G: [Non-text content: thoughts; content_type=thoughts]

G: [Non-text content: reasoning_recap; content_type=reasoning_recap]

G: Yes. And the first distinction I'd make for the model is that “CPAP became unnecessary after weight loss” and “snoring disappeared after weight loss” aren't necessarily the same proposition. Weight loss can dramatically improve obstructive sleep apnea (OSA), but it doesn't necessarily remove every anatomical or behavioral cause of airway vibration. AASM guidance specifically notes that substantial weight change is a reason to reassess OSA objectively, rather than assuming its status from symptoms alone. citeturn0search8turn0search10

So I'd organize the possibilities into five buckets, roughly from things that are easiest to investigate to things that warrant actual sleep testing.

1. Something changed recently, independent of weight

This is probably the first bucket I'd interrogate if your timeline is overweight → CPAP → weight loss → no apparent problem → target weight → snoring returns.

Things that can produce or amplify snoring include:

• Nasal congestion/allergies — seasonal allergies, a cold, chronic rhinitis, etc.
• Alcohol near bedtime — relaxes upper-airway muscles.
• Sedating medications — same general mechanism.
• Sleep deprivation — increases relaxation of throat tissues.
• Change in sleeping position, especially spending more time on the back.
• Smoking/airway irritation, if applicable.

Those aren't speculative Internet-remedy explanations; they're among the standard recognized contributors to snoring. citeturn0search0turn0search1

Position is particularly interesting because OSA can be strongly positional. Mayo notes that many people with OSA have at least twice as many breathing disruptions on their backs as on their sides or stomachs. citeturn0search12

So I'd ask the friend something like: “Did anything change around the time the snoring returned—allergy season, congestion, alcohol, medication, sleep schedule, pillow/mattress, or sleeping on your back?”

That could explain a surprisingly abrupt return without anything having gone wrong with the weight loss.

2. The weight was one cause, but not the cause

This is the important conceptual category.

Obesity can worsen OSA because tissue around the upper airway makes it easier for the airway to narrow or collapse. Losing that weight therefore improves the airway. But other pieces of the person's anatomy remain exactly where they were:

jaw shape → tongue → soft palate/uvula → tonsils → nasal passages → throat diameter

Someone can have a naturally narrow airway, elongated/soft palate, large tongue relative to the jaw, enlarged tonsils, deviated septum, etc. Those can cause ordinary snoring and/or OSA regardless of body weight. citeturn0search0turn0search3

So there's a very plausible model:

Original OSA = anatomical predisposition + excess-weight contribution + other factors.

Weight loss removes a large contributor:

anatomical predisposition + other factors = below apnea threshold

But then something relatively modest—congestion, back sleeping, alcohol, aging, etc.—could move them sufficiently toward obstruction that snoring returns without necessarily restoring their former degree of apnea.

I think that's a particularly useful way of thinking about your friend's situation.

3. They're snoring again, but the apnea has not returned

This is entirely possible.

Snoring is basically vibration produced when air moves through relaxed/narrowed upper-airway tissues. You don't have to actually stop breathing for those tissues to vibrate. citeturn0search0

So you can approximately think of a continuum:

open airway → narrowed/turbulent airway → snoring → greater obstruction → hypopnea → complete obstruction/apnea

That's simplified physiology rather than a literal sequence every patient follows, but it's useful for modeling.

Therefore, the return of snoring doesn't establish that they need CPAP again. They may have moved from “OSA + snoring” before weight loss to “little/no snoring” during one period and now to “primary snoring without clinically significant OSA.”

This would actually fit your description quite neatly.

4. The apnea never completely disappeared—or has returned

This is the category I wouldn't dismiss merely because they've reached their target weight.

Weight loss improves OSA on average, sometimes dramatically, but doesn't reliably cure it. AASM material specifically cautions against assuming that weight loss eliminates OSA; substantial residual apnea has been found even after very large weight losses. citeturn0search7turn0search10

And there's an interesting possible illusion here:

If their CPAP was discontinued because a repeat sleep study/home apnea test demonstrated resolution, that's fairly strong evidence that it really had remitted.

If instead the reasoning was:

“I lost a lot of weight, I don't snore anymore, I feel better, so I stopped using CPAP,”

then the evidentiary situation is quite different. The apnea may simply have become much milder and less obvious.

