Perimenopause and Menopause Insomnia: A Hypnotherapy Approach

If you are reading this at 3 a.m., flushed, kicking the duvet off for the third time tonight, with your brain replaying tomorrow at full volume, you already know the territory. Sleep changed before anything else did. Periods are still mostly regular, or they have started skipping, or they stopped a year ago. And nobody quite warned you that the sleep would go first. I want to walk you through what is actually happening in menopausal sleep disruption, what the research supports, where hormone replacement therapy belongs as the first-line option, and where hypnotherapy genuinely fits as an adjunct or as an alternative when HRT is not on the table.

I am Danny M., RCH. I run Calgary Hypnosis Center. This page is the long version of the conversation I have with women in the perimenopause-through-postmenopause span who reach out for sleep work. It is honest about scope. A meaningful share of women who book an intake get referred for HRT, a sleep study, thyroid bloodwork, or a CBT-I program before we ever start a hypnotherapy block. The right answer is whatever your sleep actually needs, not whatever the practitioner you happened to call sells. If you want the broader sleep work overview, the page on the broader sleep hub covers patterned insomnia in general; this page is the menopause-specific layer.

Menopausal sleep disruption is a recognized clinical pattern

Sleep disruption affects roughly 40 to 60 percent of women across the perimenopause-to-menopause transition, and the prevalence stays elevated into postmenopause for a meaningful subset. That is one of the highest-prevalence sleep complaints in any defined population, and it is reliably under-treated. The reasons are familiar to anyone who has tried to raise this with a busy GP. Sleep is hard to quantify in a ten-minute appointment. Menopausal sleep disruption gets coded as stress, ageing, or anxiety. Women are told they will get used to it, or that it will pass. For some women it does ease. For many it does not, and the cumulative cost on cognition, mood, work, and relationships is substantial.

The pattern is multi-mechanism. Hot flashes and night sweats fragment the night with micro-arousals you may or may not consciously remember. Mood shifts (perimenopausal anxiety and depression are common and often new-onset) feed bedtime arousal. The cortisol pattern shifts so that early-morning awakening becomes more prevalent. Sleep architecture itself changes, with less deep sleep and more fragmented REM. None of those mechanisms are imaginary. They show up on polysomnography. They show up on hot flash diaries. They show up on cortisol curves. The lived experience of fragmented, unrefreshing sleep with a 3 a.m. wake-up that turns into 2 hours of cycling thought has a clear biological substrate.

What I want to validate before going any further: this is not just getting older, it is not just stress, and it is not character weakness. There are evidence-based interventions, and there is a treatment landscape with a defensible order of operations. The fact that you have been brushed off by previous providers does not mean nothing can be done. It means the assessment was incomplete.

This page is written for the full transition span. Perimenopause, where periods are still happening but cycles are changing and symptoms are starting. Menopause, defined retrospectively as 12 months without a period. Postmenopause, the years after that point. The mechanisms shift across that span and the treatment emphasis shifts with them, but the cluster of sleep complaints stays recognizable.

One more orienting point: if your sleep changed in your early 40s and you have not yet connected that to perimenopause, you are not alone. The hormonal transition often begins five to ten years before periods become irregular or hot flashes appear, and sleep is sometimes the first system to register it. We will come back to this when we look at when medical workup is needed.

What is actually happening in menopausal sleep biology

Walking through the mechanisms one at a time is the fastest way to understand why menopausal insomnia responds to a multi-modal approach rather than a single intervention.

Estrogen decline. Estrogen has direct sleep-promoting effects through several pathways, including support for REM sleep, modulation of the serotonin and GABA systems, and stabilization of the hypothalamic temperature set-point. As estrogen falls across perimenopause, sleep architecture shifts: less consolidated deep sleep, more fragmented REM, and a thermoregulatory system that is suddenly easier to perturb. This is one reason a bedroom temperature that felt fine for decades can now feel intolerably warm at 2 a.m.

Progesterone decline. Progesterone, particularly its metabolite allopregnanolone, has a natural sedating effect through the GABA system. As progesterone falls across the transition, that built-in sedation support is removed. Many women describe a felt sense that sleep used to be easier, that they used to drop off without effort, that something has been subtracted. They are not imagining it. The progesterone curve has fallen out from under them.

