Thomas Kingston's Death Highlights Challenges in Linking Antidepressants to Suicide
And the necessity of being transparent about potential harms
Thomas Kingston was a British financier and former diplomat. In May 2019, he married Lady Gabriella Windsor, daughter of Prince and Princess Michael of Kent, and their wedding was attended by senior members of the royal family. On February 25, 2024, Kingston was found dead at his parents’ home in the Cotswolds. He had shot himself with a gun that was present near his body.
In January 2024, Kingston had been prescribed sertraline (an SSRI antidepressant) and zopiclone (a sedative) by a general practitioner (GP) at the Royal Mews Surgery because he had been experiencing work-related stress and sleep disturbances. After four days, he discontinued sertraline due to adverse effects: he was feeling “sleepy and low in the mornings” and “woozy and overheat” during the day (as reported by the Times). In February, when he told his doctor about this, he was prescribed citalopram, another SSRI, but after taking two doses and experiencing similar adverse reactions, he stopped the medication. The exact length of time between his use of citalopram and his suicide has not been reported in the newspapers. The coroner concluded that Kingston’s death was an impulsive act in the context of adverse reactions to the prescribed medications, noting there was no settled intention to end his life.
From the Guardian:
Recording a narrative conclusion, Katy Skerrett, senior coroner for Gloucestershire, said: “Mr Kingston took his own life … The evidence of his wife, family and business partner all supports his lack of suicidal intent. He was suffering adverse effects of medication he had recently been prescribed.”
In a statement read out at the inquest by Skerrett, Gabriella said: “[Work] was certainly a challenge for him over the years but I highly doubt it would have led him to take his own life, and it seemed much improved.
“If anything had been troubling him, I’m positive that he would have shared that he was struggling severely. The fact that he took his life at the home of his beloved parents suggests the decision was the result of a sudden impulse.”
She said she believed his death was “likely provoked” by an adverse reaction to the medication he had begun, and subsequently stopped taking, in the weeks leading up to his death…
“The lack of any evidence of inclination – it seems highly likely to me that he had an adverse reaction to the pills that led him to take his life,” Gabriella said.
“I believe anyone taking pills such as these need to be made more aware of the side-effects to prevent any future deaths.
“If this could happen to Tom, this could happen to anyone.”
From the Times:
The inquest heard Kingston has been spending the weekend at his parents’ home in Kemble, Gloucestershire, and was “in his usual ebullient spirits and good health”.
He had enjoyed several meals with his parents, attended his young niece’s birthday near Bath, and had been “light-hearted” the night before his death. His last message to his wife, who was not there that weekend, was that “all was good here”.
It was on the Sunday afternoon, when he was unpacking his father’s shotgun from his car, that he went to an upstairs bathroom in a detached outbuilding, locked the door and shot himself.
Lady Gabriella, 43, who attended the inquest with Kingston’s parents, said: “The fact he took his own life at the home of his beloved parents, where no one else would find him, suggests the decision was a result of a sudden impulse and anxious thought and this was sparked by his seeing the gun in the car boot with boxes of books to be stored away.
“To me, his final actions show he was somehow absent or taken over by an external influence in his final moments.”
Based on information that has been publicly reported so far, the link between Kingston’s SSRI use and his suicide seems rather tenuous and speculative to me. The stated reasoning is that since there was no obvious indication of suicidality and his interactions with his family around the day of his death gave no indication of severe mental distress, the suicide must have been a result of a “sudden impulse.” Since in the weeks before he had taken a few doses of two different SSRIs that had left him more anxious, therefore—it is further hypothesized—it must be the medication (which he had already stopped at the time of his death) that was cause of the sudden suicidal impulse.
This is a weak chain of inference, and I am surprised that it has been discussed so far so uncritically.
We know that a sizeable proportion of suicide deaths are preceded by no overt indication and come as a shock to family and friends. It is also to be expected that some portion of these individuals would’ve sought antidepressant treatment in the weeks preceding their death. And since worsening anxiety and activation on SSRI initiation are fairly common, it is also to be expected that some proportion of these individuals would’ve experienced SSRI-related side effects in the weeks preceding their death. When dealing with large numbers of people over time in a population, we can expect that some suicide deaths will be preceded by SSRI-related side effects based on chance alone.