AASM's current resources say follow-up polysomnography or a home sleep-apnea test may be used after clinically significant weight gain or loss of roughly 10–20%. citeturn0search8

So one thing I'd specifically find out is how they established that CPAP was no longer necessary.

5. A longer-term physiological/anatomical change

Finally there are slower-moving factors that aren't really about the weight-loss process at all.

Age itself increases OSA risk. Nasal anatomy/obstruction can change or become more important. Hormonal changes can matter, particularly menopause. Certain medical conditions and medications can alter risk. citeturn0search3turn0search11

That bucket becomes more plausible if this wasn't “six months ago everything was fine and suddenly they're snoring,” but rather several years elapsed between stopping CPAP and the snoring returning.

How I'd actually investigate it

Rather than trying random anti-snoring gadgets, I'd make a little causal tree.

First: establish what “snoring came back” means. Every night or occasionally? Loud or mild? Only on their back? Did it coincide with allergies/congestion? Alcohol? New medication? Poor sleep? Those variables can distinguish several of the buckets surprisingly well.

Second: ask the person who hears the snoring about its pattern. Continuous rhythmic snoring is one thing. Loud snoring → silence → snort/gasp/choking → resumed breathing is much more concerning for OSA. Daytime sleepiness, morning headache, poor concentration, restless sleep and witnessed breathing pauses also push the model toward recurrent/persistent OSA. citeturn0search0

Third: find out whether stopping CPAP followed an actual repeat sleep study. If it didn't, I'd put “residual OSA that became less obvious after weight loss” considerably higher on the board.

And if the snoring is persistent now, particularly with pauses/gasping or daytime symptoms, the clean way to settle that branch isn't guessing from the sound. It's another sleep evaluation—often a home sleep-apnea test is sufficient in an appropriate patient, while polysomnography gives considerably more information. citeturn0search1turn0search8

The main tension flag I'd keep in your model is therefore: don't let “healthy target weight” become evidence against OSA. Weight is a major risk modifier, not an on/off switch. In this particular history, the weight loss strongly suggests that weight was contributing, but it doesn't tell us whether the remaining anatomy leaves them just below, at, or above the apnea threshold now.

If you find out (1) roughly how old they are, (2) sex, (3) how long ago they stopped CPAP, (4) whether a sleep study cleared them to stop it, and (5) what the new snoring sounds like, I can take those variables and turn this into a much tighter differential—basically rank the five buckets rather than just enumerate them.

G: Understood. I’ll treat the timeline as: overweight + CPAP → weight loss + CPAP no longer needed → target weight reached → snoring has now returned, and I’ll rebuild the answer from scratch around documented causes of snoring/OSA recurrence after weight loss.

G: [Non-text content: thoughts; content_type=thoughts]

G: [Non-text content: reasoning_recap; content_type=reasoning_recap]

G: Starting over with exactly that timeline, the key fact from the medical literature is that weight loss can reduce or even eliminate obstructive sleep apnea, but reaching and maintaining a healthy weight does not guarantee permanent protection from either snoring or OSA. Weight is only one contributor to how collapsible the upper airway is. The American Thoracic Society explicitly says that when OSA is caused substantially by excess weight, weight loss can sometimes make it go away completely; NIH likewise treats healthy weight as one part of prevention and treatment, not the sole determinant. citeturn826868search5turn826868search3

So for your friend's pattern—

overweight → OSA/CPAP → substantial weight loss → CPAP apparently unnecessary → continued healthy/target weight → snoring returns

—I would divide the explanations into these categories.

1. A non-weight trigger has appeared or intensified

This is the simplest category and probably the first one worth looking through.

Official clinical sources identify several things that can narrow or destabilize the airway even without weight gain:

• Nasal congestion, including allergies, colds, sinus problems, or chronic rhinitis.
• Sleeping on the back. Gravity lets the tongue and soft palate fall backward and narrows the airway.
• Alcohol, especially near bedtime, because it relaxes the throat musculature.
• Sedative or sleeping medications, for essentially the same reason.
• Sleep deprivation, which can increase relaxation of throat tissues.
• Smoking or airway irritation/inflammation. citeturn826868search0turn610999search5turn610999search8

This category makes particular sense if the return of snoring was fairly abrupt.

For example:

same body weight + new allergy season → greater nasal resistance → more negative pressure needed to inhale → throat tissues vibrate/collapse more readily → snoring

ENT guidance specifically notes that some people snore only during allergy season or during a cold or sinus infection. citeturn610999search5

2. The weight loss removed one major cause, but another anatomical predisposition remained

This is probably the most important modeling point.

