Science Fact vs. Science Fiction: Can You Tell the Difference?
A portrait of skepticism while reading information online.
Today's growing distrust of science is not an academic problem. It can be a matter of life and death.
Take, for example, the tragic incident in 2016 when at least 10 U.S. children died and over 400 were sickened after they tried homeopathic teething medicine laced with a poisonous herb called "deadly nightshade." Carried by CVS, Walgreens, and other major American pharmacies, the pills contained this poison based on the alternative medicine principle of homeopathy, the treatment of medical conditions by tiny doses of natural substances that produce symptoms of disease.
Such "alternative medicines" take advantage of the lack of government regulation and people's increasing hostility toward science.
These children did not have to die. Numerous research studies show that homeopathy does not work. Despite this research, homeopathy is a quickly-growing multi-billion dollar business.
Such "alternative medicines" take advantage of the lack of government regulation and people's increasing hostility toward science. Polling shows that the number of people who believe that science has "made life more difficult" increased by 50 percent from 2009 to 2015. According to a 2017 survey, only 35 percent of respondents have "a lot" of trust in scientists; the number of people who do "not at all" trust scientists increased by over 50 percent from a similar poll conducted in December 2013.
Children dying from deadly nightshade is only one consequence of this crisis of trust. For another example, consider the false claim that vaccines cause autism. This belief has spread widely across the US, and led to a host of problems. For instance, measles was practically eliminated in the US by 2000. However, in recent years outbreaks of measles have been on the rise, driven by parents failing to vaccinate their children in a number of communities.
The Internet Is for… Misinformation
The rise of the Internet, and more recently social media, is key to explaining the declining public confidence in science.
Before the Internet, the information accessible to the general public about any given topic usually came from experts. For instance, researchers on autism were invited to talk on mainstream media, they wrote encyclopedia articles, and they authored books distributed by large publishers.
The Internet has enabled anyone to be a publisher of content, connecting people around the world with any and all sources of information. On the one hand, this freedom is empowering and liberating, with Wikipedia a great example of a highly-curated and accurate source on the vast majority of subjects. On the other, anyone can publish a blog piece making false claims about links between vaccines and autism or the effectiveness of homeopathic medicine. If they are skilled at search engine optimization, or have money to invest in advertising, they can get their message spread widely. Russia has done so extensively to influence elections outside of its borders, whether in the E.U. or the U.S.
Unfortunately, research shows that people lack the skills for differentiating misinformation from true information. This lack of skills has clear real-world effects: U.S. adults believed 75 percent of fake news stories about the 2016 US Presidential election. The more often someone sees a piece of misinformation, the more likely they are to believe it.
To make matters worse, we all suffer from a series of thinking errors such as the confirmation bias, our tendency to look for and interpret information in ways that conform to our intuitions.
Blogs with falsehoods are bad enough, but the rise of social media has made the situation even worse. Most people re-share news stories without reading the actual article, judging the quality of the story by the headline and image alone. No wonder research has indicated that misinformation spreads as much as 10 times faster and further on social media than true information. After all, creators of fake news are free to devise the most appealing headline and image, while credible sources of information have to stick to factual headlines and images.
To make matters worse, we all suffer from a series of thinking errors such as the confirmation bias, our tendency to look for and interpret information in ways that conform to our intuitions and preferences, as opposed to the facts. Our inherent thinking errors combined with the Internet's turbine power has exploded the prevalence of misinformation.
So it's no wonder we see troubling gaps between what scientists and the public believe about issues like climate change, evolution, genetically modified organisms, and vaccination.
What Can We Do?
Fortunately, there are proactive steps we can take to address the crisis of trust in science and academia. The Pro-Truth Pledge, founded by a group of behavioral science experts (including myself) and concerned citizens, calls on public figures, organizations, and private citizens to commit to 12 behaviors listed on the pledge website that research in behavioral science shows correlate with truthfulness.
Signers are held accountable through a crowdsourced reporting and evaluation mechanism while getting reputational rewards because of their commitment. The scientific consensus serves as a key measure of credibility, and the pledge encourages pledge-takers to recognize the opinions of experts - especially scientists - as more likely to be true when the facts are disputed.
The pledge "really does seem to change one's habits," encouraging signers to have attitudes "of honesty and moral sincerity."
Launched in December 2016, the pledge has surprising traction. Over 6200 private citizens took the pledge. So did more than 500 politicians, including members of US state legislatures Eric Nelson (PA), James White (TX), and Ogden Driskell (WY), and national politicians such as members of U.S. Congress Beto O'Rourke (TX), Matt Cartwright (PA), and Marcia Fudge (OH). Over 700 other public figures, such as globally-known public intellectuals Peter Singer, Steven Pinker, Michael Shermer, and Jonathan Haidt, took the pledge, as well as 70 organizations such as Media Bias/Fact Check, Fugitive Watch, Earth Organization for Sustainability, and One America Movement.
