing in a chart to make a broader point, she talks to her patients constantly about climate change and the environment. “As a family doctor, my jam is habit change. This is what I do,” she says. “So my thought with climate change is, can I start peppering my conversations with patients all the time with an argument that habit change is good for them on a personal level, but also good for the environment?”
In the case of Merritt’s patient, this talk might not have done much. There was nothing she could do about her conditions, no habit change she could make to avoid the scorching heat. Like many in her community, she likely couldn’t afford to install air-conditioning in her trailer, and beyond that there was little to be done. In cases like these, Ray says that maybe a climate change talk isn’t warranted. “They can feel helpless because there’s nothing that they can do,” she says. “They are literally living, and just living is making them sick.”
This reality can make things feel bleak for both doctors and patients. And to address these connections between health and structural conditions like climate change and racism, doctors will need to ask not simply what they can do for each individual patient, but also what they can change about medicine to account for and reckon with these links. Today, there is no diagnostic code for climate change, no way to link these cases up or track them in any way, but perhaps there should be.
“There’s all sorts of ICD-10 codes that are completely inane,” says Spears. “If you ever want to entertain yourself, you just start looking at ICD 10 codes. ‘Fall from a spacecraft’ is one. And so it would make perfect sense that there would be an ICD-10 code for climate change illness.” Being able to track these additional, systemic determinants of health could make it easier to prove the links, and do something about them.
Having more data doesn’t always mean making change—the impact that race and income have on health have been well proven for years, but still haven’t adequately been addressed. And Ray says that adding these codes shouldn’t stop with climate. “If you live in a poor area, then you are likely living with more environmental impacts. Are we going to start now having a code for low income? Is there going to be a code for: You don’t have enough money to live in a safe home and so you are experiencing environmental toxins? Is improper housing also going to be coded? So I just wonder how far we are willing to take it.”
This might be the silver lining in the story of Merritt’s patient. When we spoke, he told me he had recently gotten an email from Health Canada, asking to talk to him about creating a diagnostic code for climate change that doctors could use to track these impacts.
Writing “climate change” in one patient’s chart isn’t going to save the world, or even a single life—Merritt is the first to admit that—but it can start a conversation about how much the medical system is willing to adapt to the threats that its patients truly face. “I’ve learned a lot about how big of an impact a story can make,” he says.
Research shows that a positive attitude to ageing can lead to a longer, healthier life, while negative beliefs can have hugely detrimental effects
For more than a decade, Paddy Jones has been wowing audiences across the world with her salsa dancing. She came to fame on the Spanish talent show Tú Sí Que Vales (You’re Worth It) in 2009 and has since found success in the UK, through Britain’s Got Talent; in Germany, on Das Supertalent; in Argentina, on the dancing show Bailando; and in Italy, where she performed at the Sanremo music festival in 2018 alongside the band Lo Stato Sociale.
Jones also happens to be in her mid-80s, making her the world’s oldest acrobatic salsa dancer, according to Guinness World Records. Growing up in the UK, Jones had been a keen dancer and had performed professionally before she married her husband, David, at 22 and had four children. It was only in retirement that she began dancing again – to widespread acclaim. “I don’t plead my age because I don’t feel 80 or act it,” Jones told an interviewer in 2014.
According to a wealth of research that now spans five decades, we would all do well to embrace the same attitude – since it can act as a potent elixir of life. People who see the ageing process as a potential for personal growth tend to enjoy much better health into their 70s, 80s and 90s than people who associate ageing with helplessness and decline, differences that are reflected in their cells’ biological ageing and their overall life span.
Of all the claims I have investigated for my new book on the mind-body connection, the idea that our thoughts could shape our ageing and longevity was by far the most surprising. The science, however, turns out to be incredibly robust. “There’s just such a solid base of literature now,” says Prof Allyson Brothers at Colorado State University. “There are different labs in different countries using different measurements and different statistical approaches and yet the answer is always the same.”
If I could turn back time
The first hints that our thoughts and expectations could either accelerate or decelerate the ageing process came from a remarkable experiment by the psychologist Ellen Langer at Harvard University.
In 1979, she asked a group of 70- and 80-year-olds to complete various cognitive and physical tests, before taking them to a week-long retreat at a nearby monastery that had been redecorated in the style of the late 1950s. Everything at the location, from the magazines in the living room to the music playing on the radio and the films available to watch, was carefully chosen for historical accuracy.
The researchers asked the participants to live as if it were 1959. They had to write a biography of themselves for that era in the present tense and they were told to act as independently as possible. (They were discouraged from asking for help to carry their belongings to their room, for example.) The researchers also organised twice-daily discussions in which the participants had to talk about the political and sporting events of 1959 as if they were currently in progress – without talking about events since that point. The aim was to evoke their younger selves through all these associations.
To create a comparison, the researchers ran a second retreat a week later with a new set of participants. While factors such as the decor, diet and social contact remained the same, these participants were asked to reminisce about the past, without overtly acting as if they were reliving that period.
Most of the participants showed some improvements from the baseline tests to the after-retreat ones, but it was those in the first group, who had more fully immersed themselves in the world of 1959, who saw the greatest benefits. Sixty-three per cent made a significant gain on the cognitive tests, for example, compared to just 44% in the control condition. Their vision became sharper, their joints more flexible and their hands more dextrous, as some of the inflammation from their arthritis receded.
As enticing as these findings might seem, Langer’s was based on a very small sample size. Extraordinary claims need extraordinary evidence and the idea that our mindset could somehow influence our physical ageing is about as extraordinary as scientific theories come.
Becca Levy, at the Yale School of Public Health, has been leading the way to provide that proof. In one of her earliest – and most eye-catching – papers, she examined data from the Ohio Longitudinal Study of Aging and Retirement that examined more than 1,000 participants since 1975.
The participants’ average age at the start of the survey was 63 years old and soon after joining they were asked to give their views on ageing. For example, they were asked to rate their agreement with the statement: “As you get older, you are less useful”. Quite astonishingly, Levy found the average person with a more positive attitude lived on for 22.6 years after the study commenced, while the average person with poorer interpretations of ageing survived for just 15 years. That link remained even after Levy had controlled for their actual health status at the start of the survey, as well as other known risk factors, such as socioeconomic status or feelings of loneliness, which could influence longevity.
The implications of the finding are as remarkable today as they were in 2002, when the study was first published. “If a previously unidentified virus was found to diminish life expectancy by over seven years, considerable effort would probably be devoted to identifying the cause and implementing a remedy,” Levy and her colleagues wrote. “In the present case, one of the likely causes is known: societally sanctioned denigration of the aged.”
Later studies have since reinforced the link between people’s expectations and their physical ageing, while dismissing some of the more obvious – and less interesting – explanations. You might expect that people’s attitudes would reflect their decline rather than contribute to the degeneration, for example. Yet many people will endorse certain ageist beliefs, such as the idea that “old people are helpless”, long before they should have started experiencing age-related disability themselves. And Levy has found that those kinds of views, expressed in people’s mid-30s, can predict their subsequent risk of cardiovascular disease up to 38 years later.
The most recent findings suggest that age beliefs may play a key role in the development of Alzheimer’s disease. Tracking 4,765 participants over four years, the researchers found that positive expectations of ageing halved the risk of developing the disease, compared to those who saw old age as an inevitable period of decline. Astonishingly, this was even true of people who carried a harmful variant of the APOE gene, which is known to render people more susceptible to the disease. The positive mindset can counteract an inherited misfortune, protecting against the build-up of the toxic plaques and neuronal loss that characterise the disease.
How could this be?
Behaviour is undoubtedly important. If you associate age with frailty and disability, you may be less likely to exercise as you get older and that lack of activity is certainly going to increase your predisposition to many illnesses, including heart disease and Alzheimer’s.
Importantly, however, our age beliefs can also have a direct effect on our physiology. Elderly people who have been primed with negative age stereotypes tend to have higher systolic blood pressure in response to challenges, while those who have seen positive stereotypes demonstrate a more muted reaction. This makes sense: if you believe that you are frail and helpless, small difficulties will start to feel more threatening. Over the long term, this heightened stress response increases levels of the hormone cortisol and bodily inflammation, which could both raise the risk of ill health.
The consequences can even be seen within the nuclei of the individual cells, where our genetic blueprint is stored. Our genes are wrapped tightly in each cell’s chromosomes, which have tiny protective caps, called telomeres, which keep the DNA stable and stop it from becoming frayed and damaged. Telomeres tend to shorten as we age and this reduces their protective abilities and can cause the cell to malfunction. In people with negative age beliefs, that process seems to be accelerated – their cells look biologically older. In those with the positive attitudes, it is much slower – their cells look younger.
For many scientists, the link between age beliefs and long-term health and longevity is practically beyond doubt. “It’s now very well established,” says Dr David Weiss, who studies the psychology of ageing at Martin-Luther University of Halle-Wittenberg in Germany. And it has critical implications for people of all generations.
Our culture is saturated with messages that reinforce the damaging age beliefs. Just consider greetings cards, which commonly play on of images depicting confused and forgetful older people. “The other day, I went to buy a happy 70th birthday card for a friend and I couldn’t find a single one that wasn’t a joke,” says Martha Boudreau, the chief communications officer of AARP, a special interest group (formerly known as the American Association of Retired Persons) that focuses on the issues of over-50s.
She would like to see greater awareness – and intolerance – of age stereotypes, in much the same way that people now show greater sensitivity to sexism and racism. “Celebrities, thought leaders and influencers need to step forward,” says Boudreau.
We could all, in other words, learn to live like Paddy Jones.
When I interviewed Jones, she was careful to emphasise the potential role of luck in her good health. But she agrees that many people have needlessly pessimistic views of their capabilities, over what could be their golden years, and encourages them to question the supposed limits. “If you feel there’s something you want to do, and it inspires you, try it!” she told me. “And if you find you can’t do it, then look for something else you can achieve.”
Whatever our current age, that’s surely a winning attitude that will set us up for greater health and happiness for decades to come.
This is an edited extract fromThe Expectation Effect: How your Mindset Can Transform Your Life by David Robson, published by Canongate on 6 January (£18.99).
HUMANS ARE lucky to live a hundred years. Oak trees may live a thousand; mayflies, in their adult form, a single day. But they are all alive in the same way. They are made up of cells which embody flows of energy and stores of information. Their metabolisms make use of that energy, be it from sunlight or food, to build new molecules and break down old ones, using mechanisms described in the genes they inherited and may, or may not, pass on.
It is this endlessly repeated, never quite perfect reproduction which explains why oak trees, humans, and every other plant, fungus or single-celled organism you have ever seen or felt the presence of are all alive in the same way. It is the most fundamental of all family resemblances. Go far enough up any creature’s family tree and you will find an ancestor that sits in your family tree, too. Travel further and you will find what scientists call the last universal common ancestor, LUCA. It was not the first living thing. But it was the one which set the template for the life that exists today.
And then there are viruses. In viruses the link between metabolism and genes that binds together all life to which you are related, from bacteria to blue whales, is broken. Viral genes have no cells, no bodies, no metabolism of their own. The tiny particles, “virions”, in which those genes come packaged—the dot-studded disks of coronaviruses, the sinister, sinuous windings of Ebola, the bacteriophages with their science-fiction landing-legs that prey on microbes—are entirely inanimate. An individual animal, or plant, embodies and maintains the restless metabolism that made it. A virion is just an arrangement of matter.
The virus is not the virion. The virus is a process, not a thing. It is truly alive only in the cells of others, a virtual organism running on borrowed hardware to produce more copies of its genome. Some bide their time, letting the cell they share the life of live on. Others immediately set about producing enough virions to split their hosts from stem to stern.
The virus has no plan or desire. The simplest purposes of the simplest life—to maintain the difference between what is inside the cell and what is outside, to move towards one chemical or away from another—are entirely beyond it. It copies itself in whatever way it does simply because it has copied itself that way before, in other cells, in other hosts.
That is why, asked whether viruses are alive, Eckard Wimmer, a chemist and biologist who works at the State University of New York, Stony Brook, offers a yes-and-no. Viruses, he says, “alternate between nonliving and living phases”. He should know. In 2002 he became the first person in the world to take an array of nonliving chemicals and build a virion from scratch—a virion which was then able to get itself reproduced by infecting cells.
The fact that viruses have only a tenuous claim to being alive, though, hardly reduces their impact on things which are indubitably so. No other biological entities are as ubiquitous, and few as consequential. The number of copies of their genes to be found on Earth is beyond astronomical. There are hundreds of billions of stars in the Milky Way galaxy and a couple of trillion galaxies in the observable universe. The virions in the surface waters of any smallish sea handily outnumber all the stars in all the skies that science could ever speak of.
Back on Earth, viruses kill more living things than any other type of predator. They shape the balance of species in ecosystems ranging from those of the open ocean to that of the human bowel. They spur evolution, driving natural selection and allowing the swapping of genes.
They may have been responsible for some of the most important events in the history of life, from the appearance of complex multicellular organisms to the emergence of DNA as a preferred genetic material. The legacy they have left in the human genome helps produce placentas and may shape the development of the brain. For scientists seeking to understand life’s origin, they offer a route into the past separate from the one mapped by humans, oak trees and their kin. For scientists wanting to reprogram cells and mend metabolisms they offer inspiration—and powerful tools.
II A lifestyle for genes
THE IDEA of a last universal common ancestor provides a plausible and helpful, if incomplete, answer to where humans, oak trees and their ilk come from. There is no such answer for viruses. Being a virus is not something which provides you with a place in a vast, coherent family tree. It is more like a lifestyle—a way of being which different genes have discovered independently at different times. Some viral lineages seem to have begun quite recently. Others have roots that comfortably predate LUCA itself.
