How AI Will Rewire Us


Fears about how robots might transform our lives have been a staple of science fiction for decades. In the 1940s, when widespread interaction between humans and artificial intelligence still seemed a distant prospect, Isaac Asimov posited his famous Three Laws of Robotics, which were intended to keep robots from hurting us. The first—“a robot may not injure a human being or, through inaction, allow a human being to come to harm”—followed from the understanding that robots would affect humans via direct interaction, for good and for ill. Think of classic sci-fi depictions: C-3PO and R2-D2 working with the Rebel Alliance to thwart the Empire in Star Wars, say, or HAL 9000 from 2001: A Space Odyssey and Ava from Ex Machina plotting to murder their ostensible masters. But these imaginings were not focused on AI’s broader and potentially more significant social effects—the ways AI could affect how we humans interact with one another.

Radical innovations have previously transformed the way humans live together, of course. The advent of cities sometime between 5,000 and 10,000 years ago meant a less nomadic existence and a higher population density. We adapted both individually and collectively (for instance, we may have evolved resistance to infections made more likely by these new circumstances). More recently, the invention of technologies including the printing press, the telephone, and the internet revolutionized how we store and communicate information.

As consequential as these innovations were, however, they did not change the fundamental aspects of human behavior that comprise what I call the “social suite”: a crucial set of capacities we have evolved over hundreds of thousands of years, including love, friendship, cooperation, and teaching. The basic contours of these traits remain remarkably consistent throughout the world, regardless of whether a population is urban or rural, and whether or not it uses modern technology.

But adding artificial intelligence to our midst could be much more disruptive. Especially as machines are made to look and act like us and to insinuate themselves deeply into our lives, they may change how loving or friendly or kind we are—not just in our direct interactions with the machines in question, but in our interactions with one another.

Consider some experiments from my lab at Yale, where my colleagues and I have been exploring how such effects might play out. In one, we directed small groups of people to work with humanoid robots to lay railroad tracks in a virtual world. Each group consisted of three people and a little blue-and-white robot sitting around a square table, working on tablets. The robot was programmed to make occasional errors—and to acknowledge them: “Sorry, guys, I made the mistake this round,” it declared perkily. “I know it may be hard to believe, but robots make mistakes too.”

As it turned out, this clumsy, confessional robot helped the groups perform better—by improving communication among the humans. They became more relaxed and conversational, consoling group members who stumbled and laughing together more often. Compared with the control groups, whose robot made only bland statements, the groups with a confessional robot were better able to collaborate.

In another, virtual experiment, we divided 4,000 human subjects into groups of about 20, and assigned each individual “friends” within the group; these friendships formed a social network. The groups were then assigned a task: Each person had to choose one of three colors, but no individual’s color could match that of his or her assigned friends within the social network. Unknown to the subjects, some groups contained a few bots that were programmed to occasionally make mistakes. Humans who were directly connected to these bots grew more flexible, and tended to avoid getting stuck in a solution that might work for a given individual but not for the group as a whole. What’s more, the resulting flexibility spread throughout the network, reaching even people who were not directly connected to the bots. As a consequence, groups with mistake-prone bots consistently outperformed groups containing bots that did not make mistakes. The bots helped the humans to help themselves.

Both of these studies demonstrate that in what I call “hybrid systems”—where people and robots interact socially—the right kind of AI can improve the way humans relate to one another. Other findings reinforce this. For instance, the political scientist Kevin Munger directed specific kinds of bots to intervene after people sent racist invective to other people online. He showed that, under certain circumstances, a bot that simply reminded the perpetrators that their target was a human being, one whose feelings might get hurt, could cause that person’s use of racist speech to decline for more than a month.

But adding AI to our social environment can also make us behave less productively and less ethically. In yet another experiment, this one designed to explore how AI might affect the “tragedy of the commons”—the notion that individuals’ self-centered actions may collectively damage their common interests—we gave several thousand subjects money to use over multiple rounds of an online game. In each round, subjects were told that they could either keep their money or donate some or all of it to their neighbors. If they made a donation, we would match it, doubling the money their neighbors received. Early in the game, two-thirds of players acted altruistically. After all, they realized that being generous to their neighbors in one round might prompt their neighbors to be generous to them in the next one, establishing a norm of reciprocity. From a selfish and short-term point of view, however, the best outcome would be to keep your own money and receive money from your neighbors. In this experiment, we found that by adding just a few bots (posing as human players) that behaved in a selfish, free-riding way, we could drive the group to behave similarly. Eventually, the human players ceased cooperating altogether. The bots thus converted a group of generous people into selfish jerks.

Let’s pause to contemplate the implications of this finding. Cooperation is a key feature of our species, essential for social life. And trust and generosity are crucial in differentiating successful groups from unsuccessful ones. If everyone pitches in and sacrifices in order to help the group, everyone should benefit. When this behavior breaks down, however, the very notion of a public good disappears, and everyone suffers. The fact that AI might meaningfully reduce our ability to work together is extremely concerning.

Already, we are encountering real-world examples of how AI can corrupt human relations outside the laboratory. A study examining 5.7 million Twitter users in the run-up to the 2016 U.S. presidential election found that trolling and malicious Russian accounts—including ones operated by bots—were regularly retweeted in a similar manner to other, unmalicious accounts, influencing conservative users particularly strongly. By taking advantage of humans’ cooperative nature and our interest in teaching one another—both features of the social suite—the bots affected even humans with whom they did not interact directly, helping to polarize the country’s electorate.

Other social effects of simple types of AI play out around us daily. Parents, watching their children bark rude commands at digital assistants such as Alexa or Siri, have begun to worry that this rudeness will leach into the way kids treat people, or that kids’ relationships with artificially intelligent machines will interfere with, or even preempt, human relationships. Children who grow up relating to AI in lieu of people might not acquire “the equipment for empathic connection,” Sherry Turkle, the MIT expert on technology and society, told The Atlantic’s Alexis C. Madrigal not long ago, after he’d bought a toy robot for his son.

As digital assistants become ubiquitous, we are becoming accustomed to talking to them as though they were sentient; writing in these pages last year, Judith Shulevitz described how some of us are starting to treat them as confidants, or even as friends and therapists. Shulevitz herself says she confesses things to Google Assistant that she wouldn’t tell her husband. If we grow more comfortable talking intimately to our devices, what happens to our human marriages and friendships? Thanks to commercial imperatives, designers and programmers typically create devices whose responses make us feel better—but may not help us be self-reflective or contemplate painful truths. As AI permeates our lives, we must confront the possibility that it will stunt our emotions and inhibit deep human connections, leaving our relationships with one another less reciprocal, or shallower, or more narcissistic.

All of this could end up transforming human society in unintended ways that we need to reckon with as a polity. Do we want machines to affect whether and how children are kind? Do we want machines to affect how adults have sex?

Kathleen Richardson, an anthropologist at De Montfort University in the U.K., worries a lot about the latter question. As the director of the Campaign Against Sex Robots—and, yes, sex robots are enough of an incipient phenomenon that a campaign against them isn’t entirely premature—she warns that they will be dehumanizing and could lead users to retreat from real intimacy. We might even progress from treating robots as instruments for sexual gratification to treating other people that way. Other observers have suggested that robots could radically improve sex between humans. In his 2007 book, Love and Sex With Robots, the iconoclastic chess master turned businessman David Levy considers the positive implications of “romantically attractive and sexually desirable robots.” He suggests that some people will come to prefer robot mates to human ones (a prediction borne out by the Japanese man who “married” an artificially intelligent hologram last year). Sex robots won’t be susceptible to sexually transmitted diseases or unwanted pregnancies. And they could provide opportunities for shame-free experimentation and practice—thus helping humans become “virtuoso lovers.” For these and other reasons, Levy believes that sex with robots will come to be seen as ethical, and perhaps in some cases expected.