The pledge is effective in changing behaviors. A candidate for Congress, Michael Smith, took the Pro-Truth Pledge. He later posted on his Facebook wall a screenshot of a tweet by Donald Trump criticizing minority and disabled children. However, after being called out that the tweet was a fake, he went and searched Trump's feed. He could not find the original tweet, and while Trump may have deleted it, the candidate edited his own Facebook post to say, "Due to a Truth Pledge I have taken, I have to say I have not been able to verify this post." He indicated that he would be more careful with future postings.
U.S. Army veteran and pledge-taker John Kirbow described how the pledge "really does seem to change one's habits," helping push him both to correct his own mistakes with an "attitude of humility and skepticism, and of honesty and moral sincerity," and also to encourage "friends and peers to do so as well."
His experience is confirmed by research on the pledge. Two research studies at Ohio State University demonstrated the effectiveness of the pledge in changing the behavior of pledge-takers to be more truthful with a strong statistical significance.
Taking the pledge yourself, and encouraging people you know and your elected representatives to do the same, is an easy and effective way to fight misinformation and to promote a culture that values the truth.
Gene Transfer Leads to Longer Life and Healthspan
In August, a study provided the first proof-of-principle that genetic material transferred from one species to another can increase both longevity and healthspan in the recipient animal.
The naked mole rat won’t win any beauty contests, but it could possibly win in the talent category. Its superpower: fighting the aging process to live several times longer than other animals its size, in a state of youthful vigor.
It’s believed that naked mole rats experience all the normal processes of wear and tear over their lifespan, but that they’re exceptionally good at repairing the damage from oxygen free radicals and the DNA errors that accumulate over time. Even though they possess genes that make them vulnerable to cancer, they rarely develop the disease, or any other age-related disease, for that matter. Naked mole rats are known to live for over 40 years without any signs of aging, whereas mice live on average about two years and are highly prone to cancer.
Now, these remarkable animals may be able to share their superpower with other species. In August, a study provided what may be the first proof-of-principle that genetic material transferred from one species can increase both longevity and healthspan in a recipient animal.
There are several theories to explain the naked mole rat’s longevity, but the one explored in the study, published in Nature, is based on the abundance of large-molecule high-molecular mass hyaluronic acid (HMM-HA).
A small molecule version of hyaluronic acid is commonly added to skin moisturizers and cosmetics that are marketed as ways to keep skin youthful, but this version, just applied to the skin, won’t have a dramatic anti-aging effect. The naked mole rat has an abundance of the much-larger molecule, HMM-HA, in the chemical-rich solution between cells throughout its body. But does the HMM-HA actually govern the extraordinary longevity and healthspan of the naked mole rat?
To answer this question, Dr. Vera Gorbunova, a professor of biology and oncology at the University of Rochester, and her team created a mouse model containing the naked mole rat gene hyaluronic acid synthase 2, or nmrHas2. It turned out that the mice receiving this gene during their early developmental stage also expressed HMM-HA.
The researchers found that the effects of the HMM-HA molecule in the mice were marked and diverse, exceeding the expectations of the study’s co-authors. High-molecular mass hyaluronic acid was more abundant in kidneys, muscles and other organs of the Has2 mice compared to control mice.
In addition, the altered mice had a much lower incidence of cancer. Seventy percent of the control mice eventually developed cancer, compared to only 57 percent of the altered mice, even after several techniques were used to induce the disease. The biggest difference occurred in the oldest mice, where the cancer incidence for the Has2 mice and the controls was 47 percent and 83 percent, respectively.
With regard to longevity, Has2 males increased their lifespan by more than 16 percent and the females added 9 percent. “Somehow the effect is much more pronounced in male mice, and we don’t have a perfect answer as to why,” says Dr. Gorbunova. Another improvement was in the healthspan of the altered mice: the number of years they spent in a state of relative youth. There’s a frailty index for mice, which includes body weight, mobility, grip strength, vision and hearing, in addition to overall conditions such as the health of the coat and body temperature. The Has2 mice scored lower in frailty than the controls by all measures. They also performed better in tests of locomotion and coordination, and in bone density.
Gorbunova’s results show that a gene artificially transferred from one species can have a beneficial effect on another species for longevity, something that had never been demonstrated before. This finding is “quite spectacular,” said Steven Austad, a biologist at the University of Alabama at Birmingham, who was not involved in the study.