Disparate origins are matched by disparate architectures for information storage and retrieval. In eukaryotes—creatures, like humans, mushrooms and kelp, with complex cells—as in their simpler relatives, the bacteria and archaea, the genes that describe proteins are written in double-stranded DNA. When a particular protein is to be made, the DNA sequence of the relevant gene acts as a template for the creation of a complementary molecule made from another nucleic acid, RNA. This messenger RNA (mRNA) is what the cellular machinery tasked with translating genetic information into proteins uses in order to do so.
Because they, too, need to have proteins made to their specifications, viruses also need to produce mRNAs. But they are not restricted to using double-stranded DNA as a template. Viruses store their genes in a number of different ways, all of which require a different mechanism to produce mRNAs. In the early 1970s David Baltimore, one of the great figures of molecular biology, used these different approaches to divide the realm of viruses into seven separate classes (see diagram).
In four of these seven classes the viruses store their genes not in DNA but in RNA. Those of Baltimore group three use double strands of RNA. In Baltimore groups four and five the RNA is single-stranded; in group four the genome can be used directly as an mRNA; in group five it is the template from which mRNA must be made. In group six—the retroviruses, which include HIV—the viral RNA is copied into DNA, which then provides a template for mRNAs.
Because uninfected cells only ever make RNA on the basis of a DNA template, RNA-based viruses need distinctive molecular mechanisms those cells lack. Those mechanisms provide medicine with targets for antiviral attacks. Many drugs against HIV take aim at the system that makes DNA copies of RNA templates. Remdesivir (Veklury), a drug which stymies the mechanism that the simpler RNA viruses use to recreate their RNA genomes, was originally developed to treat hepatitis C (group four) and subsequently tried against the Ebola virus (group five). It is now being used against SARS–CoV-2 (group four), the covid-19 virus.
Studies of the gene for that RNA-copying mechanism, RdRp, reveal just how confusing virus genealogy can be. Some viruses in groups three, four and five seem, on the basis of their RdRp-gene sequence, more closely related to members of one of the other groups than they are to all the other members of their own group. This may mean that quite closely related viruses can differ in the way they store their genomes; it may mean that the viruses concerned have swapped their RdRp genes. When two viruses infect the same cell at the same time such swaps are more or less compulsory. They are, among other things, one of the mechanisms by which viruses native to one species become able to infect another.
How do genes take on the viral lifestyle in the first place? There are two plausible mechanisms. Previously free-living creatures could give up metabolising and become parasitic, using other creatures’ cells as their reproductive stage. Alternatively genes allowed a certain amount of independence within one creature could have evolved the means to get into other creatures.
Living creatures contain various apparently independent bits of nucleic acid with an interest in reproducing themselves. The smallest, found exclusively in plants, are tiny rings of RNA called viroids, just a few hundred genetic letters long. Viroids replicate by hijacking a host enzyme that normally makes mRNAs. Once attached to a viroid ring, the enzyme whizzes round and round it, unable to stop, turning out a new copy of the viroid with each lap.
Viroids describe no proteins and do no good. Plasmids—somewhat larger loops of nucleic acid found in bacteria—do contain genes, and the proteins they describe can be useful to their hosts. Plasmids are sometimes, therefore, regarded as detached parts of a bacteria’s genome. But that detachment provides a degree of autonomy. Plasmids can migrate between bacterial cells, not always of the same species. When they do so they can take genetic traits such as antibiotic resistance from their old host to their new one.
Recently, some plasmids have been implicated in what looks like a progression to true virus-hood. A genetic analysis by Mart Krupovic of the Pasteur Institute suggests that the Circular Rep-Encoding Single-Strand-DNA (CRESS–DNA) viruses, which infect bacteria, evolved from plasmids. He thinks that a DNA copy of the genes that another virus uses to create its virions, copied into a plasmid by chance, provided it with a way out of the cell. The analysis strongly suggests that CRESS–DNA viruses, previously seen as a pretty closely related group, have arisen from plasmids this way on three different occasions.
Such jailbreaks have probably been going on since very early on in the history of life. As soon as they began to metabolise, the first proto-organisms would have constituted a niche in which other parasitic creatures could have lived. And biology abhors a vacuum. No niche goes unfilled if it is fillable.
It is widely believed that much of the evolutionary period between the origin of life and the advent of LUCA was spent in an “RNA world”—one in which that versatile substance both stored information, as DNA now does, and catalysed chemical reactions, as proteins now do. Set alongside the fact that some viruses use RNA as a storage medium today, this strongly suggests that the first to adopt the viral lifestyle did so too. Patrick Forterre, an evolutionary biologist at the Pasteur Institute with a particular interest in viruses (and the man who first popularised the term LUCA) thinks that the “RNA world” was not just rife with viruses. He also thinks they may have brought about its end.
The difference between DNA and RNA is not large: just a small change to one of the “letters” used to store genetic information and a minor modification to the backbone to which these letters are stuck. And DNA is a more stable molecule in which to store lots of information. But that is in part because DNA is inert. An RNA-world organism which rewrote its genes into DNA would cripple its metabolism, because to do so would be to lose the catalytic properties its RNA provided.
An RNA-world virus, having no metabolism of its own to undermine, would have had no such constraints if shifting to DNA offered an advantage. Dr Forterre suggests that this advantage may have lain in DNA’s imperviousness to attack. Host organisms today have all sorts of mechanisms for cutting up viral nucleic acids they don’t like the look of—mechanisms which biotechnologists have been borrowing since the 1970s, most recently in the form of tools based on a bacterial defence called CRISPR. There is no reason to imagine that the RNA-world predecessors of today’s cells did not have similar shears at their disposal. And a virus that made the leap to DNA would have been impervious to their blades.
Genes and the mechanisms they describe pass between viruses and hosts, as between viruses and viruses, all the time. Once some viruses had evolved ways of writing and copying DNA, their hosts would have been able to purloin them in order to make back-up copies of their RNA molecules. And so what began as a way of protecting viral genomes would have become the way life stores all its genes—except for those of some recalcitrant, contrary viruses.
III The scythes of the seas
IT IS A general principle in biology that, although in terms of individual numbers herbivores outnumber carnivores, in terms of the number of species carnivores outnumber herbivores. Viruses, however, outnumber everything else in every way possible.
This makes sense. Though viruses can induce host behaviours that help them spread—such as coughing—an inert virion boasts no behaviour of its own that helps it stalk its prey. It infects only that which it comes into contact with. This is a clear invitation to flood the zone. In 1999 Roger Hendrix, a virologist, suggested that a good rule of thumb might be ten virions for every living individual creature (the overwhelming majority of which are single-celled bacteria and archaea). Estimates of the number of such creatures on the planet come out in the region of 1029-1030. If the whole Earth were broken up into pebbles, and each of those pebbles smashed into tens of thousands of specks of grit, you would still have fewer pieces of grit than the world has virions. Measurements, as opposed to estimates, produce numbers almost as arresting. A litre of seawater may contain more than 100bn virions; a kilogram of dried soil perhaps a trillion.
Metagenomics, a part of biology that looks at all the nucleic acid in a given sample to get a sense of the range of life forms within it, reveals that these tiny throngs are highly diverse. A metagenomic analysis of two surveys of ocean life, the Tara Oceans and Malaspina missions, by Ahmed Zayed of Ohio State University, found evidence of 200,000 different species of virus. These diverse species play an enormous role in the ecology of the oceans.
A litre of seawater may contain 100bn virions; a kilogram of dried soil perhaps a trillion
On land, most of the photosynthesis which provides the biomass and energy needed for life takes place in plants. In the oceans, it is overwhelmingly the business of various sorts of bacteria and algae collectively known as phytoplankton. These creatures reproduce at a terrific rate, and viruses kill them at a terrific rate, too. According to work by Curtis Suttle of the University of British Columbia, bacterial phytoplankton typically last less than a week before being killed by viruses.
This increases the overall productivity of the oceans by helping bacteria recycle organic matter (it is easier for one cell to use the contents of another if a virus helpfully lets them free). It also goes some way towards explaining what the great mid-20th-century ecologist G. Evelyn Hutchinson called “the paradox of the plankton”. Given the limited nature of the resources that single-celled plankton need, you would expect a few species particularly well adapted to their use to dominate the ecosystem. Instead, the plankton display great variety. This may well be because whenever a particular form of plankton becomes dominant, its viruses expand with it, gnawing away at its comparative success.
It is also possible that this endless dance of death between viruses and microbes sets the stage for one of evolution’s great leaps forward. Many forms of single-celled plankton have molecular mechanisms that allow them to kill themselves. They are presumably used when one cell’s sacrifice allows its sister cells—which are genetically identical—to survive. One circumstance in which such sacrifice seems to make sense is when a cell is attacked by a virus. If the infected cell can kill itself quickly (a process called apoptosis) it can limit the number of virions the virus is able to make. This lessens the chances that other related cells nearby will die. Some bacteria have been shown to use this strategy; many other microbes are suspected of it.
There is another situation where self-sacrifice is becoming conduct for a cell: when it is part of a multicellular organism. As such organisms grow, cells that were once useful to them become redundant; they have to be got rid of. Eugene Koonin of America’s National Institutes of Health and his colleagues have explored the idea that virus-thwarting self-sacrifice and complexity-permitting self-sacrifice may be related, with the latter descended from the former. Dr Koonin’s model also suggests that the closer the cells are clustered together, the more likely this act of self-sacrifice is to have beneficial consequences.
For such profound propinquity, move from the free-flowing oceans to the more structured world of soil, where potential self-sacrificers can nestle next to each other. Its structure makes soil harder to sift for genes than water is. But last year Mary Firestone of the University of California, Berkeley, and her colleagues used metagenomics to count 3,884 new viral species in a patch of Californian grassland. That is undoubtedly an underestimate of the total diversity; their technique could see only viruses with RNA genomes, thus missing, among other things, most bacteriophages.
Metagenomics can also be applied to biological samples, such as bat guano in which it picks up viruses from both the bats and their food. But for the most part the finding of animal viruses requires more specific sampling. Over the course of the 2010s PREDICT, an American-government project aimed at finding animal viruses, gathered over 160,000 animal and human tissue samples from 35 countries and discovered 949 novel viruses.
The people who put together PREDICT now have grander plans. They want a Global Virome Project to track down all the viruses native to the world’s 7,400 species of mammals and waterfowl—the reservoirs most likely to harbour viruses capable of making the leap into human beings. In accordance with the more-predator-species-than-prey rule they expect such an effort would find about 1.5m viruses, of which around 700,000 might be able to infect humans. A planning meeting in 2018 suggested that such an undertaking might take ten years and cost $4bn. It looked like a lot of money then. Today those arguing for a system that can provide advance warning of the next pandemic make it sound pretty cheap.
IV Leaving their mark
THE TOLL which viruses have exacted throughout history suggests that they have left their mark on the human genome: things that kill people off in large numbers are powerful agents of natural selection. In 2016 David Enard, then at Stanford University and now at the University of Arizona, made a stab at showing just how much of the genome had been thus affected.
He and his colleagues started by identifying almost 10,000 proteins that seemed to be produced in all the mammals that had had their genomes sequenced up to that point. They then made a painstaking search of the scientific literature looking for proteins that had been shown to interact with viruses in some way or other. About 1,300 of the 10,000 turned up. About one in five of these proteins was connected to the immune system, and thus could be seen as having a professional interest in viral interaction. The others appeared to be proteins which the virus made use of in its attack on the host. The two cell-surface proteins that SARS–CoV-2 uses to make contact with its target cells and inveigle its way into them would fit into this category.
The researchers then compared the human versions of the genes for their 10,000 proteins with those in other mammals, and applied a statistical technique that distinguishes changes that have no real impact from the sort of changes which natural selection finds helpful and thus tries to keep. Genes for virus-associated proteins turned out to be evolutionary hotspots: 30% of all the adaptive change was seen in the genes for the 13% of the proteins which interacted with viruses. As quickly as viruses learn to recognise and subvert such proteins, hosts must learn to modify them.
A couple of years later, working with Dmitri Petrov at Stanford, Dr Enard showed that modern humans have borrowed some of these evolutionary responses to viruses from their nearest relatives. Around 2-3% of the DNA in an average European genome has Neanderthal origins, a result of interbreeding 50,000 to 30,000 years ago. For these genes to have persisted they must be doing something useful—otherwise natural selection would have removed them. Dr Enard and Dr Petrov found that a disproportionate number described virus-interacting proteins; of the bequests humans received from their now vanished relatives, ways to stay ahead of viruses seem to have been among the most important.
Viruses do not just shape the human genome through natural selection, though. They also insert themselves into it. At least a twelfth of the DNA in the human genome is derived from viruses; by some measures the total could be as high as a quarter.
Retroviruses like HIV are called retro because they do things backwards. Where cellular organisms make their RNA from DNA templates, retroviruses do the reverse, making DNA copies of their RNA genomes. The host cell obligingly makes these copies into double-stranded DNA which can be stitched into its own genome. If this happens in a cell destined to give rise to eggs or sperm, the viral genes are passed from parent to offspring, and on down the generations. Such integrated viral sequences, known as endogenous retroviruses (ERVs), account for 8% of the human genome.
This is another example of the way the same viral trick can be discovered a number of times. Many bacteriophages are also able to stitch copies of their genome into their host’s DNA, staying dormant, or “temperate”, for generations. If the cell is doing well and reproducing regularly, this quiescence is a good way for the viral genes to make more copies of themselves. When a virus senses that its easy ride may be coming to an end, though—for example, if the cell it is in shows signs of stress—it will abandon ship. What was latent becomes “lytic” as the viral genes produce a sufficient number of virions to tear the host apart.
