CBD Oil for Sleep and Ankylosing Spondylitis: Nocturnal Axial Inflammatory Pain, Early Morning Awakening, and the Sacroiliac-Spine Circadian Pattern | PureCraft CBD

CBD Oil and AS Medications: NSAIDs as the Cornerstone, Biologics for Refractory AS, and the Gastroprotection Consideration

NSAIDs (naproxen, indomethacin, diclofenac, celecoxib — first-line AS pharmacotherapy) — no CYP interaction, additive GI mucosal risk, pharmacodynamic complementarity: NSAIDs are the first-line pharmacological treatment for AS — their COX-1 and COX-2 inhibition reduces the prostaglandin-mediated inflammatory response at the entheseal attachment sites, reducing the pain and stiffness of active AS. Unlike RA, where NSAIDs are bridging or adjunctive agents to DMARDs and biologics, continuous NSAID therapy in AS is endorsed by guidelines as disease-modifying (evidence suggests that continuous NSAID use slows radiographic spinal ankylosis progression compared to as-needed use). The CYP interaction profile: no significant CYP-mediated pharmacokinetic interaction between CBD and standard NSAIDs. The pharmacodynamic consideration: additive GI mucosal risk — NSAID COX-1 inhibition reduces gastroprotective prostaglandin synthesis, and CBD's modest prokinetic GI effects may compound GI mucosal irritability in patients on continuous NSAIDs. For AS patients on continuous NSAID therapy (the most common pharmacological scenario): taking CBD oil sublingually (absorbed through oral mucosa, bypassing most GI first-pass) minimizes the additive GI mucosal exposure. For solid-form CBD (softgels, gummies): taking with food and a proton pump inhibitor (if the treating rheumatologist has prescribed gastroprotection with the NSAID) is the standard approach. Celecoxib's COX-2 selectivity provides lower GI mucosal risk than non-selective NSAIDs, making it the most favorable NSAID combination partner for CBD in terms of GI safety. The pharmacodynamic complementarity: NSAIDs suppress prostaglandin-mediated inflammation at the enthesis (COX pathway); CBD suppresses TNF-α and IL-17A production from entheseal macrophages and neutrophils (CB2/NF-κB pathway). These are mechanistically complementary rather than duplicative — the combination addresses the entheseal inflammation through two distinct molecular pathways, which is the basis for the additive benefit that many AS patients report when using CBD alongside NSAIDs.

Biologic TNF inhibitors (etanercept, adalimumab, infliximab, certolizumab, golimumab) for refractory AS — no CYP interaction, mechanistically complementary: TNF inhibitors are the first biologic class for NSAID-refractory AS, with high efficacy for both axial inflammatory pain and enthesitis. As in RA, TNF inhibitor biologics are large-molecule proteins metabolized proteolytically — no CYP interaction with CBD. The mechanistic complementarity: anti-TNF biologic blocks already-produced TNF-α at its receptor (systemic TNF blockade); CBD CB2/NF-κB suppresses TNF-α production by entheseal macrophages (source suppression). The combination provides both production suppression and receptor blockade of TNF-α — additive in a beneficial pharmacodynamic direction. AS patients on TNF inhibitors who add CBD for sleep support represent the most common AS + biologic + CBD scenario, and no specific safety concern beyond the standard CBD precautions applies.

IL-17A inhibitors (secukinumab, ixekizumab) for AS — no CYP interaction, unique mechanistic relevance: IL-17A inhibitors are highly effective for AS — secukinumab and ixekizumab target IL-17A, the cytokine that is particularly dominant in the entheseal inflammatory process of AS (more so than in RA, making IL-17A inhibitors more effective in AS than in RA). These are large-molecule biologics with no CYP interaction with CBD. The mechanistic note: CBD's CB2/NF-κB mechanism suppresses macrophage and neutrophil NF-κB activation, which reduces IL-17A production upstream of the IL-17A inhibitor's receptor blockade target — the combination suppresses IL-17A production and blocks the remaining IL-17A at its receptor. This complementarity makes the IL-17A inhibitor + CBD combination mechanistically rational for AS.

JAK inhibitors (tofacitinib, upadacitinib) for AS — CYP3A4 substrates, interaction monitoring appropriate: JAK inhibitors are increasingly used for AS, with upadacitinib showing high efficacy for both axial and peripheral manifestations. As covered in the RA post (P11-236), JAK inhibitors are CYP3A4 substrates; CBD's modest CYP3A4 inhibition may modestly elevate JAK inhibitor plasma levels. Disclosure to the rheumatologist managing JAK inhibitor therapy is appropriate for CBD initiation in AS, and starting CBD at a lower dose with monitoring for JAK inhibitor side effect amplification is prudent.