OSA isn't simply:

too much body fat → apnea

It's more like:

airway anatomy + tissue characteristics + muscle tone + sleep state + position + weight + other influences → degree of airway narrowing/collapse

NIH lists structural factors such as a large tongue, large tonsils, large neck, or naturally narrow upper airway as independent OSA risks. Mayo similarly identifies a low/thick soft palate, elongated uvula, deviated septum, and other airway anatomy as causes of snoring. citeturn610999search8turn826868search0

So she could have originally been something like:

baseline anatomy 4 + obesity 4 + miscellaneous factors 2 = 10 → clinically significant OSA

After losing weight:

4 + 0–1 + 2 = 6 → no longer enough obstruction to need CPAP

And now some other variable changes:

4 + 1 + 4 = 9 → snoring or OSA again

Those numbers are purely illustrative, but the additive/multifactor model is much closer to the physiology than thinking of obesity as an on/off cause.

This also explains why losing weight could genuinely have eliminated the original problem without anything being “wrong” about that earlier conclusion.

3. Ordinary snoring has returned, but OSA has not

This deserves its own category because snoring and apnea aren't interchangeable.

Snoring results when airflow makes relaxed/narrowed tissues of the tongue, palate and throat vibrate. OSA requires repeated episodes of sufficiently severe narrowing or collapse that breathing is substantially reduced or stopped. Mayo explicitly says that not everyone who snores has OSA. citeturn826868search0

So she could now have crossed only the snoring threshold, rather than crossing back over the apnea threshold.

A useful conceptual continuum would be:

widely open airway → mild narrowing → turbulent airflow/snoring → substantial narrowing/hypopnea → complete or near-complete obstruction/apnea

Again, that's a model rather than a formal clinical staging system.

This possibility becomes more likely if the snoring is fairly steady and there are no witnessed breathing pauses, choking/gasping awakenings, morning headaches, major daytime sleepiness, or other OSA symptoms. Those symptoms make recurrent OSA more suspicious. citeturn826868search7

4. OSA has actually returned despite the maintained weight loss

This is absolutely possible.

The medically important point is that healthy weight reduces risk; it doesn't reduce risk to zero. NIH explicitly says sleep apnea can occur in people without obesity and identifies age, airway anatomy, hormone levels, alcohol, smoking, and other factors independently. citeturn610999search8

So weight loss could have produced a genuine remission, and later changes could move her back across the OSA threshold without regaining the lost weight.

That's different from saying the OSA never went away.

If she had an actual sleep study showing that it resolved after losing weight, then I'd regard true remission followed by recurrence as a perfectly coherent model.

If she simply stopped CPAP because she stopped snoring/felt better, there's more uncertainty about whether it ever completely disappeared.

5. Aging itself can move the threshold

This is one I would put higher on the list if several years have passed.

NIH says OSA risk increases with age. Anatomical and neuromuscular changes affecting the upper airway occur with aging, and age remains an OSA risk factor separately from obesity. citeturn610999search8

So you could have:

age 35 + target weight = airway sufficiently stable

but later:

age 45/50/etc. + same weight = airway somewhat more collapsible

There doesn't need to be an obvious new illness or weight gain.

6. Because she's a woman, hormonal transition deserves a separate category

This is one that I didn't give enough prominence to in the earlier answer.

If she's anywhere around perimenopause or menopause, this becomes a quite serious candidate.

NHLBI specifically states that women's risk for sleep apnea increases during and after menopause, and attributes some of that increase to hormonal changes. Crucially for your question, this isn't simply an indirect consequence of gaining weight. citeturn610999search0

Large epidemiological studies also find menopause-related associations with OSA after accounting for body size, supporting a role for sex hormones and upper-airway physiology independent of obesity. citeturn610999search1turn610999search7

That produces an especially interesting version of your timeline:

obesity + premenopausal physiology → OSA

↓

weight loss → enough improvement for OSA to disappear

↓

same low weight + perimenopausal/postmenopausal physiological changes → airway susceptibility increases again

↓

snoring and potentially OSA return

If her age makes that biologically plausible, I'd move this quite high on the candidate list, rather than treating it as an obscure possibility.

7. A new nasal or throat structural problem

This overlaps somewhat with anatomy but is different because it can change over time.

