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When you get scared or stressed, your body sets off what’s often called the “fight
or flight” response—a series of changes which includes an increased heart rate and
faster breathing.
And for years, we’ve thought this response was kicked off by hormones from your adrenal
glands.
But research published yesterday in the journal Cell Metabolism found that a hormone released
by your bones can trigger the response all on its own.
We’ve long known that the sympathetic nervous system, one of the automated branches of your
nervous system, prepares you to respond to danger.
And this is generally thought to be controlled by the release of stress hormones like adrenaline
and cortisol from your adrenal glands on top of your kidneys.
But that doesn’t explain why people and animals that can’t release these hormones
for whatever reason can still experience a heart-pounding, breath-quickening, acute stress
response.
In fact, you can completely remove the adrenal glands from mice and they still react to threats
with what looks like true “fight or flight”.
That suggests there is another source of stress hormones in the body that can turn on the
sympathetic nervous system.
And for the past few years, one research group has suspected that source may be bones.
After all, the whole point of having a skeleton is to let us run away from predators and protect
our organs from harm.
And studies have found that a bone-derived hormone called osteocalcin improves muscle
function during exercise, so it seemed like a good place to start.
So, they took some mice, applied an electric shock to their feet to trigger a stress response,
and then looked at hormones in their blood.
Sure enough, osteocalcin levels surged to 150% in just fifteen minutes.
The researchers also exposed mice to a chemical found in fox urine.
And just like with the shocks, the mice’s osteocalcin levels shot up.
They reached a peak just a few minutes after sniffing the scent, then stayed high for hours.
And human subjects also showed a similar elevation in osteocalcin when stressed out.
This time not smelling fox pee, but asked to do, like a public speaking task.
But the team still had to tie this bone hormone to how the brain processes stress.
They found that injecting osteocalcin was enough to trigger a mouse’s stress response.
And injecting a neuron-quieting drug into the fear center of the mice’s brains prevented
the surge of osteocalcin, while removing the mice’s adrenal glands did not.
So the osteocalcin-induced response doesn’t depend on adrenal stress hormones—it’s
a complementary switch.
They also conducted experiments to figure out how the hormone turns on the fight or
flight response.
And it turns out it’s more about what it turns off.
You see, the researchers found that when they injected osteocalcin into mice, the cells
within bones called osteoblasts took up more of the neurotransmitter glutamate.
Through a string of biological events, this dampens the activity of neurons in the parasympathetic
nervous system, a part of your nervous system that works against the sympathetic nervous
system a lot of the time, like by slowing down heart rate.
So basically, osteocalcin quiets one of your body’s key regulating systems, allowing
your sympathetic nervous system do its thing unopposed.
This alternate stress response fills in some gaps in our understanding, but the researchers
say there’s a lot more to learn about bone hormones and their effects on the body.
And more research is needed on how this alternate stress pathway interacts with adrenal responses
if we want to fully understand the relationship between brain and bone.
Speaking of needing more research… vaping
Ever since vaping became a thing, scientists have been trying to figure out how it compares
with smoking in terms of health effects.
Companies that make e-cigarettes like to claim that vaping is harmless, or at least way safer
that smoking...
but what we’re finding is that it doesn’t cause the same problems that smoking does,
it causes some problems of its own.
And a paper published recently in the Journal of Clinical Investigation adds to this idea.
They found that the presence of e-cigarette vapor altered lung immune cells in mice, making
them more prone to infection.
The researchers started by exposing the mice to traditional cigarette smoke, vapor from
e-cigarettes both with and without nicotine, and then just also regular old air.
The e-cigarette smoke didn’t trigger the kind of inflammation and structural changes
to the lungs that can lead to conditions like emphysema—stuff that is seen with traditional
cigarette smoke.
So, yay.
But, when they looked at the lung tissues under a microscope, they saw something strange
was happening.
Specifically, immune cells called macrophages were getting overly fatty.
These fats, called lipids, are important components of cells, and they play crucial roles in lung
function and immunity.
You see, your lungs are coated with a goo that helps trap foreign invaders while ensuring
enough oxygen can get through.
It works because it’s composed of a special mix of lipids and proteins.
And macrophages are responsible for ensuring the goo has the right lipids in it.
If macrophages are accumulating lipids inside of them, that suggests there’s something
going wrong with the goo.
And that could leave the lungs susceptible to infection.
So, the team ran another experiment.
This time, they exposed the mice to e-cig vapor with nicotine, e-cig vapor without nicotine,
or regular air for 3 months, and then gave them a lethal dose of flu virus.
And it didn’t matter if the vapor had nicotine or not—the mice exposed to the vapors were
significantly more likely to die.
And when given sub-lethal doses, the mice exposed to e-cig vapors lost more weight,
which the researchers interpreted as a weaker immune response.
They also found increases of inflammatory markers in the lungs, so their conclusion
seemed clear — exposure to vaping impairs the lung’s immune system, even if it doesn’t
contain nicotine.
In mice, anyway.
Though, if something similar happens in people, it could help explain the recent rush of pneumonia
cases in people who vape.
You see, tests have found macrophages similarly laden with fats in patient’s lungs.
And that kind of connection between human cases and animal models is concerning.
But, it doesn’t prove that vaping is directly responsible for people’s lung infections.
Also, it’s not yet clear what it is in the vapor causes these changes to lung immune
cells.
If we can pinpoint that, we might be able to make vaping products safer by switching
up the ingredients.
Still, studies seem to keep suggesting that vaping is harmful in its own unique way—which
is why health regulatory agencies like the US FDA keep slamming companies for claiming
their products are safe.
And whether vaping is ultimately less risky than smoking unfortunately remains an open
question.
Thanks for watching this episode of SciShow News!
This episode was brought to you by today’s President of Space, Matthew Brant.
Thank you, Matthew, for your presidential support!
If you want to join Matthew in supporting this channel, you can learn how over at Patreon.com/SciShow.
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