March for Science on Earth Day to Resist Trump’s War on Facts

ENVIRONMENT
Drastic cuts to science-based agencies like the EPA are galvanizing scientists worldwide.

Environmental Protection Agency (EPA) workers and supporters protest job cuts during rally in Chicago, Illinois, March 2, 2017.
Photo Credit: John Gress Media Inc/Shutterstock

Science isn’t everything. But it is crucial to governing, decision-making, protecting human health and the environment and resolving questions and challenges around our existence.

Those determined to advance industrial interests over all else often attack science. We’ve seen it in Canada, with a decade of cuts to research funding and scientific programs, muzzling of government scientists and rejection of evidence regarding issues such as climate change.

We’re seeing worse in the United States. The new administration is proposing drastic cuts to the Environmental Protection Agency, National Institutes of Health, National Oceanic and Atmospheric Administration, NASA and others. Information about climate change and environmental protection is being scrubbed from government websites, and scientists are being muzzled. Meanwhile, the government is increasing spending on military and nuclear weapons programs.

There’s nothing wrong with challenging research, developing competing hypotheses and looking for flaws in studies. That’s how science works. But rejecting, eliminating, covering up or attacking evidence that might call into question government or industry priorities — evidence that might show how those priorities could lead to widespread harm — is unconscionable. It’s galling to me because I traded a scientific career for full-time communication work because good scientific information helps people make the best decisions to take us into the future.

Many scientists prefer to work quietly, letting their research speak for itself. But recent attacks are galvanizing scientists and supporters throughout the U.S. and elsewhere. The March for Science on Earth Day, April 22, has been building steam for months. The main march will take place in Washington, D.C., but more than 425 marches are planned around the world. That kicks off a week of action, culminating in the People’s Climate March on April 29, also focused on Washington but with satellite marches throughout the world.

The March for Science website says organizers are “advocating for evidence-based policymaking, science education, research funding, and inclusive and accessible science.”

The group’s 850,000-member Facebook page is inspiring, with “advocates, science educators, scientists, and concerned citizens” sharing personal testimonials about their reasons for marching and why science is important to them, along with ideas for posters and slogans, questions about the march, articles about science and exposés of climate disinformation sent to schools and science teachers by the anti-science Heartland Institute.

March participants are a wide-ranging group, from a neuroscientist who is marching “for the thousands of people suffering from spinal cord injury” to sci-fi fans who are marching “Because you can’t have science fiction without science!” to a scientist marching to honour “the many, many women and young girls interested or involved in science” to those marching “because we know climate change is real.”

Celebrating and advocating for science is a good way to mark Earth Day. I’ll be in Ottawa, where a march is also taking place. David Suzuki Foundation senior editor Ian Hanington and I will launch our new book, Just Cool It!, at an Ottawa Writers Festival event that also features Nishnaabeg musician, scholar and writer Leanne Betasamosake Simpson.

Climate change is one area where anti-science rhetoric and actions at the highest levels of society are endangering human health and survival. Our book is a comprehensive look at the history and implications of climate science, the barriers to confronting the crisis and the many solutions required to resolve it.

It’s discouraging to witness the current attacks on science, and the ever-increasing consequences of climate change, diminishing ocean health and other human-caused problems, but seeing so many people standing up for science and humanity is reason for optimism. Of all the many solutions to global warming and other environmental problems, none is as powerful as people getting together to demand change.

Every day should be Earth Day, but it’s good to have a special day to remind us of the importance of protecting the air, water, soil and biodiversity that we all depend on for health and survival. Politicians are supposed to work for the long-term well-being of people who elect them, not to advance the often short-sighted agendas of those who pay large sums of money to get their way regardless of the consequences. Standing together to make ourselves heard is one of the best ways to ensure they fulfill their responsibilities.

This article was originally published by the David Suzuki Foundation.

No two noses smell the same

 

 

How you sense a smell—as pleasant or offensive—may be decided by a difference at the smallest level of DNA—one amino acid on one gene, researchers say.

 

There are about 400 genes coding for the receptors in our noses, and according to the 1000 Genomes Project, there are more than 900,000 variations of those genes. These receptors control the sensors that determine how we smell odors. A given odor will activate a suite of receptors in the nose, creating a specific signal for the brain.