Though some of their genes are associated with cancers, in humans ERVs do not burst back into action in later generations. Instead they have proved useful resources of genetic novelty. In the most celebrated example, at least ten different mammalian lineages make use of a retroviral gene for one of their most distinctively mammalian activities: building a placenta.
The placenta is a unique organ because it requires cells from the mother and the fetus to work together in order to pass oxygen and sustenance in one direction and carbon dioxide and waste in the other. One way this intimacy is achieved safely is through the creation of a tissue in which the membranes between cells are broken down to form a continuous sheet of cellular material.
The protein that allows new cells to merge themselves with this layer, syncytin-1, was originally used by retroviruses to join the external membranes of their virions to the external membranes of cells, thus gaining entry for the viral proteins and nucleic acids. Not only have different sorts of mammals co-opted this membrane-merging trick—other creatures have made use of it, too. The mabuya, a long-tailed skink which unusually for a lizard nurtures its young within its body, employs a retroviral syncytin protein to produce a mammalian-looking placenta. The most recent shared ancestor of mabuyas and mammals died out 80m years before the first dinosaur saw the light of day, but both have found the same way to make use of the viral gene.
You put your line-1 in, you take your line-1 out
This is not the only way that animals make use of their ERVs. Evidence has begun to accumulate that genetic sequences derived from ERVs are quite frequently used to regulate the activity of genes of more conventional origin. In particular, RNA molecules transcribed from an ERV called HERV-K play a crucial role in providing the stem cells found in embryos with their “pluripotency”—the ability to create specialised daughter cells of various different types. Unfortunately, when expressed in adults HERV-K can also be responsible for cancers of the testes.
As well as containing lots of semi-decrepit retroviruses that can be stripped for parts, the human genome also holds a great many copies of a “retrotransposon” called LINE-1. This a piece of DNA with a surprisingly virus-like way of life; it is thought by some biologists to have, like ERVs, a viral origin. In its full form, LINE-1 is a 6,000-letter sequence of DNA which describes a “reverse transcriptase” of the sort that retroviruses use to make DNA from their RNA genomes. When LINE-1 is transcribed into an mRNA and that mRNA subsequently translated to make proteins, the reverse transcriptase thus created immediately sets to work on the mRNA used to create it, using it as the template for a new piece of DNA which is then inserted back into the genome. That new piece of DNA is in principle identical to the piece that acted as the mRNA’s original template. The LINE-1 element has made a copy of itself.
In the 100m years or so that this has been going on in humans and the species from which they are descended the LINE-1 element has managed to pepper the genome with a staggering 500,000 copies of itself. All told, 17% of the human genome is taken up by these copies—twice as much as by the ERVs.
Most of the copies are severely truncated and incapable of copying themselves further. But some still have the knack, and this capability may be being put to good use. Fred Gage and his colleagues at the Salk Institute for Biological Studies, in San Diego, argue that LINE-1 elements have an important role in the development of the brain. In 2005 Dr Gage discovered that in mouse embryos—specifically, in the brains of those embryos—about 3,000 LINE-1 elements are still able to operate as retrotransposons, putting new copies of themselves into the genome of a cell and thus of all its descendants.
Brains develop through proliferation followed by pruning. First, nerve cells multiply pell-mell; then the cell-suicide process that makes complex life possible prunes them back in a way that looks a lot like natural selection. Dr Gage suspects that the movement of LINE-1 transposons provides the variety in the cell population needed for this selection process. Choosing between cells with LINE-1 in different places, he thinks, could be a key part of the process from which the eventual neural architecture emerges. What is true in mice is, as he showed in 2009, true in humans, too. He is currently developing a technique for looking at the process in detail by comparing, post mortem, the genomes of different brain cells from single individuals to see if their LINE-1 patterns vary in the ways that his theory would predict.
V Promised lands
HUMAN EVOLUTION may have used viral genes to make big-brained live-born life possible; but viral evolution has used them to kill off those big brains on a scale that is easily forgotten. Compare the toll to that of war. In the 20th century, the bloodiest in human history, somewhere between 100m and 200m people died as a result of warfare. The number killed by measles was somewhere in the same range; the number who died of influenza probably towards the top of it; and the number killed by smallpox—300m-500m—well beyond it. That is why the eradication of smallpox from the wild, achieved in 1979 by a globally co-ordinated set of vaccination campaigns, stands as one of the all-time-great humanitarian triumphs.
Other eradications should eventually follow. Even in their absence, vaccination has led to a steep decline in viral deaths. But viruses against which there is no vaccine, either because they are very new, like SARS–CoV-2, or peculiarly sneaky, like HIV, can still kill millions.
Reducing those tolls is a vital aim both for research and for public-health policy. Understandably, a far lower priority is put on the benefits that viruses can bring. This is mostly because they are as yet much less dramatic. They are also much less well understood.
The viruses most prevalent in the human body are not those which infect human cells. They are those which infect the bacteria that live on the body’s surfaces, internal and external. The average human “microbiome” harbours perhaps 100trn of these bacteria. And where there are bacteria, there are bacteriophages shaping their population.
The microbiome is vital for good health; when it goes wrong it can mess up a lot else. Gut bacteria seem to have a role in maintaining, and possibly also causing, obesity in the well-fed and, conversely, in tipping the poorly fed into a form of malnutrition called kwashiorkor. Ill-regulated gut bacteria have also been linked, if not always conclusively, with diabetes, heart disease, cancers, depression and autism. In light of all this, the question “who guards the bacterial guardians?” is starting to be asked.
The viruses that prey on the bacteria are an obvious answer. Because the health of their host’s host—the possessor of the gut they find themselves in—matters to these phages, they have an interest in keeping the microbiome balanced. Unbalanced microbiomes allow pathogens to get a foothold. This may explain a curious detail of a therapy now being used as a treatment of last resort against Clostridium difficile, a bacterium that causes life-threatening dysentery. The therapy in question uses a transfusion of faecal matter, with its attendant microbes, from a healthy individual to reboot the patient’s microbiome. Such transplants, it appears, are more likely to succeed if their phage population is particularly diverse.
Medicine is a very long way from being able to use phages to fine-tune the microbiome. But if a way of doing so is found, it will not in itself be a revolution. Attempts to use phages to promote human health go back to their discovery in 1917, by Félix d’Hérelle, a French microbiologist, though those early attempts at therapy were not looking to restore balance and harmony. On the basis that the enemy of my enemy is my friend, doctors simply treated bacterial infections with phages thought likely to kill the bacteria.
The arrival of antibiotics saw phage therapy abandoned in most places, though it persisted in the Soviet Union and its satellites. Various biotechnology companies think they may now be able to revive the tradition—and make it more effective. One option is to remove the bits of the viral genome that let phages settle down to a temperate life in a bacterial genome, leaving them no option but to keep on killing. Another is to write their genes in ways that avoid the defences with which bacteria slice up foreign DNA.
The hope is that phage therapy will become a backup in difficult cases, such as infection with antibiotic-resistant bugs. There have been a couple of well-publicised one-off successes outside phage therapy’s post-Soviet homelands. In 2016 Tom Patterson, a researcher at the University of California, San Diego, was successfully treated for an antibiotic-resistant bacterial infection with specially selected (but un-engineered) phages. In 2018 Graham Hatfull of the University of Pittsburgh used a mixture of phages, some engineered so as to be incapable of temperance, to treat a 16-year-old British girl who had a bad bacterial infection after a lung transplant. Clinical trials are now getting under way for phage treatments aimed at urinary-tract infections caused by Escherichia coli, Staphylococcus aureus infections that can lead to sepsis and Pseudomonas aeruginosa infections that cause complications in people who have cystic fibrosis.
Viruses which attack bacteria are not the only ones genetic engineers have their eyes on. Engineered viruses are of increasing interest to vaccine-makers, to cancer researchers and to those who want to treat diseases by either adding new genes to the genome or disabling faulty ones. If you want to get a gene into a specific type of cell, a virion that recognises something about such cells may often prove a good tool.
The vaccine used to contain the Ebola outbreak in the Democratic Republic of Congo over the past two years was made by engineering Indiana vesiculovirus, which infects humans but cannot reproduce in them, so that it expresses a protein found on the surface of the Ebola virus; thus primed, the immune system responds to Ebola much more effectively. The World Health Organisation’s current list of 29 covid-19 vaccines in clinical trials features six versions of other viruses engineered to look a bit like SARS-CoV-2. One is based on a strain of measles that has long been used as a vaccine against that disease.
Viruses engineered to engender immunity against pathogens, to kill cancer cells or to encourage the immune system to attack them, or to deliver needed genes to faulty cells all seem likely to find their way into health care. Other engineered viruses are more worrying. One way to understand how viruses spread and kill is to try and make particularly virulent ones. In 2005, for example, Terrence Tumpey of America’s Centres for Disease Control and Prevention and his colleagues tried to understand the deadliness of the influenza virus responsible for the pandemic of 1918-20 by taking a more benign strain, adding what seemed to be distinctive about the deadlier one and trying out the result on mice. It was every bit as deadly as the original, wholly natural version had been.
The use of engineered pathogens as weapons of war is of dubious utility, completely illegal and repugnant to almost all
Because such “gain of function” research could, if ill-conceived or poorly implemented, do terrible damage, it requires careful monitoring. And although the use of engineered pathogens as weapons of war is of dubious utility—such weapons are hard to aim and hard to stand down, and it is not easy to know how much damage they have done—as well as being completely illegal and repugnant to almost all, such possibilities will and should remain a matter of global concern.
Information which, for billions of years, has only ever come into its own within infected cells can now be inspected on computer screens and rewritten at will. The power that brings is sobering. It marks a change in the history of both viruses and people—a change which is perhaps as important as any of those made by modern biology. It is constraining a small part of the viral world in a way which, so far, has been to people’s benefit. It is revealing that world’s further reaches in a way which cannot but engender awe. ■
Editor’s note: Some of our covid-19 coverage is free for readers of The Economist Today, our daily newsletter. For more stories and our pandemic tracker, see our hub
This article appeared in the Essay section of the print edition under the headline “The outsiders inside”
A lack of essential nutrients is known to contribute to the onset of poor mental health in people suffering from anxiety and depression, bipolar disorder, schizophrenia and ADHD. Nutritional psychiatry is a growing discipline that focuses on the use of food and supplements to provide these essential nutrients as part of an integrated or alternative treatment for mental health disorders.
But nutritional approaches for these debilitating conditions are not widely accepted by mainstream medicine. Treatment options tend to be limited to official National Institute for Care Excellence (NICE) guidelines which recommend talking therapies and antidepressants.
Use of antidepressants
Antidepressant use has more than doubled in recent years. In England 64.7m prescriptions were issued for antidepressants in 2016 at a cost of £266.6m. This is an increase of 3.7m on the number of items prescribed in 2015 and more than double than the 31m issued in 2006.
A recent Oxford University study found that antidepressants were more effective in treating depression than placebo. The study was led by Dr Andrea Cipriani who claimed that depression is under treated. Cipriani maintains that antidepressants are effective and a further 1m prescriptions should be issued to people in the UK.
This approach suggests that poor mental health caused by social conditions is viewed as easily treated by simply dispensing drugs. But antidepressants are shunned by people whom they could help because of the social stigma associated with mental ill-health which leads to discrimination and exclusion.
Prescriptions for 64.7m items of antidepressants were dispensed in England in 2016, the highest level recorded by the NHS. Shutterstock
More worrying is the increase in the use of antidepressants by children and young people. In Scotland, 5,572 children under 18 were prescribed antidepressants for anxiety and depression in 2016. This figure has more than doubled since 2009/2010.
But according to British psychopharmacologist Professor David Healy, 29 clinical trials of antidepressant use in young people found no benefits at all. These trials revealed that instead of relieving symptoms of anxiety and depression, antidepressants caused children and young people to feel suicidal.
Healy also challenges their safety and effectiveness in adults. He believes that antidepressants are over-prescribed and that there is little evidence that they are safe for long-term use. Antidepressants are said to create dependency, have unpleasant side effects and cannot be relied upon to always relieve symptoms.
Nutrition and poor mental health
In developed countries such as the UK people eat a greater variety of foodstuffs than ever before – but it doesn’t follow that they are well nourished. In fact, many people do not eat enough nutrients that are essential for good brain health, opting for a diet of heavily processed food containing artificial additives and sugar.
The link between poor mental health and nutritional deficiencies has long been recognised by nutritionists working in the complementary health sector. However, psychiatrists are only now becoming increasingly aware of the benefits of using nutritional approaches to mental health, calling for their peers to support and research this new field of treatment.
It is now known that many mental health conditions are caused by inflammation in the brain which ultimately causes our brain cells to die. This inflammatory response starts in our gut and is associated with a lack of nutrients from our food such as magnesium, omega-3 fatty acids, probiotics, vitamins and minerals that are all essential for the optimum functioning of our bodies.
Recent research has shown that food supplements such as zinc, magnesium, omega 3, and vitamins B and D3 can help improve people’s mood, relieve anxiety and depression and improve the mental capacity of people with Alzheimer’s.
Magnesium is one of most important minerals for optimal health, yet many people are lacking in it. One studyfound that a daily magnesium citrate supplement led to a significant improvement in depression and anxiety, regardless of age, gender or severity of depression. Improvement did not continue when the supplement was stopped.
Omega-3 fatty acids are another nutrient that is critical for the development and function of the central nervous system – and a lack has been associated with low mood, cognitive decline and poor comprehension.
Research has shown that supplements like zinc, magnesium and vitamins B and D can improve the mental capacity of people with Alzheimer’s. Shutterstock
These over-the-counter” supplements are widely available in supermarkets, chemists and online health food stores, although the cost and quality may vary. For people who have not responded to prescription drugs or who cannot tolerate the side effects, nutritional intervention can offer hope for the future.
