New therapies, better access and personalized care

Q: What is your opinion on the new orexin antagonists and what place they may have in the future treatment of COMISA?

Dr. Sweetman: I’m excited to see how the field develops with the new dual orexin receptor antagonist. From a comorbid insomnia and sleep apnea (COMISA) perspective, there are only a couple of studies so far, maybe two or three. These medications appear to have fewer side effects and a lower risk of dependence compared to benzodiazepines, which is a big plus. But the meta-analytic data on their effectiveness is a bit underwhelming.

For example, the most common outcome measure in insomnia trials is the Insomnia Severity Index (ISI) in which a six-point reduction is considered clinically meaningful. But with orexin antagonists, meta-analyses report reductions of only 1.5 to 2 points, which is below that threshold. Similarly, sleep outcomes like time to fall asleep or time awake during the night might improve by 5 to 15 minutes. But for someone who’s awake two or three hours every night, that kind of improvement is not particularly meaningful.

So yes, they’re safer and less habit-forming than other medications, which is promising. But their clinical impact so far appears modest.

Q: Neurostimulation for insomnia is now FDA-approved. How do you see this fitting into future treatment approaches?

Dr. Sweetman: It’s great to see novel treatments like neurostimulation emerging, along with third-wave psychological therapies like mindfulness-based approaches and acceptance and commitment therapy (ACT).

While cognitive behavioral therapy for insomnia (CBT-I) remains the gold standard, it doesn’t work for everyone. About 20–30% of people with insomnia don’t respond to CBT-I, so it’s essential to develop and support alternatives with evidence behind them.

We absolutely need more research in this space. But given my passion and interest, I’m still deeply focused on improving access to CBT-I. It’s backed by hundreds of clinical trials and more than 40 meta-analyses, yet only about 1% of people with insomnia access it.

New treatments are important and exciting, but we can’t lose sight of the fact that the most evidence-backed therapy still isn’t reaching the majority of people who need it.

Q: Is there a specific population for whom CBT-I may not work well? Could this be a subgroup that may benefit from these alternative therapies?

Dr. Sweetman: I think the better question is, “Who responds to CBT-I, and why?”

I’m speculating a little here and stepping outside the direct evidence, but I imagine it comes down to the underlying causes of insomnia for each person. CBT-I is designed to target the psychological and behavioral factors that maintain chronic insomnia. If insomnia is driven by those mechanisms, CBT-I tends to work well. But if the root causes are biological, medical or something else, CBT-I may be less effective.

Of course, that’s a bit of an oversimplification. Most cases sit somewhere on a continuum. Some are psychological, biological or environmental, and many are mixed.

This is an emerging area of research. I’ve been working with a group at Deakin University and Reconnexion in Australia, where a DPsych student, Monique Smith, has been doing fantastic work conducting a comprehensive review exploring a very large number of different predictors of which patients with insomnia are most likely to respond to CBT-l.

Q: New pharmacological treatments for OSA are in the clinical trial pipeline. However, insomnia is sometimes reported as a side effect. What are your thoughts on treating one condition and potentially triggering another?

Dr. Sweetman: Yes, this highlights why we need a holistic approach, not a siloed, disorder-specific one.

We can’t just ask, “Is this treatment effective for sleep apnea?” without also asking, “How does it affect insomnia?” We need to look at improving overall sleep health. It's a good reminder that we need to assess insomnia symptoms not just at baseline, but also during and after treatment for sleep apnea.

There hasn’t been much research in this area yet, but I suspect that positive airway pressure (PAP) therapy may actually cause new-onset insomnia symptoms in some patients. It’s something we need to understand better, and it reinforces how complex sleep disorders are.

Q: Your work focuses heavily on insomnia and COMISA research. What are you currently working on, and where do you see this heading in the future?

Dr. Sweetman: A big focus for me is fostering more collaboration within the healthcare system. Right now, COMISA isn’t well-managed in isolation. It needs a multidisciplinary approach.

First, we need better recognition. Then, we need care models that allow different types of clinicians to work together closely in managing COMISA.

Another area I’ve become more passionate about in recent years is digital CBT-I (dCBT-I). It has huge potential to improve access. One key question we’re exploring is: Which patients with COMISA are appropriate and safe candidates for self-guided digital CBT-I, and which ones need referral and care from a clinician?

It could depend on symptom severity, daytime functioning, workplace safety and other factors. We want to be able to triage people effectively to either digital or in-person CBT-I.

We’re also exploring timing and treatment combinations. How should CBT-I be combined with sleep apnea treatments, whether it’s PAP, oral appliances, positional therapy or even emerging medications? What are the best sequences or combinations? And which patients respond best to which combinations?

It all comes back to personalizing care and figuring out the right combination for each person. That’s where I see a lot of my future work heading. And that’ll probably keep me busy until the end of my career.