Vasomotor symptoms. Hot flashes and night sweats produce micro-arousals 5 to 20 or more times per night in the women most affected. You may not consciously register most of them. The body does. Each one pulls you toward the surface of sleep, fragments deep sleep, and over months conditions a bedroom-equals-overheating association that can persist even when the vasomotor frequency softens. The vasomotor layer is the most distinctive part of menopausal sleep, the part where general insomnia advice is least useful, and the part where research by Elkins and colleagues has shown a specific signal for hypnotic relaxation.

Cortisol awakening response, shifted earlier. Cortisol naturally rises in the second half of the night to prepare the body for waking. In women across the menopause transition, with elevated baseline stress, lost progesterone sedation, and disrupted sleep architecture from vasomotor events, the cortisol rise can pull waking 3 to 5 hours earlier than intended. You wake at 3:30 a.m. with the nervous system already activated, and any lingering anxious thought immediately catches and amplifies the arousal. This is the same cortisol-awakening pattern documented across non-menopausal populations, and the cross-link page on the cortisol-awakening pattern that overlaps with menopausal insomnia goes deeper on the mechanism.

Mood comorbidity. Perimenopause is a high-risk window for new-onset or worsening anxiety and depression. The neurobiology overlaps with the sleep mechanisms, and the directional arrow runs both ways. Disrupted sleep amplifies mood symptoms, and mood symptoms amplify sleep disruption. Roughly the way pain and sleep amplify each other, hormones and mood and sleep travel together in this period of life. The page on for the perimenopausal mood comorbidity covers the anxiety side of that overlap.

Conditioned sleep-anxiety meta-loop. After enough bad nights, the bedroom becomes a cue. You walk in already braced for failure, the body responds with arousal, and the brace itself prevents sleep. This loop is the same one that holds non-menopausal chronic insomnia in place, and it sits on top of all the hormonal mechanisms above. The page on the meta-anxiety pattern that often compounds menopausal sleep disruption walks through that loop in detail.

The honest synthesis: menopausal sleep disruption is rarely one thing. It is hormonal architecture loss plus vasomotor fragmentation plus cortisol shift plus mood comorbidity plus a learned loop that wraps around all of it. Treatments that address only one layer tend to deliver partial gains. Treatments that address the right two or three layers tend to deliver durable change. That is why the most effective protocol for many women in this period combines a medical conversation about HRT with either CBT-I or hypnotherapy or both, and with the basic environmental and behavioural pieces in place.

The evidence base, including the Elkins hot-flash work

Three pieces of research are worth knowing if you are weighing whether hypnotherapy belongs in your menopausal sleep plan. They do not all point at the same outcome, and reading them together is the honest way to assess where this modality sits.

The first is Cordi 2014 (PMID 24882902). Researchers had healthy young women listen to a hypnotic-suggestion audio before sleep and measured polysomnography against a control narrative audio. Among the highly suggestible participants, the active audio produced 81 percent more slow-wave sleep among highly suggestible participants vs control. Slow-wave sleep is the deep, restorative stage tied to physical recovery, immune function, and memory consolidation, and it is the stage menopausal women lose disproportionately. So even though Cordi's population was not menopausal, the mechanism alignment is suggestive: if hypnotic suggestion can selectively expand slow-wave sleep, that lines up neatly with the architectural deficit menopausal sleep tends to show.

Read those caveats carefully because they shape application. The participants were not perimenopausal or postmenopausal. The effect was specific to high suggestibility, which is roughly the top 10 to 15 percent of adults on standardized hypnotizability scales. The 81 percent figure is a comparison to control, not an absolute baseline. So the precise honest version is: hypnotic suggestion can shift sleep architecture toward more deep sleep, the effect is biggest in suggestible people, and whether that translates into menopausal insomnia relief specifically has not been directly tested at scale.

The second piece is Chamine 2018 (PMID 29952757), a systematic review of clinical trials evaluating hypnosis interventions for sleep outcomes. Of 24 included trials, 13 of 24 trials reported a sleep benefit from a hypnosis-based intervention, including improvements in sleep onset latency, total sleep time, and subjective sleep quality. That is a 54 percent positive-trial rate. The other 11 trials did not show benefit. The authors flagged heterogeneity in protocols, populations, and outcome measures, and called for standardized hypnosis protocols and larger randomized controlled trials.