Long before most of us encounter AI dilemmas this intimate, we will wrestle with more quotidian challenges. The age of driverless cars, after all, is upon us. These vehicles promise to substantially reduce the fatigue and distraction that bedevil human drivers, thereby preventing accidents. But what other effects might they have on people? Driving is a very modern kind of social interaction, requiring high levels of cooperation and social coordination. I worry that driverless cars, by depriving us of an occasion to exercise these abilities, could contribute to their atrophy.

Not only will these vehicles be programmed to take over driving duties and hence to usurp from humans the power to make moral judgments (for example, about which pedestrian to hit when a collision is inevitable), they will also affect humans with whom they’ve had no direct contact. For instance, drivers who have steered awhile alongside an autonomous vehicle traveling at a steady, invariant speed might be lulled into driving less attentively, thereby increasing their likelihood of accidents once they’ve moved to a part of the highway occupied only by human drivers. Alternatively, experience may reveal that driving alongside autonomous vehicles traveling in perfect accordance with traffic laws actually improves human performance.

Either way, we would be reckless to unleash new forms of AI without first taking such social spillovers—or externalities, as they’re often called—into account. We must apply the same effort and ingenuity that we apply to the hardware and software that make self-driving cars possible to managing AI’s potential ripple effects on those outside the car. After all, we mandate brake lights on the back of your car not just, or even primarily, for your benefit, but for the sake of the people behind you.

In 1985, some four decades after Isaac Asimov introduced his laws of robotics, he added another to his list: A robot should never do anything that could harm humanity. But he struggled with how to assess such harm. “A human being is a concrete object,” he later wrote. “Injury to a person can be estimated and judged. Humanity is an abstraction.”

Focusing specifically on social spillovers can help. Spillovers in other arenas lead to rules, laws, and demands for democratic oversight. Whether we’re talking about a corporation polluting the water supply or an individual spreading secondhand smoke in an office building, as soon as some people’s actions start affecting other people, society may intervene. Because the effects of AI on human-to-human interaction stand to be intense and far-reaching, and the advances rapid and broad, we must investigate systematically what second-order effects might emerge, and discuss how to regulate them on behalf of the common good.

Already, a diverse group of researchers and practitioners—computer scientists, engineers, zoologists, and social scientists, among others—is coming together to develop the field of “machine behavior,” in hopes of putting our understanding of AI on a sounder theoretical and technical foundation. This field does not see robots merely as human-made objects, but as a new class of social actors.

The inquiry is urgent. In the not-distant future, AI-endowed machines may, by virtue of either programming or independent learning (a capacity we will have given them), come to exhibit forms of intelligence and behavior that seem strange compared with our own. We will need to quickly differentiate the behaviors that are merely bizarre from the ones that truly threaten us. The aspects of AI that should concern us most are the ones that affect the core aspects of human social life—the traits that have enabled our species’ survival over the millennia.

The Enlightenment philosopher Thomas Hobbes argued that humans needed a collective agreement to keep us from being disorganized and cruel. He was wrong. Long before we formed governments, evolution equipped humans with a social suite that allowed us to live together peacefully and effectively. In the pre-AI world, the genetically inherited capacities for love, friendship, cooperation, and teaching have continued to help us to live communally.

Unfortunately, humans do not have the time to evolve comparable innate capacities to live with robots. We must therefore take steps to ensure that they can live nondestructively with us. As AI insinuates itself more fully into our lives, we may yet require a new social contract—one with machines rather than with other humans.

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Toxic emissions down, but people still dying from air pollution – it’s time for something radical


The UK has made much progress in its efforts to clean the air of toxic pollutants, but while the thick, dirty haze of the 1952 great London smog no longer fills the city streets, air pollution remains a silent killer. In the UK, poor air quality is responsible for some 40,000 deaths each year. It has been linked to diseases such as cancer, asthma, stroke and heart disease, diabetes, obesity and dementia. The health problems from exposure to air pollution are costing the nation more than £20 billion every year.

Dirty air also causes acid rain, which affects historical monuments, land and aquatic systems, and the excessive release of soil nutrients, which stimulates algae growth in lakes and water courses. It can even form a ground-level ozone gas that damages plants, crops and forests.

Getting clean

The latest update to the UK national air pollution statistics shows that there has been a long-term decrease in emissions from power stations, transport, household heating, agriculture and industrial processes.

Over the past four decades, emissions of key pollutants such as sulphur dioxide, nitrogen oxides, non-methane organic compounds and particulate matter have fallen by between 66% and 92%. But emissions of ammonia from the agriculture sector rose by 3% between 2015 and 2016. This has been blamed on manure from larger dairy herds and using fertilisers.

Despite the decline in air pollutants, the UK remains in breach of European limits on nitrogen dioxide (NO₂) in 16 cities, mainly due to diesel fumes from road transport. In 2018, London reached its legal air pollution limit for the whole year within one month: on Brixton Road, South London, NO₂ levels exceed average hourly limits 18 times – the maximum allowed under European air quality rules.

Health warning.

A decision on potential legal proceedings against the UK is expected from the European Commission in mid-March.

Trips for free

If air quality is to improve, people must change the way they move around their cities. The UK government intends to ban the sale of all petrol and diesel cars and vans from 2040. The rigging of emission tests by car manufacturers has already resulted in consumers ditching diesel – sale of diesel cars fell by 25% in January 2018 compared with the previous year.

In contrast, sales of electric vehicles are growing – though this trend will need to accelerate if 60% of all new cars and vans are to be electric by 2030, as the UK Committee on Climate Change hopes. While electric vehicles will improve air quality by reducing NO₂ emissions, they still produce half of all transport-related particulate matter emissions because of the fine particles released from their brakes, clutches and tyres, as well as the dust thrown up from the roads.

Having fewer cars on the roads would be even better than having cleaner cars. Attitudes may be changing, alongside the rise of the sharing economy. Younger people are using apps to take part in car club schemes, ride-sharing and car-sharing as a way of opting out of the expense and hassle of owning a car. But there’s also a clear need to provide infrastructure that encourages more walking, cycling and public transport.

If the British people want a more radical solution, then they could consider making public transport in cities free. This is already happening in Seoul on days with severe pollution. Germany is reported to be mulling over plans to make public transport free to address air pollution and reduce the number of private cars.

But this doesn’t always work as planned: one analysis of a fare-free public transport scheme in Tallin found that the increase in use was largely from people who normally walk, rather than drive a car.

While the overall drop in air pollutants is welcome, the UK needs to make further progress to ensure that everyone can breathe clean air.

London air pollution is restricting children’s lung development – new research


Air pollution is known to contribute to early deaths from respiratory and cardiovascular disease. There is also mounting evidence to show that breathing polluted air increases the risk of dementia. Children are vulnerable, too: exposure to air pollution has been associated with babies being born underweight, as well as poorer cognitive development and lung function during childhood.

Cities including London are looking to tackle the social, economic and environmental costs of air pollution by improving urban air quality using low emission zones. In these zones, the most polluting vehicles are restricted from entering, or drivers are penalised to encourage them to take up lower emission technologies. London’s low emission zone was rolled out in four stages from February 2008 to January 2012, affecting mainly heavy and light goods vehicles, such as delivery trucks and vans.

But our new research, involving more than 2,000 children in four of London’s inner-city boroughs, reveals that while these measures are beginning to improve air quality, they do not yet protect children from the harmful effects of air pollution. It is the most detailed assessment of how a low emission zone has performed to date.

