3 March 2025
If you’ve been reading my work for a while, you’ll know that I’m not the world’s biggest fan of antidepressant medications. Not only do they cause profound sexual dysfunction that may persist even after patients stop taking them, birth defects and an increased risk of premature birth in offspring of mothers who take them, hip fractures and upper gastrointestinal bleeds, but the rationale for prescribing them (the ‘biochemical imbalance’ theory of depression) is utterly baseless, the clinical trial data show that they don’t relieve the symptoms of depression any better than placebos, and they can cause debilitating withdrawal effects including flu-like symptoms, intractable insomnia, nausea, persistent electric shock-like sensations dubbed ‘brain zaps’, anxiety, irritability and impaired concentration. Apart from all that though, they’re great </sarcasm>.
But just in case the COVID jab debacle didn’t open your eyes to this sad fact, most doctors don’t seem to have any objection to prescribing drugs that don’t work but do cause horrendous adverse effects. And one of the patient groups most at risk of inappropriate and harmful prescriptions is elderly people. Back in 2019, I wrote about a British study which found that more than twice as many people over 65 had been prescribed antidepressants in 2011 compared to 1991, and that most of them did not actually have depression, according to a validated psychiatric diagnostic instrument called AGECAT. Gee, I wonder if the doctors who wrote those prescriptions conducted a proper informed consent discussion with their elderly patients.
There’s yet another serious harm inflicted on elderly people by antidepressants: they appear to accelerate cognitive decline in patients with dementia. In a study based on data from dementia patients registered in the Swedish Registry for Cognitive/Dementia Disorders (SveDem), researchers identified a dose-response relationship between antidepressant use and cognitive decline. Furthermore, taking antidepressants was associated with heightened risk of severe dementia, all-cause mortality and bone fractures.
Noting that previous observational studies investigating the impact of antidepressants on cognitive function had produced contradictory results, the authors set out to design a study that addressed the limitations of these earlier studies, including short follow-up time and enrolment of patients who did not yet have a dementia diagnosis. They took advantage of Sweden’s highly-centralised health care system, which maintains nationwide registries of patients with particular diagnoses, inpatient and specialised outpatient care records, cause of death and dispensation of prescription medications from all pharmacies. From these registries, they were able to sift out 18 740 individuals who
- Had received a dementia diagnosis between 1 May 2007 and 16 October 2018;
- Had undergone a Mini-Mental State Examination (MMSE) to assess the severity of their dementia at diagnosis, and on at least one follow-up visit;
- Were new users of antidepressants – that is, they had not been taking antidepressants any earlier than six months before their dementia diagnosis; and
- Were not prescribed multiple antidepressants, either of the same or different classes.
23 per cent of the 18 740 patients were issued at least one prescription for an antidepressant during the study period. Just six drugs accounted for 99 per cent of all antidepressant prescriptions: citalopram (a selective serotonin uptake inhibitor, or SSRI), mirtazapine (a tetracyclic antidepressant), sertraline (SSRI), escitalopram (SSRI), amitriptyline (a tricyclic antidepressant, or TCA), and venlafaxine ( a serotonin norepinephrine reuptake inhibitor, or SNRI).
Using MMSE scores at baseline and follow-up to track patients’ rate of deterioration, the use of any type of antidepressant was associated with faster cognitive decline, in all subtypes of dementia except for frontotemporal and Lewy body dementia:
Comparing classes of antidepressants, and individual antidepressants, the drugs that were significantly associated with cognitive decline were SSRIs, the non-SSRI/SNRI/TCA group classified as ‘others’, sertraline, citalopram, escitalopram and mirtazapine:
Comparing rates of cognitive decline in the subgroup of patients who were all taking some type of antidepressant, escitalopram was associated with the fastest deterioration, followed by citalopram and sertraline. Mirtazepine had less cognitive impact than these three SSRIs.
