THE PURE CRAFT JOURNAL

CBD Gummies for Heart Health and Cardiovascular Support: What Research Shows

October 20, 2026

By PureCraft Editorial Team | PureCraft CBD | Updated October 2026

Cardiovascular disease remains the leading cause of death globally, driven by a convergence of modifiable risk factors — hypertension, chronic inflammation, oxidative stress, dyslipidemia, endothelial dysfunction, and the cortisol-driven autonomic dysregulation of chronic psychological stress. The endocannabinoid system (ECS) is deeply embedded in cardiovascular physiology: CB1 and CB2 receptors are expressed throughout the heart, coronary vasculature, and the autonomic nervous system that governs cardiac rhythm and vascular tone. Far from being peripheral to heart health, the ECS is one of the primary regulators of cardiovascular homeostasis — with endocannabinoids modulating heart rate, blood pressure, vascular inflammation, platelet aggregation, and the neuroendocrine stress response that represents the most direct pathway from psychological stress to heart disease. This article examines the cardiac ECS, CBD's cardiovascular mechanisms, and what the evidence actually supports — while being transparent about the distinction between preclinical data and human evidence, and the specific drug interactions that matter most in cardiovascular health management.

The Cardiac ECS: How the Endocannabinoid System Governs Heart Function

CB1 in the Heart and Vasculature

CB1 receptors are expressed in cardiomyocytes (cardiac muscle cells), the sinoatrial node (the heart's pacemaker), vascular smooth muscle cells, and cardiac sympathetic nerve terminals. In metabolic disease, chronic stress, and heart failure, cardiac CB1 becomes chronically overactivated — contributing to negative inotropy (reduced contractile force), reduced heart rate variability (a marker of autonomic cardiovascular health), and maladaptive cardiac remodeling. CB1 activation at sympathetic nerve terminals inhibits norepinephrine release — this has vasodilatory effects that are acutely beneficial but become dysregulated in chronic overactivation. CBD's negative allosteric CB1 modulation — reducing CB1 signaling efficiency without blocking the receptor — has documented acute cardiovascular effects in humans, including modest blood pressure reduction and attenuation of the blood pressure and heart rate response to psychological stress.

CB2 in Cardiac and Vascular Tissue

CB2 receptors in the cardiovascular system are expressed primarily on cardiac macrophages, vascular endothelial cells, and circulating immune cells recruited to atherosclerotic plaques. CB2 activation exerts directly anti-atherosclerotic effects: suppression of vascular macrophage NF-κB inflammatory activation (macrophage foam cell formation is the cellular basis of atherosclerotic plaque); reduction of VCAM-1 and ICAM-1 endothelial adhesion molecule expression (which recruit circulating monocytes to the arterial wall — a key early step in atherogenesis); suppression of inflammatory cytokine production (TNF-α, IL-6, IL-1β) in plaque-associated macrophages; and reduction of plaque vulnerability through anti-inflammatory stabilization of the fibrous cap. CBD's CB2 modulation engages this vascular anti-inflammatory pathway directly relevant to atherosclerosis prevention and progression.

TRPV1 and Anandamide: Vascular Tone Regulation

TRPV1 channels are expressed throughout the vascular system, where their activation by endocannabinoids — particularly anandamide — produces vasodilation through release of calcitonin gene-related peptide (CGRP) and substance P from perivascular nerve fibers, and through direct endothelial nitric oxide (NO) release. CBD desensitizes TRPV1 (reducing its activation threshold) and inhibits FAAH (the enzyme that degrades anandamide), increasing anandamide bioavailability at vascular TRPV1 receptors. This anandamide-TRPV1-NO pathway is a well-characterized endogenous vasodilatory mechanism — CBD's dual action (TRPV1 desensitization + FAAH inhibition → more anandamide at vascular receptors) contributes to its documented acute antihypertensive effect in human studies.

CBD and Blood Pressure: The Human Evidence

Of all CBD's cardiovascular mechanisms, the blood pressure data is the most directly supported by human clinical evidence. A notable 2017 randomized, double-blind, placebo-controlled crossover study (Jadoon et al., Journal of Clinical Investigation Insight) found that a single 600 mg CBD dose reduced resting systolic blood pressure by 6 mmHg in healthy volunteers, and — crucially — significantly attenuated the blood pressure increase produced by cold stress testing (the sympathetically-mediated blood pressure spike: reduced by ~5 mmHg vs placebo). Heart rate response to stress was also attenuated.