Young lungs

Our study focused mainly on the boroughs of Tower Hamlets and Hackney, but also included primary schools in the City of London and Greenwich. All of these areas experienced high levels of air pollution from traffic, and exceeded the annual EU limit for nitrogen dioxide (NO₂). What’s more, they have a very young demographic and are among the UK’s most deprived areas.

Between 2008-9 and 2013-14, we measured changes to air pollution concentrations in London, while also conducting a detailed examination of children’s lung function and respiratory symptoms in these areas.

Every year for five years, we measured the lung function in separate groups of 400 children, aged eight to nine years old. We then considered these measurements alongside the children’s estimated exposure to air pollution, which took into account where they lived, and the periods they spent at home and at school.

Our findings confirmed that long-term exposure to urban air pollution is related to smaller lung volumes among children. The average exposure for all children over the five years of our study was 40.7 micrograms of NO₂ per cubic metre of air, which was equivalent to a reduction in lung volume of approximately 5%.

A long-term effect. Shutterstock.

Changes of this magnitude would not be of immediate clinical significance; the children would be unaware of them and they would not affect their daily lives. But our results show that children’s lungs are not developing as well as they could. This is important, because failure to attain optimal lung growth by adulthood often leads to poor health in later life.

Over the course of the study, we also observed some evidence of a reduction in rhinitis (a constant runny nose). But we found no reduction in asthma symptoms, nor in the proportion of children with underdeveloped lungs.

Air pollution falls

While the introduction of the low emission zone did relatively little to improve children’s respiratory health, we did find positive signs that it was beginning to reduce pollution. Using data from the London Air Quality Network – which monitors air pollution – we detected small reductions in concentrations of NO₂, although overall levels of the pollutant remained very high in the areas we looked at.

The maximum reduction in NO₂ concentrations we detected amounted to seven micrograms per cubic metre over the five years of our study, or roughly 1.4 micrograms per cubic metre each year. For context, the EU limit for NO₂ concentrations is 40 micrograms per cubic metre. Background levels of NO₂ for inner city London, where our study was located, decreased from 50 micrograms to 45 micrograms per cubic metre, over five years. NO₂ concentrations by the roadside experienced a greater reduction, from 75 micrograms to 68 micrograms per cubic metre, over the course of our study.

By the end of our study in 2013-14, large areas of central London still weren’t compliant with EU air quality standards – and won’t be for some time at this rate of change.

We didn’t detect significant reductions in the level of particulate matter over the course of our study. But this could be because a much larger proportion of particulate matter pollution comes from tyre and brake wear, rather than tail pipe emissions, as well as other sources, so small changes due to the low emission zone would have been hard to quantify.

The route forward

Evidence from elsewhere shows that improving air quality can help ensure children’s lungs develop normally. In California, the long-running Children’s Health Study found that driving down pollution does reduce the proportion of children with clinically small lungs – though it’s pertinent to note that NO₂ concentrations in their study in the mid-1990s were already lower than those in London today.

Our findings should encourage local and national governments to take more ambitious actions to improve air quality, and ultimately public health. The ultra-low emission zone, which will be introduced in central London on April 8, 2019, seems a positive move towards this end.

The scheme, which will be expanded to the boundaries set by the North and South circular roads in October 2021, targets most vehicles in London – not just a small fraction of the fleet. The low emission zone seems to be the right treatment – now it’s time to increase the dose.

Your exposure to air pollution could be much higher than your neighbour’s – here’s why


Each year, tens of thousands of people in the UK die early due to air pollution, which is linked to asthma, heart disease and lung cancer. The health risk presented by air pollution depends on how much dirty air we breathe over time. Pollution levels in UK cities regularly exceed the limits set by the World Health Organisation. But people’s exposure to pollution can vary greatly between people living on the same street, or even the same house.

Currently, health authorities estimate exposure to air pollution based on outdoor pollution at a person’s home address. But we don’t just sit outside our front doors all day – we each follow our personal daily schedules. The environment at home, in transit and at work or school all affect our exposure to pollution. Knowing this can help governments to create more effective policies and provide better advice to the public on how to reduce their exposure.

By equipping volunteers with portable pollution sensors, scientists have shown that exposure to air pollution during the day can vary substantially. For example, commuting during peak hour can account for a significant proportion of the pollution we’re exposed to – even though commuting only takes up a small part of our day.

By contrast, being indoors is often associated with lower exposure to pollution, because buildings provide some protection against outdoor pollutants. But gas cookers, wood burners and household cleaning products can also create high levels of indoor pollution.

How habits influence exposure

With all these different sources and levels of pollution around us, our daily activities and habits have a big influence on how much polluted air we breathe. Even couples who live together can have different exposures: a person who stays at home may experience up to 30% less pollution than their partner who commutes to work.

A 24-hour measurement of a person’s pollution exposure, which varies throughout the day. McCreddin et al., CC BY-SA

Small changes in our daily routines can significantly reduce our exposure to air pollution. In a study in London, participants were able to decrease their exposure during commuting by 25% to 90% by choosing alternative routes or modes of transport. Active commuters who walk or cycle are usually less exposed to pollution than people travelling by car or bus – this might be because vehicles travel in a queue, so air pollution from the vehicle directly in front gets drawn in through ventilation systems and trapped inside. The air is also much cleaner on overground trains than on the underground.

Displaying public information about pollution hot spots and ways to avoid them can help. The Wellbeing Walk is a signposted backstreet walking route taking ten to 15 minutes between London’s Euston and King’s Cross stations, which exposes walkers to 50% less pollution than the main road. Since its launch in 2015, the number of people taking the healthier path has tripled. There need to be many more initiatives like this in cities.

Modelling human movements

Being able to tell when and where people are most exposed to pollution makes it possible to compare the benefits of different solutions. That’s why scientists have created computer models to simulate different scenarios. By combining information on outdoor pollution, pollution on transport and people’s travel routes, these models help us understand how people’s movements contribute to their personal exposure.

Computer exposure models for cities, including London, Leicester and Hong Kong among others, are beginning to give us a better picture of how people are exposed to harmful pollution. But the answers they provide are often complicated.

Commuting: the shorter the better. Harry Green/Shutterstock.

For example, the model for London suggests that on average citizens are exposed to less pollution than previously estimated. But many individuals still experience extremely high pollution during long periods on transport – so a lengthy commute by car, bus or underground could mean you’re among the most affected.

What’s more, the model does not yet account for pollution created indoors through cooking or wood burning. Including these additional sources of pollution may well shake up the results.

More data, please

The UK’s clean air strategy aims to halve the number of people exposed to particulate pollution above World Health Organisation guidelines by 2025. But surprisingly little is known about pollution levels inside our homes, schools and workplaces. If the strategy is to meet its goal, the government will need more data and better methods to estimate people’s exposure to air pollution.

Any model needs to be confirmed using actual measurements, to ensure we can trust what the model predicts about our exposure. Although the technology is advancing, portable pollution sensors are still bulky and heavy. Recruiting volunteers to carry these sensors wherever they go can be difficult. Phone-integrated sensors could make this easier in the future, but their reliability is still debated among scientists.

Improving outdoor air quality is currently a top priority in cities across Europe – and rightly so. But measurements and computer models are indicating that our exposure to pollution is much more varied and complex than currently estimated. We should build on this knowledge to develop measures that deliver the greatest reduction in human exposure and empower citizens to make healthier choices in their daily routines.

