I’m going to guess that you’ve been on the internet before, and thus you’ve seen
plenty of ads for treatments that supposedly help you lose weight, “using one weird trick.”
Or you might have seen recent news about research claiming to have discovered what’s been
described as “exercise in a pill.”
Sign me up!
If those things really worked, I’d be speaking for everybody when I said, SHUT UP AND TAKE
MY MONEY!
Unfortunately, there’s very little scientific evidence that any drug will make you lose
weight in a significant amount, safely and healthily.
However!
There really are some promising treatments in development right now that do at least
SOMETHING to help people lose weight, based on new insights into how your body absorbs
nutrients, and uses energy.
So sit down, enjoy your little bacon sandwich there, while we walk you through the facts
and fictions of weight-loss in a pill.
Let’s start with what your doctor can do for real, today.
Because: You actually can get medications for weight loss, by prescription, and they
come in two basic categories: appetite suppressants and fat blockers.
Appetite suppressants work by blocking your body’s ability re-absorb the chemical signals
that your brain uses, called neurotransmitters, to regulate hunger.
You’ve probably heard of a couple of these neurotransmitters -- serotonin and norepinephrine.
They’re released by your hypothalamus to make you feel ‘full.’
So, if a chemical can block your body’s ability to reabsorb those chemicals, you would
feel more full, and eat less.
Do they work?
Well, sort of.
And only for a while.
When combined with diet and exercise, studies have shown that prescription appetite suppressants
can lead to losing around one and a half to maybe a little over 2 kilograms of extra weight.
But after six to eight weeks, the appetite control center in your brain adjusts to the
new levels of those neurotransmitters, and the weight loss benefits disappear.
Fat blockers work differently.
They inhibit an enzyme called lipase.
When you eat food that has fat in it, those fat molecules need to be broken down into
their constituent parts - glycerol and fatty acids - before they can pass through the walls
of your intestines.
That’s because fat molecules are too big to pass through the membranes of your cells
on their own.
Lipases are enzymes that break down those fat molecules.
And in order to do that, they need to bind with them.
Fat-blocking drugs work by bonding with lipases, which prevents them from bonding with fat.
And without lipases to break it down, fat passes through your intestines and out of
your body without ever being absorbed.
So do they work?
Pretty well, actually.
Studies have shown that they stop about 30% of the fat in your food from getting taken
into your body.
And over the course of two years, people who took a fat blocking drug lost, on average,
about two and half kilograms more than people who didn’t.
But there can be some serious...and kinda gross...side effects.
Because fat blockers keep the fat in your intestines, using the toilet can become a
messier, oilier business.
So...those are your current prescription options.
Then you’ve got your over-the-counter weight loss supplements.
And I’m going to be honest with you here: nearly all of these are bogus.
There’s very little good science that suggests that any of them will help you lose weight...at
all.
According to the Office of Dietary Supplements at the National Institutes of Health, the
only - yes, ONLY - one of these that has stood up to reputable trials AND is legal in the
United States is green tea.
Green tea contains both caffeine and an organic compound known as catechin.
Separately, these two things don’t contribute to any statistically significant amount of
weight loss, but when you put them together, they appear to act synergistically.
Caffeine stimulates the nervous system, which has a thermogenic effect: basically, heating
up your body by getting your nervous system to tell everything to go a little faster.
And catechins inhibit the action of lipases, which gives them a minor fat blocking effect.
They also stimulate the production of norepenephrine, which helps with hunger control.
So together, these compounds have a mild appetite suppressant effect that works the same way
as prescription appetite suppressants.
And there are apparently other mechanisms that seem to be affected by green tea as well,
but we don’t understand them all yet.
So...great news, right?
Just start drinking lots of green tea.
I like green tea.
Well, don’t go expecting a miracle.
Especially if you put a bunch of sugar in it like I do.
Even the most optimistic studies suggest that drinking green tea leads to losing a couple
extra kilos over about twelve weeks.
And even so, lots of caffeine can be dangerous.
So, when it comes to what’s on the market today, that’s it.
But what about stuff that ISN’T on the market?
Most scientists involved in making the fat-busting drugs of the future believe that a commercially
viable option is at least ten years away.
But we do know a bit about how they might work.
One weight loss treatment currently in development aims to work by targeting your body’s circadian
rhythm.