There is currently much debate over the effectiveness of antidepressants. The use of food supplements offer an alternative approach that has the potential to make a significant difference to the mental health of all age groups.
The emerging scientific evidence suggests that there should be a bigger role for nutritional psychiatry in mental health within conventional health services. If the burden of mental ill health is to be reduced, GPs and psychiatrists need to be aware of the connection between food, inflammation and mental illness.
Medical education has traditionally excluded nutritional knowledge and its association with disease. This has led to a situation where very few doctors in the UK have a proper understanding of the importance of nutrition. Nutritional interventions are thought to have little evidence to support their use to prevent or maintain well-being and so are left to dietitians, rather than doctors, to advise on.
But as the evidence mounts up, it is time for medical education to take nutrition seriously so that GPs and psychiatrists of the future know as much about its role in good health as they do about anatomy and physiology. The state of our mental health could depend on it.
Pesquisadora da Unicamp alerta para influência da indústria farmacêutica no crescimento do número de diagnósticos de transtornos mentais
Dados do National Institute of Mental Health (NIMH, 2012) apontam que 46% dos norte-americanos preenchem os critérios de diagnóstico de um transtorno mental. Na Europa essa porcentagem corresponde a 38%. Nos Estados Unidos, o diagnóstico de transtorno bipolar em crianças e adolescentes aumentou 40 vezes, entre 1994 e 2003, e uma entre cinco crianças tem um surto de transtorno mental por ano, de acordo com dados do Centro de Controle de Doenças, daquele país (CDC, 2013).
Há pesquisas que indicam que 10% da população mundial teria algum tipo de transtorno, um número que segundo a médica pediatra, Maria Aparecida Affonso Moysés, da Faculdade de Medicina da Universidade Estadual de Campinas (Unicamp), inviabiliza qualquer esforço de política pública. “Temos que começar a questionar como esses números são construídos. Na verdade, mudanças nos critérios do diagnóstico se tornaram muito frouxos nos últimos anos”, afirmou a médica, em sua conferência na Reunião Anual da SBPC. “É muito difícil qualquer um de nós não se encaixar nos critérios. Os testes que detectam algumas dessas doenças são verdadeiras armadilhas”, alertou.
Ela refutou a ideia de que vivemos uma epidemia de doenças mentais. “O que temos é uma epidemia de diagnósticos de transtornos mentais”, disse. Na primeira vez em que foi publicado pela Associação Americana de Psiquiatria, em 1952, o Manual Diagnóstico e Estatístico de Transtornos Mentais (DSM), tinha 106 categorias de transtornos mentais. Em sua última edição, em 2013, foram listadas 300 categorias. “Alterar as normas para caracterização de um transtorno e criar doenças novas contribuíram para essa epidemia amplamente patrocinada pela indústria farmacêutica”, declarou Moysés. “Antes de vender remédios, o departamento de marketing da indústria de fármacos trabalha para vender doenças”, diz. Déficit de atenção, transtorno de descontrole de humor, transtorno de aprendizagem, depressão, transtorno opositor desafiante, hiperatividade, são algumas dessas doenças fabricadas para vender medicamentos. “Onde está a ciência e ética nesse campo?”, questionou a médica. Segundo ela, esses medicamentos são largamente receitados para crianças e adultos, como se fossem 100% seguros, mas boa parte deles provoca dependência química.
Um exemplo é o metilfenidato, base de uma classe de estimulantes do sistema nervoso central, vendido entre outras, com a marca “Ritalina”. O medicamento age inibindo a receptação de dopamina na sinapse, o que teria como resultado o aumento do nível de concentração. Conforme explicou Moysés, ele é receitado para crianças com Transtorno do Déficit de Atenção com Hiperatividade (TDAH), não pelo seu efeito terapêutico, mas pelas reações adversas. No sistema nervoso central o metilfenidato provoca o efeito “zombie like”, quando a pessoa fica contida em si mesma. “Eu comparo esse fármaco a uma droga da obediência porque o indivíduo perde a capacidade de questionar, de sentir. É um tipo de contenção química. O aumento de concentração, tão propagado, é, na verdade, uma redução do foco da atenção, isto é, a pessoa presta atenção em uma coisa de cada vez”, afirmou. “Não existe uma pílula que nos faça prestar atenção. Para isso, precisamos de bons professores com boas condições de trabalho”.
Na opinião da pesquisadora da Unicamp, vivemos em um projeto de sociedade que estimula e premia comportamentos homogêneos, punindo as singularidades. “Não é à toa que assistimos cortes significativos nos orçamentos da ciência e da educação. Temos que ser iguais porque as diferenças incomodam cada vez mais. Entretanto, neutralizar os sonhadores, os que pensam diferente é um genocídio do futuro”, disse.
O combate ao que a médica chama de patologização da sociedade passa pelos campos da saúde, da educação e por uma revisão das políticas públicas para que elas não sejam submissas ao mercado. Outro setor é o da formação profissional. Nas escolas de medicina, a técnica não pode se sobrepor à ética e ao aspecto humano. Toda avaliação e diagnóstico têm que respeitar saberes, valores, história e a cultura porque “a vida não é mercadoria”, finalizou.
Why do people pay for experiences deliberately marketed as painful? According to a new study, consumers will pay big money for extraordinary — even painful — experiences to offset the physical malaise resulting from today’s sedentary lifestyles.
Why do people pay for experiences deliberately marketed as painful? According to a new study in the Journal of Consumer Research, consumers will pay big money for extraordinary — even painful — experiences to offset the physical malaise resulting from today’s sedentary lifestyles.
“How do we explain that on the one hand consumers spend billions of dollars every year on analgesics and opioids, while exhausting and painful experiences such as obstacle races and ultra-marathons are gaining in popularity?” asked authors Rebecca Scott (Cardiff University), Julien Cayla (Nanyang Technological University), and Bernard Cova (KEDGE Business School).
Tough Mudder is a grueling adventure challenge involving about 25 military-style obstacles that participants — known as Mudders — must overcome in half a day. Among others, its events entail running through torrents of mud, plunging into freezing water, and crawling through 10,000 volts of electric wires. Injuries have included spinal damage, strokes, heart attacks, and even death.
Through extensive interviews with Mudders, the authors learned that pain helps individuals deal with the reduced physicality of office life. Through sensory intensification, pain brings the body into sharp focus, allowing participants who spend much of their time sitting in front of computers to rediscover their corporeality.
In addition, the authors write, pain facilitates escape and provides temporary relief from the burdens of self-awareness. Electric shocks and exposure to icy waters might be painful, but they also allow participants to escape the demands and anxieties of modern life.
“By leaving marks and wounds, painful experiences help us create the story of a fulfilled life spent exploring the limits of the body,” the authors conclude. “The proliferation of videos recording painful experiences such as Tough Mudder happens at least partly because a fulfilled life also means exploring the body in its various possibilities.”
Rebecca Scott, Julien Cayla, Bernard Cova. Selling Pain to the Saturated Self. Journal of Consumer Research, 2017; DOI: 10.1093/jcr/ucw071
Um babuíno sobreviveu por dois anos e meio após ter um coração de porco transplantado em seu abdômen. Em pesquisas anteriores, primatas sobreviviam no máximo 500 dias. O recorde foi divulgado na última terça-feira (5) na revista Nature Communications e abre espaço para transplantes entre suínos e humanos no futuro.
O método utilizou uma combinação de modificação genética e drogas imunossupressoras em cinco babuínos. Os corações dos porcos não substituíam os dos primatas — que continuaram com a função de bombear o sangue, mas estavam ligados ao sistema circulatório por meio de dois grandes vasos sanguíneos no abdômen.
Muitas vezes, o sistema imunológico do receptor rejeita o coração do doador por reconhecê-lo como estranho e, portanto, uma ameaça. Na pesquisa com babuínos, os corações dos porcos foram geneticamente modificados para ter alta tolerância à resposta imune. Os cientistas norte-americanos e alemães também adicionaram uma assinatura genética humana para ajudar a prevenir a coagulação do sangue.
Apenas um dos babuínos atingiu a marca de 945 dias vivo. A média entre os cinco foi de 298 dias. A equipe pensa em estender a pesquisa para a substituição dos órgãos.
Transplantes em humanos
Os cientistas têm feito experiências com transplante de rins, coração e fígados de primatas em seres humanos desde a década de 1960. Nenhum sobreviveu por mais de alguns meses.
Por conta da proximidade genética, os primatas eram os melhores candidatos a doadores. Mas não há uma grande quantidade de macacos criados em cativeiro.
Os corações dos porcos são anatomicamente semelhantes aos corações humanos. Os suínos também crescem rápido e são amplamente domesticados.
With several of its marquee players retiring early after a cascade of frightening concussions, the league formed a committee in 1994 that would ultimately issue a succession of research papers playing down the danger of head injuries. Amid criticism of the committee’s work, physicians brought in later to continue the research said the papers had relied on faulty analysis.
Now, an investigation by The New York Times has found that the N.F.L.’s concussion research was far more flawed than previously known.
For the last 13 years, the N.F.L. has stood by the research, which, the papers stated, was based on a full accounting of all concussions diagnosed by team physicians from 1996 through 2001. But confidential data obtained by The Times shows that more than 100 diagnosed concussions were omitted from the studies — including some severe injuries to stars like quarterbacks Steve Young and Troy Aikman. The committee then calculated the rates of concussions using the incomplete data, making them appear less frequent than they actually were.
After The Times asked the league about the missing diagnosed cases — more than 10 percent of the total — officials acknowledged that “the clubs were not required to submit their data and not every club did.” That should have been made clearer, the league said in a statement, adding that the missing cases were not part of an attempt “to alter or suppress the rate of concussions.”
One member of the concussion committee, Dr. Joseph Waeckerle, said he was unaware of the omissions. But he added: “If somebody made a human error or somebody assumed the data was absolutely correct and didn’t question it, well, we screwed up. If we found it wasn’t accurate and still used it, that’s not a screw-up; that’s a lie.”
These discoveries raise new questions about the validity of the committee’s findings, published in 13 peer-reviewed articles and held up by the league as scientific evidence that brain injuries did not cause long-term harm to its players. It is also unclear why the omissions went unchallenged by league officials, by the epidemiologist whose job it was to ensure accurate data collection and by the editor of the medical journal that published the studies.
In 2013, the N.F.L. agreed to a $765 million settlement of a lawsuit in which retired players accused league officials of covering up the risks of concussions. Some players have appealed the settlement, asking for an examination of the committee’s concussion research.
Dr. Joseph Waeckerle, speaking to quarterback Joe Montana in 1994, was the Chiefs’ team physician and a member of the N.F.L.’s concussion committee.CreditAssociated Press
Some retired players have likened the N.F.L.’s handling of its health crisis to that of the tobacco industry, which was notorious for using questionable science to play down the dangers of cigarettes.
Concussions can hardly be equated with smoking, which kills 1,300 people a day in the United States, and The Times has found no direct evidence that the league took its strategy from Big Tobacco. But records show a long relationship between two businesses with little in common beyond the health risks associated with their products.
In a letter to The Times, a lawyer for the league said, “The N.F.L. is not the tobacco industry; it had no connection to the tobacco industry,” which he called “perhaps the most odious industry in American history.”
Still, the records show that the two businesses shared lobbyists, lawyers and consultants. Personal correspondence underscored their friendships, including dinner invitations and a request for lobbying advice.
In 1997, to provide legal oversight for the committee, the league assigned Dorothy C. Mitchell, a young lawyer who had earlier defended the Tobacco Institute, the industry trade group. She had earned the institute’s “highest praise” for her work.
A co-owner of the Giants, Preston R. Tisch, also partly owned a leading cigarette company, Lorillard, and was a board member of both the Tobacco Institute and the Council for Tobacco Research, two entities that played a central role in misusing science to hide the risks of cigarettes.
The N.F.L.’s concussion committee began publishing its findings in 2003 in the medical journal Neurosurgery. Although the database used in the studies contained numerical codes for teams and players, The Times decoded it by cross-referencing team schedules and public injury reports.
The N.F.L.’s concussion studies have faced questions since they were published, but even the league’s harshest critics have never suggested, and no evidence has ever arisen, that the underlying data set could be so faulty.
“One of the rules of science is that you need to have impeccable data collection procedures,” said Bill Barr, a neuropsychologist who once worked for the Jets and who has in the past criticized the committee’s work.
By excluding so many concussions, Mr. Barr said, “You’re not doing science here; you are putting forth some idea that you already have.”
The Work Begins
In an introduction to the first of the concussion committee’s papers, the league’s commissioner at the time, Paul Tagliabue, acknowledged the need for “independent scientific research” to better understand the risks of concussions.
“As we looked more deeply into the specific area of concussions, we realized that there were many more questions than answers,” Mr. Tagliabue wrote.
The committee’s chairman, Dr. Elliot Pellman, the team physician for the Jets, emphasized that his group aimed to produce research that was “independent” and “meticulous.”
In fact, most of the dozen committee members were associated with N.F.L. teams, as a physician, neurosurgeon or athletic trainer, which meant they made decisions about player care and then studied whether those decisions were proper. Still, the researchers stated unambiguously — in each of their first seven peer-reviewed papers — that their financial or business relationships had not compromised their work.
The committee said it analyzed all concussions diagnosed by team medical staffs from 1996 through 2001 — 887 in all. Concussions were recorded by position, type of play, time missed, even the brand of helmet.
The committee’s statements emphasized the completeness of the data.
“It was understood that any player with a recognized symptom of head injury, no matter how minor, should be included in the study,” one paper said.
And in confidential peer-review documents, the committee wrote that “all N.F.L. teams participated” and that “all players were therefore part of this study.”
Those statements are contradicted by the database.