Your exposure to air pollution could be much higher than your neighbour’s – here’s why


Each year, tens of thousands of people in the UK die early due to air pollution, which is linked to asthma, heart disease and lung cancer. The health risk presented by air pollution depends on how much dirty air we breathe over time. Pollution levels in UK cities regularly exceed the limits set by the World Health Organisation. But people’s exposure to pollution can vary greatly between people living on the same street, or even the same house.

Currently, health authorities estimate exposure to air pollution based on outdoor pollution at a person’s home address. But we don’t just sit outside our front doors all day – we each follow our personal daily schedules. The environment at home, in transit and at work or school all affect our exposure to pollution. Knowing this can help governments to create more effective policies and provide better advice to the public on how to reduce their exposure.

By equipping volunteers with portable pollution sensors, scientists have shown that exposure to air pollution during the day can vary substantially. For example, commuting during peak hour can account for a significant proportion of the pollution we’re exposed to – even though commuting only takes up a small part of our day.

By contrast, being indoors is often associated with lower exposure to pollution, because buildings provide some protection against outdoor pollutants. But gas cookers, wood burners and household cleaning products can also create high levels of indoor pollution.

How habits influence exposure

With all these different sources and levels of pollution around us, our daily activities and habits have a big influence on how much polluted air we breathe. Even couples who live together can have different exposures: a person who stays at home may experience up to 30% less pollution than their partner who commutes to work.

A 24-hour measurement of a person’s pollution exposure, which varies throughout the day. McCreddin et al., CC BY-SA

Small changes in our daily routines can significantly reduce our exposure to air pollution. In a study in London, participants were able to decrease their exposure during commuting by 25% to 90% by choosing alternative routes or modes of transport. Active commuters who walk or cycle are usually less exposed to pollution than people travelling by car or bus – this might be because vehicles travel in a queue, so air pollution from the vehicle directly in front gets drawn in through ventilation systems and trapped inside. The air is also much cleaner on overground trains than on the underground.

Displaying public information about pollution hot spots and ways to avoid them can help. The Wellbeing Walk is a signposted backstreet walking route taking ten to 15 minutes between London’s Euston and King’s Cross stations, which exposes walkers to 50% less pollution than the main road. Since its launch in 2015, the number of people taking the healthier path has tripled. There need to be many more initiatives like this in cities.

Modelling human movements

Being able to tell when and where people are most exposed to pollution makes it possible to compare the benefits of different solutions. That’s why scientists have created computer models to simulate different scenarios. By combining information on outdoor pollution, pollution on transport and people’s travel routes, these models help us understand how people’s movements contribute to their personal exposure.

Computer exposure models for cities, including London, Leicester and Hong Kong among others, are beginning to give us a better picture of how people are exposed to harmful pollution. But the answers they provide are often complicated.

Commuting: the shorter the better. Harry Green/Shutterstock.

For example, the model for London suggests that on average citizens are exposed to less pollution than previously estimated. But many individuals still experience extremely high pollution during long periods on transport – so a lengthy commute by car, bus or underground could mean you’re among the most affected.

What’s more, the model does not yet account for pollution created indoors through cooking or wood burning. Including these additional sources of pollution may well shake up the results.

More data, please

The UK’s clean air strategy aims to halve the number of people exposed to particulate pollution above World Health Organisation guidelines by 2025. But surprisingly little is known about pollution levels inside our homes, schools and workplaces. If the strategy is to meet its goal, the government will need more data and better methods to estimate people’s exposure to air pollution.

Any model needs to be confirmed using actual measurements, to ensure we can trust what the model predicts about our exposure. Although the technology is advancing, portable pollution sensors are still bulky and heavy. Recruiting volunteers to carry these sensors wherever they go can be difficult. Phone-integrated sensors could make this easier in the future, but their reliability is still debated among scientists.

Improving outdoor air quality is currently a top priority in cities across Europe – and rightly so. But measurements and computer models are indicating that our exposure to pollution is much more varied and complex than currently estimated. We should build on this knowledge to develop measures that deliver the greatest reduction in human exposure and empower citizens to make healthier choices in their daily routines.

Air pollution may be making us less intelligent


Long-term exposure to air pollution was linked to cognitive decline in elderly people.

Not only is air pollution bad for our lungs and heart, it turns out it could actually be making us less intelligent, too. A recent study found that in elderly people living in China, long-term exposure to air pollution may hinder cognitive performance (things like our ability to pay attention, to recall past knowledge and generate new information) in verbal and maths tests. As people age, the link between air pollution and their mental decline becomes stronger. The study also found men and less educated people were especially at risk, though the reason why is currently unknown.

We already have compelling evidence that air pollution – especially the tiniest, invisible particulates in pollution – damages the brain in both humans and animals. Traffic pollution is associated with dementia, delinquent behaviour in adolescents, and stunted brain development in children who attend highly polluted schools.

In animals, mice exposed to urban air pollution for four months showed reduced brain function and inflammatory responses in major brain regions. This meant the brain tissues changed in response to the harmful stimuli produced by the pollution.

We don’t yet know which aspects of the air pollution particulate “cocktail” (such as the size, number or composition of particles) contribute most to reported brain deterioration. However, there’s evidence that nanoscale pollution particles might be one cause.

These particles are around 2,000 times smaller than the diameter of a human hair, and can be moved around the body via the bloodstream after being inhaled. They may even reach the brain directly through the olfactory nerves that give the brain information about smell. This would let the particles bypass the blood-brain barrier, which normally protects the brain from harmful things circulating in the bloodstream.

Postmortem brain samples from people exposed to high levels of air pollution while living in Mexico City and Manchester, UK, displayed the typical signs of Alzheimer’s disease. These included clumps of abnormal protein fragments (plaques) between nerve cells, inflammation, and an abundance of metal-rich nanoparticles (including iron, copper, nickel, platinum, and cobalt) in the brain.

Automobiles are a major cause of the world’s air pollution.

The metal-rich nanoparticles found in these brain samples are similar to those found everywhere in urban air pollution, which form from burning oil and other fuel, and wear in engines and brakes. These toxic nanoparticles are often associated with other hazardous compounds, including polyaromatic hydrocarbons that occur naturally in fossil fuels, and can cause kidney and liver damage, and cancer.

Repeatedly inhaling nanoparticles found in air pollution may have a number of negative effects on the brain, including chronic inflammation of the brain’s nerve cells. When we inhale air pollution, it may activate the brain’s immune cells, the microglia. Breathing air pollution may constantly activate the killing response in immune cells, which can allow dangerous molecules, known as reactive oxygen species, to form more often. High levels of these molecules could cause cell damage and cell death.

The presence of iron found in air pollution may speed up this process. Iron-rich (magnetite) nanoparticles are directly associated with plaques in the brain. Magnetite nanoparticles can also increase the toxicity of the abnormal proteins found at the centre of the plaques. Postmortem analysis of brains from Alzheimer’s and Parkinson’s disease patients shows that microglial activation is common in these neurodegenerative diseases.


The latest study of the link between air pollution and declining intelligence, alongside the evidence we already have for the link between air pollution and dementia, makes the case for cutting down air pollution even more compelling. A combination of changes to vehicle technology, regulation and policy could provide a practical way to reduce the health burden of air pollution globally.

However, there are some things we can do to protect ourselves. Driving less and walking or cycling more can reduce pollution. If you have to use a car, driving smoothly without fierce acceleration or braking, and avoiding travel during rush hours, can reduce emissions. Keeping windows closed and recirculating air in the car might help to reduce pollution exposure during traffic jams as well.

Reducing vehicle use by walking or cycling instead could have a major impact on air pollution levels.

But young children are among the most vulnerable because their brains are still developing. Many schools are located close to major roads, so substantially reducing air pollution is necessary. Planting specific tree species that are good at capturing particulates along roads or around schools could help.