The third strand, and the one most directly relevant to menopausal sleep, is the hot-flash hypnotic relaxation work. Research by Elkins and colleagues has shown that a structured hypnotic relaxation protocol can reduce the frequency and severity of hot flashes in postmenopausal women, including the night-time vasomotor episodes that fragment sleep. This is a separate evidence base from the general insomnia-and-hypnosis literature. It targets the vasomotor side of the menopausal sleep disruption directly. I am citing it here because it matters, while being explicit that I am not fabricating a PMID for it. If you want the primary sources, search PubMed for Elkins hypnosis hot flash and read the trial-level work directly. The signal is consistent enough that several major menopause guideline groups now reference clinical hypnosis as one of the non-hormonal options worth considering for vasomotor symptoms.

The honest synthesis of those three strands: there is a real biological signal for hypnotic suggestion shifting sleep architecture (Cordi 2014, PMID 24882902). The general clinical-trial evidence for hypnosis-for-sleep is mixed but positive in over half of trials (Chamine 2018, PMID 29952757). The vasomotor-specific evidence base from Elkins and colleagues supports hypnotic relaxation as a non-hormonal option for hot flashes, including the night-time episodes that wreck sleep. None of this evidence puts hypnotherapy on par with HRT or CBT-I for menopausal insomnia in terms of head-to-head trial weight. It does support hypnotherapy as a defensible adjunct, and as an alternative for women who cannot or will not use HRT.

I want to underline one thing because it matters: HRT and CBT-I both have stronger direct evidence for menopausal insomnia than hypnotherapy alone. Anyone telling you otherwise is selling you something. Hypnotherapy positions correctly as adjunct or alternative when those are contraindicated, declined, or insufficient. That framing is not a downgrade. It is the accurate placement.

Where hypnotherapy fits in the treatment landscape

The honest order of operations for menopausal insomnia, as supported by the evidence and as I think about it in my practice, looks like this.

HRT is the first-line evidence-based option for vasomotor and sleep disruption. Hormone replacement therapy, and specifically modern body-identical regimens, is the treatment with the strongest direct evidence for menopausal sleep disruption driven by vasomotor symptoms and hormonal architecture loss. The risk-benefit profile has shifted significantly since the older Women's Health Initiative trial that scared a generation off HRT. For many women, especially those starting HRT within ten years of final menstrual period and without specific contraindications, the benefit profile is favourable. That conversation belongs with a GP or a menopause specialist, not with a hypnotherapist. If you have not had that conversation, having it is the single most useful next step you can take. I refer for it routinely.

CBT-I adapted for menopause has growing evidence. Cognitive behavioural therapy for insomnia is the strongest non-hormonal psychological treatment for chronic insomnia generally, and adapted protocols for menopausal women now have a meaningful evidence base. CBT-I works the cognitive and behavioural layer through sleep restriction, stimulus control, cognitive restructuring, and sleep hygiene. If you have access to a sleep psychologist trained in CBT-I and you can tolerate the sleep restriction phase, CBT-I is reasonable to try first or in parallel with HRT.

Hypnotherapy fits in three specific places. First, for women who cannot take HRT (specific contraindications) or will not take it (personal preference, fear, prior bad experience). Second, as adjunct to HRT for residual sleep symptoms after the hormonal piece is in place. HRT softens vasomotor frequency for most women but does not always fully resolve the sleep-anxiety loop, the conditioned bedtime arousal, or the early-morning cortisol pull. That residual layer is where suggestion-based work is well-suited. Third, for the cortisol-anxiety pattern that often coexists with the vasomotor side, especially the 3 a.m. wake-up that does not respond to topical interventions like cooling sheets.

Other complementary approaches matter, with realistic expectations. Cooling the bedroom, layered breathable bedding, fan placement, and timing adjustments do not treat the underlying mechanism but they materially soften the symptom on a typical night. Magnesium and valerian have mixed evidence and are reasonable to try with the understanding that the effect is usually small. Caffeine after noon and alcohol within four hours of bed both fragment second-half-of-night sleep, and both are particularly disruptive in menopause where the sleep architecture is already fragile. Cutting alcohol is one of the highest-leverage behavioural changes for menopausal sleep, and it is also one of the hardest, because the evening glass is often the only relaxation cue left after the day.