Muscle relaxants (cyclobenzaprine, methocarbamol — for AS-associated paravertebral spasm) — CYP1A2 substrate (cyclobenzaprine), additive CNS depression: Paravertebral muscle spasm — secondary to the spinal entheseal inflammation of AS — is common and contributes to nighttime pain and stiffness. Cyclobenzaprine (a tricyclic-related muscle relaxant) is a CYP1A2 substrate; CBD's modest CYP1A2 inhibition may modestly elevate cyclobenzaprine plasma levels, with additive CNS depression (sedation, anticholinergic effects). At standard supplemental CBD doses, the interaction is modest but clinically relevant for patients already experiencing significant sedation from cyclobenzaprine. Taking cyclobenzaprine at bedtime (its most common usage, for nocturnal spasm) with pre-sleep CBD oil requires awareness of the additive CNS depression — reduced alertness on nighttime awakenings (which AS patients characteristically need to move around and perform spinal exercises) could be problematic if too sedating to safely mobilize.

Active AS with Early Morning Awakenings: The Delay-the-Awakening Protocol

For people with active AS where the characteristic two to four AM early morning awakening from sacroiliac and spinal pain is the dominant sleep disruptor, the CBD protocol is structured to reduce the rate of entheseal inflammatory mediator accumulation during the nocturnal immobility period — with the practical goal of extending the period of uninterrupted sleep before the pain awakening occurs. The Nano CBD Broad Spectrum Oil taken forty-five to sixty minutes before sleep provides CB2/NF-κB suppression of entheseal macrophage and neutrophil TNF-α and IL-17A production beginning at approximately midnight, partially reducing the rate of inflammatory mediator accumulation during the early nocturnal period. The CBD+CBN+D9+Melatonin Gummies taken sixty minutes before sleep provide N3 slow-wave sleep promotion (CBN) that maximizes the depth and continuity of sleep during the period before the pain awakening — because AS patients who are going to wake at two to four AM regardless should achieve the deepest, most restorative sleep possible in the first half of the night — combined with the melatonin circadian sleep onset anchor that addresses any IL-17A-related suppression of pineal melatonin synthesis in active AS. The Nano CBD Water-Soluble Broad Spectrum Softgels at sleep onset provide sustained overnight CB2 entheseal coverage through the two to four AM peak immobility-accumulation window, potentially extending the time before the inflammatory mediator threshold for pain awakening is reached. The Nano CBD Muscle & Joint Cream applied to the lower lumbar and sacral region (the most common AS pain epicenter — directly over the sacroiliac joints and the lumbosacral junction) before sleep provides local TRPV1 desensitization at the entheseal sensory afferents accessible through the overlying skin and soft tissue of the lower back — reducing the sensitized nociceptor discharge threshold at the primary AS pain site. For AS with costovertebral enthesitis: cream applied to the anterior chest wall (lateral sternal borders, the costochondral junctions) addresses the respiratory pain from chest wall enthesitis in supine sleep.

AS on Biologics with Residual Sleep and Fatigue: The Hyperarousal-Fatigue Protocol

For people with AS in low disease activity on biologic therapy where morning stiffness has shortened, early morning awakenings are less frequent, but sleep remains non-restorative and the fatigue-hyperarousal paradox persists, the CBD protocol emphasizes the central mechanisms. The Nano CBD Broad Spectrum Oil for HPA/FAAH modulation of the chronic hyperarousal maintaining conditioned nocturnal arousal and the 5-HT1A mechanism for the serotoninergic restoration supporting the fatigue-associated mood dysregulation common in chronic AS. The CBD+CBN+D9+Melatonin Gummies for N3 architecture restoration addressing the slow-wave sleep deficit from chronic AS-related sleep fragmentation — the same CBN N3 mechanism that is valuable in AS remission as in active disease, because the sleep architecture disruption from months or years of nocturnal pain awakenings persists as an architectural deficit after the acute pain driver is controlled. The Nano CBD Broad Spectrum Gummies for daytime maintenance — both for the residual systemic AS inflammatory burden that biologic therapy partially but not always fully controls, and for the daytime fatigue management through the consistent 5-HT1A and adenosine mechanism support of daytime alertness and mood that reduces the fatigue-hyperarousal paradox. The cream remains useful for breakthrough axial pain at any disease activity level, particularly during AS flares that break through biologic therapy (a common occurrence, as biologics reduce but do not eliminate entheseal inflammatory activity).