What the Blood Pressure Evidence Actually Shows

What's established: Acute single-dose CBD (at pharmacological doses of 300–600 mg) produces measurable blood pressure reduction and attenuates stress-induced blood pressure responses in healthy adults.

The dose gap: 600 mg is 12–24× typical gummy supplement doses (25–50 mg). Whether 25–50 mg produces the same acute blood pressure effect has not been demonstrated in controlled trials.

The cumulative argument: HPA axis normalization from consistent daily dosing at supplement doses is the most plausible mechanism by which standard-dose CBD produces cardiovascular benefit — cortisol reduction over weeks reduces RAAS activation, sympathetic tone, and endothelial inflammatory stress. This is indirect but mechanistically coherent.

Honest bottom line: CBD at standard supplement doses is not a proven antihypertensive medication. It is a reasonable supplementary strategy within a broader cardiovascular health approach, with its strongest evidence at pharmacological doses and its most plausible standard-dose mechanism being the stress-cortisol pathway.

Cardiovascular Risk Factor Map: CBD Mechanisms

CV Risk Factor	Mechanism of Injury	CBD Mechanism	Evidence Level
Hypertension	Endothelial shear stress → vascular remodeling; glomerular damage; LVH; stroke risk	TRPV1/anandamide vasodilation; 5-HT1A HPA/cortisol normalization → reduced RAAS; CB1 modulation of sympathetic tone	Human (acute, pharmacological dose); mechanistic at supplement dose
Chronic stress/sympathetic overdrive	Cortisol → endothelial dysfunction, platelet hyperaggregability, RAAS activation, visceral fat → metabolic CV risk; elevated norepinephrine → arrhythmia risk	5-HT1A/HPA → cortisol reduction; CB1 modulation at sympathetic nerve terminals; GABA-A potentiation → reduced anxiety-driven sympathetic activation	Human (anxiety/cortisol); strongest standard-dose cardiovascular pathway
Atherosclerosis/inflammation	Monocyte recruitment → foam cell formation → plaque; NF-κB-driven endothelial VCAM-1/ICAM-1 → adhesion; oxidized LDL → macrophage activation; plaque rupture → ACS	CB2/NF-κB vascular macrophage suppression; VCAM-1/ICAM-1 reduction; direct antioxidant (LDL oxidation reduction); Nrf2/HO-1 endothelial protection	Preclinical (atherosclerosis models); CB2 atherosclerosis data well-established in rodents
Oxidative vascular stress	Superoxide quenching of NO → endothelial dysfunction; LDL oxidation → foam cell formation; ROS-mediated endothelial apoptosis	Direct radical scavenging; Nrf2 upregulation of SOD/catalase/GSH; endothelial NO preservation	Preclinical; Nrf2/HO-1 mechanism well-characterized
Sleep deprivation	Short sleep (≤6h) independently doubles cardiovascular mortality risk; sleep deprivation raises inflammatory markers (CRP, IL-6), blood pressure, insulin resistance, cortisol, and sympathetic tone	CBD/CBN sleep quality support; adenosine A1/A2A modulation; cortisol reduction (lower evening cortisol → faster sleep onset → better deep sleep architecture → reduced nocturnal blood pressure dipping failure)	Human (sleep); cardiovascular link through nocturnal BP and inflammatory marker pathway

The Stress-Heart Connection: CBD's Most Clinically Relevant Cardiovascular Pathway

Psychological stress is a well-established independent cardiovascular risk factor — not merely a background variable but a direct causal driver through multiple physiological pathways. The Interheart study, which enrolled 15,152 heart attack patients across 52 countries, found that psychosocial stress was the second largest population-attributable risk factor for acute myocardial infarction, behind only dyslipidemia. CBD's most thoroughly documented human mechanism — HPA axis modulation and cortisol reduction via 5-HT1A agonism — is therefore directly cardiovascular relevant through the following cascade:

1. Cortisol → endothelial dysfunction: Cortisol reduces endothelial nitric oxide synthase (eNOS) activity, decreasing NO production and impairing the endothelium's ability to vasodilate and resist inflammatory adhesion — a foundational step in atherogenesis. CBD's cortisol-lowering effect preserves eNOS activity and NO bioavailability.