We’ve talked about this before: Your circadian clock regulates rhythms in many of your body’s
processes: including food intake, as well as fat and sugar metabolism.
And when your circadian clock says it’s time to burn fuel, it activates a protein
in your body called REV-ERB-α.
This protein works by boosting the number of mitochondria in your cells.
Mitochondria are like your cells’ power plants: they take in fuel, and turn it into
energy that your body can use.
And your body breaks down the fat molecules in your fat cells to fuel your mitochondria.
So, to figure out what role REV-ERB-α could play in weight loss, researchers injected
it into some super wimpy mice.
Like, I don’t know what else to call them.
These mice were just...not athletic.
They had poor endurance, their muscles were 60% weaker than normal mice, and their muscle
cells had fewer mitochondria.
They were like what we’d be like if we were sitting on the couch all day eating chips.
The researchers injected these mice with REV-ERB.
And all of their cells began producing lots of mitochondria.
Soon, the mice could run significantly further and longer than untreated mice.
Obese mice given REV-ERB lost weight, too, and their cholesterol even improved.
Essentially, REV-ERB provided a whole-body boost to their metabolism: like what happens
when you get lots of regular exercise.
It made it so that the mice’s bodies just burned calories at a faster rate.
Even when they were doing nothing.
Excellent!
Put that in a pill.
Give it to me.
I want to take it.
So, there’s a problem right?
Just tell me what the problem is.
Well...in low doses, REV-ERB doesn’t seem to do anything.
And in high doses...it’s toxic.
While it speeds up the development of mitochondria in the short term, it impairs your cell’s
ability to produce healthy mitochondria in the long term.
And your cells need healthy mitochondria to...stay alive.
Since rampant cell death is something we want to avoid...a weight loss treatment based on
REV-ERB is going to need more work.
Other treatments in development seek to take advantage of the calorie-burning wizardry
of brown fat.
Brown fat is good fat.
Yes, there’s good fat.
You actually have two different kinds of fat cells in your body: White fat cells just hang
on to fat for whenever your body needs it.
It’s the kind of fat that gives you the love handles and makes you jiggle.
Brown fat cells are different.
They’re not supposed to STORE fat: they’re supposed to BURN it.
Brown fat raises your body temperature when it gets cold by breaking down fat into chemicals
that release heat.
It can do that because it’s packed with mitochondria.
Which, are brown; that’s why they’re called ‘brown fat cells.’
And the mitochondria in brown fat have a protein in them called UCP1 that tells them to act
like tiny fat-burning furnaces.
So...what if there were a way to turn white fat cells into brown fat cells?
Actually...there is!
Maybe!
The key is a hormone whose existence in the human body was only confirmed early in 2015:
It’s called irisin.
Irisin turns out to be one of the many hormones released by your body when you exercise, along
with more well-known ones like testosterone and adrenaline.
But while testosterone stimulates muscle growth and repair, and adrenaline stimulates the
breakdown of fat and sugar in your bloodstream for energy, irisin stimulates the production
of mitochondria and UCP1 in your white fat cells.
Which turns them into brown fat cells.
So, if scientists can figure out how to stick that stuff into a pill or a syringe, they’d
theoretically be able to kick your brown fat cell production into overdrive.
Which would mean lots of fat being burned without you needing to do a thing.
But, since they’ve only just figured out that irisin in humans exists, that’s a long
way off.
Another potential treatment involves developing a way to inject brown fat stem cells into
white fat cells, to teach the white fat cells how to produce more mitochondria on their
own.
Researchers at Harvard have developed a compound that lets the brown fat stem cells do this.
And I’d really love to tell you how, or even what that compound is; but since it’s
probably worth billions of dollars, it’s kind of a secret.
And .. we do know already know at least one downside to this possible fat-burning drug:
the compound also happens to be an immunosuppressant.
It interferes with your body’s natural inflammatory responses.
Which is really bad.
Because you need your inflammatory response to let your immune cells reach invading bacteria
and stuff.
Without that response, even minor infections could potentially become really serious.
But other scientists elsewhere are working on lots of other things to allow you to someday
be both lazy and have a healthy weight at the same time.
Still, you shouldn’t hang up your running shoes anytime soon.
For now...we’re stuck with getting and staying in shape the old fashioned way.
More running; less bacon.
But thanks for watching this episode of SciShow, which was brought to you by our patrons on
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