5 Key Questions to Consider Before Sending Your Child Back to School
Consider community, school district policies, family health, risks/benefits, and necessity of schools before making the difficult decision.
[Editor's Note: This essay is in response to our current Big Question, which we posed to several experts: "Under what circumstances would you send a child back to school, given that the virus is not going away anytime soon?"]
It is August. The start date of school is quickly approaching. Decisions must be made about whether to send our children back. As a physician, a public health researcher, and the mother of two school-aged children, I have few clear answers.
To add insult to injury, a spate of recent new data suggests that - as many of us suspected all along - kids are susceptible to COVID-19, they transmit COVID-19, and they can get really sick from COVID-19.
Let me start with the obvious. My kids, and all kids, deserve a safe, in-person school year. We know the data on the adverse effects of school closure on kids, particularly for those who are already vulnerable. I also know, on a personal level, that distance learning is no substitute for in-person schooling. Homeschooling may be great for those with the privilege to do it, but I - like many Americans - am unable to quit my job, and children need more than a screen to learn.
Moreover, safe school reopening should not be an impossible dream. I and many other physicians, teachers, and scientists have described the bare minimum that we need to safely reopen schools: a stable, low rate of COVID-19 in the community; funding and mandates for basic public health precautions (like universal masking and small, stable classes) in the schools; and easy access to testing for kids and teachers. This has been achieved, successfully, in other countries.
Unfortunately, the United States has squandered its opportunity to do right by families. Across our country, rates of COVID-19 are rising. Few states have been able to sustain a test positivity rate of less than 5 percent - the maximum that most of us, in the public health world, would tolerate. Delays in testing are rampant. Systemic under-funding of public schools means that many schools simply can't afford to put basic public health measures in place. Worst, science denialism (and the spread of quack conspiracy theories online) means that many communities are fighting even the most basic of safety precautions.
To add insult to injury, a spate of recent new data suggests that - as many of us suspected all along - kids are susceptible to COVID-19, they transmit COVID-19, and they can get really sick from COVID-19. This data increases the risk calculus. Our kids are not immune, and neither are we.
Given that the necessary societal interventions simply have not happened, most American families are therefore left making an individual choice: do I send my kid to school? Or not? There are five key questions for parents to ponder when making the difficult choice about what to do.
First, we must look at our community. Knowing that testing is difficult to obtain, a true estimate of community prevalence of COVID-19 is nearly impossible. But with a test positivity rate of more than 5 percent, it's safe to assume that in a school of 500 people, at least 1 will be positive for COVID-19. That is too high for safety. Whether or not the local government does the right thing, I would not send my child to in-person school if my community had these high rates of test positivity.
Second, we must look at our school district's policies. Will the school mandate masks? Are they cohorting students and teachers in small, stable groups? Do they have contact tracing and isolation policies in place for when a student or teacher inevitably tests positive? Do they have procedures to protect vulnerable teachers and staff? If not, I would not send my child to school. If the district is doing all of the above, I would consider it.
Third, we must look at the health profile of our own kids and families. If my child had chronic medical issues, or if I lived with my elderly parents or were myself at high risk of severe disease, I would not send my child to in-person school.
It is therefore unlikely that schools anywhere in the U.S. will be open by October.
Fourth, we must do the difficult, ethical weighing of the non-zero risk of infection (even in the safest communities) with the needs of our children. Even in low-prevalence states, there will be infections in the school setting. That said, the small risk of a severe infection may be outweighed by the social, emotional, and financial risk of keeping a child home. This decision must be made on a family-by-family basis. I know my answer; but I cannot provide this answer for others.
Finally, we must call attention to the fact that many kids and families have no options. There are far too many American children who literally depend on their school system for physical, nutritional, emotional, and academic safety. There are too many parents who have no way to earn an income and keep their kids safe without in-person learning. If anyone deserves to be prioritized for in-person schooling, it should be them. (And yes, we should also work to fix the social safety net that leaves these children high and dry.)
As I write this on August 2nd, 2020, I am planning to send my two children back to our public schools for in-person education. We have low rates of infection in our community, we have masking and stable cohorts in place, and my family is relatively healthy. We also depend on the schools to keep my children safe and engaged while I'm working in the ER! I will not hesitate, however, to pull my children out of school should any of these considerations change, if local test positivity rates go up, or if my children report that masking is not the norm in the classroom.
And sadly, I expect that this discussion will soon be a moot point. We continue to fail as a nation at basic public health policies. It is therefore unlikely that schools anywhere in the U.S. will be open by October. Our country has not shown the willpower to control the virus, leaving us all with, literally, no choice to make.
[Editor's Note: Here's the other essay in the Back to School series: Masks and Distancing Won't Be Enough to Prevent School Outbreaks, Latest Science Suggests.]
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