 

But the receptors don’t work the same for all of us, says Hiroaki Matsunami, associate professor of molecular genetics and microbiology at the Duke University School of Medicine. In fact, when comparing the receptors in any two people, they should be about 30 percent different.

 

“There are many cases when you say you like the way something smells and other people don’t. That’s very common,” says Matsunami, who is also a member of the Neurobiology Graduate Program and the Duke Institute for Brain Sciences.

 

But what the researchers found is that no two people smell things the same way. “We found that individuals can be very different at the receptor levels, meaning that when we smell something, the receptors that are activated can be very different (from one person to the next) depending on your genome.”

 

The study didn’t look at the promoter regions of the genes, which are highly variable, or gene copy number variation, which is very high in odor receptors, so the 30 percent figure for the difference between individuals is probably conservative, Matsunami says.

 

Flavors, fragrance, food

 

While researchers had earlier identified the genes that encode for odor receptors, it has been a mystery how the receptors are activated. To determine what turns the receptors on, researchers cloned more than 500 receptors each from 20 people that had slight variations of only one or two amino acids and systematically exposed them to odor molecules that might excite the receptors.

 

By exposing each receptor to a very small concentration—1, 10, or 100 micromoles—of 73 odorants, such as vanillin or guaiacol, the group was able to identify 27 receptors that had a significant response to at least one odorant.

 

The finding, published in the December issue of Nature Neuroscience, doubles the number of known odorant-activated receptors, bringing the number to 40. The research could have a big impact for the flavors, fragrance, and food industries.

 

“These manufacturers all want to know a rational way to produce new chemicals of interest, whether it’s a new perfume or new-flavored ingredient, and right now there’s no scientific basis for doing that,” Matsunami says.

 

“To do that, we need to know which receptors are being activated by certain chemicals and the consequences of those activations in terms of how we feel and smell.”

 

Researchers from University of Pennsylvania School of Medicine, Rockefeller University, and Monell Chemical Senses Center in Philadelphia contributed to the study that was funded by the National Institutes of Health.

 

Source: Duke University

The Biggest Losers

Op-Ed Columnist

The pundit consensus seems to be that Republicans lost in the just-concluded budget deal. Overall spending will be a bit higher than the level mandated by the sequester, the straitjacket imposed back in 2011. Meanwhile, Democrats avoided making any concessions on Social Security or Medicare. Call this one for Team D, I guess.

Fred R. Conrad/The New York Times

But if Republicans arguably lost this round, the unemployed lost even more: Extended benefits weren’t renewed, so 1.3 million workers will be cut off at the end of this month, and many more will see their benefits run out in the months that follow. And if you take a longer perspective — if you look at what has happened since Republicans took control of the House of Representatives in 2010 — what you see is a triumph of anti-government ideology that has had enormously destructive effects on American workers.

First, some facts about government spending.

One of the truly remarkable things about American political discourse at the end of 2013 is the fixed conviction among many conservatives that the Obama era has been one of enormous growth in government. Where do they think this surge in government spending has taken place? Well, it’s true that one major new program — the Affordable Care Act — is going into effect. But it’s not nearly as big as people imagine. Once Obamacare is fully implemented, the Congressional Budget Office estimates that it will add only about 3 percent to overall federal spending. And, if you ask people ranting about runaway government what other programs they’re talking about, you draw a blank.

Meanwhile, the actual numbers show that over the past three years we’ve been living through an era of unprecedented government downsizing. Government employment is down sharply; so is total government spending (including state and local governments) adjusted for inflation, which has fallen almost 3 percent since 2010 and around 5 percent per capita.

And when I say unprecedented, I mean just that. We haven’t seen anything like the recent government cutbacks since the 1950s, and probably since the demobilization that followed World War II.

What has been cut? It’s a complex picture, but the most obvious cuts have been in education, infrastructure, research, and conservation. While the Recovery Act (the Obama stimulus) was in effect, the federal government provided significant aid to state and local education. Then the aid went away, and local governments began letting go of hundreds of thousands of teachers.

Meanwhile, public investment fell sharply — so sharply that many observers refer to it as a “collapse” — as state and local governments canceled transportation projects and deferred maintenance. Researchers, like those at the National Institutes of Health, also took large cuts. And there was a major cut in spending on land and water conservation.

There are three things you need to know about these harsh cuts.