The Times found that most teams failed to report all of their players’ concussions. Over all, at least 10 percent of head injuries diagnosed by team doctors were missing from the study, including two sustained by Jets receiver Wayne Chrebet, who retired several years later after more concussions. Dr. Pellman, the Jets’ physician, led the research and was the lead author on every paper.
With the proposed connection between the Zika virus and Brazil’s outbreak of microcephaly in new born babies looking increasingly tenuous, Latin American doctors are proposing another possible cause: Pyriproxyfen, a pesticide used in Brazil since 2014 to arrest the development of mosquito larvae in drinking water tanks. Might the ‘cure’ in fact be the poison?
Malformations detected in thousands of children from pregnant women living in areas where the Brazilian state added Pyriproxyfen to drinking water are not a coincidence, even though the Ministry of Health places direct blame on the Zika virus.
The World Health Organization view that the microcephaly outbreak in Brazil’s impoverished northeast is caused by the Zika virus has, so far, received few challenges.
Brazil’s Health Minister, Marcelo Castro, has gone so far as to say that he has “100% certainty”that there is a link between Zika and microcephaly, a birth defect in which babies are born with small heads.
The view is widely supported in the medical community worldwide, including by the US’s influential Center for Disease Control. But there is no hard evidence of the link, rather a mixture of epidemiological indications and circumstantial evidence.
One of the key scientific papers, by A S Oliveira Melo et al in the journal Ultrasound in Obstetrics & Gynecology, found Zika virus in the amniotic fluids and other tissues of the affected babies and their mothers. But only two women were examined, far too small a number to establish a statistically significant link.
The New York Times also reported on 3rd February on the outcome of analyses by Brazil’s Health Ministry: “Of the cases examined so far, 404 have been confirmed as having microcephaly. Only 17 of them tested positive for the Zika virus. But the government and many researchers say that number may be largely irrelevant, because their tests would find the presence of the virus in only a tiny percentage of cases.”
And last weekend, the most powerful indicator yet that the microcephaly may have another cause altogether was announced by Colombia’s president, Juan Manuel Santos, as reported by the Washington Post. Colombian public health officials, stated Santos, have so far diagnosed 3,177 pregnant women with the Zika virus- but in no case had microcephaly been observed in the foetus.
Argentine doctors: it’s the insecticide
Now a new report has been published by the Argentine doctors’ organisation, Physicians in the Crop-Sprayed Towns (PCST),  which not only challenges the theory that the Zika virus epidemic in Brazil is the cause of the increase in microcephaly among newborns, but proposes an alternative explanation.
According to PCST, the Ministry failed to recognise that in the area where most sick people live, a chemical larvicide that produces malformations in mosquitoes was introduced into the drinking water supply in 2014.
This pesticide, Pyriproxyfen, is used in a state-controlled programme aimed at eradicating disease-carrying mosquitos. The Physicians added that the Pyriproxyfen is manufactured by Sumitomo Chemical, a Japanese ‘strategic partner‘ of Monsanto. – a company they have learned to distrust due to the vast volume of the company’s pesticides sprayed onto Argentina’s cropland.
Pyriproxyfen is a growth inhibitor of mosquito larvae, which alters the development process from larva to pupa to adult, thus generating malformations in developing mosquitoes and killing or disabling them. It acts as an insect juvenile hormone or juvenoid, and has the effect of inhibiting the development of adult insect characteristics (for example, wings and mature external genitalia) and reproductive development.
The chemical has a relatively low risk profile as shown by its WHO listing, with low acute toxicity. Tests carried out in a variety of animals by Sumitomo found that it was not a teratogen (did not cause birth defects) in the mammals it was tested on. However this cannot be taken as a completely reliable indicator of its effects in humans – especially in the face of opposing evidence.
The PCST commented: “Malformations detected in thousands of children from pregnant women living in areas where the Brazilian state added Pyriproxyfen to drinking water are not a coincidence, even though the Ministry of Health places a direct blame on the Zika virus for this damage.”
They also noted that Zika has traditionally been held to be a relatively benign disease that has never before been associated with birth defects, even in areas where it infects 75% of the population.
Brazilian doctors also suspect pyriproxyfen
Pyriproxyfen is a relatively new introduction to the Brazilian environment; the microcephaly increase is a relatively new phenomenon. So the larvicide seems a plausible causative factor in microcephaly – far more so than GM mosquitos, which some have blamed for the Zika epidemic and thus for the birth defects.
The PCST report, which also addresses the Dengue fever epidemic in Brazil, concurs with the findings of a separate report on the Zika outbreak by the Brazilian doctors’ and public health researchers’ organisation, Abrasco. 
Abrasco also names Pyriproxyfen as a possible cause of the microcephaly. It condemns the strategy of chemical control of Zika-carrying mosquitoes, which it says is contaminating the environment as well as people and is not decreasing the numbers of mosquitoes.
Instead Abrasco suggests that this strategy is in fact driven by the commercial interests of the chemical industry, which it says is deeply integrated into the Latin American ministries of health, as well as the World Health Organization and the Pan American Health Organisation.
Abrasco names the British GM insect company Oxitec as part of the corporate lobby that is distorting the facts about Zika to suit its own profit-making agenda. Oxitec sells GM mosquitoes engineered for sterility and markets them as a disease-combatting product – a strategy condemned by the Argentine Physicians as “a total failure, except for the company supplying mosquitoes.”
Both the Brazilian and Argentine doctors’ and researchers’ associations agree that poverty is a key neglected factor in the Zika epidemic. Abrasco condemned the Brazilian government for its “deliberate concealment” of economic and social causes: “In Argentina and across America the poorest populations with the least access to sanitation and safe water suffer most from the outbreak.” PCST agrees, stating, “The basis of the progress of the disease lies in inequality and poverty.”
Abrasco adds that the disease is closely linked to environmental degradation: floods caused by logging and the massive use of herbicides on (GM) herbicide-tolerant soy crops – in short, “the impacts of extractive industries.”
The notion that environmental degradation may a factor in the spread of Zika finds backing in the view of Dino Martins, PhD, a Kenyan entomologist. Martins said that “the explosion of mosquitoes in urban areas, which is driving the Zika crisis” is caused by “a lack of natural diversity that would otherwise keep mosquito populations under control, and the proliferation of waste and lack of disposal in some areas which provide artificial habitat for breeding mosquitoes.”
The Argentine Physicians believe that the best defence against Zika is “community-based actions”. An example of such actions is featured in a BBC News report on the Dengue virus in El Salvador.
A favourite breeding place for disease-carrying mosquitoes is storage containers of standing water. El Salvadorians have started keeping fish in the water containers, and the fish eat the mosquito larvae. Dengue has vanished along with the mosquitoes that transmit the disease. And so far, the locals don’t have any Zika cases either.
Simple yet effective programmes like this are in danger of being neglected in Brazil in favour of the corporate-backed programmes of pesticide spraying and releasing GM mosquitoes. The latter is completely unproven and the former may be causing far more serious harm than the mosquitoes that are being targeted.
In fact, the wellness craze has deep roots. Beginning in the middle of the 19th century, the leisure class grew infatuated with a particular type of healthy getaway: the water cure. By the 1850s, a constellation of spa villages had emerged across 20 states. By 1930, the country had over 2,000 hot- and cold-spring resorts.
Neither the practice nor the result of the treatment—which evolved out of a newfound enthusiasm for bathing—was strictly defined. Hydropathy encompassed everything from a spell in the tub to highly regimented procedures supervised by water doctors with stopwatches. According to its boosters, who were some of the most distinguished medical men of the day, water could cure everything from hiccups to cancer (and even hydrophobia!).Renowned water-lovers included John Roebling, the engineer of the Brooklyn Bridge, who liked to wrap himself in a damp, cold sheet, and most famously, President Franklin Roosevelt, whose interest in taking the waters long predated his visits to Warm Springs, Georgia.
Most of these “procedures” could have been performed at public baths, or at suburban facilities like the Harrogate spa, four miles out of Philadelphia. But part of the lure was always to get out of the city. For one thing, hydropathy was cast as a cure for the peculiar ailments of the well-off urbanite—a remedy for bourgeois decadence, to heal, as Carl Smith writes in City Water, City Life, the ill effects of the “overly refined life characteristic of cities.” (The equivalent of a modern farm vacation, maybe.)
“Taking the Waters at Saratoga”—a Harper’s cover in 1890 (Yates Collection of Saratogiana, Skidmore College)
For another thing, as Thomas Chambers suggests in Drinking the Waters, “taking the waters” was simply an excuse to have fun. And so a vast network of scenic spa towns emerged along the railroads. Built around grand bathhouses, they offered a much more social experience than bathing at home.
Some of these places, like Saratoga Springs, New York, or Palm Springs, California, blossomed into small cities, with diverse leisure cultures and other economic engines. But most fell into a state of prolonged decline in the 20th century. The trains stopped running; the visitors stopped arriving; the grand hotels closed, collapsed, or burned.
Not surprisingly, the perceived medical value of hydropathy dropped after the discovery of penicillin and the polio vaccine. But there were other factors at work, too. Bathing, like other old-time leisure pursuits, simply wasn’t cool anymore. Americans had taken up other, more exhilarating physical activities. And the automobile and the airplane opened up exciting new vacation possibilities.
But some spa towns are turning around, finding renewed interest in their quaint charms—and their water.
Hot Springs, Arkansas, is one of those places. A town of 35,000 about halfway between Memphis and Dallas, Hot Springs was once a major destination for high rollers from Chicago and St. Louis.
In 1946, visitors took 649,000 baths on Bathhouse Row, the parade of elegant spas abutting the main drag. By 1979, that number had fallen to just 79,000. Retail occupancy downtown in the 1980s was below 10 percent. All but one of the bathhouses closed between 1962 and 1985.
That surviving establishment, the Buckstaff, continues to offer an old-time water-cure to visitors. But it’s no longer the only game in town: In 2007, investors rehabilitated the neighboring Quapaw into a luxe modern spa. Three years ago, the Superior spa reopened as a brewery, producing the world’s only thermal beer.
The number of visitors to Hot Springs is steadily rising, and the retail occupancy rate is now over 90 percent. Historic architecture is no small part of its charm. “It’s totally a nostalgic story,” says Cole McCaskill, the downtown development director for the Hot Springs Metro Partnership. But, he adds, the city has done a good job diversifying its water-tourism offerings: A stay in Hot Springs now might include a trip to a nearby water park or aquarium.
Earlier visitors would have supplemented their health vacation with a little gambling, or a visit to an ostrich or alligator farm. This was typical, Chambers explains. “People wanted to find ways to have leisure, but culture told them they couldn’t do anything wasteful or not productive. You could say you were going to the springs for your health, but you were really going there to try and find a spouse or gamble.”
The Vanderbilts moved on years ago from Sharon Springs, New York, one of a handful of smaller, quieter resort towns west of Saratoga Springs. Now small-town appeal has drawn investors to revitalize the bathing industry there. A Korean investment group is restoring a long-dormant spa complex for Korean tourists, which has coincided with a general sense of civic renewal.
“We’re thrilled they’re doing something,” says Ron Ketelson, a California transplant who purchased the nearby Roseboro Hotel last year. “The bathhouse is being saved.”
For Ketelson, New York’s spa-town past represents something more personal than moth-balled grandeur. Not long after he purchased the Roseboro, Ketelson found an old postcard revealing that—unbeknownst to him—his own grandfather, suffering from breathing problems, had come to take the waters in Sharon Springs.
Doenças associadas à poluição do ar deixaram sete milhões de pessoas mortas em 2012, segundo a OMS. Foto: Banco Mundial / Curt Carnemark
Doenças relacionadas à presença de partículas na atmosfera provocaram a morte 7 milhões de pessoas em 2012. Aumento dos preços dos combustíveis poderia reduzir emissões de carbono, cortar pela metade mortes causadas por poluição e gerar 3 trilhões de dólares por ano, mais da metade dos gastos de saúde do planeta.
A Organização Mundial da Saúde (OMS) destacou nesta terça-feira (17) que as mudanças climáticas já causam milhares de mortes todos os anos, provocadas por fenômenos extremos, enchentes e secas e pela degradação da qualidade do ar, da água e dos alimentos. Segundo a agência da ONU, a situação tende a se agravar, caso os Estados-membros não adotem ações decisivas na Conferência do Clima de Paris, em dezembro.
De acordo com previsões da OMS, as mudanças climáticas poderão provocar, entre 2030 e 2050, 25 mil mortes por ano, associadas a infecções como malária e diarreia, a ondas de calor e a subnutrição. Outro fator preocupante é a poluição do ar. Doenças relacionadas à presença de partículas na atmosfera deixaram 7 milhões de pessoas mortas em 2012. Mulheres, crianças e os mais pobres em países de baixa renda serão os mais afetados no futuro.
Para a OMS, ações de combate às mudanças climáticas, como o investimento em desenvolvimento de baixo carbono e o uso de energias renováveis, trazem ganhos tanto para o meio ambiente, quanto para a saúde de todos. Segundo a agência, intervenções que reduzam as emissões de poluentes como o carbono negro e o metano e que restrinjam as emissões de veículos podem salvar 2,4 milhões de vidas por ano e reduzir em 0,5ºC o aquecimento do planeta até 2050.
A agência também afirmou que a atribuição de preços mais altos para combustíveis poluentes, de modo a compensar impactos de saúde negativos, pode reduzir as emissões de dióxido de carbono em 20% e cortar pela metade o número de mortes causadas pela poluição do ar. As restrições poderiam gerar lucros de 3 trilhões de dólares por ano, valor que representa mais da metade dos gastos de saúde de todos os governos do mundo. (ONU Brasil/ #Envolverde)
A situação é surreal. Decisões judiciais têm obrigado a USP a produzir e fornecer a pessoas com câncer uma substância cujos efeitos não são conhecidos, que não teve sua eficácia comprovada e, pior, jamais foi submetida a testes de segurança em seres humanos.