ENT guidance specifically points to nasal obstruction, septal problems, enlarged tonsillar/adenoidal tissue, allergy-related swelling, infection, and obstruction at several different levels of the upper airway. citeturn610999search5

So something like chronic nasal inflammation could make a previously adequate airway functionally narrower even though her weight hasn't changed.

An ENT examination can sometimes identify this category directly.

Put together, I think the most useful model is not “why did weight loss stop working?”

It's:

Weight loss moved her comfortably away from an obstruction threshold. Something else has subsequently moved her toward that threshold again.

The plausible things doing the moving break roughly into:

temporary/environmental: congestion, allergies, sleep deprivation, alcohol, medications
behavioral/mechanical: sleeping position
structural: nose, palate, tongue, jaw/throat anatomy
time-dependent physiological: aging
female-specific physiological: perimenopause/menopause
disease recurrence: OSA itself returning despite sustained weight loss

And there's one important fork you can't resolve from snoring alone:

snoring returned
→ airway vibrates again, but ventilation remains adequate
or
→ airway is once again collapsing enough to qualify as OSA

Given her previous documented need for CPAP, persistent renewed snoring is a stronger reason for reassessment than it would be in somebody who had never had OSA. A home sleep-apnea test or sleep study is what actually separates those last two branches; listening to the snoring can't reliably do it. citeturn826868search4turn610999search5

If you tell me roughly her age, how long the weight loss took, how long she was free of the CPAP/snoring before this returned, and whether anything like menopause, allergies, medications or sleeping-position changes line up temporally, I can use those facts to rank these mechanisms rather than merely categorize them.

G: [Non-text content: thoughts; content_type=thoughts]

G: [Non-text content: reasoning_recap; content_type=reasoning_recap]

G: Yes. If we completely bracket the previous sleep apnea and ask only, “What can make someone who wasn't snoring start snoring?”, the list gets cleaner.

Snoring itself is just airflow making relaxed/narrowed tissues in the upper airway vibrate. It does not require apnea. Mayo and Cleveland Clinic give essentially the same major causes. citeturn0search0turn0search1

Besides back-sleeping, I'd rank the broad categories like this:

1. Sleep deprivation / unusually deep sleep. Your suspicion here is legitimate. When someone is sleep-deprived, the throat muscles can relax more when they finally sleep, increasing snoring. Both Mayo and Cleveland Clinic explicitly identify inadequate sleep as a cause/risk factor. citeturn0search0turn0search1 Importantly, the reason for the sleep deprivation could certainly be psychological—stress, anxiety, disrupted schedule, insomnia, etc. The psychological state wouldn't directly make the throat vibrate; psychological problem → inadequate sleep → greater relaxation during subsequent sleep → snoring is the plausible chain.

2. Nasal obstruction. Allergies, a cold, sinus inflammation, chronic rhinitis, dry/irritated nasal passages, or a deviated septum can reduce nasal airflow and promote mouth breathing/snoring. This can appear even if nothing else about the person changes. citeturn0search0turn0search8

3. Anything increasing muscle relaxation. Alcohol is the classic example, particularly near bedtime. Sedatives and some other medications can do something similar. citeturn0search1turn0search2

4. Anatomical/physiological changes. A naturally narrow airway, large tongue or tonsils, long/soft palate, elongated uvula, nasal structural problems, etc. can predispose someone to snoring. Aging also gradually decreases upper-airway muscle tone, so somebody who didn't previously snore can eventually begin doing so without gaining weight. citeturn0search0turn0search1

5. Weight/tissue distribution. Still relevant to ordinary snoring even if we're ignoring apnea, although in her case maintained weight loss obviously makes this a less immediately satisfying explanation unless her body composition or fat distribution has changed. citeturn0search0

So if you're looking specifically for something that could cause a fairly recent onset, I'd put my first investigative attention on:

sleep deprivation → nasal congestion/allergies → alcohol/medication changes → sleep-position/neck-position changes → longer-term anatomical/age-related changes.

And yes, psychologically caused sleep deprivation survives this reframing quite well. It's specifically documented that insufficient sleep can increase snoring because of increased throat relaxation; we'd just need to establish whether she's actually getting substantially less or poorer sleep. citeturn0search0turn0search2

Now I'm curious what your suspicions were, because with the apnea assumption removed we can test them against this mechanism rather than trying to force everything back through her old OSA.