2. Cortisol → platelet hyperaggregability: Elevated cortisol increases platelet thromboxane A2 sensitivity and reduces prostacyclin production, shifting the thrombosis/thrombolysis balance toward clot formation — relevant to acute coronary syndrome risk from vulnerable plaque rupture. CBD's cortisol reduction shifts this balance toward the protective end.

3. Cortisol → RAAS activation: Cortisol has mineralocorticoid-like effects that amplify aldosterone signaling, sodium retention, and RAAS activation — raising blood pressure and increasing glomerular filtration pressure. CBD's HPA/cortisol reduction reduces RAAS activation through this pathway.

4. Stress → sympathetic overdrive → arrhythmia: Acute psychological stress activates the sympathetic nervous system, elevating norepinephrine levels that increase heart rate, reduce heart rate variability (HRV), and can precipitate arrhythmias in susceptible individuals. CBD's GABA-A potentiation and CB1 modulation at sympathetic nerve terminals blunt sympathetic outflow, contributing to the HRV improvement and heart rate attenuation seen in the Jadoon stress study.

5. Chronic stress → visceral fat → metabolic CV risk: HPA-driven cortisol chronically promotes visceral adipose deposition, insulin resistance, dyslipidemia, and the full metabolic syndrome that represents the most common modern cardiovascular risk profile. CBD's cortisol normalization disrupts this stress-metabolic-cardiovascular risk cascade at its endocrine origin point.

Practical Protocol: CBD Gummies for Cardiovascular Health Support

Cardiovascular Health Support Protocol — CBD Gummies

Daily stress-cortisol-cardiovascular foundation: Broad Spectrum CBD Gummies (25 mg daily) — consistent daily CBD for sustained HPA normalization and sympathetic tone modulation. The cardiovascular case for CBD is most compelling when framed through the stress-cortisol-endothelial pathway, where consistent daily dosing over 2–6 weeks produces the cumulative HPA modulation most relevant to cardiovascular benefit. Morning dosing with food to maximize absorption; nanoemulsion formulation in all PureCraft products improves the consistent bioavailability that steady-state HPA effects require.

Vascular anti-inflammatory phytocannabinoid support: Full Spectrum Berry Gummies add beta-caryophyllene (direct CB2 agonist with documented vascular anti-inflammatory activity — directly relevant to the CB2/NF-κB atherosclerotic plaque macrophage suppression mechanism), CBG (PPARγ activity that complements endothelial anti-inflammatory effects), and CBC (TRPA1/TRPV1 activity that complements vascular tone regulation). The full terpene-cannabinoid entourage provides maximal CB2 vascular engagement — particularly relevant for individuals with family history of cardiovascular disease or elevated inflammatory markers (hsCRP, IL-6).

Antioxidant vascular protection: CBD Elderberry Gummies add elderberry anthocyanins with directly cardioprotective antioxidant and anti-inflammatory properties — elderberry anthocyanins (particularly cyanidin-3-glucoside) have been shown in human studies to reduce LDL oxidation, improve endothelial function (flow-mediated dilation), and reduce serum hsCRP. These elderberry cardiovascular benefits are independent of CBD and complement CBD's vascular mechanisms through overlapping antioxidant and anti-inflammatory pathways. The Water Soluble CBD Softgels provide an alternative delivery format with enhanced nanoemulsion bioavailability for individuals who prefer softgels over gummies for consistent cardiovascular supplement routines.

Sleep architecture and nocturnal blood pressure: CBD+CBN+Melatonin Gummies — nocturnal blood pressure dipping (the normal 10–20% blood pressure reduction during sleep) is a critical cardiovascular protective phenomenon: "non-dippers" (individuals whose blood pressure does not fall adequately during sleep) have significantly elevated cardiovascular event risk independent of daytime blood pressure. Sleep architecture quality — particularly slow-wave sleep, which requires adequate melatonin and adenosine signaling — governs the depth of nocturnal BP dipping. CBD+CBN's sleep quality support and melatonin's circadian regulation of nocturnal BP dipping together address this underappreciated cardiovascular sleep-health connection. The Broad Spectrum CBD Oil allows flexible sublingual dosing — useful for split dosing strategies where morning CBD supports cortisol awakening response management and evening CBD supports the pre-sleep cortisol reduction that facilitates nocturnal BP dipping.

