Trauma is usually treated as something you carry, manage, work through, and sometimes facilitate. It is rarely something that can be stopped before it takes hold. That’s what a A group of researchers in Munich and Stockholm set out to test.
They begin to make the first days of life difficult. The mother mice were given much less nesting material and bedding than usual. This was enough to make mothers moody and unpredictable in the first days of life. The mice raised in these difficult conditions grew up looking completely healthy, with no obvious disease or anything obviously wrong.
The researchers then put them into groups and watched what happened. Repeatedly, these mice ended up at the bottom. They were pushed to the lowest ranks of the social hierarchy, first as teenagers, then again as adults. The difficult childhood left no visible mark, but it determined the position they would occupy for the rest of their lives.
When the researchers gave each other a drug, the pattern disappeared.
The study, published in June, was co-led by Mathias Schmidt at Harvard University Max Planck Institute of Psychiatry In Munich and Juan Pablo Lopez in Karolinska Institute in Stockholm.
How does childhood trauma affect the brain and body?
Start with cortisol, the body’s main stress hormone. When something stressful happens, cortisol floods the system. This is a standard protective response.
What’s equally important is the off switch. The body needs to register that the danger is over and stop the response. It does this through cortisol receptors, which are parts of cells that detect the hormone and signal the system to stop.
A protein called FKBP51 controls the sensitivity of these receptors. Research indicates that early hardship causes the body to produce more of it. This makes it difficult to stimulate the receptors, so the step-down signal never fully arrives, and The stress response remains on Much longer than it should be.
Schmidt’s point is that none of this is something anyone can feel.
“Your cortisol response is something you don’t feel,” he said. “You may think you can handle stress, but your body is secreting cortisol, and you don’t know it.”
Can medication prevent the effects of a difficult childhood?
The researchers used a compound called SAFit2, which blocks FKBP51. It is given to mothers during a period of stress, and reaches the offspring through breast milk.
The treated mice continued to perform similarly, within their social groups, to mice that faced no adversity at all, erasing the social cost of the difficult start.
The effect appeared in the brain as well as in behavior. The team examined gene activity in six stress-related regions and found that early adversity left a broad imprint. The medication has largely reversed this, most clearly in two parts: the medial prefrontal cortex and the nucleus accumbens, regions involved in emotional control and reward.
Can childhood trauma be reversed?
Not on this evidence.
In the Munich study, the compound was given during the stress period itself, rather than after it. What the study shows is prevention, not reform.
Other studies have shown behavioral effects when the drug is used in adult animals, but complete reversal of already existing trauma remains unproven. Prevention only works if you can identify people at risk before harm occurs, a problem this research does not address.
Will this drug actually work on humans?
It’s too early to say.
The study only tested male mice, so it is not yet known whether the same applies to females. SAFit2 remains an investigational compound 3 that is effective in animals but has not yet been developed or tested for safety for human use. However, Schmidt sees a realistic path toward clinical application within the next decade, noting that the mechanisms of stress are “very similar in animals and humans.”
How is trauma treated now, and why doesn’t it always work?
Current treatments for stress-related disorders, including PTSD and trauma-related depression, rely largely on selective serotonin reuptake inhibitors, or SSRIs. These medications target serotonin pathways. It is effective for many patients, but the mechanism is not fully understood, and a large portion of patients do not respond at all.
By contrast, targeting FKBP51 means treating the disease at its source. “We will actually treat not only the symptoms, but also the cause of the disorder by acting directly [on] “Stress mechanism,” Schmidt said. “These types of drugs are not currently on the market.”
In the long term, Schmidt envisions a more targeted approach: identifying individuals genetically susceptible to stress whose FKBP51 expression is already high, and treating that group specifically afterward. Acute traumatic events.
At the other end of the spectrum, there are people who, through genetics or past experience, have proven to be remarkably resilient even under extreme conditions, and may not need medication at all. Understanding who needs it, and reaching them in a timely manner, is where the research is headed next, Schmidt said.
What are the signs of unresolved trauma?
Schmidt ensures that trauma is highly individual, both psychological and physiological. The rough guide he gives is duration, not intensity.
A strong stress reaction immediately after a car accident or violent event is normal – the body is doing its job. What worries doctors is when the response continues much further: They still can’t cross the street after a month, and they still can’t sleep after six weeks. These are illustrative examples he gives, not diagnostic thresholds, but the principle remains. If the stress response does not fade, it is recommended to speak to a doctor.
This remains a practical guideline at present. The emergence of a drug, if it exists, will take at least a decade – and, according to current evidence, it must come before the damage is done, not after.
Editor: Kawkab Shirani
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