How a Wrinkle Treatment Began as a Poison
Botulinum toxin is the most poisonous substance known to science, and it is injected into millions of faces every year. The path between those two facts runs through a nineteenth-century German doctor investigating bad sausages, an ophthalmologist trying to straighten crossed eyes, and a Vancouver couple who noticed something their patients kept mentioning. Understanding that history explains a great deal about how the treatment is dosed, why it wears off, and why the person holding the syringe matters more than the brand on it.
Botulinum toxin is the most poisonous substance we know of. It is also injected into millions of faces every year. The road between those two facts runs through a German doctor in the 1800s looking into bad sausages, an eye surgeon trying to straighten crossed eyes, and a husband and wife in Vancouver who noticed something their patients kept saying. That story explains a lot: why the dose is so tiny, why the effect fades, and why the person holding the needle matters far more than the brand name on the box.
How a Wrinkle Treatment Began as a Poison: the essentials
The short version
1820s, by Justinus Kerner, from outbreaks traced to spoiled sausage
In the 1820s, by a German doctor called Justinus Kerner, after people died from eating badly kept sausage.
Latin botulus, meaning sausage
From botulus, the Latin word for sausage.
1970s and 1980s, injected by Alan Scott to treat strabismus
In the 1970s and 1980s, when Dr Alan Scott injected it to straighten crossed eyes.
Observed by Jean and Alastair Carruthers while treating eyelid spasm; published 1992
Noticed by Jean and Alastair Carruthers while they were treating eyelid twitching, and written up in 1992.
Blocks acetylcholine release at the neuromuscular junction, so the muscle receives no instruction to contract
It blocks the chemical message a nerve uses to tell a muscle to squeeze, so the muscle never gets the order.
The nerve terminal regenerates its signalling machinery over months; the effect is temporary by design
The nerve rebuilds itself over a few months. The effect is meant to be temporary.
The doctor who studied bad sausages
In the early 1800s a district medical officer in Wรผrttemberg named Justinus Kerner began investigating a pattern of deaths that followed the eating of poorly preserved sausage. Between 1817 and 1822 he documented well over a hundred cases with an exactness that still reads as modern: drooping eyelids, double vision, a dry mouth, difficulty swallowing, and then a paralysis that spread while the mind stayed entirely clear.
In the early 1800s, a local doctor in Wurttemberg, in what is now Germany, named Justinus Kerner started looking into a run of deaths. They all followed a meal of badly kept sausage. Between 1817 and 1822 he wrote up more than a hundred cases, and his notes still read like a modern doctor’s: drooping eyelids, double vision, a dry mouth, trouble swallowing, and then a creeping paralysis, while the person’s mind stayed completely clear.
Kerner did more than describe it. He fed extracts to animals, then to himself, and worked out that whatever the poison was, it interrupted the signal between nerve and muscle while leaving sensation and consciousness untouched. That is a precise description of what the toxin does, arrived at seventy years before anyone could see a bacterium responsible.
Kerner did not stop at describing it. He gave extracts to animals, then took some himself, and worked out that the poison cut the signal between nerve and muscle while leaving feeling and thinking untouched. That is exactly what the toxin does. He got there seventy years before anyone could even see the germ that makes it.
He then wrote something extraordinary. If the substance could switch off a muscle, he suggested, it might one day be used deliberately in conditions where a muscle contracts when it should not. He had no way to purify it, no way to dose it, and no way to test the idea. He simply saw where it led. It took roughly a century and a half for medicine to catch up with him.
Then he wrote something remarkable. If this stuff can switch a muscle off, he said, perhaps one day it could be used on purpose, in illnesses where a muscle tightens when it should not. He had no way to clean it up, no way to measure out a dose, and no way to test the idea. He simply saw where it led. Medicine took about a hundred and fifty years to catch up with him.
Finding the organism
Finding the germ behind it
The bacterium was identified in 1895 by Emile van Ermengem, a Belgian microbiologist, after thirty-four people fell ill at a funeral dinner in the village of Ellezelles. He traced the illness to salted ham, isolated an anaerobic organism from it, and named it after the sausage that had given the disease its name.
The germ was found in 1895 by a Belgian scientist, Emile van Ermengem, after thirty four people fell ill at a funeral dinner in the village of Ellezelles. He traced it to salted ham, grew the germ from it, and named it after the sausage that had already given the illness its name.
The organism, now called Clostridium botulinum, grows only where there is no oxygen, which is exactly the environment inside a sealed sausage or an improperly canned jar. It does not poison by infecting the person. It produces a protein while it grows, and the protein does the damage. That distinction matters: the toxin can be separated from the organism, purified, measured and eventually used on purpose, which is what makes any of the medicine that follows possible.