First, they were unnecessary. The Washington establishment may have hyperventilated about debt and deficits, but markets have never shown any concern at all about U.S. creditworthiness. In fact, borrowing costs have stayed at near-record lows throughout.

Second, the cuts did huge short-term economic damage. Small-government advocates like to claim that reducing government spending encourages private spending — and when the economy is booming, they have a point. The recent cuts, however, took place at the worst possible moment, the aftermath of a financial crisis. Families were struggling to cope with the debt they had run up during the housing bubble; businesses were reluctant to invest given the weakness of consumer demand. Under these conditions, government cutbacks simply swelled the ranks of the unemployed — and as family incomes fell, so did consumer spending, compounding the damage.

The result was to deepen and prolong America’s jobs crisis. Those cuts in government spending are the main reason we still have high unemployment, more than five years after Lehman Brothers fell.

Finally, if you look at my list of major areas that were cut, you’ll notice that they mainly involve investing in the future. So we aren’t just looking at short-term harm, we’re also looking at a long-term degradation of our prospects, reinforced by the corrosive effects of sustained high unemployment.

So, about that budget deal: yes, it was a small victory for Democrats. It was also, possibly, a small step toward political sanity, with some Republicans rejecting, provisionally, the notion that a party controlling neither the White House nor the Senate can nonetheless get whatever it wants through extortion.

But the larger picture is one of years of deeply destructive policy, imposing gratuitous suffering on working Americans. And this deal didn’t do much to change that picture.

 

 

“The E. Coli Made Me Do It”

November 11, 2013

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In May of 2000, heavy rains pummeled Walkerton, Ontario, a town of around five thousand people located a hundred miles northeast of Toronto. Excrement from cattle containing the bacteria E. coli and campylobacter washed into the municipal water supply. An epidemic of bacterial dysentery ensued; nearly half the residents became ill and seven people died.

Two years later, Canadian researchers began surveying the exposed population. One question they asked was: Since the outbreak, have you been told for the first time by a doctor or a health-care professional that you’ve developed depression, anxiety disorder, panic disorder, or post-traumatic-stress disorder? Residents who had diarrhea after being exposed to the contaminated water were more likely to answer yes than those who hadn’t had any gastrointestinal symptoms.

This association could simply represent a natural response to a serious illness. It’s often the case that if you get sick one year, you get depressed the next. Or, maybe, people who suffered gastrointestinal distress were inclined to respond affirmatively about any symptom—particularly given their pending lawsuits against the city. The researchers dealt with this potential bias by inserting a control question on ear-buzzing, for which the rates of the two groups were the same. This allowed the researchers to raise a third possibility: Could the bacteria itself cause depression?

A lot of public and scientific attention has been paid recently to the idea that the microbiome—the collection of bacteria, viruses, fungi, and other microbes that share our bodies, outnumbering our own cells ten to one—can cause diseases widely conceptualized as non-communicable. According to well-designed, peer-reviewed studies on rodents and humans, the microbiome appears to be a major contributor to obesity, diabetes, atherosclerosis, malnutrition, hypertension, asthma, rheumatoid arthritis, colon cancer, ulcers, inflammatory bowel disease, lymphoma, liver cancer, psoriasis, and even ear wax. We are, in many ways, a result of the organisms that live inside us. (Michael Specter wrote a feature on the microbiome in the magazine last year.)

But the link between the microbiome and how we feel and behave seems far more tenuous, if only because diseases of the mind are influenced by so many factors, and often elude clear biological pathways. A number of elegant studies, however, suggest that the microbiome may have as many implications for our brains and behavior as it does for more easily defined diseases.

At a recent National Institutes of Health conference on the topic, Ted Dinan, an avuncular, scholarly psychiatrist from Cork, Ireland, explained one way that bacteria in our gut could alter our behavior. Many organisms are capable of making neurotransmitters such as norepinephrine; nerves need to communicate with each other, and neurotransmitters serve as the key facilitators of this communication. Many people are familiar with the neurotransmitter serotonin, for instance, because it is targeted by widely used antidepressants, like Prozac. What many don’t realize, however, is that gut bacteria are actually the body’s major producer of serotonin.

