My oldest son, Michael, is my scientist of the litter. At 16, he’s already forged firm plans for the future that include studying theoretical physics at Columbia. Although I’m extraordinarily proud of his ambition and academic focus, I wonder if his always-calculating cranium has taken a moment to contemplate the cost of attending the second most expensive university in the United States. I am really trying to avoid playing the part of the old fogey, reminding him that money doesn’t grow on trees:
“Listen here, laddie: That’s the problem with you kids today—always have your head in the clouds, or cloud, or i-cloud. You can’t grasp the reality of simple math and finance.”
I really hope I don’t sound like that. Ughhh!
Anyway, to help him in his endeavors – and possibly me if he can get at least a partial scholarship – Kelsy and I got Michael a subscription to Scientific American magazine. SA has been around for nearly two centuries and has a really interesting history that you can read about on their website, www.scientificamerican.com. They describe themselves as the “award-winning authoritative source for the science discoveries and technology innovations that matter.” I can’t argue otherwise.
The household mail is usually dumped on my desk each day, so I get a chance to scan the cover of each new issue to see if anything piques my interest. Most of the time, I pass as the topics are pretty thick and require more cognitive energy than I can procure at the end of the day. But every once in a while, something catches my eye and Michael gets his issue a day or two late.
A couple of days ago, we got the February 2018 issue, and Michael still hasn’t seen it. I was immediately drawn to an article titled, “Are smart phones really destroying the adolescent brain?” Knowing that Michael would extract key details from this article to use in future parent-child arguments, I figured I had to get the entire scoop so I would be able to keep pace with him.
About half-way through the article, I was stopped dead in my tracks. In the middle of the big debate over whether smartphones are rotting our kids’ brains, a hypothesis was tossed out there that could have painfully negative implications for teenage diabetics. Larry D. Rosen, psychology professor at California State University, posits that the “technological anxiety” teens experience during the 50 times each day that they check their phones is leading to potentially high cortisol levels. According to Rosen, after someone checks in and then stops looking at the phone, “cortisol leaks into the system out of the adrenal glands.” Cortisol levels rise, increasing anxiousness. “The only way to quell that feeling,” Rosen says, “is to check the phone again.”
This becomes a cyclical compulsion that most of us deem addiction. This really jumped out at me because I had just talked about the negative effects of cortisol for diabetics in my last post. Small amounts of cortisol are fine for most people, but large amounts can have a serious effect on us. Sustained high cortisol levels have been linked to heart disease, obesity, type 2 diabetes, and as I discussed last week, insulin resistance. That’s the short list. The full list of potential health problems is long—very long!
So, if Rosen is right, then higher cortisol levels could lead to perpetual insulin resistance that is causing blood sugar control problems with many of our teens. In fact, it might be time for us to get a little selfish and start thinking about how we’re affected as adults. I know that the 142 spammy sales calls I get each day don’t do much to keep my stress and cortisol levels in check.
But then what are we to do? Smartphones are a permanent part of our world and an appendage that’s as real as our right arm. In fact, I think many would sacrifice their right arm if it meant keeping their smartphone. Have we created a technological monster that’s destined to do us in? Or, can we curb the compulsion to check our phones at every opportunity? In the end, Rosen’s hypothesis is just that. But, it does point to some issues that should concern us as parents and as people.
Onward.
After a lively conversation with Kelsy about the smartphone article, she asked me what I had thought about the diabetes one. I gave her a dumbfounded look and said, “What diabetes article?” Apparently, I had gotten so caught up in the perils of phone usage that I had missed an equally compelling article titled, “Vanquishing Diabetes.”
This article explores the “hygiene hypothesis,” which attributes rising rates of certain medical conditions to the environmental improvements we’ve made in sanitation and cleanliness and the subsequent reduced exposure to microbes and viruses. It may be that our soaps have helped wash away an important means of defense and left people with certain genetic predispositions vulnerable to auto-immune attacks.
Back to Bacteria
As parents, we do a lot to protect our young children: We buy top-of-the-line car seats with special 5-point safety harnesses; we baby-proof our homes to keep little ones out of dangerous cabinets and electrical outlets; and we strive to provide a clean and sterile environment so they spend less time sick and more time getting to be kids.
But according to professors Drescher and Tracy, our kids might be needing a good dose of bacteria to reduce the likelihood of developing type 1 diabetes. More specifically, a group of pathogens called enteroviruses that, interestingly, can either prevent or trigger type 1 diabetes, depending on the age when infected.
Now their research was performed on mice, but some amazing observations were recorded during their studies. “Some enteroviruses are able to replicate in the pancreas, inflaming areas adjacent to where the islets cells, which produce insulin, reside.” These inflamed regions produce autoimmune T cells that can attack the nearby islet cells, thus bringing on diabetes. Although there are over 100 known enteroviruses, Drescher and Tracy focused on a group of six (called the Coxsackie B viruses) that are suspected to be likely triggers for type 1 diabetes.
The researchers infected very young mice with Coxsackie B viruses. Over time, these mice showed a much reduced incidence of type 1 diabetes than mice that were uninfected. This supports their belief that early exposure to the microbes somehow protects against the development of type 1 diabetes.
However, when older mice were infected, the likelihood of developing type 1 diabetes increased, rather than decreased. The conclusion drawn was that the pancreas of these mice was already inflamed due to a genetically-induced autoimmune T cell attack. This leaves the pancreas vulnerable to the virus and speeds the development of type 1 diabetes once infected.
The research cited that really puts this into perspective is that of immunologist Matthias von Herrath. He and his colleagues posited that “enterovirus infections early in life (before an autoimmune attack is launched) can stimulate the production of regulatory T cells, which persist into adulthood. The Tregs suppress the production of autoimmune T cells and thereby protect against type 1 diabetes. But if the pancreas is already inflamed with autoimmune T cells – as would naturally happen in older mice – the virus is able to replicate, damaging the insulin-producing islet cells and precipitating diabetes.” So, depending on the age at infection, enteroviruses could either protect against or trigger type 1 diabetes.
Ultimately, the objective in this research is to study the possibility of creating a vaccine for type 1 diabetes, much like was done for another group of enteroviruses called polioviruses. When was the last time you heard of someone contracting polio? Maybe someday soon we can ask that same question about type 1 diabetes.
For the record, I have not been asked or paid to endorse Scientific American. However, if this magazine would like to cough up some cash for extra promotion, I’m sure I could write a glowing testimonial based on our family’s experiences. After all, I have upcoming tuition bills and my money tree is looking rather ill.
-Tad