The AS Sleep Protocol: Entheseal Coverage Through the Nocturnal Accumulation Window + Movement Integration

Integrate CBD with the pre-sleep spinal mobility routine: AS patients are already taught (by physical therapists and rheumatologists) to maintain a spinal extension exercise routine — a critical non-pharmacological pillar of AS management that counters the tendency toward flexion deformity and maintains spinal mobility. The ideal AS pre-sleep protocol integrates CBD with the spinal mobility routine: perform pre-sleep spinal extension exercises first (ten to fifteen minutes — the mechanical entheseal circulation from movement reduces the residual intra-articular inflammatory mediator load before sleep), then apply the CBD cream to the lower lumbar and sacral region (while the periarticular tissue is warm and vasodilated from the exercise, enhancing transdermal CBD delivery), then take the sublingual oil, then take the gummies and softgels. This sequence maximizes the mechanical clearance from movement before beginning the overnight CBD entheseal suppression — starting from the lowest possible inflammatory mediator baseline before the overnight immobility period begins.

Sleep positioning optimization complements CBD in AS: Unlike most sleep conditions in this series, AS patients have specific, medically recommended sleep positioning requirements: sleeping on a firm mattress (to support the spine in extension during sleep), avoiding the fetal flexion position (which places the lumbar spine in the flexion that promotes ankylosis), using no pillow or a flat pillow (to avoid cervical flexion), and sleeping supine with legs extended (or prone in early AS if cervical spine is unaffected). These positioning guidelines reduce the accumulation of entheseal inflammatory stress from nocturnal flexion posture — combining the mechanical benefits of optimal sleep positioning with the pharmacological benefit of overnight CBD entheseal suppression provides the most comprehensive approach to the nocturnal inflammatory mediator accumulation problem.

BASDAI sleep sub-score as CBD response tracking metric: The BASDAI question on fatigue and sleep quality provides a validated, AS-specific tracking tool for CBD response in axial spondyloarthritis — analogous to morning stiffness duration in RA. Logging the BASDAI score (available as a free questionnaire online or in AS patient apps) at baseline and monthly during CBD use provides an objective disease-specific metric for tracking the sleep quality component of AS management response. Ideally, the treating rheumatologist reviews BASDAI scores at appointments — consistent improvements in the sleep and fatigue sub-scores with CBD use are clinically relevant information for the rheumatology team's overall AS management assessment.

Rheumatologist disclosure — NSAID context most important: For AS patients on continuous NSAIDs (the most common AS pharmacological scenario), disclosure of CBD use to the rheumatologist is important for the GI monitoring context — if GI symptoms develop during continuous NSAID + CBD use, both agents are potential contributors, and the rheumatologist's gastroprotection assessment (proton pump inhibitor, NSAID dose adjustment, switching to celecoxib) is the appropriate response.

Why does CBD oil for ankylosing spondylitis sleep need to address the early morning awakening specifically — why is it so predictable?

The early morning awakening of AS is predictable because it reflects the intersection of two precise biological clocks — the circadian nadir of cortisol (two to four AM, when the anti-inflammatory effect of cortisol is at its lowest) and the accumulation clock of the overnight entheseal inflammatory mediator buildup. During upright waking activity, the mechanical loading and movement of the spine continuously circulates the interstitial fluid in the entheseal tissue at the sacroiliac joints and spinal facets, clearing TNF-α, IL-17A, and prostaglandins as fast as the inflamed entheseal macrophages and neutrophils produce them. This dynamic equilibrium prevents any single time point from accumulating enough inflammatory mediators to trigger the pain threshold. When sleep begins and movement stops, the mechanical clearance ceases. The entheseal macrophages and neutrophils continue producing inflammatory mediators at the same rate they did during the day, but now those mediators accumulate in the stagnant interstitial space around the entheseal nociceptors. After three to four hours of immobility — consistently landing around two to four AM depending on when the person fell asleep — the accumulated inflammatory mediator concentration reaches the activation threshold of the sensitized TRPV1 and other nociceptors at the entheseal attachment sites, generating the pain signal that produces full awakening. The cortisol nadir in this window removes the last anti-inflammatory brake that might otherwise delay the awakening. This predictability is diagnostically useful: it is one of the four criteria for inflammatory back pain (IBP) that rheumatologists use to distinguish AS from mechanical back pain. It is also therapeutically targetable: if you know when the accumulation threshold will be reached, you can design the CBD dosing timeline to maximize CB2 entheseal suppression during the accumulation window. The sequential pre-sleep oil (active from midnight) and sleep-onset softgels (active from two to four AM) are timed to cover exactly the accumulation window that produces the characteristic AS early morning awakening. The practical goal is not to eliminate the underlying entheseal inflammation (that requires NSAID and biologic therapy) but to reduce the rate of inflammatory mediator accumulation enough to either push the awakening time later (from two AM to four AM, for example) or reduce its intensity so that it can be slept through rather than forcing full awakening.