The germ, now called Clostridium botulinum, only grows where there is no air. That is exactly what it is like inside a sealed sausage, or a jar that was canned badly. It does not harm you by infecting you. As it grows it makes a protein, and the protein does the damage. That difference is the key to everything that came later: a protein can be separated from the germ, cleaned up, measured out, and eventually used on purpose.
The eye surgeon who used it first
In the 1970s an ophthalmologist in San Francisco named Alan Scott was looking for an alternative to surgery for strabismus, where the eyes do not point in the same direction because one set of muscles pulls harder than the other. Working with toxin purified by the biochemist Edward Schantz, he injected minute quantities into the overactive muscle to weaken it, and the eye moved.
In the 1970s, an eye surgeon in San Francisco called Alan Scott was looking for something other than an operation to fix a squint, where the eyes do not point the same way because one set of eye muscles pulls harder than the other. Using toxin cleaned up by a chemist, Edward Schantz, he injected tiny amounts into the stronger muscle to weaken it. The eye moved.
It is worth pausing on the size of the doses. Scott was working in units measured in billionths of a gram, in a substance where the difference between a treatment and a catastrophe is a matter of decimal places. Everything the field later learned about careful dosing, precise placement and respecting the muscle you are not treating comes from this period, when the margin for error was the entire subject.
It is worth stopping to think about how small those doses were. Scott was working in billionths of a gram, with a substance where the gap between a treatment and a disaster is a decimal point. Everything this field later learned about careful dosing, exact placement, and leaving alone the muscles you are not treating comes from those years, when there was no room at all for a mistake.
American regulators approved the toxin for strabismus and for blepharospasm, an involuntary forcible closing of the eyelids, in 1989. Both are conditions where a muscle contracts against the person’s wishes. Nothing about the approval had anything to do with appearance.
In 1989, American regulators approved the toxin for crossed eyes, and for a condition where the eyelids clamp shut against the person’s will. Both are problems where a muscle tightens when the person does not want it to. None of it had anything to do with looks.
The observation that changed everything
The chance discovery that changed everything
Jean Carruthers, an ophthalmologist in Vancouver, was treating patients for blepharospasm. Her patients kept telling her that the frown lines between their eyebrows had softened. She mentioned it to her husband Alastair, a dermatologist. In 1992 they published the observation, and the cosmetic use of botulinum toxin began with a doctor listening to what her patients volunteered rather than what she had asked about.
Jean Carruthers, an eye doctor in Vancouver, was treating people whose eyelids kept clamping shut. Her patients kept telling her that the frown lines between their eyebrows had softened. She mentioned it to her husband Alastair, a skin doctor. In 1992 they published what she had noticed. The whole cosmetic use of this treatment started with a doctor paying attention to something her patients brought up on their own.
American approval for the cosmetic treatment of frown lines between the eyebrows followed in 2002, a full decade later. Approvals for forehead lines, for the lines at the outer corners of the eyes, and for the vertical cords of the neck came later still, each one requiring its own trials. That sequence is why a treatment being common is not the same as it being approved for the particular place it is being used, a distinction a good practitioner will explain rather than blur.
American approval to treat frown lines between the eyebrows came in 2002, a full ten years later. Approval for forehead lines, for the lines at the outer corners of the eyes, and for the cords in the neck came later again, and each one needed its own trials. This is why a treatment being common is not the same thing as it being approved for the exact spot it is being used on. A good practitioner will tell you which is which instead of glossing over it.
What it actually does, in one paragraph
What it actually does, in plain terms
A nerve tells a muscle to contract by releasing acetylcholine into the tiny gap between them. Releasing it requires a set of proteins that dock the packet of chemical against the nerve’s outer membrane. Botulinum toxin enters the nerve ending and cuts one of those proteins. The packet cannot dock, the message is never sent, and the muscle stays where it is.
A nerve tells a muscle to squeeze by releasing a chemical into the tiny gap between them. To let that chemical out, the nerve needs a set of proteins that push the little packet of it up against the nerve’s outer wall. Botulinum toxin gets inside the nerve ending and cuts one of those proteins. The packet cannot get out, the message is never sent, and the muscle simply stays as it is.
The nerve is not destroyed. Over the following months it rebuilds the machinery and, in some cases, sprouts new endings, and the muscle begins to receive instructions again. This is why the effect fades, why it fades gradually rather than switching off, and why nobody can promise a permanent result. It is also, from a safety point of view, the single most reassuring thing about the treatment: the body undoes it.
The nerve is not killed. Over the next few months it rebuilds those parts, and sometimes grows new endings, and the muscle starts getting its orders again. That is why the effect fades, why it fades slowly instead of stopping all at once, and why nobody can promise you a permanent result. It is also the most reassuring thing about the treatment from a safety point of view: your own body undoes it.