A dose-response relationship was observed for both SSRIs and the ‘other’ category of antidepressants, with higher dispensed dosages associated with a faster rate of cognitive decline. Furthermore, patients with the lowest initial MMSE scores (indicating worse dementia) suffered the greatest subsequent cognitive decline if they were prescribed antidepressants.
And just to cap it all off, dementia patients taking antidepressants were 7 per cent more likely to die, and 18 per cent more likely to have a bone fracture than those who weren’t; once again a dose-response relationship was observed, with those on the highest doses of antidepressants being 18 per cent more likely to die and 25 per cent more likely to have a fracture.
Cause or effect?
One of the chief weaknesses of association studies such as this one is indication bias, also known as confounding by indication. Confounding by indication is highly likely when a particular medicine is linked to the outcome of interest in a study. In this case, it is well-established that people with depression are more likely to become cognitively impaired and to develop dementia. Hence, it could be the case that patients who were prescribed antidepressants were already at heightened risk of cognitive decline, because they were depressed, and that those prescribed the highest doses of antidepressants were the most depressed, and therefore could be expected to deteriorate faster. In other words, maybe depression caused both antidepressant prescription and faster cognitive decline.
To reduce the impact of confounding by indication, the researchers separated out the subgroup of patients who were prescribed antidepressants but who had not been diagnosed with depression1, and found no difference in the rate of cognitive decline between them, and the patients who were depressed. Furthermore, the study excluded patients who were taking antidepressants prior to the six months before their dementia diagnosis, in order to minimise the effect of pre-existing depression on the subsequent rate of cognitive decline. Still, no study design or statistical technique can completely neutralise indication bias.
The authors acknowledge that they certainly have not proven that antidepressants accelerate cognitive decline in patients with dementia, and call for more research into “the complex interplay between antidepressant use, dementia severity, and cognitive decline.” They also suggest that their study might “help doctors and other healthcare professionals choose antidepressants that are better adapted for patients with dementia.”
Sure, that interplay is complex and more research would help to elucidate it. But let’s not lose sight of the crucial fact that people don’t become depressed because they’re suffering from antidepressant deficiency. As I wrote in More elderly people are taking antidepressants, but they’re just as depressed,
“From my point of view, prescribing antidepressants to older people who show signs of psychological distress rather than attempting to understand and address the causes of that distress is irrational, inhumane and a flagrant waste of health care resources.
Poor diet, lack of exercise and disrupted sleep are major contributing factors to depressed mood, and should be addressed as part of a comprehensive lifestyle intervention.
Loneliness, poverty and loss of a sense of meaning and purpose in life are also key factors in depression. It is beyond ridiculous – not to mention profoundly dehumanising and insulting to suffering individuals – to maintain the fiction that the consequences of social and spiritual isolation and economic deprivation can simply be medicated away.”
More elderly people are taking antidepressants, but they’re just as depressed
Furthermore, the same diet and lifestyle factors that increase the risk of depression, are also implicated in dementia. As Dr Dean Ornish’s Alzheimer’s study showed, getting people with mild cognitive impairment or early dementia onto a comprehensive program incorporating a wholefood plant-based diet, daily exercise, stress management and sleep optimisation, and emotional and social support, can actually reverse cognitive decline, with the greatest benefits occurring in those with the greatest adherence to the program. Huh. It’s almost as if we need to eat wholesome food, move our bodies around regularly, get to bed on time and have meaningful connections with other human beings, in order to be physically, cognitively, emotionally and spiritually healthy. Damn, if only that were patentable.
Over the last year or so, I’ve been seeing many more clients with early cognitive decline, thanks to my collaboration with Alzheimer’s recovery coach, John Bransby. I’ve seen, up close and personal, the dramatic benefits of diligently implementing a multimodal diet and lifestyle plan. You can’t drug a person into being happy, nor can you medicate a deteriorating brain into health. But as it turns out, addressing the underlying drivers of both depression and cognitive decline works where pharmaceuticals fail. Who woulda thunk it???
- Patients with dementia are often prescribed antidepressants to manage their anxiety, aggressiveness, and sleep disturbances, rather than for depression. ↩︎
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