Indoor pollution can also cause health problems, so ventilation is needed while cooking. Open fires (both indoors and outdoors) are a significant source of particulate pollution, with woodburning stoves producing a large percentage of outdoor air pollution in the winter. Using dry, well-seasoned wood, and an efficient ecodesign-rated stove is essential if you don’t want to pollute the atmosphere around your home. If you live in a naturally-ventilated house next to a busy road, using living spaces at the back of the house or upstairs will reduce your pollution exposure daily.

Finally, what’s good for your heart is good for your brain. Keeping your brain active and stimulated, eating a good diet rich in antioxidants, and keeping fit and active can all build up resilience. But as we don’t yet know exactly the mechanisms by which pollution causes damage to our brains – and how, if possible, their effects might be reversed – the best way we can protect ourselves is to reduce or avoid pollution exposure as much as possible.

Air Pollution, Forest Fires, and Industrial Toxins: Your Best Detox Strategies


Poor air quality from industrial activities and the recent wildfires is a looming health risk for us all. Here are evidence-based strategies for removing toxic compounds from your body and mitigating the health risks of air pollution. 

Besides the tragic loss of life and property, casualties to wildlife, and devastation to nature wrought by the recent wildfires, a toll to human health will be an inevitable consequence. Without taking into account the recent impact of these natural disasters, air pollution already claims more than two million lives per year (1).

Particulate Matter Emission from Forest Fires

Especially troubling is the particulate matter content of air pollution, which is connected to a litany of adverse health outcomes (2). Airborne particulate matter, which “consists of a heterogeneous mixture of solid and liquid particles suspended in air that varies continuously in size and chemical composition in space and time,” is more dangerous than both ground-level ozone and carbon monoxide (3). Among the constituents of particulate matter are biological components such as cell fragments and endotoxin, crustal material, heavy metals, particle-bound water, sulfates, nitrates, organic and elemental carbon, and dangerous combustion byproducts called polycyclic aromatic hydrocarbons such as naphthalene and benzo(a)pyrene (3, 4).

Anthropogenic, or manmade sources, such as construction sites, cooking, vehicle exhaust, agricultural or industrial byproducts, road erosion, mining operations, and combustion of solid-fuels including coal, oil, gasoline, biomass, and lignite can generate particulate matter (5, 6, 7, 8). However, particulate matter production can also emerge from natural sources such as sea spray, vegetation, volcanoes, dust storms, windblown soil, and most relevant to recent current events: forest fires (9).

Size Matters: PM-2.5 in Airborne Pollution Poses Massive Health Risks

The Environmental Protection Agency (EPA) classified particulate matter into ultra-fine (PM-0.1), fine (PM-2.5), and coarse (PM-10) based on its aerodynamic diameter in micrometers, which in turn influences its dissemination in the atmosphere and respiratory penetrance when inhaled by a living organism (10). For comparison, the average human hair and particle of fine beach sand have diameters of 70 and 90 micrometers, respectively (11). Fine particulate matter, which can be either directly released into the air or converted from gaseous precursors, poses monumental risks to health due to its suspension in air for weeks to months and its ability to be transported hundreds or thousands of kilometers (12).

The nasal cilia and mucus filter coarse particulates, and the coarse particulates that do settle in the trachea or bronchi of the respiratory passages are expelled via sneezing and coughing reflexes (13). However, the smaller particulates tend to lodge in the respiratory tract at increased rates, depositing deep within sites of gaseous exchange such as the respiratory bronchioles and the alveoli of the lungs, and ultimately translocate into tissue and circulation (14, 15).

At a mechanistic level, tissue damage to airways and inflammation can occur due to transition metals present in particulate matter, which induce production of electron-stealing, tissue-damaging reactive oxygen species (ROS) (3). Similarly, transition metals such as iron elicit genotoxic effects, damaging cellular genetic material (16). Disruption of cell membrane integrity is a consequence of the elemental components of particulate matter, which can lead to pulmonary fibrosis (17).

Particulate matter-mediated induction of pro-inflammatory cytokines, or intercellular signaling molecules which can elicit systemic inflammation, is implicated in cardiovascular disease (18). PM-2.5 alters vascular endothelial cells membranes, promoting permeability and consequent development of atherosclerotic lesions (19). Furthermore, PM-2.5 induces cardiac hypoxia, or oxygen deprivation, which can modify the function of vascular endothelial cell membranes and lead to plaque deposition (20). Specifically, “translocation of PM-2.5 from the lung…directly into the blood exacerbates the progression of atherosclerosis by initiating acute inflammatory responses” (19).

In addition, oxidative stress and inflammation caused by particulate matter may promote apoptosis, or programmed cell death (3). Lipopolysaccharide from gram-negative bacteria present in particulate matter can induce pathologic intestinal permeability, the precursor to autoimmune disease, as well as generate a milieu of metabolic endotoxemia which favors the development of airway dysfunction, obesity, metabolic syndrome, atherogenesis, and cardiovascular disease (21, 22).

The Correlation Between PM-2.5 and Disease

Cardiovascular disorders, including acute coronary syndrome, hypertension, venous thrombosis (blood clots), arrhythmia, stroke, exacerbation of congestive heart failure, increased rates of heart attacks, and aberrations in cholesterol profiles, can manifest from PM-2.5 exposure (3, 23, 24, 25, 26). Increases in PM-2.5 are associated with increased carotid intimal-media thickness, a measure of cardiovascular risk and marker for the accumulation of atheromas, or abnormal masses of fatty material in the arterial wall (27). Decreased tone of the anti-inflammatory ‘rest and digest’ parasympathetic arm of the nervous system, as exhibited by depressed heart rate variability, is also associated with exposure to PM-2.5 (28).

Particulate matter is likewise correlated with adult diabetes, even after accounting for other risk factors such as ethnicity and obesity (29). PM-2.5 is also associated with reduced lung function, elevated respiratory-related mortality, and increased hospital admissions for pneumonia, asthma, and chronic obstructive pulmonary disease (COPD) (11, 24, 30). In fact, at a global level, particulate matter is responsible for approximately 5% of deaths due to lung cancer and 3% of cardiopulmonary deaths (31). PM-2.5 in particular reduces lifespan by an estimated 8.6 months (32). This is not withstanding the financial toll incurred by particulate matter, which cost China and the United States $106.5 billion and $29 billion, respectively, in one year alone (3).

Optimize Phase II Detoxification to Protect Yourself

In the first phase of hepatic detoxification, toxins undergo chemical modifications such as oxidation, reduction, or hydrolysis, and are therefore rendered even more reactive with the potential to wreak havoc. The second phase, thus, is essential in order to render phase I metabolites more hydrophilic, or water-soluble, so that they can be excreted. Sulfation, acetylation, glucuronidation, and glutathione conjugation are examples of phase II processes whereby the phase I intermediate is attached to a conjugating agent by a transferase enzyme, in order for the toxicant to be eliminated from the body.

Genetic polymorphisms, as well as liver congestion due to over-burdening of the detoxification systems, can create a bottleneck where phase I outpaces phase II, which leads to an accumulation of free radicals that deplete the body of the master endogenous antioxidant, glutathione (33). Signaling is then directed down pathways that activate mitogen activated protein kinase (MAPK) and nuclear factor kappa beta (NFkB), which leads to a pro-inflammatory cascade (34).

In order to promote removal of harmful substances from the body, it is essential to ensure phase II detoxification is running unimpeded. As a fundamental endogenous defense system against oxidative stress, phase II enzymes scavenge reactive oxygen species, metabolize foreign compounds, and have demonstrated protective effects against xenobiotics including ozone, tobacco smoke, and diesel exhaust particles (35, 36, 37).