Can CBD oil help with the morning stiffness in ankylosing spondylitis the same way it might in rheumatoid arthritis?

CBD oil addresses morning stiffness in AS through the same general CB2 cytokine suppression rationale as in RA but with important mechanistic differences that make the tracking and the timeline different. In RA, morning stiffness reflects intra-articular cytokine accumulation in small peripheral joint spaces (hands, wrists, knees) that resolves with joint movement within minutes to hours as synovial fluid circulates. In AS, morning stiffness reflects entheseal cytokine accumulation in the sacroiliac joints and the entire axial skeleton — a larger anatomical target, a more mechanically constrained clearance pathway, and a tissue (the enthesis, not the synovium) that is inherently less vascular and less efficiently cleared than synovial fluid. This means AS morning stiffness typically: (1) lasts longer than RA morning stiffness in comparable disease activity — two to four hours in active AS versus one to two hours in active RA; (2) requires more active resolution (specific spinal extension exercises, not just gentle joint movement); and (3) involves the axial skeleton's range of motion rather than peripheral finger/wrist/knee stiffness. The BASDAI morning stiffness sub-score, measured in both intensity and duration, is the AS equivalent of RA morning stiffness duration as a CBD response tracking metric. If consistent nightly CBD use reduces the BASDAI morning stiffness sub-score over four to eight weeks (with stable pharmacological therapy), this is evidence of reduced overnight entheseal cytokine accumulation. The timeline is similar to RA: acute effects on pre-sleep hyperarousal and TRPV1-mediated pain sensitivity within one to two weeks; progressive CB2 entheseal macrophage modulation showing up as reduced morning stiffness intensity and duration over four to eight weeks; full sleep architecture improvement (CBN N3 restoration) at six to twelve weeks. AS morning stiffness will not resolve from CBD alone — it requires the combination of CBD's CB2 entheseal suppression, adequate NSAID and/or biologic disease control, and the regular spinal extension exercise program that is the mechanical clearance mechanism for the accumulated entheseal cytokines. CBD is the pharmacological complement to the exercise program's mechanical clearance — working together, they address both the production rate (CB2 suppresses it) and the clearance rate (exercise accelerates it) of the overnight entheseal inflammatory mediator accumulation.

Is CBD oil safe with the NSAIDs I take continuously for ankylosing spondylitis?

Continuous NSAID therapy and CBD are pharmacokinetically compatible — there is no CYP-mediated interaction between CBD and naproxen, indomethacin, diclofenac, or celecoxib. The relevant concern is pharmacodynamic: additive gastrointestinal mucosal risk. NSAIDs reduce GI mucosal protection by inhibiting COX-1-mediated prostaglandin synthesis (prostaglandins maintain the protective mucus layer and blood flow to the stomach and small intestine lining). Continuous NSAID use already carries a meaningful GI mucosal risk that rheumatologists manage through patient selection, the lowest effective NSAID dose, proton pump inhibitor co-prescription in high-risk patients, and switch to celecoxib (COX-2 selective, lower GI risk). CBD itself does not directly inhibit COX enzymes, but its GI prokinetic effects and the potential for sublingual oil to partially irritate the upper GI mucosa if swallowed adds a modest additional GI mucosal concern in the context of continuous NSAIDs. The practical management approach: take the sublingual CBD oil properly (under the tongue for sixty to ninety seconds, absorbed through the oral mucosa — minimizing the amount that is swallowed and reaches the GI tract); take solid-form CBD (softgels, gummies) with food to reduce GI mucosal exposure; if you are on continuous NSAIDs and develop any new GI symptoms (nausea, epigastric pain, dark stools) after adding CBD, report to the rheumatologist promptly for evaluation; consider requesting a switch to celecoxib if you are on a non-selective NSAID and adding CBD (celecoxib's COX-2 selectivity provides the best GI safety profile for the continuous NSAID + CBD combination). The pharmacodynamic complementarity of NSAIDs and CBD is the more clinically interesting aspect: NSAIDs reduce prostaglandin-mediated entheseal inflammation through the COX pathway; CBD reduces TNF-α and IL-17A through the CB2/NF-κB pathway. These two pathways are distinct and together provide broader entheseal inflammation suppression than either agent alone. Many AS patients report that the CBD + NSAID combination provides better nocturnal pain management than the NSAID alone — the separate mechanisms complement each other at the entheseal inflammatory site.