As liminares concedidas não só ignoram princípios básicos da pesquisa científica como também colocam em risco a vida dos mais de mil pacientes autorizados a receber um composto a respeito do qual praticamente nada se sabe.
Estudada por um professor do Instituto de Química da USP de São Carlos, a fosfoetanolamina só passou por experimentos em células e animais, nos quais mostrou algum potencial contra certos cânceres.
Noticia-se que o docente, seguro das possibilidades terapêuticas da substância –que não pode ser considerada um remédio–, a distribuía por conta própria. Em 2014, uma portaria da universidade interrompeu o fornecimento.
Iniciou-se, então, uma disputa judicial. Centenas de liminares determinando que a USP providenciasse a droga foram concedidas na primeira instância, mas, em setembro, terminaram suspensas pelo Tribunal de Justiça de São Paulo.
No começo de outubro, o ministro Luiz Edson Fachin, do Supremo Tribunal Federal, ordenou que um paciente recebesse cápsulas de fosfoetanolamina. Ato contínuo, o presidente do TJ-SP, José Renato Nalini, reconsiderou a suspensão de entrega da substância.
A argumentação dos magistrados denuncia profundo desconhecimento dos protocolos universalmente adotados para o desenvolvimento de fármacos.
Fachin, por exemplo, parece considerar o registro na Anvisa (Agência Nacional de Vigilância Sanitária) um detalhe desimportante. Não é. Trata-se de garantia de que a droga passou por todos os testes devidos –razão pela qual nem sequer há pedido de registro da fosfoetanolamina na agência.
Nalini, por sua vez, afirma que “não se podem ignorar os relatos de pacientes que apontam melhora no quadro clínico”. Ocorre que a ausência de testes controlados torna impossível saber se os alegados progressos decorreram de propriedades do composto.
Mais: sem as pesquisas apropriadas, não se podem descartar efeitos colaterais e graves problemas gerados pela interação com substâncias presentes em medicamentos.
Compreende-se que a luta contra o câncer leve pacientes a buscar todo tipo de tratamento –mas essa é uma questão individual. O Poder Judiciário, entretanto, ao decidir casos dessa natureza, não pode atropelar as normas de validação científica.
Levantamento aponta uso de drogas pela categoria. Intenção dos vereadores era redigir uma moção de apoio aos trabalhadores
Atualizado em 22 de setembro de 2015 às 11h45
Dois presidentes de sindicatos ligados ao Porto de Santos protestaram, na sessão de ontem da Câmara, contra a divulgação de uma pesquisa feita pela Universidade Federal Paulista (Unifesp) apontando o consumo de entorpecentes e ingestão de álcool entre os trabalhadores avulsos do cais.
As críticas partiram do presidente do Sindicato dos Operários Portuários (Sintraport), Claudiomiro Machado, o Miro, e do presidente do Sindicato dos Estivadores, Rodnei Oliveira, o Nei da Estiva. Eles afirmaram que o levantamento feito pela universidade feriu a honra da “família portuária”.
Quase todos os vereadores apoiaram a fala dos sindicalistas e questionaram o método de como a pesquisa foi feita. A pesquisa apontaria que 25% dos trabalhadores avulsos usam crack ou cocaína e 80% fazem ingestão de bebida alcoólica.
Miro questionou, por exemplo, o local onde o levantamento foi feito. “Dentro do Porto o acesso é liberado apenas ao trabalhador. Não foram lá entrevistar trabalhador portuário”.
O presidente do Sintraport relatou o drama vivido por um associado, cujo filho foi questionado na escola sobre a profissão do pai. “Falaram para o garoto: teu pai é portuário? Então ele usa cocaína, usa crack”.
Já Nei da Estiva se mostrou indignado pelo fato de nenhum sindicato ter sido procurado para comentar os dados da pesquisa.
Intenção dos vereadores era redigir uma moção de apoio aos trabalhadores ( Foto: Matheus Tagé/DL)
O vereador Antônio Carlos Banha Joaquim (PMDB) lembrou que a Unifesp já foi alvo de uma investigação de uma Comissão de Inquérito aberta na casa, que apurou contratos da universidade com a Prefeitura. “Um trabalho científico tem de ser feito com metodologia”, comentou.
Banha também se disse atingido com o resultado da pesquisa. “Meu avô era trabalhador portuário. Ele deve estar rolando no caixão”, comentou, antes de sugerir que a Unifesp seja questionada judicialmente sobre o levantamento.
Para o vereador Benedito Furtado (PSB), o resultado da pesquisa “dá a entender que 80% dos portuários são alcoólatras”. Ele também atacou ferozmente a universidade. “Essa tal de Unifesp não cumpre lei municipal”.
Ressaltando ser filho de estivador, Geonísio Pereira de Aguiar, o Boquinha (PSDB), além de questionar a seriedade da pesquisa, disse que quase todos os alunos da instituição não são de Santos e, por isso, devem conhecer pouco o cais.
Igor Martins de Melo, o Professor Igor (PSB), foi outro a lembrar que os pesquisadores precisam ter autorização para entrar na área portuária. “Quer dizer, então, que o maior porto da América Latina é tocado por um bando de irresponsáveis? O que é isso?”
Vereador e professor de Matemática, José Lascane (PSDB) disse que é preciso tomar extremo cuidado ao se fazer um levantamento feito pela Unifesp. “A amostra precisa ser bem avaliada, bem como a formulação da pergunta, que precisa ser bem clara”.
Marcelo Del Bosco (PPS) deu uma sugestão ao líder do Governo na Câmara, Sadao Nakai (PSDB): o secretário municipal de Assuntos Portuários e Marítimos, José Eduardo Lopes, deve se manifestar sobre o levantamento.
Roberto Oliveira Teixeira, o Pastor Roberto (PMDB), disse que as esposas dos trabalhadores portuários “se sentiram humilhadas com o resultado dessa pesquisa”.
What is it that makes you, you? While you’re made up of 10 trillion human cells, 100 trillion microbial cells also live on you and in you. This vast array of microscopic bugs may be your defining feature, and scientists around the world are racing to find out more. Amanda Smith reports.
Microbes, it seems, are the next big thing. Around the world, scientists are researching the human microbiome—the genes of our microbes—in the hope of unlocking quite a different way to understand sickness and health.
At the Microbiome Initiative at the University of California, San Diego, Rob Knight runs the American Gut Project, a citizen science initiative where you can get your microbiome sequenced.
Breast milk is meant to present the baby with a manageable dose of everything in the environment. It samples the entire environment—everything the mother eats, breathes, touches.
MAUREEN MINCHIN, AUTHOR OF MILK MATTERS.
‘What we can do right now is put you on this microbial map, where we can compare your microbes to the microbes of thousands of other people we’ve already looked at,’ he says. ‘But what we need to do is develop more of a microbial GPS that doesn’t just tell you where you are, but tells you where you want to go and what you need to do, step by step, in order to get there.’
The Australian Centre for Ecogenomics is also setting up a service where you can get your gut microbes analysed. The centre’s director, Phillip Hugenholtz, predicts that in years to come such a process will be a diagnostic procedure when you go to the doctor, much like getting a blood test.
‘I definitely think that’s going to become a standard part of your personalised medicine’, he says. ‘Micro-organisms are sometimes a very good early indicator of things occurring in your body and so it will become something that you’d go and get done maybe once or twice a year to see what’s going on.’
While this level of interest in the microbiome is new, the first person to realise we’re all teeming with micro-organisms was Dutchman Anton Leeuwenhoek, way back in 1676. Leeuwenhoek was interested in making lenses, and constructed himself a microscope.
‘He was looking at the scum from his teeth, and was amazed to see in this scraped-off plaque from inside his own mouth what he called hundreds of different “animalcules swimming a-prettily”,’ says Tim Spector, professor of genetic epidemiology at Kings College London.
‘He was the first to describe this, and it took hundreds of years before people actually believed that we were completely full of these microbes and we’d co-evolved with them.’
Microbes have come a long way over the last century. Until recent advances in DNA sequencing, all tummy bugs were considered bad.
‘We used to think that there was no such thing as a good microbe in our guts, that they were all out to do us no good, and we’ve basically spent the last 100 years trying to eliminate them with disinfectants and then the last 50 years with antibiotics,’ says Spector.
This has given rise to the ‘hygiene hypothesis’, which contends that by keeping ourselves too clean, we’re denying ourselves the microbes necessary to keep our immune system balanced, resulting in all sorts of chronic diseases.
‘Over the last half-century, as infectious diseases like polio and measles and hepatitis and so-on have plummeted in their frequency, chronic diseases—everything from obesity to diabetes to inflammatory bowel disease—have been skyrocketing,’ says the Microbiome Initiative’s Rob Knight.
‘So the idea is that potentially without exposure to a diverse range of healthy microbes our immune systems might be going into overdrive and attacking our own cells, or overreacting to harmless things we find in the environment.’
In terms of human DNA, we’re all 99.99 per cent identical. However our microbial profiles can differ enormously. We might share just 10 per cent of our dominant microbial species with others.
According to Knight, some of the differences are explained by method of birth.
‘If you come out the regular way you get coated with microbes as you’re passing through your mother’s birth canal,’ he says.
Babies delivered by Caesarian section, on the other hand, have microbes that are mostly found on adult skin, from being touched by different doctors and nurses.
‘One thing that’s potentially interesting about that is differences between C-section and vaginally delivered babies have been reported: higher rates in C-section babies of asthma, allergies, atopic disease, even obesity. All of those have been linked to the microbiome now.’
Also important to the development of healthy microbiota in babies is breastfeeding, according to Maureen Minchin, the author of Milk Matters.
‘We’ve known for over 100 years that breast milk and formula result in very, very different gut flora in babies, but it’s only very recently that anyone has thought to look and see what breast milk does contain, and at last count there were well over 700 species of bacteria in breast milk,’ she says.
According to Minchin, breastfeeding is the bridge between the womb and the world for babies.
‘Breast milk is meant to present the baby with a manageable dose of everything in the environment. It samples the entire environment—everything the mother eats, breathes, touches. Her microbiome is present in that breast milk and will help create the appropriate microbiome in the baby.’
Minchin is an advocate of the World Health Organisation’s recommendation to breastfeed exclusively to six months and then continue breastfeeding while introducing other foods through the first and second year.
So if what babies are fed is important for their microbiome, what about adults? Tim Spector says research into microbes is yielding new information about healthy eating.
‘It’s going to soon revolutionise how we look at food and diet. This is one of the most exciting things in science at the moment, because it’s obviously much easier to change your microbes than it is to change your genes.’
‘Most processed foods only contain about five ingredients, and in a way our epidemic of the last 30 years of obesity and allergy is that our diets have become less and less diverse.’
According to Spector, studies of people with various chronic diseases, obesity and diabetes show a common feature, which is that their gut microbes have a much-reduced diversity compared to healthy people.
He likes to use the analogy of a garden: ‘A neglected garden has very few species, not much fertilised soil, and this allows weeds to take over in great numbers,’ he says.
‘I think this is a nice concept because we’re very good gardeners, humans, and I think we need to start using those principles—fertilising, adding soil, experimenting and avoiding adding nasty toxins to our own bodies as we would our gardens.’
Notícia de poucos dias atrás (Diário Digital, 19/4) dá conta de pesquisa (relatada pela revista Science) de um grupo de cientistas que, trabalhando na fronteira Brasil-Venezuela com índios ianomâmis, conclui que eles têm anticorpos resistentes a agentes externos – “um microbioma com o nível mais alto de diversidade bacteriana” jamais registrado em qualquer outro grupo. Por isso mesmo, “seu sistema imunológico apresenta mais microrganismos e de todas as bactérias que o dos demais grupos humanos conhecidos” – como demonstrou o sequenciamento de DNA e de bactérias encontradas na pele, na boca e nos intestinos.
Essas análises foram confirmadas por pesquisas em universidades norte-americanas, que recentemente devolveram aos ianomâmis 2.693 amostras de sangue levadas para os Estados Unidos em 1962 – e que agora foram sepultadas pelos índios em cerimoniais respeitosos. Segundo os pesquisadores, na relação com outros grupos humanos esses índios perdem a diversidade de microrganismos e se tornam vulneráveis a doenças que antes não conheciam.
A memória dá um salto e retorna a 1979, quando o autor destas linhas, então chefe da redação do programa Globo Repórter, da Rede Globo, foi pela primeira vez ao Parque Indígena do Xingu documentar um trabalho que ali vinha sendo feito por uma equipe de médicos da Escola Paulista de Medicina (hoje Universidade Federal de São Paulo), liderada pelo professor Roberto Baruzzi. Os pesquisadores acompanhavam a saúde de cada índio de várias etnias do sul do Xingu, mantinham fichas específicas de todos e as comparavam com a visita anterior. A conclusão era espantosa: não havia ali um só caso de doenças cardiovasculares – exatamente porque, vivendo isolados, os índios não tinham nenhum dos chamados fatores de risco dessas doenças: não fumavam, não bebiam álcool, não tinham vida sedentária nem obesidade, não apresentavam hipertensão, não consumiam sal (só sal vegetal, feito com aguapé) nem açúcar de cana. Saindo do Xingu, fomos documentar grupos de índios caingangues e guaranis aculturados que viviam nas proximidades de Bauru (SP). Os que trabalhavam eram boias-frias e os demais, mendigos, alcoólatras, com perturbações mentais. Praticamente todos eram hipertensos, obesos, com taxas de mortalidade altas e precoces. A comparação foi ao ar num documentário, As Razões do Coração, que teve índices altíssimos de audiência.