As noted by Fahey and colleagues, “Induction of phase 2 detoxication enzymes [e.g., glutathione transferases, epoxide hydrolase, NAD(P)H: quinone reductase, and glucuronosyltransferases] is a powerful strategy for achieving protection against carcinogenesis, mutagenesis, and other forms of toxicity of electrophiles and reactive forms of oxygen” (33). Researchers propose that induction of phase II enzymes may represent a powerful strategy to combat the oxidative stress resulting from oxidant pollutants (37).

Eat More Cruciferous Vegetables

Some of the cruciferous vegetables, belonging to the Brassicaceae or mustard family, include arugula, broccoli, Brussel sprouts, red, green, Chinese, and savoy cabbage, cauliflower, chard, collard greens, radish, rapini, rutabaga, turnip and turnip greens, wasabi, and watercress.

Sulforaphane, an isothiocyanate compound enriched in all cruciferous or Brassica vegetables, but particularly concentrated in broccoli sprouts, is the most potent inducer of phase II enzymes yet identified (33, 37). In fact, “3-day-old sprouts of cultivars of certain crucifers including broccoli and cauliflower contain 10-100 times higher levels of glucoraphanin (the glucosinolate of sulforaphane) than do the corresponding mature plants” (33, p. 10367).

Amplifying the levels of phase II enzymes with sulforaphane can inhibit diesel exhaust particle-stimulated production of inflammatory cytokines by airway epithelial cells (61). As a chemoprotective agent, sulforaphane also decreases the incidence, number, and rate of development of mammary tumors in rats treated with the carcinogenic chemical dimethylbenz(a)anthracene (33).

Proof of concept was provided by a twelve-week randomized clinical trial which evaluated the effects of a broccoli sprout-derived beverage on the urinary excretion of airborne pollutants in participants from the Yangtze River delta region of China notorious for air pollution (38). Based on increased appearance of glutathione-derived conjugates of the pollutants benzene and acrolein in the urine of those who received the broccoli sprout beverage, the researchers concluded, “intervention with broccoli sprouts enhances the detoxication of some airborne pollutants and may provide a frugal means to attenuate their associated long-term health risks” (38).

In a similar study, subjects recruited from the polluted Qidong, China, consumed either a glucoraphanin-rich or sulforaphane-rich broccoli sprout-derived beverage in a randomized cross-over clinical trial (39). Excretion of glutathione-derived conjugates of several pollutants, including acrolein, crotonaldehyde and benzene, were significantly increased compared to baseline (39). In other words, the broccoli sprout intervention enhanced phase II, glutathione-mediated elimination of toxic air pollutants.

Consume Botanical Agents that Enhance Phase II Detoxification

Cinnamon

Cinnamaldehyde, the flavonoid that imparts a characteristic odor and flavor to cinnamon, causes the transcription factor called nuclear erythroid 2-related factor 2 (Nrf2) to translocate to the cell nucleus and bind to a sequence known as the antioxidant response element (ARE), which “regulates the expression of a large battery of genes involved in the cellular antioxidant and anti-inflammatory defense as well as mitochondrial protection” (40). Activation of ARE, in turn, stimulates glutathione production and induces expression of phase II enzymes to promote detoxification (40). Not only does this cinnamon compound have the chemopreventative potential to protect cells from the toxic effects of chemotherapy drugs, but it also may support the detoxification of air pollution.

Rooibos and Honeybush Teas

In addition, rooibos and honeybush teas have been demonstrated to significantly augment activity of phase II enzymes such as glutathione S-transferase, as well as increase the ratio of reduced to oxidized glutathione, both of which are important for limiting the damage done by heavy metals, free radicals, and lipid peroxides (41, 42). In this way, these natural agents may be able to confer protection against the oxidative damage and mutagenesis resulting from particulate matter exposure.

Holy Basil

Another traditional herb, Indian holy basil, significantly increases levels of glutathione (GSH) and the antioxidant enzymes glutathione transferase (GST), glutathione peroxidase (GSPx), and glutathione reductase (GSRx), the catalysts which detoxify xenobiotic substrates, neutralize oxidative stress, and regenerate glutathione, respectively (43). Likewise, holy basil increases levels of superoxide dismutase (SOD), an enzyme which neutralizes cell-damaging reactive oxygen species (43). Holy basil also maintains levels of glutathione as well as all of the aforementioned enzymes in the face of gamma radiation and reduces the level of lipid peroxidation (oxidative deterioration of lipids) induced by radiation (43).

Curcumin

A powerhouse botanical which prevents glutathione depletion is curcumin, a yellow compound in turmeric root (44, 62). In a rat model, curcumin extract protected against liver injury after exposure to the toxic chemical carbon tetrachloride (CCl4) by improving levels of glutathione, superoxide dismutase, and glutathione peroxidase (44). As a result, damage to cell membranes, as indicated by lipid peroxidation, was reduced, and CCl4-mediated elevation in the liver enzyme AST was prevented (44). Curcumin has similarly been demonstrated to prevent mitochondrial dysfunction and reduce hepatoxicity induced by metals such as arsenic, lead, mercury, copper, chromium, and cadmium (45).

Ginger, Resveratrol, and Quercetin

Along similar lines, ginger rhizome protects against liver fibrosis induced by the toxin CCl4 by significantly increasing glutathione and superoxide dismutase (46). In this study, ginger also significantly decreased levels of the mutagenic and carcinogenic compound malondialdehyde, indicating that ginger suppressed CCl4-mediated damage to lipids (46). Resveratrol, on the other hand, from foods such as grapes, blueberries, and cranberries, increases expression of the antioxidant enzymes superoxide dismutase and glutathione peroxidase in a concentration-dependent manner, which accounts for the vascular protective effects of this phytonutrient (47). In another in vitro study, both resveratrol and quercetin (a flavonoid found in plant foods such as apples and onions) increased levels of glutathione and antioxidant defense enzymes including superoxide dismutase, glutathione transferase, and glutathione peroxidase, as well as adiponectin, an anti-inflammatory signaling molecule secreted by fat cells (48).

Increase Antioxidant Supplementation

Emissions of particulate matter are associated with excess generation of reactive oxygen species (ROS), agents which perpetuate pathology and require antioxidants for neutralization (49). In South Brazil subjects exposed to particulate matter from a coal electric-power plant, surrogate markers for oxidative stress including byproducts of lipid degradation called thiobarbituric acid reactive substances (TBARS) and protein carbonyls (PC), reflecting oxidative damage to proteins, were elevated (49). Levels of endogenous antioxidants, including reduced glutathione (GSH) and vitamin E, were also compromised in those exposed to coal combustion (49).

All of these biomarkers normalized after daily supplementation with 500 mg vitamin C and 800 mg vitamin E, indicating that, “The antioxidant intervention was able to confer a protective effect of vitamins C and E against the oxidative insult associated with airborne contamination derived from coal burning of an electric-power plant” (49, p. 175).

Consume More of the Most Antioxidant-Rich Foods

In addition to targeted supplementation under the guidance of a licensed physician, increasing consumption of colorful plant foods is a therapeutic strategy to increase antioxidant intake. Phytochemicals, or bioactive constituents derived from plants, can be classified as antioxidants due to their participation in redox reactions where electrons are exchanged (50). Not only do plant antioxidants defend against reactive oxygen and nitrogen species, but they also favorably modulate gene expression and promote cell maintenance, repair of genetic material, and longevity (51, 52, 53).