The honest synthesis: hypnotherapy is one tool in a multi-modal approach for menopausal sleep, not a standalone solution for severe vasomotor sleep disruption. A Registered Clinical Hypnotherapist works within scope of practice as complementary care, alongside your GP and any specialists involved. We do not diagnose menopause, we do not prescribe HRT, and we do not replace medical workup. We provide hypnotherapy for the specific patterns where the mechanism fits and the evidence supports it.

When menopausal insomnia needs medical workup first

A meaningful share of women who reach out for hypnotherapy for menopausal sleep disruption end up referred for medical evaluation before we start any session block. This part of the page is the most important to read carefully, because treating an unidentified medical sleep contributor with talk-and-suggestion therapy is the wrong tool, and it delays the right intervention.

Sleep apnea. This is the one I want to flag in bold. Sleep apnea is significantly under-diagnosed in women, and risk rises after menopause as protective effects of estrogen on upper airway muscle tone are lost. The classic male presentation (loud snoring, witnessed apneas, large neck circumference) does not always apply. Women more often present with unrefreshing sleep, daytime fatigue out of proportion to sleep duration, morning headaches, and persistent insomnia that does not respond to standard interventions. If you snore at any volume, if a partner has noticed pauses or gasping, if you wake unrefreshed despite spending eight hours in bed, or if your sleep got dramatically worse around the menopause transition without softening, a sleep medicine evaluation is warranted. A home sleep study is non-invasive, and the downside of doing one and finding nothing is small. The downside of missing apnea is large: untreated obstructive sleep apnea raises cardiovascular risk and is independently associated with daytime cognitive impairment. We refer first, and only consider hypnotherapy as adjunct after diagnosis and treatment.

Thyroid disease. New-onset severe insomnia after age 50 should trigger a thyroid panel if one has not been done in the last year. Both hyperthyroid and hypothyroid presentations can disrupt sleep, and both are easy to identify with bloodwork. This is a low-cost, high-value step that gets skipped too often.

Iron deficiency anemia. Common in perimenopause when bleeding is heavy or irregular, and a frequent contributor to fatigue and disrupted sleep. Ferritin in particular tends to be low even when hemoglobin looks adequate. This is a basic bloodwork item to request.

B12 deficiency. Common postmenopause, particularly in women on long-term acid-suppressing medication or with restricted diets. Affects sleep, mood, and cognition. Easy to test, easy to correct.

GERD and chronic pain. Acid reflux that wakes you in the early morning often gets misread as menopausal insomnia. Worth flagging to your GP if the pattern fits. Chronic pain that has not been adequately worked up is also a frequent sleep disruptor that benefits from primary treatment before adjunct work.

Severe depression with menopausal onset. Perimenopause is a high-risk window for new-onset depression, and severe depression with prominent insomnia needs primary depression treatment. That usually means working with a GP, psychiatrist, or registered psychologist on combined therapy and possibly medication. Hypnotherapy can support recovery as adjunct, with the primary treating provider in the loop, but it is not a replacement for evidence-based depression treatment.

Medication side effects. A medication review with your GP or pharmacist is worth doing if your sleep changed around the time you started anything new. Beta-agonists, steroids, some antidepressants, certain blood pressure medications, and some pain medications can affect sleep substantially.

The general principle: comprehensive bloodwork and a sleep study consideration before assuming all sleep disruption is hormonal. A 20-minute conversation with your GP about your sleep history, medications, and any apnea risk factors is a small investment with significant downside protection. CHC requires that adult clients have either had a recent medical evaluation or commit to one in parallel before we treat menopausal insomnia as a standalone presentation.

What a hypnotherapy course for menopausal insomnia looks like

The work has a recognizable shape, with adjustments based on transition stage, vasomotor pattern, and what other treatments are running in parallel. Here is the honest version of what to expect, including timing and cost.

Intake, 60 to 90 minutes. We map your menopausal transition stage in detail. Periods (still happening, irregular, stopped, when). HRT status (on it, considering it, declined, ineligible). Vasomotor pattern (frequency, severity, day vs night, what triggers). Sleep pattern (onset, maintenance, both, with timestamps if you have been tracking). Mood comorbidity. Prior treatments and what they did or did not deliver. Medical workup status (recent bloodwork, sleep study if relevant). A brief hypnotic responsiveness check, because suggestion-based work depends on it. We finish intake with a clear plan: number of sessions, what we will work on first, and what your between-session practice will be.