Dinan’s own work relies heavily on observations of mice. Mice don’t have the same personality variations as people, but they do exhibit fear, anxiety, risk-taking, and depression, among other traits. Dinan and his colleagues, for example, have performed a so-called forced-swim test, where mice are made to swim along a cylinder. They will pause periodically and become immobile; this immobility is considered a sign of hopelessness. Reporting in the Proceedings of the National Academy of Science, Dinan and colleagues found that feeding mice lactobacillus, a bacteria commonly found in yogurt, resulted in shorter immobility times, suggesting less hopelessness. When they severed the vagus nerve, which transmits signals from the gut to the brain, the mice became hopeless again.

Other studies that used mice raised in germ-free facilities and fed only sterilized food and water have convincingly shown that microbes in the bowel affect the emotional states, and consequent behaviors, of the specimens. A commentary by Elizabeth Pennisi published earlier this year in Science noted that germ-free mice are hyperactive, and that this behavior was reversed if the mice were colonized with specific bacteria introduced at a critical age.

Microbes, it seems, also make mice fat, and recent data suggest that this association depends, at least in part, on the microbiome’s influence on the animals’ behavior. The genes of the innate immune system create a defense similar to the Coast Guard, vigilantly protecting the body from microbial invasion; if these immune-system genes are altered, the microbes that survive in the colon also change. Matam Vijay-Kumar, a scientist at Emory who studies the immune system, made the surprising observation that one such gene-altered mouse developed obesity and diabetes. When he gave similarly altered mice antibiotics, their metabolic abnormalities disappeared. And when he placed normal, germ-free mice in the same cage as mice with the altered innate immune system, the previously healthy mice became obese. It seemed that the tendency to become obese and diabetic was literally contagious.

Why would the microbiome have this effect? There are several possible underlying mechanisms: the bacteria might make cells resistant to insulin, for instance, or they could extract calories from undigested food, thus adding to the organism’s weight. Intriguingly, however, the link between bacteria and weight-gain was largely mediated by behavior—the mice with the altered microbiome ate significantly more. We are a long way from treating obesity with a dose of penicillin, but the possibility that our microbiomes can determine how hungry we feel, or how poorly we cope, certainly warrants further investigation.

As intriguing as this early evidence may be, targeting the microbiome in order to treat mental illness or change stubborn behaviors will be complicated by the fact that the role of bacteria in human behavior may begin long before any signs of illness appear. We are host to a hundred trillion or so bacteria, and every portion of the bowel represents a different microbial ecosystem. Organisms that are present when we’re two months old may have shaped our brain, but they have long since disappeared when we hit twenty or forty or sixty. Indeed, while a recent summary in the journal JAMA Pediatrics suggests that bowel bacteria may provide insight into “autism, schizophrenia and anxiety,” the authors also emphasize the role that timing plays in the microbiome’s influence over the developing brain. Designing interventions, then, will depend not only on identifying the bacterial links to diseases but on understanding when such an influence occurs.

Identifying which bacteria are critical and which are bystanders, which strains affect which behaviors, by which pathways, in whom and when, is a formidable task. But we now have reason to believe that it is not impossible. The Walkerton epidemic is a milestone, because it provides human epidemiological data to bear on the association between the microbiome and personality change. And, it has biological plausibility because of earlier basic science research in mice. Fifteen years ago, Mark Lyte and his colleagues, a microbiology team from the Minneapolis Medical Research Foundation, studied the effect of infecting mice with campylobacter, one of the bacteria implicated in the Walkerton epidemic. The dose of bacteria was high enough to be detected in the intestine, but not so high that the mice developed overt illness. You probably won’t be surprised to learn that the campylobacter-infected mice exhibited more anxiety when navigating a maze than the control mice.

Because such mass bacterial exposures are rare, gathering human evidence of the mind-microbial connection will take time and ingenuity. It’s too soon to know whether a cleanse might contribute to your insomnia, or whether swallowing dirt will keep you lean. But next time you are served a delicious meal and fall asleep before doing the dishes, it wouldn’t hurt to try a new excuse: “The E. coli made me do it.”

James T. Rosenbaum is a professor of ophthalmology, medicine, and cell biology at Oregon Health & Science University, where he holds the Edward E. Rosenbaum Chair for inflammation research, and the chief of ophthalmology at the Legacy Devers Eye Clinic, in Portland, Oregon, where he holds the Chenoweth Chair.

Photograph: Zoran Kolundzija