Just as in lifespan, the effects in various organs and systems varied between the sexes, a common occurrence in longevity research, according to Austad, who authored the book Methuselah’s Zoo and specializes in the biological differences between species. “We have ten drugs that we can give to mice to make them live longer,” he says, “and all of them work better in one sex than in the other.” This suggests that more attention needs to be paid to the different effects of anti-aging strategies between the sexes, as well as gender differences in healthspan.
According to the study authors, the HMM-HA molecule delivered these benefits by reducing inflammation and senescence (cell dysfunction and death). The molecule also caused a variety of other benefits, including an upregulation of genes involved in the function of mitochondria, the powerhouses of the cells. These mechanisms are implicated in the aging process, and in human disease. In humans, virtually all noncommunicable diseases entail an acceleration of the aging process.
So, would the gene that creates HMM-HA have similar benefits for longevity in humans? “We think about these questions a lot,” Gorbunova says. “It’s been done by injections in certain patients, but it has a local effect in the treatment of organs affected by disease,” which could offer some benefits, she added.
“Mice are very short-lived and cancer-prone, and the effects are small,” says Steven Austad, a biologist at the University of Alabama at Birmingham. “But they did live longer and stay healthy longer, which is remarkable.”
As for a gene therapy to introduce the nmrHas2 gene into humans to obtain a global result, she’s skeptical because of the complexity involved. Gorbunova notes that there are potential dangers in introducing an animal gene into humans, such as immune responses or allergic reactions.
Austad is equally cautious about a gene therapy. “What this study says is that you can take something a species does well and transfer at least some of that into a new species. It opens up the way, but you may need to transfer six or eight or ten genes into a human” to get the large effect desired. Humans are much more complex and contain many more genes than mice, and all systems in a biological organism are intricately connected. One naked mole rat gene may not make a big difference when it interacts with human genes, metabolism and physiology.
Still, Austad thinks the possibilities are tantalizing. “Mice are very short-lived and cancer-prone, and the effects are small,” he says. “But they did live longer and stay healthy longer, which is remarkable.”
As for further research, says Austad, “The first place to look is the skin” to see if the nmrHas2 gene and the HMM-HA it produces can reduce the chance of cancer. Austad added that it would be straightforward to use the gene to try to prevent cancer in skin cells in a dish to see if it prevents cancer. It would not be hard to do. “We don’t know of any downsides to hyaluronic acid in skin, because it’s already used in skin products, and you could look at this fairly quickly.”
“Aging mechanisms evolved over a long time,” says Gorbunova, “so in aging there are multiple mechanisms working together that affect each other.” All of these processes could play a part and almost certainly differ from one species to the next.
“HMM-HA molecules are large, but we’re now looking for a small-molecule drug that would slow it’s breakdown,” she says. “And we’re looking for inhibitors, now being tested in mice, that would hinder the breakdown of hyaluronic acid.” Gorbunova has found a natural, plant-based product that acts as an inhibitor and could potentially be taken as a supplement. Ultimately, though, she thinks that drug development will be the safest and most effective approach to delivering HMM-HA for anti-aging.
A new study provides key insights in what causes Alzheimer's: a breakdown in the brain’s system for clearing waste.
In recent years, researchers of Alzheimer’s have made progress in figuring out the complex factors that lead to the disease. Yet, the root cause, or causes, of Alzheimer’s are still pretty much a mystery.
In fact, many people get Alzheimer’s even though they lack the gene variant we know can play a role in the disease. This is a critical knowledge gap for research to address because the vast majority of Alzheimer’s patients don’t have this variant.
A new study provides key insights into what’s causing the disease. The research, published in Nature Communications, points to a breakdown over time in the brain’s system for clearing waste, an issue that seems to happen in some people as they get older.
Michael Glickman, a biologist at Technion – Israel Institute of Technology, helped lead this research. I asked him to tell me about his approach to studying how this breakdown occurs in the brain, and how he tested a treatment that has potential to fix the problem at its earliest stages.
Dr. Michael Glickman is internationally renowned for his research on the ubiquitin-proteasome system (UPS), the brain's system for clearing the waste that is involved in diseases such as Huntington's, Alzheimer's, and Parkinson's. He is the head of the Lab for Protein Characterization in the Faculty of Biology at the Technion – Israel Institute of Technology. In the lab, Michael and his team focus on protein recycling and the ubiquitin-proteasome system, which protects against serious diseases like Alzheimer’s, Parkinson’s, cystic fibrosis, and diabetes. After earning his PhD at the University of California at Berkeley in 1994, Michael joined the Technion as a Senior Lecturer in 1998 and has served as a full professor since 2009.
Dr. Michael Glickman