It also explains the most common disappointment. Botulinum toxin softens a line that is made by movement. A line that has become etched into the skin, or a fold created by lost volume or loose skin, is a different problem with a different answer. A practitioner who treats every line with the same syringe will produce a face that moves less without looking better.
It also explains why some people end up disappointed. This treatment softens a line that is made by movement. A line that has become carved into the skin, or a fold caused by lost fullness or loose skin, is a different problem and needs a different answer. Someone who treats every line with the same syringe will give you a face that moves less without looking better.
Why any of this matters to a patient
Why this matters to you
Because the history is a two-hundred-year argument for precision. Every advance in this story came from someone reducing a dose, narrowing a target or paying closer attention, and every disaster came from the opposite.
Because the whole story, across two hundred years, is an argument for being careful. Every step forward came from someone using less, aiming more precisely, or looking more closely. Every disaster came from the opposite.
Practically, three things follow. Units are not interchangeable between brands, because each product is measured against its own reference and a unit of one is not a unit of another. Where the injection goes matters more than how much goes in, because the muscles of the face are layered and neighbouring ones do different jobs. And the goal is a chosen pattern of softening rather than the absence of movement, which is a judgement about anatomy and about what the person actually wants their face to do.
Three practical things follow. First, units are not the same between brands. Each product is measured against its own yardstick, so ten units of one is not ten units of another. Second, where the injection goes matters more than how much goes in, because the muscles of the face sit in layers and the ones next door do different jobs. Third, the aim is to soften certain movements on purpose, not to stop your face moving at all. That is a judgement about your anatomy, and about what you actually want your face to be able to do.
This is a prescription medicine. That is a conversation to have with a physician who can examine you, not a decision to make from a price list.
This is a prescription medicine. That is a conversation to have with a doctor who can examine you, not a decision to make off a price list.
Questions patients ask
Is botulinum toxin really the same poison that causes botulism?
Is this really the same poison that causes botulism?
It is the same protein, produced by the same organism, purified and measured in quantities many orders of magnitude smaller than a poisoning dose and placed into a specific muscle rather than swallowed. The dose and the route are the whole difference, which is why it is a prescription medicine administered by a clinician.
It is the same protein, made by the same germ. What differs is the amount and where it goes. A treatment dose is a tiny fraction of a poisoning dose, and it is placed into one muscle rather than eaten. That is the whole difference, and it is why this is a prescription medicine given by a clinician.
Why does it take a few days to work?
The toxin has to be taken into the nerve ending and cut its target protein, and the muscle only quietens as the existing signalling is used up. Onset is typically over several days, with the full effect usually judged at around two weeks.
The toxin has to get inside the nerve ending and cut its target before anything changes, and the muscle only goes quiet once the messages already waiting have been used up. Most people notice it over several days, and the full effect is usually judged at about two weeks.
Why can I not simply have more so it lasts longer?
Why can I not just have more, so it lasts longer?
Duration is governed by how quickly the nerve rebuilds, not by how much was given. More product spreads further, affects muscles that were not the target, and raises the risk of an unwanted result without meaningfully extending the effect.
How long it lasts depends on how fast your nerve rebuilds itself, not on how much you were given. Extra product spreads further, reaches muscles that were never the target, and raises the chance of a result you did not want. It does not meaningfully add to the time.
Are the different brands interchangeable?
Can the different brands be swapped for each other?
No. Each product has its own potency reference, so units cannot be converted between them, and each carries its own approved uses. A clinician chooses between them on the basis of the area, the pattern of movement and the product’s labelling.
No. Each product is measured against its own yardstick, so you cannot convert units from one to another, and each is approved for its own list of uses. A clinician chooses between them based on the area being treated, how your face moves, and what each product is approved for.
Does it prevent lines from forming?
Does it stop lines from forming?
Repeatedly softening a movement can reduce how deeply a line becomes etched over time, which is why some people start earlier. It is not a guarantee, it does not address sun damage or volume loss, and starting a lifelong treatment is a decision worth making deliberately rather than by drift.
Softening a movement again and again can keep a line from being carved in as deeply over the years, which is why some people start young. It is not a guarantee. It does nothing about sun damage or lost fullness. And starting a treatment you may keep up for life is worth deciding on purpose, rather than drifting into.
Where to go next
Talk it through with a physician first.
Every plan starts with an assessment of your skin, your anatomy and what you actually want to change.
This page is general health information, not medical advice. It cannot tell you whether a treatment is right for you. Approved uses, risks and results differ from person to person, and product labelling changes. Ask us at Dermatology and Laser Centre about your own situation, or make an appointment, and seek urgent care for any serious symptom.