G: [Non-text content: thoughts; content_type=thoughts]

G: [Non-text content: reasoning_recap; content_type=reasoning_recap]

G: Yes—now I see the mechanism you're proposing much more clearly:

Regular exercise → better/deeper sleep → less responsiveness/more upper-airway relaxation → recurrence of snoring in somebody already anatomically predisposed to it.

I checked specifically for evidence for that chain. Pieces of it are real, but the complete chain isn't well supported, and one part actually points in the opposite direction.

Exercise really can alter sleep architecture. A meta-analysis found both acute and chronic exercise associated with more slow-wave sleep and longer total sleep, along with faster sleep onset. citeturn0search12turn0search13 So your intuition that somebody who has become physically active might sleep differently/deeper isn't imaginary.

Where I'd modify the model is the “physical collapse makes the airway sloppier” part. When researchers actually study exercise in people susceptible to obstructive breathing, exercise generally improves rather than worsens airway obstruction during sleep, even when the exercise doesn't produce meaningful additional weight loss. Multiple meta-analyses find reductions in apnea/hypopnea events following exercise training independent of substantial BMI changes. citeturn0search2turn0search4turn0search5 A 2026 randomized resistance-training trial similarly found fewer respiratory events and fewer micro-arousals after training. citeturn0search11

So I wouldn't put $5 on “she's exercising so hard that when she sleeps her throat muscles collapse from exhaustion.” There's a plausible-sounding physiological story there, but the empirical evidence doesn't seem to cooperate with it.

There is, however, a nearby version of your hypothesis that I'd leave on the board:

exercise → changed sleep architecture/deeper or more consolidated sleep → an existing snoring tendency becomes expressed differently

That isn't the same as exercise causing the airway problem. She could already possess the anatomy capable of snoring—as her previous history rather strongly suggests—and changes in sleep depth/stage distribution could change when and how much she snores. The literature establishes that snoring/upper-airway behavior varies across sleep stages, although it doesn't give me good evidence for the simple rule “more deep sleep = more snoring.” That's the part I wouldn't promote from plausible mechanism to documented explanation.

And your other bracket—too little sleep—is considerably better documented. Sleep deprivation can increase upper-airway relaxation and snoring. So if the recent inadequate sleep occurred after the snoring had already returned, as you think, it can't explain the onset—but it could now be amplifying an already-present snoring problem.

The combination I'd find more interesting given the extra fact you supplied is actually:

preexisting susceptible airway + major weight loss removes the original aggravating factor + perimenopausal physiological changes gradually increase susceptibility + ordinary variations in sleep depth/position/congestion/etc. finally make snoring audible again.

That doesn't require her OSA to have returned. Nor does it require exercise to be harmful. In fact, the gym is probably pushing in the favorable direction overall, while simultaneously improving/consolidating her sleep enough that you might notice changes in how she sleeps. The perimenopause and prior OSA tell us that her airway wasn't starting from a completely neutral baseline.

So if we're assigning your hypothetical $5 at this point, I'd put very little on “exercise exhaustion directly causes snoring,” somewhat more on “changes in sleep pattern expose an existing tendency,” and considerably more on “preexisting airway susceptibility + perimenopausal/other physiological change, with current sleep deprivation potentially making it louder.”

The really interesting next question would be whether perimenopause can cause snoring to emerge independently of weight gain and independently of full-blown OSA. That's narrow enough that I can dig into the actual hormonal/upper-airway literature rather than the generic menopause–OSA association.

G: [Non-text content: thoughts; content_type=thoughts]

G: [Non-text content: reasoning_recap; content_type=reasoning_recap]

G: Yes. With that clarification, both things you're proposing have real counterparts in the sleep literature, although I'd modify the airway idea slightly.

1. Can a basically adequate airway snore just because tissue is vibrating?

Yes—with an important semantic qualification. Snoring doesn't require the airway to become obstructed in the apnea sense. Medicine calls snoring without apnea primary/simple/isolated snoring. The sound is vibration of structures such as the soft palate, uvula and pharyngeal tissues as air passes them. citeturn1search0turn1search7

There ordinarily is some local narrowing or altered airflow involved, so I wouldn't quite call the airway physically identical to a fully awake, maximally open airway. But that can be a perfectly functional airway: air continues moving adequately, oxygenation is fine, breathing doesn't stop, yet some compliant tissue flutters.

