Based on an interview with Dr Jon-Paul Khoo, psychiatrist, co-owner and director at the Toowong Specialist Clinic, Brisbane held at the Annual Women and Children’s Health Update, Melbourne, March 2018
Modern antidepressant medication is efficacious and effective for sufferers of major depressive disorder.
However, residual symptoms, even in those who appear to be in remission, are common and can contribute to ongoing distress. Sexual dysfunction is one particularly relevant example. Up to a quarter of the general population report this, and the rate increases to about half of those who are depressed but not on treatment.
Sexual dysfunction may affect up to 80% of treated depressed people and is affected by their background, the depression itself and the treatment. Even when mood recovery occurs, sexual dysfunction can persist. As GPs are the main prescribers of antidepressants in Australia, before choosing a medication, they need to feel informed and comfortable when discussing the impact of depression and its treatment on all aspects of functioning, specifically sexual functioning.
Following a complete assessment, the GP may feel that antidepressant medication is indicated. This would be an opportune time to ask about current sexual function. It is likely to be a more comfortable discussion if the patient and doctor are already acquainted, but even if this is not the case, it a straight-forward approach with some advance warning about the need for personal questions often helps.
“We have to introduce the topic of sexual dysfunction as very few patients will spontaneously bring up this topic”, says psychiatrist Dr Jon-Paul Khoo.
Sexual behaviour in humans is complex, individual and highly personal. Nothing should be assumed about the patient’s sexual habits. It may be necessary to discuss relationship problems, at-risk behaviour, sociocultural issues and medical conditions affecting sexual function.
It should also be discussed with patients that many people in the general population who are not depressed have sexual dysfunction.
Given this, the usual sexual dysfunction associated with antidepressant use in women is lack of desire and difficulty achieving orgasm. The usual sexual dysfunction associated with antidepressant use in men is lack of desire, erectile dysfunction and delayed or absent ejaculation. The impact of these side-effects may be more severe for men than for women (although sexual side-effects occur more commonly in women).
People who have less supportive relationships, those in the older age groups, those with medical conditions and those with sexual problems prior to the depression, or because of it, are most likely to be adversely affected sexually by antidepressant medication.
On the positive side, antidepressants may be beneficial in patients who have premature ejaculation. Furthermore, judicious decision-making about antidepressant type may allow those with pre-existing impotence, pain disorders and sexual dysfunction due to other causes to undertake effective treatment without a worsening of sexual dysfunction
We are familiar with efficacy data and the overall clinical utility of antidepressant medications, but we are less well-educated regarding the adverse sexual effects of treatment.
Although there are minimal efficacy differences between antidepressant therapies in the treatment of major depressive disorder, there are distinct tolerability differences. The propensity for causing sexual dysfunction varies both between and within antidepressant subtypes.
A brief summary of antidepressant-induced sexual dysfunction is that approximately 80% of people taking (most types of) selective serotonin reuptake inhibitors (SSRI) or venlafaxine, a serotonin noradrenaline reuptake inhibitor (SNRI), will report some sort of adverse sexual effect.
A more moderate risk of sexual dysfunction occurs with imipramine, as well as escitalopram and fluvoxamine (both SSRIs) and duloxetine (an SNRI).
The lowest rates of sexual dysfunction (placebo-equivalent rates) in controlled studies are reported with agomelatine, moclobemide, mirtazapine (though sedation may affect desire) and vortioxitine (on pooled analysis).
In comparison, atypical antipsychotics have a higher rates of sexual dysfunction than antidepressant therapies, probably related to their propensity to elevate prolactin. It is wise to exclude or manage drug and alcohol issues, and to discuss with the patient the adverse effect of these regarding both the remission of depression and adequate sexual functioning.
Patients at high risk of, or who already have, pre-existing sexual dysfunction should be commenced on a low-risk antidepressant when clinically reasonable.
If a higher risk medication is working well for mood stability, the patient may decide not to change treatments.
Commonly cited strategies of waiting for sexual dysfunction to improve with time, or scheduling sexual activity against dosing, have limited benefit for the majority of patients. Similarly, dose reduction and ‘drug holidays’ are not generally effective.
The most gain in arresting sexual dysfunction occurs with changing the antidepressant to a lower risk alternative. Augmenting the antidepressant therapy with an intervention that might improve any induced sexual dysfunction is probably the next best option.
For women, this might include exercise 30 minutes prior to sexual activity, as may increasing the frequency of sexual activity. For men, the best augmentation strategy appears to be prostaglandin E inhibitors. There are data for both sildenafil and tadalafil, both of which are indicated in men who have sexual dysfunction.
Finally, it is also suggested that involving the partner, where appropriate, may help reduce stigma and increase support and understanding for patients affected by sexual dysfunction.
With the cost of developing a new drug to market estimated at US$2.6 billion, the burden of family planning looks to remain firmly on the shoulders of women for now.
Adam Watkins, Assistant Professor, University of Nottingham
This article was originally published on The Conversation. Read the original article.
On the savings side, there was also no move yet on the private health insurance rebate which some experts think could be scrapped.
Kees Van Gool, Health economist, University of Technology Sydney; Andrew Wilson, Co-Director, Menzies Centre for Health Policy, University of Sydney; Helen Dickinson, Associate Professor, Public Service Research Group, UNSW; Lesley Russell, Adjunct Associate Professor, Menzies Centre for Health Policy, University of Sydney; Peter Sivey, Associate Professor, School of Economics, Finance and Marketing, RMIT University, and Rosalie Viney, Professor of Health Economics, University of Technology Sydney
This article was originally published on The Conversation. Read the original article.