I have chest pain and trouble breathing deeply when I sleep — is this from my ankylosing spondylitis and can CBD oil help?

Chest pain and restricted deep breathing during sleep in AS almost certainly reflects costovertebral enthesitis — the inflammation at the attachment points of the ribs to the thoracic vertebrae (costovertebral joints) and at the front of the chest where the ribs meet the sternum (costochondral and costosternal junctions). This is a well-recognized but often underappreciated feature of AS, affecting thirty to sixty percent of patients at some point in the disease course. The sleep implications are direct: in the supine position, the thoracic cage normally expands freely during inspiration. When the costovertebral joints are inflamed and the entheseal attachment points at the rib-sternum junctions are painful, the normal inspiratory expansion of the chest becomes painful during sleep, and the combination of reduced chest wall compliance from entheseal stiffness and the respiratory muscle relaxation of sleep (particularly in REM sleep when intercostal muscle tone is minimal) produces the sensation of chest tightness, restricted breathing, and pain with deep breaths that wakes AS patients from sleep or makes the supine position intolerable. Before attributing chest pain in AS to costovertebral enthesitis, it is essential to ensure that cardiovascular and pulmonary causes have been evaluated — chest pain always warrants physician assessment, and AS itself carries elevated cardiovascular risk (aortitis and cardiac conduction abnormalities are recognized AS extra-articular manifestations). Once costovertebral enthesitis is confirmed as the cause of chest wall pain, CBD oil's CB2/NF-κB mechanism addresses the entheseal inflammatory process at the costovertebral and costosternal attachment sites through the same mechanism as at the sacroiliac and spinal entheses — reducing macrophage TNF-α and IL-17A production at the chest wall inflammatory sites. The most targeted approach: applying the CBD Muscle & Joint Cream directly to the anterior chest wall — along the lateral borders of the sternum, over the costochondral junctions (feel for the tender points where the cartilaginous ribs meet the sternum), and along the lower rib margins — before sleep provides TRPV1 desensitization at the sensory afferents in the periosteal and entheseal tissue of the chest wall, reducing the nocturnal nociceptor discharge from the inflamed costovertebral and costosternal attachments. This chest wall cream application is unique to AS among all the conditions in this series. Sleep positioning — slightly elevated head and trunk (a wedge pillow under the upper back) rather than completely flat supine — reduces the costovertebral joint compression that occurs in full supine and may reduce the pain with inspiration enough to maintain the supine position recommended for spinal health in AS.

I'm exhausted during the day from my AS but can't sleep well at night — why doesn't being so tired help me sleep better?