São informações que deveriam fazer parte de nossas discussões de hoje, quando estamos às voltas com várias crises na área de saúde – epidemias de dengue (mais de 220 casos novos por hora, 257.809, ou 55% do total, em São Paulo), índices altíssimos de obesidade, inclusive entre jovens e crianças, doenças cardiovasculares entre as mais frequentes causas de morte. Mas em lugar de prestar atenção aos modos de viver de indígenas, enquanto ainda na força de sua cultura, continuamos a tratá-los como seres estranhos, que vivem pelados, não falam nossas línguas, não trabalham segundo nossos padrões. A ponto de eles terem agora de se rebelar para que não se aprove no Congresso Nacional, sob pressão principalmente da “bancada ruralista”, uma proposta de emenda constitucional que lhes retira parte de seus direitos assegurados pela constituição de 1988 e transfere da Funai para o Congresso o poder de demarcar ou não terras indígenas.
Com esses rumos acentuaremos o esquecimento de que eles foram os “donos” de todo o território nacional, do qual foram gradativamente expulsos. Mas ainda são quase 1 milhão de pessoas de 220 povos, que falam 180 línguas, em 27 Estados. Agora avança, inclusive no Judiciário, a tese de que só pode ser reconhecido para demarcação território já ocupado efetivamente por eles antes de 1988. E assim cerca de 300 áreas correm riscos.
Só que nos esquecemos também dos relatórios da ONU, do Banco Mundial e de outras instituições segundo os quais as áreas indígenas são os lugares mais eficazes em conservação da biodiversidade – mais que as reservas legais e outras áreas protegidas. Que seus modos de viver são os que mais impedem desmatamentos – esse problema tão angustiante por sua influência na área do clima e dos regimes de chuvas.
Isso não tem importância apenas para o Brasil. A própria ONU, por meio de sua Agência para a Alimentação e Agricultura (FAO), afirma (Eco-Finanças, 17/4) que a “crise da água” afetará dois terços da população mundial em 2050 (hoje já há algum nível de escassez para 40% da população). E que o fator principal será o maior uso da água para produzir 60% mais alimentos que hoje.
Mas há diferenças de um lugar para outro. Os países ditos desenvolvidos, com menos de 20% da população mundial, consomem quase 80% dos recursos físicos; os Estados Unidos, com 5% da população, respondem por 40% do consumo. Segundo a sua própria Agência de Proteção Ambiental, os EUA jogam no lixo 34 milhões de toneladas anuais de alimentos. No mundo, um terço dos alimentos é desperdiçado (FAO, 5/2), enquanto mais de 800 milhões de pessoas passam fome e mais de 2 bilhões vivem abaixo da linha de pobreza. No Brasil mesmo, 3,4 milhões de pessoas passam fome (Folha de S.Paulo, 22/9/2014). A elas podemos somar mais de 40 milhões de pessoas que vivem do Bolsa Família.
Diante de tudo isso, vale a pena lembrar o depoimento do saudoso psicanalista Hélio Pellegrino, no livro Noel Nutels – Memórias e Depoimentos, sobre o médico que dedicou sua vida a grupos indígenas. “Se estamos destruindo os índios”, escreveu Hélio Pellegrino, “é porque nossa brutalidade chegou a um nível perigoso para nós próprios. Os índios representam a possibilidade humana mais radical e íntima de transar com a natureza (…). Homem e natureza são casados (…). Dissolvido esse casamento, o homem tomba num exílio feito de poeira amarga e estéril”. (O Estado de S. Paulo/ #Envolverde)
* Washington Novaes é jornalista. E-mail: firstname.lastname@example.org.
Energia liberada pelas mãos consegue curar malefícios, afirma pesquisa da USP
25/11/2011 – 08h58 . Gazeta de Ribeirão
A missionária Marta Brisa transmite as técnicas de Johrei em Ana Paula Politi
(Foto: Lucas Mamede/Da Gazeta de Ribeirão)
Um estudo desenvolvido recentemente pela USP (Universidade de São Paulo), em conjunto com a Unifesp (Universidade Federal de São Paulo), comprova que a energia liberada pelas mãos tem o poder de curar qualquer tipo de mal estar. O trabalho foi elaborado devido às técnicas manuais já conhecidas na sociedade, caso do Johrei, utilizada pela igreja Messiânica do Brasil e ao mesmo tempo semelhante à de religiões como o espiritismo, que pratica o chamado “passe”.
Todo o processo de desenvolvimento dessa pesquisa nasceu em 2000, como tema de mestrado do pesquisador Ricardo Monezi, na Faculdade de Medicina da USP. Ele teve a iniciativa de investigar quais seriam os possíveis efeitos da prática de imposição das mãos. “Este interesse veio de uma vivência própria, onde o Reiki (técnica) já havia me ajudado, na adolescência, a sair de uma crise de depressão”, afirmou Monezi, que hoje é pesquisador da Unifesp.
Segundo o cientista, durante seu mestrado foram investigado os efeitos da imposição em camundongos, nos quais foi possível observar um notável ganho de potencial das células de defesa contra células que ficam os tumores. “Agora, no meu doutorado que está sendo finalizado na Unifesp, estudamos não apenas os efeitos fisiológicos, mas também os psicológicos”, completou.
A constatação no estudo de que a imposição de mãos libera energia capaz de produzir bem-estar foi possível porque a ciência atual ainda não possui uma precisão exata sobre esse efeitos. “A ciência chama estas energias de ‘energias sutis’, e também considera que o espaço onde elas estão inseridas esteja próximo às frequências eletromagnéticas de baixo nível”, explicou.
As sensações proporcionadas por essas práticas analisadas por Monezi foram a redução da percepção de tensão, do stress e de sintomas relacionados a ansiedade e depressão. “O interessante é que este tipo de imposição oferece a sensação de relaxamento e plenitude. E além de garantir mais energia e disposição.”
Neste estudo do mestrado foram utilizados 60 ratos. Já no doutorado foram avaliados 44 idosos com queixas de stress.
O processo de desenvolvimento para realizar este doutorado foi finalizado no primeiro semestre deste ano. Mas a Unifesp está prestes a iniciar novas investigações a respeito dos efeitos do Reiki e práticas semelhantes a partir de abril do ano que vem.
Pesquisa da Unesp estuda união entre tratamento espiritual e médico. Trabalho é realizado por médicos da Associação Espírita de Botucatu (SP).
Do G1 Bauru e Marília
Passe simples sendo aplicado pelo grupo mediúnico (Foto: Isabela Ribeiro/ G1)
Um grupo de oito médicos da Associação Espírita de Médicos de Botucatu (SP) se reuniu para pesquisar a influência da terapêutica energética do “passe” espírita na redução da ansiedade. A técnica, originada das práticas de cura do cristianismo primitivo, consiste basicamente na imposição de mãos sobre uma pessoa, a fim de transferir boas energias e tratar o lado espiritual de quem recebe o “passe”.
A pesquisa teve início em 2014 e está em fase de desenvolvimento na Faculdade de Medicina de Botucatu/Unesp (FMB). De acordo com o médico infectologista Ricardo de Souza Cavalcante, a inspiração para a pesquisa surgiu de outro grupo de médicos, de São Paulo, que iniciou um estudo sobre a eficácia de uma técnica semelhante, o Reiki, de origem japonesa.
Passistas preparados iniciar sessão do passe conjugado (Foto: Isabela Ribeiro/ G1)
O estudo sobre o “passe” é feito com voluntários, não necessariamente espíritas ou praticantes de alguma religião, que não estejam fazendo nenhum tipo de tratamento psicológico ou psiquiátrico. “Primeiramente, nós fazemos uma avaliação médica para verificar se o voluntário tem realmente o diagnóstico de ansiedade. Se confirmado, o paciente passa a frequentar a sala de estudos uma vez por semana, durante oito semanas, para receber o ‘passe’ ”, explica Ricardo.
Ainda de acordo com o médico, antes de iniciar o tratamento, os participantes passam por um tempo de meditação e concentração. Música ambiente é utilizada para relaxar e, por 5 minutos, um terapeuta impõe as mãos sobre a cabeça, tórax e barriga do voluntário. São levados em conta, na análise, níveis de depressão, qualidade de vida e grau de espiritualidade do paciente.
Os voluntários respondem a um questionário ao final de cada sessão e, alguns deles, passam por exames de eletroencefalograma, para medir as variações das ondas cerebrais antes, durante e depois do procedimento.
Passe conjugado, com dois ou mais passistas (Foto: Isabela Ribeiro/ G1)
Ciência e espiritualidade
Nas últimas décadas, muitos estudos científicos têm sido feitos a fim de demonstrar os benefícios de aliar o trabalho com a espiritualidade ao tratamento médico convencional.
“Houve uma separação histórica, mas eu acredito que essas coisas precisam caminhar juntas. O ser humano deve ser visto como um todo. Nós não somos só um amontoado de células. Temos, comprovadamente, um lado emocional, espiritual”, pontua Ricardo.
A dona de casa Silvia Helena Vieira da Silva, de 47 anos, é uma das voluntárias que participarão da pesquisa. Católica, ela acredita que as práticas espíritas podem colaborar para o bem-estar. “Nós estamos tão ansiosos, nos medicando tanto, que eu gostaria de experimentar algo que não fosse medicamento, até porque remédios atacam meu organismo. Se eu puder fugir, eu fujo”, declara Silvia, que sofre as consequências físicas da ansiedade.
“Nós que temos filhos, estamos sempre na expectativa de algo. É um convívio constante com a ansiedade. Quando ela aparece, meu intestino solta, sinto dores no estômago e na cabeça. Quero muito que esta iniciativa dê certo”, conta.
“Muitos voluntários estão participando da pesquisa. Eles precisaram demonstrar ter ansiedade e não esteja em tratamento psicológico pode participar. Nosso objetivo não é converter ninguém”, explica o médico.
Os interessados em participar da pesquisa podem obter informações pelo telefone (14) 3811- 6547.
Leopoldo Zanardi, diretor de comunicação do Centro Espírita Amor e Caridade (Foto: Isabela Ribeiro/ G1)
Passe na Dourtina Espírita
De acordo com Leopoldo Zanardi, diretor de comunicação do Centro Espírita Amor e Caridade, de Bauru (SP), o “passe” trata-se de uma assistência espiritual, denominada de fluidoterapia, e que não anula a necessidade do tratamento médico. Este nome é dado por ser uma transferência de energias. “As mãos são colocadas de 10 a 15 centímetros acima da cabeça, não há toque físico. A Federação Espírita brasileira aconselha que as mãos sejam colocadas apenas sobre a cabeça”, conta Leopoldo.
Ele explica também que, na doutrina espírita, acredita-se que além das boas energias passadas pelo passista, existe também a atuação de espíritos que identificam e agem diretamente no problema de quem está recebendo o passe, seja ele físico, emocional ou espiritual. O procedimento pode ser individual (“passe simples”) ou em grupo (“passe conjugado” – 2 ou mais passistas realizam o procedimento). Mas quanto mais pessoas estiverem juntas, melhor, de acordo com Leopoldo.
Prece feita pelo grupo mediúnico antes de dar início ao procedimento (Foto: Isabela Ribeiro/ G1)
No Centro Espírita, o passe simples pode ser tomado por qualquer um que desejar, sem a necessidade de entrevista. Mas, para aqueles que querem tratar algo específico, é necessário passar pelo atendimento, onde será identificada a necessidade de cada pessoa.
Em seguida a pessoa recebe um papel que dá direito a oito passes, que devem ser tomados uma vez por semana. Em ambos os casos, os pacientes entram em uma sala, após um período de oração do grupo mediúnico (responsável por aplicar os passes), sentam-se nas cadeiras e estendem as duas mãos para frente, como quem está para receber algo.
Os passistas, como também são chamados os membros do grupo mediúnico, impõe as mãos sobre a cabeça das pessoas, uma nova prece é anunciada e, após poucos minutos de silêncio, tudo está feito. Depois de dispensar as pessoas, os passistas fazem outra oração de agradecimento e encerram o procedimento. “É importante ressaltar que não se deve abrir mão do tratamento médico. Nós oferecemos uma assistência espiritual. Também não basta apenas ‘tomar o passe’. É necessário assistir às palestras, mudar o pensamento, buscar ser melhor a cada dia. Dominar as más inclinações e fazer caridade. Precisamos estar em constante evolução”, completa Leopoldo.
Iole Angelo Cintra fala de sua experiência com o passe espírita (Foto: Isabela Ribeiro/ G1)
Para a dona de casa Iole Angelo Cintra, de 46 anos, tomar os “passes” trouxe melhora para problemas de insônia e dor de cabeça que, segundo ela, tinham raiz espiritual.
“Eu não dormia direito à noite. Aqui no centro descobri que eu tinha ‘desdobramento’, que é uma espécie de mediunidade que me faz sair do meu corpo. Eu me via dormindo à noite e andava pela minha casa. Quando comecei a tomar os passes, as dores de cabeça sumiram e eu pude controlar mais esse desdobramento. O efeito do passe é ótimo, mas também depende da pessoa se esforçar para ser alguém melhor”, contou Iole.
Aplicação do passe simples pelo grupo mediúnico (Foto: Isabela Ribeiro/ G1)
One long-ago summer, I joined the legion of teens helping harvest our valley’s peach crop in western Colorado. My job was to select the best peaches from a bin, wrap each one in tissue, and pack it into a shipping crate. The peach fuzz that coated every surface of the packing shed made my nose stream and my eyelids swell. When I came home after my first day on the job, my mother was so alarmed she called the family doctor. Soon the druggist was at the door with a vial of Benadryl (diphenhydramine) tablets. The next morning I was back to normal and back on the job. Weeks later, when I collected my pay (including the ½-cent-per-crate bonus for staying until the end of the harvest), I thanked Benadryl.
