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Pain sucks.
And if that wasn’t bad enough, the best painkillers we have
tend to be incredibly addictive and can pose other dangers, too.
So scientists are on the lookout for alternatives.
And a new study in the journal Cell may have just found
an unlikely ally in the hunt: hunger.
On Thursday, biologists from the University of Pennsylvania
reported that mice going without food for a day
felt far less inflammatory pain than their fully-fed counterparts.
The team was curious about how animal brains prioritize competing needs.
Previous research had shown that hungry mice
don’t react as much to painful stimuli, but it wasn’t clear why.
So they made some mice hungry by taking away their food for a day,
while others were allowed to eat normally.
Then they injected their paws with a painful chemical,
which causes both acute and inflammatory pain.
Acute pain is the sharp ouch that happens right away in response to injury,
while inflammatory pain is the duller throb
associated with things like swelling, and takes a little while to kick in.
It’s also one of the major causes of chronic pain in people.
Both fully-fed and starved mice noticed the acute pain of the injection,
and weren’t huge fans—they kept licking their paws.
Which suggests immediate threats to the body take top billing in the brain.
But the starved mice seemed much less bothered over time,
when they should have felt the inflammatory pain kicking in.
It was sort of like they’d been given painkillers!
The next step was tracking down which neurons in the brain
were involved in the pain relief.
They used a technique called optogenetics to genetically modify cells
involved in brain hunger responses so they could be turned on with laser light.
They started by activating all of these neurons,
which, as expected, had the pain-killing effect.
Then they went through more specific circuits of neurons one by one,
using a tiny little fiber to shine the light on certain areas of the brain.
And they found that activating just one particular set of 300 neurons
provided pain relief for the mice, without causing the animals to eat more food.
And while the results are just in mice,
researchers think the same basic mechanism probably exists in humans.
And if it does, studying the neurons involved could reveal new ways
to dull long-term, chronic pain—without forcing people to starve themselves,
which is always a plus.
Therapies based on this would be decades away,
but given the number of people struggling with chronic pain,
this small set of neurons is an exciting find.
Next, we’re continuing the theme of hunger-related evolution,
this time in little fish called Mexican tetra.
Some of these tetra live in caves, and after millions of years
of living in the dark, they’ve lost their eyes.
But some might argue this isn’t their most dramatic adaptation to cave life.
This week, a study in the journal Nature reveals that these fish
have all the markings of being diabetic—and yet, they’re super healthy.
It’s an evolutionary puzzle that may help us figure out
how to better treat certain metabolic diseases.
Despite millions of years apart from their river-dwelling kin,
the tetra that live in caves aren’t their own species.
And each cave has separately adjusted to cavern life,
which makes the species a good species to study adaptive evolution.
In this case, the researchers were looking at how the fish survive starvation.
Their caves are too dark for plants to grow in, which makes food a rarity.
So cavefish may eat only once or twice a year,
when seasonal floods bring in nutrients or when bat poop lands in the water.
And to survive this starvation, previous studies had found that
compared to river fish, cavefish store more fat when they’re fed,
and lose less weight when deprived of food.
To figure out how they manage to pull this off,
the team gave a jolt of sugar to three groups
of independently evolved cavefish and their river-dwelling cousins.
When they checked the fishes’ blood after 8 hours,
the levels of glucose in the cavefish remained high,
while the river fish’s glucose had returned to normal.
In humans, that kind of result would be a clear indicator of insulin resistance:
a reduced response to the hormone insulin,
which signals cells to remove sugar from the bloodstream.
It’s one of the hallmarks of type 2 diabetes.
And sure enough, when biologists injected the animals
with compounds that stimulate insulin release or insulin itself,
glucose levels only dropped in the river fish.
The researchers suspect this is what allows the cavefish
to quickly put on weight and use their reserves more slowly,
which is key to surviving those long periods between meals.
But they’re not sure how the fish avoid the downsides of being diabetic.
If you’re a person, having high blood sugar
and being insulin resistant is a bad thing.
But the cavefish didn’t seem any worse for wear.
In fact, they seem to age more slowly than their river counterparts.
When the researchers raised the fish in tanks,
they found by their middle teens, the river fish had the telltale signs
of fish aging—a hunched back, loose skin, and raggedy fins—
whereas the cavefish were still going strong.
The key seems to be that the cavefish somehow limit glycation:
the binding of sugar molecules to proteins,
which occurs during long periods of high blood sugar.
Glycation can change how proteins function, damaging tissues,
and it’s thought to be a major driver of diabetes-related complications.
The cavefish studied had about the same number of glycated proteins
as river fish despite their lasting elevated sugar levels.
If researchers can figure out how the fish prevent glycation,
they might be able to do the same in people with diabetes.
Like hunger-based painkillers, it would take a while
to translate the research to humans.
But these little diabetic fish show that
there is a way to live a long, healthy life with high blood sugar.
We just have to figure out how they do it.
These amazing discoveries are also thanks to some pretty state-of-the-art tech.
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