To go beyond speculation, we need some evidence of a clinical causal link. Such a link would be present in Kingston’s case if there was evidence of persistent agitation, anxiety, restlessness, or suicidality. If Kingston had been observed to be “light-hearted” and “in his usual ebullient spirits and good health” by his family in the day prior to his death, we cannot reasonably say that Kingston was suffering from persisting agitation or akathisia from the discontinued SSRI.
I accept that in some circumstances SSRI can indeed lead to suicidality, suicide attempts, or suicide deaths. SSRI-related suicide deaths in adults at the population level seem to be uncommon enough that observational studies of adults do not show a conclusive link, but I do not deny that it happens. (In RCTs and observational studies, SSRIs seem to neither increase nor decrease suicide rates in adults on average—which could either mean that there is no substantial effect either way or that the two effects are roughly equal in magnitude and cancel out).
In my clinical work, I frequently encounter individuals who tell me that they have experienced suicidality on antidepressants. This experience is often restricted to a particular antidepressant, and a different one is tolerated well, but not always. In some cases, antidepressants generally seem to provoke suicidality.
The scenarios of SSRI-related suicidality I have observed and heard about from patients tend to fall into the following:
Initiation of antidepressant leads to intense anxiety or dysphoria that produces (or exacerbates existing) suicidality
Treatment with antidepressant leads to manic or mixed symptoms, which lead to suicidality
Antidepressants make the person feel emotionally indifferent, and in the context of existing suicidal thoughts, it leads them to act on the suicidal thoughts because the usual emotional aversion to suicidal thoughts gets replaced by, “Eh, so what if I die?”
Stopping an antidepressant abruptly (in someone who has been on them for a prolonged period) leads to a sudden exacerbation of mood and suicidality (withdrawal-related suicidality)
I am yet to meet a patient who told me that they had SSRI-related anxiety/agitation, stopped the SSRI, were fine, and then out of nowhere had a “sudden impulse” to die by suicide.
Lady Gabriella said: “I believe anyone taking pills such as these need to be made more aware of the side-effects to prevent any future deaths.” But here’s the thing. There is no way to guard against a putative sudden suicidal impulse that comes even after one has stopped the medication, and that turns a person in ebullient spirits into something like an automaton who commits suicide. If the official story reported in the media is correct, Thomas Kingston had already done the right thing. He stopped sertraline after 4 doses and stopped citalopram after 2 doses. He had the presence of mind to discontinue as soon as he noticed a problem.
The more plausible scenario is either that Thomas Kingston was experiencing persistent agitation from the SSRI that went unobserved and led to suicide or that he had been contemplating suicide for some time and decided to proceed with it after unsuccessful attempts at medication treatment. In either case, we are filling in the gaps with what may have been the case. We don’t know.
What could’ve been done differently? Psychiatrist David Healy suggested in his statements to the press that once Kingston experienced anxiety on sertraline, he should not have been tried on another SSRI again. Current clinical opinion is that tolerability varies among SSRI agents, and if a patient experiences anxiety/hyperactivation from an SSRI, it is reasonable to try a different one. I have switched a patient from one SSRI to another for this reason numerous times, usually starting with half the normal dose, and this strategy works well enough in clinical practice that I stick to it. But of course, as noted, they are patients who don’t generally respond well to any serotonergic antidepressant, and it’s basically impossible to know in advance unless there is some clear risk factor, like established bipolarity, or SSRI-induced manic or mixed symptoms suggesting latent bipolarity, or pharmacogenomic data indicating poor metabolism across SSRIs, etc. As far as I know, this question has also not been properly studied in research. While we have some research on the efficacy and tolerability of switching to a different antidepressant once a patient has had limited benefit with the initial antidepressant (e.g., see Boyce et al. 2020; Ruhe et al. 2006), we don’t really know what percentage of people fail to tolerate a second SSRI if they haven’t tolerated the first SSRI and how this changes based on the nature of adverse effects experienced.