Your word “resonant” is actually a useful intuitive model. ENT literature even describes a long soft palate/uvula as acting rather like a “flutter valve” during relaxed breathing. citeturn1search1

And I found something particularly interesting for your hypothesis. NIH discussed research showing the initially counterintuitive observation that:

snoring increases during slow-wave (deep) sleep even though the airway is less prone to collapse then.

Conversely, REM makes the airway more collapsible, yet snoring is less frequent. Researchers found that respiratory drive—the strength of the effort to breathe—also contributes to snoring loudness, rather than snoring simply measuring how obstructed the airway is. citeturn1search3

That's surprisingly close to what you've been proposing.

So a plausible model is:

deeper slow-wave sleep + relaxed vibratable tissue + sufficiently vigorous airflow → vibration/noise

without:

airway collapse → inadequate ventilation → apnea.

In other words, a louder snore isn't necessarily a gauge showing how close the airway is to closing.

And exercise gives you one possible route into the first part. Meta-analyses find modest increases in slow-wave sleep following exercise, although the effect varies and isn't enormous. citeturn0search0turn0search4

I therefore wouldn't say “the gym caused her snoring.” But your more precise hypothesis—

exercise changes/consolidates sleep → more/deeper slow-wave sleep → existing mechanically snore-capable airway makes noise during otherwise effective breathing

—is physiologically plausible, and there is actual evidence connecting each of those pieces. I didn't find a study demonstrating that entire causal chain specifically.

2. Can the body objectively sleep while the person nevertheless doesn't experience restorative sleep?

Very much yes. And the bipolar-disorder part makes your second idea substantially more interesting.

There's an important distinction between objective sleep physiology and subjective sleep experience. How many hours somebody slept, what stages they entered, and how efficiently they slept don't perfectly determine whether they report feeling rested.

There's actually research specifically on bipolar disorder demonstrating unusually large subjective–objective sleep discrepancies. In one study, objectively measured total sleep time in symptomatic bipolar participants didn't significantly correlate with their subjective estimate of how much they'd slept, while it did in healthy controls. Greater depressive symptoms predicted greater discrepancy. citeturn0search10

And a much larger 2025 meta-analysis found sleep abnormalities even during euthymia—periods when bipolar patients aren't in an obvious manic or depressive episode. It found worse subjective sleep quality, greater variability in sleep duration/continuity, and differences between sleep-diary reports and objective measurements. During depressive phases, insomnia was extremely common; manic/mixed phases showed shorter and less efficient sleep. citeturn0search12

So I wouldn't model this as “her psychology prevents deep sleep from penetrating into consciousness.” That's evocative, but physiologically it mixes two different systems.

I'd separate them:

Objective sleep:
Did she actually enter N3/slow-wave sleep? How much? How fragmented was it? What was her REM architecture?

Subjective restoration:
Does her brain subsequently generate the experience “I slept well and am restored”?

Those variables correlate, but they aren't identical.

There's also a third variable you're already circling: circadian regularity. Bipolar disorder is particularly associated with variability in sleep/wake timing, sleep onset and sleep continuity even between mood episodes. citeturn0search16 So somebody could accumulate a reasonable quantity of objectively real sleep while having an irregular schedule and disturbed sleep architecture and nevertheless experience poor/restless/unrefreshing sleep.

Which produces an interesting combined model

I wouldn't yet claim this is what's happening to her, but your observations no longer require a contradiction:

regular gym activity
→ potentially somewhat more consolidated/slow-wave sleep
→ more opportunity for benign tissue vibration/snoring

while independently:

bipolar physiology + perimenopause + irregular sleep schedule/current psychological state
→ altered sleep timing/architecture and/or subjective perception of sleep
→ “I'm not getting enough/good sleep.”

Those two arrows can coexist. Her making snoring noises characteristic of deeper sleep doesn't establish that she ought to wake feeling wonderfully rested.

There's actually a nice tension flag here: the return of snoring and the complaint of poor sleep could be causally unrelated despite occurring in the same person. Our brains naturally want one to explain the other. Your revised hypothesis allows the snoring to be a mechanical consequence of how she's sleeping while the tiredness is a separate circadian/mood/sleep-quality phenomenon.

The one thing her history prevents us from doing is assuming the snoring is benign primary snoring. Previous OSA means recurrent OSA remains a candidate that a sleep study could distinguish. But as a modeling exercise, “adequate airway + tissue vibration during deeper sleep” is a legitimate branch, not something we have to force into apnea. citeturn1search6turn1search7