The fatigue-hyperarousal paradox of AS is one of the most frustrating aspects of the condition, and it is mechanistically explicable — not a paradox at all once the biology is understood. The exhaustion in AS comes from multiple converging sources: the systemic metabolic cost of the chronic inflammatory process (the immune system's continuous activation consumes significant energy), the direct brain effects of systemic TNF-α and IL-17A that produce the sickness behavior fatigue similar to the fatigue of infection, and the sleep fragmentation from chronic nocturnal pain awakenings that accumulates a sleep debt over months and years. This is genuine biological exhaustion — not depression, not laziness. The hyperarousal that prevents consolidated sleep in AS despite this exhaustion comes from different mechanisms: the chronic pain produces the same conditioned anticipatory arousal that any chronic nocturnal pain condition produces over time (the nervous system learns that going to sleep means waking in pain, and increases the baseline cortical arousal to prepare for the expected nocturnal awakening — a maladaptive but neurobiologically explicable response); the systemic TNF-α and IL-17A directly activate the HPA axis, maintaining cortisol variability and hypothalamic CRH release that sustains physiological hyperarousal; and the chronic sleep fragmentation itself activates the cortical arousal system through the same homeostatic pressure mechanism (sleep pressure builds from fragmentation, but the hyperarousal system simultaneously becomes more sensitized, preventing consolidation of the accumulated sleep pressure into continuous sleep). The fundamental problem: in people without sleep disorders, exhaustion reliably overcomes arousal because the sleep homeostatic system (the rising adenosine sleep pressure from extended wakefulness) overpowers arousal thresholds. In AS (as in other chronic pain and inflammatory conditions), the arousal system is chronically upregulated to the point where even the extreme exhaustion from systemic inflammation and sleep fragmentation cannot fully overcome it. CBD addresses this from both directions: the FAAH/anandamide and 5-HT1A mechanisms reduce the hyperarousal by dampening HPA CRH release and restoring serotoninergic tone; the CB2/NF-κB mechanism reduces the systemic AS inflammatory burden that is sustaining the arousal through cytokine HPA stimulation; and the adenosine reuptake inhibition mechanism amplifies the sleep homeostatic pressure (the accumulating adenosine signal for sleep onset) that exhaustion generates. The result, after consistent use, is a gradual convergence of the exhaustion and the arousal — with sleep onset becoming easier as the hyperarousal is moderated, and sleep continuity improving as the pain awakenings become less frequent or less intense.

How long does CBD oil take to work for ankylosing spondylitis sleep, and what is realistic to expect?

The timeline for CBD oil's effects in AS sleep follows a similar pattern to RA but with some AS-specific expectations. In the first one to two weeks: the most immediate benefits are typically in sleep onset (HPA/5-HT1A reduction in pre-sleep hyperarousal making falling asleep easier) and in the subjective intensity of the nocturnal pain awakening (TRPV1 desensitization from oil and cream reducing the peak pain intensity that wakes the patient, even if the awakening itself still occurs). The characteristic two to four AM awakening may not be eliminated in the first weeks but the pain intensity that triggers it may be reduced, and the ability to return to sleep after moving around may be easier. Over four to eight weeks: the progressive CB2 entheseal macrophage M1→M2 polarization shift accumulates — the macrophages in the entheseal tissue that are persistently activated in AS gradually show reduced pro-inflammatory cytokine production with consistent CB2 activation, reducing the rate of overnight inflammatory mediator accumulation. This may manifest as the early morning awakening shifting later (from two AM to three or four AM) or becoming less frequent (every other night rather than every night). The BASDAI morning stiffness sub-score may begin to improve as the overnight entheseal cytokine accumulation is reduced. Over eight to twelve weeks: the CBN N3 sleep architecture restoration from the gummies begins showing in improved sleep quality scores and daytime energy — the slow-wave sleep architectural deficit from chronic AS sleep fragmentation gradually reverses with consistent N3-promoting CBD use and reduced nocturnal awakening frequency. Realistic expectations: CBD will not make the AS early morning awakening disappear in active disease — that requires effective biologic or NSAID disease control as the primary treatment. The realistic CBD contribution is: reduced pain awakening intensity and frequency, extended time before the overnight accumulation threshold is reached, improved pre-awakening sleep quality, and better daytime energy and fatigue management. The combination of CBD (for CB2 entheseal suppression and sleep architecture) + NSAIDs/biologics (for overall disease control) + spinal extension exercises (for mechanical entheseal clearance) + optimal sleep positioning (for reduced costovertebral and sacroiliac joint pressure during sleep) is the comprehensive AS sleep management approach that produces the best overall outcome.

Medical Disclaimer

This article is for informational and educational purposes only. It is not intended to diagnose, treat, cure, or prevent any disease or medical condition, including ankylosing spondylitis, axial spondyloarthritis, inflammatory back pain, or any sleep disorder. CBD oil is not a substitute for physician-directed NSAID, DMARD, or biologic therapy for ankylosing spondylitis. Chest pain in AS patients should be evaluated by a physician before being attributed to costovertebral enthesitis — cardiac and pulmonary causes must be excluded. Patients on continuous NSAIDs, biologic agents, or JAK inhibitors for AS must discuss CBD use with their rheumatologist before initiating. The statements in this article have not been evaluated by the Food and Drug Administration. CBD products are not intended to diagnose, treat, cure, or prevent any disease. Individual responses to CBD vary significantly.