Not Vaccinating Your Kids Endangers Public Health
A pediatrician gives a one-year-old child a vaccine.
[Editor's Note: This opinion essay is in response to our current Big Question, which we posed to experts with different viewpoints: "Where should society draw the line between requiring vaccinations for children and allowing parental freedom of choice?"]
Society has a right and at times an obligation to require children to be vaccinated. Vaccines are one of the most effective medical and public health interventions. They save lives and prevent suffering. The vast majority of parents in the United States fully vaccinate their children according to the recommended immunization schedule. These parents are making decisions so that the interests of their children and the interest of society are the same. There are no ethical tensions.
"Measles is only a plane ride away from American children."
A strong scientific basis supports the recommended immunization schedule. The benefits of recommended vaccines are much bigger than the risks. However, a very small proportion of parents are ideologically opposed to vaccines. A slightly larger minority of parents do not believe that all of the recommended vaccines are in their child's best interests.
Forgoing vaccinations creates risk to the child of contracting diseases. It also creates risk to communities and vulnerable groups of people who cannot be vaccinated because of their age or health status.
For example, many vaccines are not able to be given to newborns, such as the measles vaccine which is recommended at 12-15 months of age, leaving young children vulnerable. Many diseases are particularly dangerous for young children. There are also some children who can't be vaccinated, such as pediatric cancer patients who are undergoing chemotherapy or radiation treatment. These children are at increased risk of serous complication or death.
Then there are people who are vaccinated but remain susceptible to disease because no vaccine is 100% effective. In the case of measles, two doses of vaccines protect 97% of people, leaving 3% still susceptible even after being fully vaccinated. All of these groups of people – too young, not eligible, and vaccinated but still susceptible – are dependent on almost everyone else to get vaccinated in order for them to be protected.
Sadly, even though measles has been largely controlled because most people get the very safe and very effective vaccine, we are now seeing dangerous new outbreaks because some parents are refusing vaccines for their children, especially in Europe. Children have died. Measles is only a plane ride away from American children.
There have been repeated measles outbreaks in the United States – such as the Disneyland outbreak and six outbreaks already this year - because of communities where too many parents refuse the vaccine and measles is brought over, often from Europe.
The public health benefits cannot be emphasized enough: Vaccines are not just about protecting your child. Vaccines protect other children and the entire community. Vaccine-preventable diseases (with the exception of tetanus) are spread from person to person. The decision of a parent to not vaccinate their child can endanger other children and vulnerable people.
As a vaccine safety researcher for 20 years, I believe that the community benefit of vaccination can provide justification to limit parental autonomy.
Given these tensions between parental autonomy and the protective value of vaccines, the fundamental question remains: Should society require all children to submit to vaccinations? As a vaccine safety researcher for 20 years, I believe that the community benefit of vaccination can provide justification to limit parental autonomy.
In the United States, we see this balancing act though state requirements for vaccinations to enter school and the varying availability of non-medical exemptions to these laws. Mandatory vaccination in the United States are all state laws. All states require children entering school to receive vaccines and permit medical exemptions. There are a lot of differences between states regarding which vaccines are required, target populations (daycare, school entry, middle school, college), and existence and types of non-medical (religious or philosophical) exemptions that are permitted.
Amid recent measles outbreaks, for instance, California eliminated all non-medical exemptions, making it one of three states that only permit medical exemptions. The existence and enforcement of these school laws reflect broad public support for vaccines to protect the community from disease outbreaks.
I worry about how many kids must suffer, and even die, from diseases like measles until enough is enough. Such tragedies have no place in the modern era. All parents want to do right by their children. All parents deserve autonomy when it comes to decision-making. But when their choices confer serious risks to others, the buck should stop. Our nation would be better off—both medically and ethically—if we did not turn our backs on our most vulnerable individuals.
[Editor's Note: Read the opposite viewpoint here.]
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