Berries have high antioxidant potential due to active phytochemical constituents including lignans, phenolic acids, stibenoids, tannins, and flavonoids such as anthocyanidins (54). Ranking highest in antioxidant capacity are dried varieties of amla (Indian gooseberry), dog rose, and bilberries, but fresh black currants, blackberries, cranberries, crowberries, goji berries, strawberries, and zebeck (red sour berries) also rank high (50). In an analysis of 581 fruits and vegetables, artichokes, green and red chili peppers, lemon skin, curly kale, and okra flour, as well as dried varieties of apples, plums, and apricots, were classified as antioxidant-rich (50).

Although herbs and spices make up a small proportion of a meal, they also represent a potent source of antioxidants. Researchers state, “Sorted by antioxidant content, clove has the highest mean antioxidant value, followed by peppermint, allspice, cinnamon, oregano, thyme, sage, rosemary, saffron and estragon, all dried and ground” (50). Traditional botanical medicines are also reservoirs of antioxidants, which explains their therapeutic properties. Half of the plant medicine products analyzed ranked in the 90th percentile or higher for antioxidant capacity (50).

Beverages worthy of inclusion for boosting antioxidant levels are unprocessed tea powders, tea leaves, and coffee beans. The antioxidant content in coffee is attributable to heterocyclic and volatile aromatic compounds, caffeine, and polyphenols, whereas monomer catechins such as epigallocatechin gallate (EGCG) and polymerized catechin such as theaflavin and thearubigen predominate in green tea and black tea, respectively (50). Chocolate is likewise a prominent source of antioxidants, with antioxidant content correlating directly with percentage cocoa (50).

Include Healthy Fats and Oils

Even short-term exposure to PM-2.5 is associated with dysfunction in endothelial cells, or the thin layer of simple squamous cells that lines blood vessels and lymphatic vessels, interfacing between luminal contents and the vessel wall (55, 56). A disturbance in flow mediated dilation (FMD), or the capacity of a blood vessel to dilate with increased blood flow, reflects endothelial dysfunction, a key change in the development of atherosclerosis (57).

Olive Oil

In middle-age volunteers, supplementation with three grams per day of olive oil for four weeks prior to exposure to concentrated ambient particulate (CAP) matter has been shown to prevent the reduction in FMD induced by particulate matter (58). Not only that, but this olive oil intervention blunted the adverse changes in blood markers associated with vasoconstriction (the narrowing of vessels) and fibrinolysis (the enzymatic break-down of blood clots) (58). The researchers suggest that dietary inclusion of olive oil may “prevent deleterious effects of CAP exposure on vascular function and might, therefore, represent a practical approach to reduce the mortality and morbidity of cardiovascular diseases associated with PM exposure” (58).

Fish Oil

In another randomized, double-blinded, controlled study of healthy middle-aged participants by the same group, supplementation with three grams per day of fish oil, but not olive oil, prevented deleterious changes in lipids, cardiac rhythm, and heart rate variability resulting from exposure to particulate matter (23). A recent study also underscored how omega-3 fatty acids prevent systemic and pulmonary inflammation as well as oxidative stress induced by fine particulate matter, when administered either before or after exposure (59). The authors conclude, “Our findings demonstrate that elevating tissue omega-3 levels can prevent and treat fine particle-induced health problems and thereby present an immediate, practical solution for reducing the disease burden of air pollution” (59).

Therefore, it is prudent to incorporate high quality, extra virgin olive oil, as well as omega-3 fatty acids from wild-caught, low-mercury fatty fish such as salmon, mackerel, herring, or sardines. Omega-3s can also be obtained from pasture-raised eggs and grass-fed meat, the latter of which has been shown to predictably raise plasma and platelet long chain omega-3 polyunsaturated fatty acid status (60). Although supplementing with a professional-grade, molecularly distilled fish oil is a viable option with physician approval, consuming whole foods sources of omega-3s provides the added benefit of B vitamins, minerals, and amino acids, phospholipids, required for detoxification.

When used as part of a comprehensive regimen that incorporates an anti-inflammatory diet, stress management, exercise, and sleep optimization, these food, herb, and nutraceutical-based strategies can minimize the deleterious effects of exposure to air pollution, and optimize detoxification pathways to protect us from the onslaught of modern-day toxicant exposures.

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Air pollution may affect your menstrual cycle: Study


https://speciality.medicaldialogues.in/air-pollution-may-affect-your-menstrual-cycle-study/

STUDY PROVES REFINED SUGAR IS RESPONSIBLE FOR REMARKABLE RATE OF DISEASE


refined sugar
  • Sugar has become a daily habit in the past 100 years, during which rates of obesity, Type 2 diabetes, cancer, heart disease and other chronic illnesses have skyrocketed
  • Recent research demonstrates cancer cells use sugar as their primary fuel and are functionally starved when sugar is withheld, upholding previous research by German biochemist, Otto Warburg
  • The metabolic theory of cancer holds sugar damages mitochondrial function and energy production, triggering cell mutations that are then fed by ongoing sugar consumption
  • Your healthiest choice is to avoid or eliminate refined sugar from your diet by eating whole, organic foods, and carefully reading labels of any packaged foods you buy

Refined sugar was not consumed on a daily basis until the past 100 years. Before that, it was a treat afforded only by the very rich as sugar cane was a difficult crop to grow. In the past 100 years, rates of obesityheart diseaseType 2 diabetes and numerous other chronic diseases have skyrocketed.

When sugar and tobacco were introduced by Native Americans to Europeans as they began to settle America, the average life span was relatively short.1 This meant health consequences from sugar and tobacco were easily buried in the myriad of other life challenges the early settlers faced.

As early as the 1920s, research documented the damage sugar does to your body. To this day, tobacco continues to be a leading a cause of premature death.2 Unfortunately, while the Centers for Disease Control and Prevention (CDC) call tobacco the leading cause of preventable death in the U.S., that title may well belong to sugar. Yet people who would never consider smoking may have little concern over the amount of sugar and starch eaten each day.

From a nutritional standpoint, your body does not need refined sugar. Although you need glucose, your body manufactures the glucose it needs in your liver through a process called gluconeogenesis. If you never ate another morsel of candy, sugar or starch again, you would live quite comfortably and likely in far better health.

Sugar Feeds the Growth of Cancer Cells

 

Recent research reported in this short news video demonstrates that the amount of sugar you eat each day should be an important consideration in your nutritional plan. In 1926, German biochemist Otto Warburg observed cancer cells fermented glucose to lactic acid, even in the presence of oxygen (known as the Warburg effect), and theorized it might be the fundamental cause of cancer.3 This led to the idea that tumor growth could be disturbed by cutting off the energy supply, namely sugar.

For decades, scientists and researchers dismissed the idea, and the sugar industry backed them up. Warburg received the Nobel Prize in Physiology or Medicine in 1931 for his work in cellular respiration and energy production. His life’s mission was to find a cure for cancer, but his findings were largely ignored by the conventional medical community as they were considered simplistic and didn’t fit the genetic model of disease that was widely accepted.

Recent research from Belgium4 shows there is indeed a strong link between glucose overstimulation and mutated proteins often found inside human tumor cells, which make the cells grow faster.5 The study began in 2008, triggered by the researchers’ desire to gain a greater understanding of the Warburg effect.

The rapid breakdown of glucose in tumor cells is not seen in healthy cells, making glucose the primary energy source for cancer. Researcher Johan Thevelein, Ph.D., a molecular biologist from LU Leuven in Belgium, commented on the results of the study in a press release, saying:6

“Our research reveals how the hyperactive sugar consumption of cancerous cells leads to a vicious cycle of continued stimulation of cancer development and growth. Thus, it is able to explain the correlation between the strength of the Warburg effect and tumor aggressiveness.