NSAID-reduction strategy: CBD Muscle and Joint Cream — regular NSAID use (particularly COX-2 inhibitors like celecoxib, but also ibuprofen and naproxen with regular use) carries documented cardiovascular risk through prostaglandin I2 suppression (prostacyclin — a vasodilatory and platelet-inhibiting prostaglandin) without equivalent COX-1-derived thromboxane A2 suppression, shifting the balance toward vasoconstriction and platelet aggregation. Topical CBD for musculoskeletal pain management reduces systemic NSAID reliance and thereby reduces this cardiovascular prostanoid imbalance risk — an indirect but practically significant cardiovascular benefit for individuals with both joint pain and cardiovascular risk factors.

Delta-8 note: Delta-8 Gummies are not recommended for cardiovascular health support. THC analogs including delta-8 produce acute tachycardia (elevated heart rate), variable blood pressure effects (initial rise then fall), and autonomic dysregulation that are the opposite of cardiovascular-supportive. Regular THC/THC-analog use has been associated with increased cardiovascular event risk in epidemiological data. Individuals with cardiovascular disease or significant cardiovascular risk factors should prioritize CBD-dominant formulations without THC analogs.

Frequently Asked Questions

Can CBD gummies help lower blood pressure?

Research suggests CBD gummies may support healthy blood pressure through several mechanisms, with the strongest human evidence at pharmacological doses and the most plausible standard-dose mechanism being the stress-cortisol pathway — making honest expectations essential. The human evidence: a 2017 randomized crossover study (Jadoon et al.) found a single 600 mg CBD dose reduced resting systolic blood pressure by ~6 mmHg and significantly attenuated stress-induced blood pressure response compared to placebo in healthy volunteers. This is direct human evidence for CBD's antihypertensive effect — but at a dose 12–24 times typical gummy supplement doses. Whether 25–50 mg produces similar acute blood pressure effects has not been established in controlled trials. The cumulative mechanism: at standard supplement doses, the most plausible blood pressure pathway is HPA axis normalization over weeks of consistent daily dosing — CBD's 5-HT1A agonism reduces cortisol output, which reduces RAAS activation (cortisol has mineralocorticoid-like aldosterone-amplifying effects), reduces sympathetic tone, and reduces the endothelial dysfunction that raises vascular resistance. This is an indirect but well-mechanistically-supported pathway. For context: a 5–6 mmHg sustained systolic BP reduction is clinically meaningful — a 5 mmHg population-level reduction in systolic BP is estimated to reduce stroke risk by ~34% and coronary heart disease risk by ~21%. CBD is not a hypertension medication and should not substitute for prescribed antihypertensives. It is a reasonable supplementary strategy with its strongest mechanism in individuals where stress and HPA dysregulation are significant contributors to their blood pressure elevation — and where lifestyle modification (weight loss, sodium reduction, aerobic exercise, stress management) are the primary interventions CBD complements.

Can CBD gummies help with heart palpitations or irregular heartbeat?

Research suggests CBD gummies may support healthy heart rhythm through autonomic nervous system modulation — particularly in the context of stress-driven or anxiety-related palpitations — but CBD is not an antiarrhythmic medication and cardiac arrhythmias require medical evaluation. Heart palpitations have multiple causes: stress/anxiety-driven sympathetic activation causing sinus tachycardia or premature beats (the most common cause in healthy young adults); electrolyte imbalances (magnesium, potassium deficiency); thyroid dysfunction; structural heart disease; and true cardiac arrhythmias (atrial fibrillation, SVT, ventricular arrhythmias). CBD's mechanism is most relevant to the sympathetic/autonomic subtype: CBD's GABA-A potentiation (reducing anxiety-driven sympathetic outflow), 5-HT1A agonism (anxiolytic), and CB1 modulation at sympathetic nerve terminals reduce the elevated norepinephrine and sympathetic tone that drives sinus tachycardia and stress-induced premature beats. CBD has shown antiarrhythmic effects in preclinical cardiac ischemia/reperfusion models — reducing ischemia-induced arrhythmias through CB1 modulation at cardiac sympathetic terminals and direct membrane effects. Human evidence for CBD reducing clinically significant arrhythmias is limited. Practical guidance: individuals with occasional stress-related palpitations may find CBD's anxiolytic and autonomic-modulating effects reduce palpitation frequency — this is a reasonable use case with supporting mechanisms. Individuals with persistent palpitations, documented arrhythmias, atrial fibrillation, or any structural heart disease must consult their cardiologist before CBD supplementation — not because CBD is arrhythmogenic (it is not) but because (a) CBD's CYP3A4 inhibition affects many antiarrhythmic and cardiovascular medications, and (b) arrhythmias warrant diagnosis, not supplementation-first management.