Anticholinergic drugs block the action of acetylcholine. This substance transmits messages in the nervous system. In the brain, acetylcholine is involved in learning and memory. In the rest of the body, it stimulates muscle contractions. Anticholinergic drugs include some antihistamines, tricyclic antidepressants, medications to control overactive bladder, and drugs to relieve the symptoms of Parkinson’s disease.
What the study found
A team led by Shelley Gray, a pharmacist at the University of Washington’s School of Pharmacy, tracked nearly 3,500 men and women ages 65 and older who took part in Adult Changes in Thought (ACT), a long-term study conducted by the University of Washington and Group Health, a Seattle healthcare system. They used Group Health’s pharmacy records to determine all the drugs, both prescription and over-the-counter, that each participant took the 10 years before starting the study. Participants’ health was tracked for an average of seven years. During that time, 800 of the volunteers developed dementia. When the researchers examined the use of anticholinergic drugs, they found that people who used these drugs were more likely to have developed dementia as those who didn’t use them. Moreover, dementia risk increased along with the cumulative dose. Taking an anticholinergic for the equivalent of three years or more was associated with a 54% higher dementia risk than taking the same dose for three months or less.
The ACT results add to mounting evidence that anticholinergics aren’t drugs to take long-term if you want to keep a clear head, and keep your head clear into old age. The body’s production of acetylcholine diminishes with age, so blocking its effects can deliver a double whammy to older people. It’s not surprising that problems with short-term memory, reasoning, and confusion lead the list of anticholinergic side effects, which also include drowsiness, dry mouth, urine retention, and constipation.
The University of Washington study is the first to include nonprescription drugs. It is also the first to eliminate the possibility that people were taking a tricyclic antidepressant to alleviate early symptoms of undiagnosed dementia; the risk associated with bladder medications was just as high.
“This study is another reminder to periodically evaluate all of the drugs you’re taking. Look at each one to determine if it’s really helping,” says Dr. Sarah Berry, a geriatrician and assistant professor of medicine at Harvard Medical School. “For instance, I’ve seen people who have been on anticholinergic medications for bladder control for years and they are completely incontinent. These drugs obviously aren’t helping.”
Many drugs have a stronger effect on older people than younger people. With age, the kidneys and liver clear drugs more slowly, so drug levels in the blood remain higher for a longer time. People also gain fat and lose muscle mass with age, both of which change the way that drugs are distributed to and broken down in body tissues. In addition, older people tend to take more prescription and over-the-counter medications, each of which has the potential to suppress or enhance the effectiveness of the others.
What should you do?
In 2008, Indiana University School of Medicine geriatrician Malaz Boustani developed the anticholinergic cognitive burden scale, which ranks these drugs according to the severity of their effects on the mind. It’s a good idea to steer clear of the drugs with high ACB scores, meaning those with scores of 3. “There are so many alternatives to these drugs,” says Dr. Berry. For example, selective serotonin re-uptake inhibitors (SSRIs) like citalopram (Celexa) or fluoxetine (Prozac) are good alternatives to tricyclic antidepressants. Newer antihistamines such as loratadine (Claritin) can replace diphenhydramine or chlorpheniramine (Chlor-Trimeton). Botox injections and cognitive behavioral training can alleviate urge incontinence.
One of the best ways to make sure you’re taking the most effective drugs is to dump all your medications — prescription and nonprescription — into a bag and bring them to your next appointment with your primary care doctor.
Mas e em 2015, o que veremos? Apostamos em cinco coisas que poderão aparecer neste ano.
Se queremos colonizar Marte, não adianta passagem só de ida. Esses foguetes, capazes de ir e voltar, são a promessa para transformar o futuro das viagens espaciais. Veremos se a empresa SpaceX, que já está nessa, consegue.
Robôs em casa
Os japoneses da Softbank começam a vender, em fevereiro, um robô humanoide chamado Pepper. Ele usa inteligência artificial para reconhecer o humor do dono e fala quatro línguas. Apesar de ser mais um ajudante do que um cara que faz, logo logo aprenderá novas funções.
O Grande Colisor de Hádronsvai voltar a funcionar em março e terá potência duas vezes maior de quebrar partículas. Uma das possibilidades é que ele ajude a descobrir novas superpartículas que, talvez, componham a matéria escura. Seria o primeiro novo estado da matéria descoberto em um século.
Cura para o ebola
Depois da crise de 2014, pode ser que as vacinas para o ebola comecem a funcionar e salvem muitas vidas na África. Vale o mesmo para a aids. O HIV está cercado, esperamos que a ciência finalmente o vença neste ano.
2014 foi um dos mais quentes da história e, do jeito que a coisa vai, 2015 seguirá a mesma trilha. Em dezembro, o mundo vai discutir um acordo para tentar reverter o grau de emissões de gases em Paris. São medidas para ser implementadas a partir de 2020. Que sejam sensatos nossos líderes.
Mothers’ stress during 1998 ice storm shows up in children’s DNA, study says (Fox News)
By John Johnson
Published October 20, 2014
File photo of the aftermath of an ice storm. (AP Photo/Matt Rourke)
Just how bad was an epic 1998 ice storm in Canada? You can read all about it in the DNA of kids who were born around that time.
An intriguing study in PLoS One finds that women who were especially stressed during the storm gave birth to kids whose immune cells have telltale signs of their mothers’ trouble, reports Raw Story.
The storm was brutal, leaving people without power for more than a month. Researchers at the time surveyed expectant moms to gauge their “objective” distress, measuring things such as how many days they went without electricity.
Then they tracked down their kids more than a decade later and found that moms who were in the most distress bore children whose DNA had specific markers as a result.
The genes affected are related to immune function and sugar metabolism. Toronto’s Globe and Mail has a nice explanation of what’s going on, with help from Suzanne King of McGill University.
It involves “epigenetics,” as opposed to genetics:
“An individual’s genetics are like a musical score, and what’s written comes from the mother and father. … Although nothing can change what’s written on the page, environmental factors act as an orchestral conductor might, amplifying some aspects and tempering others, leaving markings, or methylation of the DNA.”
This isn’t necessarily a bad thing.
A pregnant woman in a famine, for instance, might “amplify” traits that would give her child a better chance of surviving—traits that could then backfire in terms of health if the famine goes away.
It’s not clear what, if any, health effects the Canadian kids will see as a result, explains a post at McGill University. But given the genes affected, they might have a greater risk of developing asthma, diabetes, or obesity.
Summary: The cycling of mercury through soil and water has been studied as it impacts atmospheric loadings, researchers report. Recent studies that show increasing levels of mercury in the ocean’s upper levels, along with news reports of Arkansas lakes as a hotspot for mercury in fish, have heightened awareness of the potential harm mercury poses.
The professor and chair of the University of Arkansas at Little Rock Department of Chemistry has recently completed an in-depth review of atmospheric mercury in Energy and Emissions Control Technologies, an open access peer-review journal published by Dove Press.
Dr. Jeffrey S. Gaffney and his co-author Nancy A. Marley stressed in their article the many forms that atmospheric mercury takes and how its levels are in balance with mercury levels found in our water, soil, and the biosphere.
Recent studies that show increasing levels of mercury in the ocean’s upper levels, along with news reports of Arkansas lakes as a hotspot for mercury in fish, have heightened awareness of the potential harm mercury poses.
The article, titled “In-depth review of atmospheric mercury: sources, transformations, and potential sink,” has seen extensive online traffic since it was first published Aug. 6.
Gaffney said the high volume of page visits was likely tied to the recent news concerning the rising levels of mercury in the oceans. Mercury is a toxic, heavy metal found naturally throughout the global environment.
Increased levels of mercury in the water could be caused by atmospheric deposition primarily in precipitation, something not usually considered when measuring mercury levels, according to the authors.
This timely review outlines the chemistry of mercury in gas, aqueous, and solid phases, including inorganic, organic, and complexed mercury species. The research particularly brings attention to the wet reaction of gaseous mercury with hydrogen peroxide that can occur in clouds and on wet aerosol surfaces.
The sources and fate of mercury in the atmosphere, including the cycling of mercury through soil and water as it impacts atmospheric loadings, are also examined in the review, as well as recommendations for future studies.
Jeffrey Gaffney, Nancy Marley. In-depth review of atmospheric mercury: sources, transformations, and potential sinks. Energy and Emission Control Technologies, 2014; 1 DOI: 10.2147/EECT.S37038
That cockroaches will inherit our despoiled earth is just a tired misconception. The real champions will be disease-carrying rats.
Even though cockroaches seem to be of inexhaustible supply, their invertebrate ilk are actually suffering a fairly rapid decline—and the rodents are rising up. In a recent and widely-discussed study in Science, researchers examined a process called defaunation—remember that term, it’s likely to prove as vital as ‘Arctic ice melt’ or ‘habitat loss’ to understanding our planet’s ecological collapse—that describes how the majority of the world’s animals are vanishing at a rapid pace.
Led by Rodolfo Dirzo, a professor of biology at Stanford University, a team of scientists documented the rate that fauna are going extinct in the modern era. Since the year 1500 AD, at least 320 vertebrate species have been extinguished, primarily due to human activity. Those that remain have seen their total populations decline by 25 percent. Even more striking is the decline of insects: In the past 35 years alone, the scientists found that the number of invertebrates have plummeted 45 percent. The researchers cite the drops as further evidence that we are bearing witness to the unfurling of the Anthropocene Extinction event—the planet’s sixth great mass extinction.
So who wins, besides humans, when the bees and the tigers and the bears lose? Rats.
“Where human density is high, you get high rates of defaunation, high incidence of rodents, and thus high levels of pathogens, which increases the risks of disease transmission,” Dirzo said in a statement upon the study’s publication. “Who would have thought that just defaunation would have all these dramatic consequences? But it can be a vicious circle.”
Hilary Young, one of the study’s authors, has conducted previous research examining how rodents thrived after a large species went extinct.
RATS COULD GROW LARGER THAN SHEEP
“What we found was that these areas quickly experienced massive increases of rodents,” Young told The Current. “All the grass and shrubs normally eaten by this megafauna was, instead, available for rodents—both as food and as shelter. Consequently, the number of rodents doubled—and so did the abundance of the disease-carrying ectoparasites that they harbored.”
Twice the rats. And twice the ectoparasites. A 2013 study in the International Journal of Current Microbiology and Applied Sciences examined how parasite-carrying rats are instrumental in transporting disease: “Rodents together with arthropod ectoparasites can play an important role in the distribution of the arboviruses, streptococcal infections, choriomeningitis, plague, tularemia, leptospirosis, spirochaetosis etc.,” the authors wrote.
“Ectoparasites include insects and acarnies (fleas and mites),” the 2013 study continued, “some of them are permanent like lice, while most of the mature ticks and fleas are temporary parasites. Rats are known to harbor four groups of arthropod ectoparasites: fleas, ticks, mites and lice… Some of the ectoparasites can biologically or mechanically transfer infectious agents to the human or animals and results in the spread of infection.”
In other words, rats carry a lot of parasites, which carry a lot of diseases. Here, according to the Centers for Disease Control, is a quick list of the diseases rats are currently responsible for spreading in the United States:
Hantavirus Pulmonary Syndrome
Hemorrhagic Fever with Renal Syndrome
Lymphocytic Chorio-meningitis (LCM)
Omsk Hemorrhagic Fever
South American Arenaviruses (Argentine hemorrhagic fever, Bolivian hemorrhagic fever, Sabiá-associated hemorrhagic fever, Venezuelan hemorrhagic fever)
It’s an ugly list. And in light of their impending dominance, it’s worth remembering that rats played a key role in helping spread the bubonic plague during the Black Death. Crammed, unhygienic living conditions helped it become such a devastating killer, but it was an ectoparasite—a flea—that brought the plague.
“The bubonic plague, a disease still present in some areas of the world, is now known to have spread via fleas living on rats,” Mark Ormrod, a professor of history at the University of York, wrote for the BBC.
Our hygiene and health-care are much improved from Medieval times, but we are headed towards a future marked by shared, maybe cramped, living spaces: More than half the world’s population currently lives in cities, billions are slated to join them, and so, the megacities are growing. More urban living, paired with more rats, could beget similar, if not as deadly, health woes.
And Dirzo and his crew aren’t the only ones who worry about the rise of the rats. In fact, just earlier this year, another group of scientists determined that rodents would be the species most likely to outlast all others.
Dr. Jan Zalasiewicz, a geologist at the University of Leicester, believes that rats are the animal best suited to repopulate the world in the event of a mass extinction.
“[Rats] are now on many, if not most, islands around the world,” he explained, “and once there, have proved extraordinarily hard to eradicate. They’re often there for good, essentially. Once there, they have out-competed many native species and at times have driven them to extinction. As a result, ecospace is being emptied—and rats are in a good position to re-fill a significant chunk of it, in the mid to far geological future.”
For many of us, that future is exceedingly easy to imagine. By some counts, in New York, there are twice as many rats as human residents. They are a scourge in other cities, too, of course.
As humans continue to knock out the larger fauna, and the number of rats “double” to fill the void, we can, theoretically, look forward to seeing more of all of the above. And even if you’re not concerned with the health implications, there’s the simple fact that we’re hacking away at our immense, spectacular biodiversity, and trading it in for a deeply unpleasant, rat-centric monotony.
Beyond defaunation, there’s evidence that climate change is improving conditions for rats in general in many regions, too. It’s also probably worth adding at this point that warmer temperatures are causing some rat species to grow larger, too, thus adding another potential population booster. Zalasiewicz, for his part, imagines that once its competition is scarce, rats could become larger than sheep.
So that, then, is a foreboding slice of the Anthropocene: Giant, parasite-and-disease-carrying rats, multiplying in droves while everything else goes extinct.