One reasonable question here is: did Thomas Kingston need to be on an SSRI to begin with? According to the Times, he told his GP he was suffering stress at work and had trouble sleeping. GP diagnosed him as suffering from “acute anxiety.” We are told that there is no prior history of mental health problems. It is quite likely that there are additional clinical details that we are not privy to. Hence, my discussion is limited by what is publicly available and may be rendered inapplicable if new details emerge. But if that is all Kingston was dealing with, then treatment with SSRI could reasonably have been deferred. SSRIs are great options neither for acute anxiety nor insomnia. They perform best, IMO, when the problem is chronic—generalized anxiety, dysthymia, adjustment disorder with high neuroticism—or sufficiently severe, e.g., major depression. Stress-related anxiety that is mild and anticipated to be self-limiting is best addressed via supportive interventions or short-term use of quick-acting medications, such as sedatives. SSRIs can still be reasonable options in such situations, but the risk-benefit considerations are not quite straightforward.
Such things make physicians uncomfortable, but I’ll say so clearly: on starting an antidepressant (as well as going off them abruptly), some patients can experience worsening anxiety, agitation, restlessness, irritability, mood lability, or akathisia. These can subsequently induce or exacerbate suicidal thoughts, which in some cases can lead to suicide attempts and, rarely, suicide deaths. In my clinical experience of working with people with complicated mood and anxiety disorders, these issues with antidepressants are common enough that I try to see patients soon after starting an SSRI so that I can address early issues with tolerability. The idea of just starting an antidepressant and seeing them a month (or months) later worries me. As a psychiatrist, I get to see more complicated cases, and my experience doesn’t generalize to primary care, but I do think that even in primary care, it should be anticipated that a substantial number will struggle with SSRI-initiation and that a close follow-up after starting an SSRI is a useful general strategy.
We accept all kinds of risks in our lives. We drive cars on roads, we fly on planes, we drink alcohol socially, we use tobacco and cannabis, we invest in stocks, we undergo general anesthesia for surgical procedures, etc., etc. When my son was an infant, he loved being in a particular bouncer. We used it all the time. This is despite the fact that there was a warning prominently displayed on it. “Fall Hazard: Babies have suffered skull fractures falling while in and from bouncers.” Essentially, we accepted a very small risk of a catastrophic event because of the tremendous everyday convenience the bouncer offered us. Such considerations are ubiquitous in healthcare.
Every time a person uses an antidepressant, there is a small possibility that their experience may go very badly, sometimes in life-altering ways (e.g., suicide, mania, persisting sexual dysfunction, protracted withdrawal). Risk is ubiquitous in medicine; the possibility of iatrogenic harm is unavoidable. This will not stop people from using antidepressants. I have worked with many patients who experienced serious adverse effects with an antidepressant in the past but were still interested in trying others because they were desperate for relief.
But being transparent with the public about these risks accomplishes two things.
First, if patients and clinicians are aware of the possibility of harm, they can recognize the problem early and stop the medication before it progresses.
Second, it serves as a reminder that the condition being treated should be distressing enough or severe enough for the person that they are willing to accept the possibility of uncommon but serious adverse events. The threshold for what counts as distressing enough or severe enough will be different for different people, but what that threshold is in any particular situation for any particular person is worth giving some thought to.
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Thanks for commenting on this difficult story. I had a similar reaction in terms of the link between SSRIs and this tragic outcome.
More generally, I think it’s so tricky to talk about rare, serious side-effects from medical interventions (eg vaccines) because, for the person unfortunate to have such an adverse effect, it is little comfort to know they were particularly unlucky and on the whole most people experience a net benefit. As medical professionals it can feel easier to deny such rare side-effects even occur at all.
Why not address the actual cause of death? The gun. Was he competent with firearms? Why wasn’t it in a safe? We cannot talk about causal inference of completed suicide and not talk about means.