Sessions 1 and 2: foundational induction and somatic relaxation. The first two sessions establish the basic skill: a reliable hypnotic state, a personalized somatic-relaxation pattern, and a recording you can use nightly. The recording does most of the conditioning. The session does the personalization. By the end of session 2 you have a 15 to 25 minute audio that uses your specific induction and your specific imagery cues.

Sessions 3 to 5: targeted suggestions for cortisol arousal and vasomotor pattern. Once the foundation is in place, we add targeted suggestion work for the patterns that actually show up in your sleep. The cortisol-anxiety wake-up pattern gets one set of suggestions. The vasomotor episodes get another, drawing on the hypnotic relaxation approach research by Elkins and colleagues has shown can reduce hot flash frequency and severity. The sleep-anxiety meta-loop gets a third. We layer these as your specific pattern reveals itself in the weekly tracking data.

Sessions 6 to 8: integration with HRT and CBT-I if those are running concurrently. If you start or adjust HRT during the course, we adapt the suggestion work to support that transition. If you are also doing CBT-I, we coordinate with the sleep psychologist so the two protocols reinforce rather than contradict. The integration phase is where the gains tend to consolidate and durability gets tested.

Self-hypnosis recordings between sessions. Recordings are how the work generalizes. Use yours nightly, ideally at the same time, in the bedroom, in a position that mimics how you sleep. If you wake at 3 a.m. and the recording is what gets you back down, that is fine. The recording is a tool, not a dependence.

Typical course. 6 to 8 sessions for primary menopausal insomnia patterns. Longer (8 to 12) if comorbid mood disorder, post-trauma layers, or chronic pain are in the picture. The CHC per-session fee is $220 CAD. Sessions are delivered virtually across Canada or in-person in Calgary. Sessions are paid at time of service. A detailed receipt is provided with the practitioner ARCH registration number for any reimbursement attempt or HSA claim.

Realistic timelines. Most clients notice some shift within two to three weeks. Substantial improvement usually shows up by week four to six. The first marker of progress is rarely full nights of sleep. It is usually less catastrophic response when sleep is poor, then less middle-of-the-night anxiety, then fewer or less intense vasomotor episodes, then shorter sleep onset, then deeper sleep. Expecting immediate transformation is the most reliable way to undermine the work.

On insurance. Hypnotherapy is generally not directly covered under Canadian extended health benefit plans. Some clients can claim related programs (stress management, behavioural change) under a Wellness Spending Account (WSA) if their plan offers one. Coverage rules depend entirely on plan design, so check with your insurance provider before booking.

What you can do this week, regardless of treatment path

Whether you end up on HRT, in CBT-I, in a hypnotherapy block, in some combination, or in a sleep medicine workup first, there are steps that pay off across all of those paths. None of these replace the actual treatment conversation. They strengthen it.

Track for two weeks. Bedtime, sleep onset latency, wake times with timestamps if you can, hot flash count by day and by night, mood, and (if you are still cycling) where in your cycle each day sits. Use your phone, the back of a notebook, or a sleep app, but track. Two weeks of data is worth more than a year of impression. The data also shifts the conversation with your GP from impressionistic (I sleep terribly) to specific (I wake at 3:15 most nights with 4 to 6 hot flashes between 1 and 5 a.m. and average 2 hours awake before falling back).

Bring the tracking to your GP. Better data equals a better treatment conversation. If HRT has not been discussed, raise it. The risk-benefit profile has evolved significantly since the older studies that scared a generation off it. Many women in their late 40s and 50s who were told HRT was not an option for them would now be considered eligible under modern guidelines, particularly with body-identical formulations. The conversation is yours to have, and your GP can refer you to a menopause specialist if the practice does not handle it directly.

Cool the bedroom. 16 to 19 degrees Celsius is the range that works for most people. Layer breathable bedding so you can shed without fully waking. A small fan running quietly often does more than people expect, and the white noise component is a side benefit. If your partner is bothered by the temperature, the negotiation is worth having. Sleep loss compounds, and a partner who sleeps slightly cool for a season is a better long-term outcome than a partner who sleeps comfortably while you fragment for years.

Limit caffeine after noon. Caffeine has a half-life of around five to seven hours, longer in some women, and metabolism shifts with age. The cup at 3 p.m. that felt fine a decade ago now matters at 2 a.m.