This link between sugar and cancer has sweeping consequences. Our results provide a foundation for future research in this domain, which can now be performed with a much more precise and relevant focus.”

Cell Mutation Not Limited to Sugar Consumption

They’re quick to point out that while they believe the presence of added sugar in your diet may increase the aggressive growth of cancer cells, their research does not prove it triggers the original mutation.7 That said, previous research has shown that the genetic mutations found in cancer cells are actually a downstream effect caused by mitochondrial dysfunction, not the original cause, and excessive sugar consumption is one of the things that triggers mitochondrial dysfunction. I’ll discuss this more in a section below.

Granted, there are thousands of manufactured chemicals in your home, car and workplace that may cause or contribute to cell mutations. Air pollutionpersonal care productsplastics and chemical treatments often contain chemicals with carcinogenic properties, and such exposures also play a role.

The mutation of a cell, fed by your daily sugar habit, may grow into cancer. Cell mutation from sugar consumption occurs after mitochondrial damage. However, sugar also provides nutrition to cells mutated by contaminant exposure, and is required for these mutated cells to grow and multiply. As such, your sugar intake becomes an important factor, and one that you have a great deal of control over.

This means that even in the absence of oxygen, tumor cells can extract energy from glucose molecules. Rapid cell division of cancer cells to fuel growth requires the presence of a lot of sugar. Warburg believed a defect in the mitochondria of cancer cells allows the cells to use glycolysis to fuel growth, which suggests cancer is actually a metabolic disease that is affected by your diet.

Research Supports Cancer Is a Metabolic Disease

In the U.S. an estimated 600,000 people will die from cancer this year, costing over $125 billion in health care expenses.9 The World Health Organization finds cancer is the second leading cause of death worldwide, responsible for nearly 8.8 million deaths in 2015.10 Imagine if that many people were dying each year from the flu or polio. This would be headline news each day. Have we become so used to the idea of cancer that 1.6 million new cases every year in the U.S. is old news?

Conventional cancer treatment focuses on surgery, chemotherapy and radiation. However, many of these treatments have only been successful at lengthening lives by months and not in curing the disease. The basis for these treatments is that cancer is a genetic problem and not one triggered and fed by mitochondrial dysfunction. As a result, the nutritional link is typically overlooked.

The featured study exposes the flaw in using only pharmaceutical, surgical and radiation treatments on tumors and other cancer growths. Warburg postulated that by cutting off the food supply cancer cells rely on for survival, you effectively starve them.

Research has also shown that genetic mutations are not the trigger for cancer growths but rather a downstream effect resulting from defective energy metabolism in cell mitochondria. This defective energy metabolism changes the way your cells function and promotes the growth of cancer cells.

In other words, if your mitochondria remain healthy, your risk of developing cancer is slim. Thomas Seyfried, Ph.D., author of “Cancer as a Metabolic Disease: On the Origin, Management and Treatment of Cancer,” has received many awards and honors through his long and illustrious career for the work he’s done expanding knowledge of how metabolism affects cancer.

He is one of the pioneers in the application of nutritional ketosis for cancer. While in nutritional ketosis, your body burns fat for fuel instead of starches and carbohydrates. By eating a healthy high-fat, low-carbohydrate and low- to moderate-protein diet, your body begins to burn fat as its primary fuel. Research from Ohio State University demonstrates athletes who eat a ketogenic diet experience significant improvements in their health and performance.11

Nutritional ketosis is also showing great promise in the treatment of neurological disorders such as Alzheimer’s disease or Parkinson’s disease,12 Type 2 diabetes13 and seizures14 that are unresponsive to medications. This recent research from Belgium confirms the work Warburg, Seyfried and others have done, and supports the hypothesis that cancer is a metabolically based disease and not a genetic problem.

Chemotherapy May Not Be the Answer

Traditional administration of chemotherapy may increase your risk of metastasis (the spread of cancer cells through your body) and may trigger additional tumor growth. Chemotherapy is sometimes recommended prior to surgery to help shrink the size of the tumor, increasing the likelihood a woman could have a lumpectomy instead of a full mastectomy.

Recent research reveals that giving chemotherapy prior to breast cancer surgery may promote metastasis of the disease, allowing it to spread to other areas of your body.15 This greatly increases the risk of dying. The study found that mice had twice the amount of cancer cells in their blood and lungs after treatment with chemotherapy. The researchers also found similar results in 20 human patients whose tumor microenvironments became more favorable to metastasis after chemotherapy.

Other studies in men with prostate cancer have demonstrated chemotherapy may cause DNA damage in healthy cells that boosts tumor growth and helps the cancer cells resist treatment.16 Research continues to reveal the effect chemotherapy has on your body and the devastating effect it has on healthy cells. At least as far back as 2004, researchers have known that “chemotherapy only makes a minor contribution to cancer survival.”17

Your Healthiest Choice Is to Avoid Sugar

Sugar is a primary factor driving the development of a number of different health conditions and chronic diseases. Sugar contributes to several of the leading causes of death in the U.S., including:18

Heart disease Hypertension Atherosclerosis Cancer
Stroke Diabetes Chronic liver disease Parkinson’s and Alzheimer’s disease19

While all forms of sugar are harmful when consumed in excess, processed fructose — the most commonly found sugar in processed foods — appears to be the worst. Manufacturers use the addictive property of sugar to drive sales, and high fructose corn syrup (HFCS) allows them to achieve their goals at a lower price. Although it tastes like sugar, HFCS gives your body a bigger sugar jolt. Dr. Yulia Johnson, family medicine physician with The Iowa Clinic, comments on the use of HFCS:20

“Your body processes high fructose corn syrup differently than it does ordinary sugar. The burden falls on your liver, which is not capable of keeping up with how quickly corn syrup breaks down. As a result, blood sugar spikes quicker. It’s stored as fat, so you can become obese and develop other health problems, such as diabetes, much faster.”

It stands to reason that if you want to live a healthier life and reduce your health care costs and your risk for cancer, you’d be wise to avoid refined sugar as much as possible, if not eliminate it from your diet entirely.

Eating real food (ideally organic), following a high-fat, low-carb, moderate-protein diet described in “Fat for Fuel,” and fasting are all things you can do to optimize your health and reduce your risk of chronic disease. For inspiring stories of others who have used a ketogenic diet to stabilize their health, read my article, “Promoting Advances in Managing Cancer as a Metabolic Disease Need Your Support.”

If you do pick up packaged foods, read the labels carefully so you can make an informed decision about the sugar you’re adding to your diet. Sugars may masquerade under several different names on food labels. Some of the more common names are listed below, but there are more than are listed here.

Labels list ingredients in order of the amount in the product. In other words, there is more of the first ingredient than the second, and so forth. When evaluating sugar, remember if it is listed in the fourth, sixth and ninth positions, the combined total may put it in the first or second position.21

Fruit juice concentrate Evaporated cane juice Cane juice crystals Blackstrap molasses
Buttered syrup Fruit juice Honey Carob syrup
Caramel Brown rice syrup Corn syrup solids Florida crystal
Golden syrup Maple syrup Molasses Refiner’s syrup
Sorghum syrup Sucanat Treacle Turbinado
Barley malt Corn syrup Dextrin Dextrose
Diastatic malt Ethyl maltol Glucose Glucose solids
Lactose Malt Syrup Maltose D-ribose
Rice syrup Galactose Maltodextrin Castor

Air pollution causes of birth defects


https://speciality.medicaldialogues.in/air-pollution-causes-of-birth-defects/