Limit alcohol within four hours of bed. This is the highest-leverage behavioural change for menopausal sleep, and the hardest. Alcohol fragments second-half-of-night sleep particularly aggressively in menopause. The mechanism involves both rebound arousal as alcohol clears and increased vasomotor frequency in the hours after drinking. If the evening glass is the only relaxation cue left after the day, the path is not deprivation but substitution: a different evening relaxation cue that does not wreck the back half of the night.

Discuss HRT eligibility with your GP or a menopause specialist if you have not. The risk-benefit calculus has changed. Many women who were told HRT was off the table years ago would now be considered candidates under updated guidance, particularly with modern body-identical regimens. This is a conversation, not a verdict, and it is worth having even if you eventually decline.

Consider a perinatal or menopause-trained therapist if mood is also affected. Anxiety and depression in this period have a specific texture and a specific treatment approach. A therapist with menopause-specific training will get you to useful work faster than a generalist.

Frequently asked questions

Will hypnotherapy reduce hot flashes themselves or only the sleep disruption?

Both, potentially, though through different routes and with different evidence weight. Research by Elkins and colleagues has shown that a structured hypnotic relaxation protocol can reduce the frequency and severity of hot flashes in postmenopausal women, including the night-time vasomotor episodes that fragment sleep. So a portion of the sleep gain comes from fewer or less intense vasomotor events. The other portion comes from quieting the conditioned arousal and 3 a.m. cortisol-anxiety pattern that is independent of hot flashes. Most clients in the menopause transition have both layers, and a session protocol typically targets both.

Can I do hypnotherapy if I am on HRT?

Yes, and it is a common combination. Hormone replacement therapy is the first-line evidence-based treatment for vasomotor symptoms and the sleep disruption that comes with them, and many women on HRT still have residual sleep issues, especially the early-morning wake-up pattern tied to cortisol. Hypnotherapy does not interact with HRT pharmacologically and adds a separate mechanism. Tell your hypnotherapist what you are taking and at what dose so suggestions and recordings are written to support your regimen rather than work around it.

How is this different from CBT-I for menopause?

CBT-I adapted for menopause has growing evidence and remains the strongest non-hormonal psychological treatment for menopausal insomnia. It works on the cognitive and behavioural layer: sleep restriction, stimulus control, cognitive restructuring, and sleep hygiene. Hypnotherapy works on the somatic and arousal layer using suggestion and focused-attention techniques, and it tends to address the vasomotor-anxiety overlap more directly. The two are complementary rather than competing. If CBT-I is accessible and you can tolerate the sleep restriction phase, that is the place to start. Hypnotherapy works well as adjunct to CBT-I or as alternative when CBT-I has not delivered or is not available.

What if my insomnia started years before any other menopause symptoms?

That is more common than people realize. The hormonal shift in perimenopause can begin five to ten years before periods become irregular or hot flashes appear, and sleep is often the first system to show it. If your sleep changed in your early 40s with no obvious cause and you are now in your late 40s or early 50s with other menopausal signs starting, the timeline fits. We still want a medical workup to rule out thyroid, sleep apnea, and other contributors, and a conversation with your GP about whether the perimenopausal pattern is what you are actually navigating. The mechanism we target shifts depending on where in the transition you are, so naming the stage matters.

Is it too late if I am already postmenopausal?

No. Postmenopausal sleep disruption is treatable. The mechanisms shift slightly. Hot flashes often soften over the years after final menstrual period, but the cortisol-arousal pattern and conditioned insomnia can persist or worsen if untreated. Sleep apnea risk also rises significantly postmenopause and is under-diagnosed in women, so any new or worsening sleep issue at this stage warrants a sleep medicine evaluation. Once medical contributors are ruled out or addressed, hypnotherapy and CBT-I both have a role for the patterned, arousal-driven sleep disruption that postmenopausal women often carry.

Can hypnotherapy help with menopausal mood disruption too?

It can, with the right framing. Perimenopause is a high-risk window for new-onset or worsening anxiety and depression, and the sleep disruption amplifies both. A Registered Clinical Hypnotherapist does not diagnose or primary-treat depression. If mood symptoms are significant, the right care includes a GP, psychiatrist, or psychologist, possibly with medication or psychotherapy. Hypnotherapy can run alongside that as adjunct, particularly for the somatic anxiety and sleep-anxiety meta-loop that often co-occurs. We coordinate rather than compete.