Do CBD gummies interact with heart medications?

CBD gummies have clinically significant interactions with several cardiovascular medications that require physician awareness and, in some cases, active monitoring. CBD is a significant CYP3A4 inhibitor and moderate CYP2C9/CYP2C19/CYP2D6 inhibitor. Key cardiovascular drug interactions: Statins (atorvastatin, simvastatin, lovastatin — CYP3A4 substrates): CBD inhibits their metabolism, raising plasma statin levels and increasing myopathy/rhabdomyolysis risk; physician monitoring warranted, particularly at higher CBD doses. Warfarin (CYP2C9 substrate): CBD increases warfarin plasma levels — INR elevation and increased bleeding risk; INR monitoring required for patients on warfarin who start CBD. Beta-blockers (metoprolol, carvedilol — CYP2D6 substrates): CBD may increase beta-blocker levels; heart rate and blood pressure monitoring warranted. Calcium channel blockers (amlodipine, diltiazem, verapamil — CYP3A4 substrates): CBD inhibition increases plasma levels; additive blood pressure-lowering effect; physician monitoring for hypotension. Antiarrhythmics (amiodarone — CYP2C9/CYP3A4; flecainide — CYP2D6): narrow therapeutic index; CBD may significantly increase plasma levels; these are among the highest-risk CBD cardiovascular drug interactions — physician supervision essential. Digoxin: P-glycoprotein substrate; limited CYP interaction, but CBD may affect P-gp; narrow therapeutic index requires physician guidance. Antiplatelet agents (clopidogrel — CYP2C19 prodrug): CYP2C19 inhibition by CBD may reduce clopidogrel activation and antiplatelet effect — potentially clinically significant in post-stent patients; cardiologist consultation required. The most important rule: anyone managing cardiovascular disease with medications should review their complete cardiac drug list with their cardiologist before adding CBD supplementation. CBD interactions in cardiovascular medicine are driven primarily by hepatic CYP enzyme inhibition, not direct cardiac effects.

Can CBD gummies help with atherosclerosis or heart disease prevention?

Research suggests CBD gummies may support cardiovascular health in ways relevant to atherosclerosis risk through anti-inflammatory, antioxidant, and endothelial-protective mechanisms — while being clear that CBD is not a proven atherosclerosis prevention strategy in humans and does not replace evidence-based cardiovascular risk reduction. The preclinical evidence for CBD's anti-atherosclerotic mechanisms is compelling: in ApoE knockout mice (the standard atherosclerosis research model), CBD administration significantly reduced atherosclerotic plaque progression, plaque macrophage infiltration (foam cell content), and vascular NF-κB inflammatory markers — with clear CB2-mediated and antioxidant mechanisms. The pathways are well-grounded: oxidized LDL is the primary atherogenic lipoprotein, and CBD's antioxidant activity (direct scavenging + Nrf2/HO-1 upregulation) reduces LDL oxidation; CB2/NF-κB suppression of vascular macrophage activation reduces foam cell formation and plaque inflammatory activity; endothelial NO preservation through TRPV1/anandamide/Nrf2 reduces the endothelial dysfunction that initiates atherosclerosis; and HPA/cortisol reduction reduces the cortisol-driven endothelial dysfunction, platelet hyperaggregability, and visceral adipose accumulation that amplify atherosclerotic risk. The translation gap to human anti-atherosclerotic efficacy has not been bridged by controlled trials. What is reasonable to say: CBD's combined anti-inflammatory, antioxidant, cortisol-lowering, and endothelial-supportive mechanisms collectively address the biological milieu in which atherosclerosis develops and progresses. This is a supportive strategy within a comprehensive cardiovascular risk reduction framework — not a substitute for evidence-based interventions: statin therapy where indicated, blood pressure management, smoking cessation, aerobic exercise, Mediterranean diet pattern, and physician-supervised cardiovascular risk management.

Can CBD gummies support recovery after a cardiac event?

Research suggests CBD gummies may offer supportive benefits during cardiac rehabilitation following a cardiovascular event — while this is a context requiring explicit cardiologist guidance before any supplement changes. The preclinical cardiac ischemia-reperfusion (IR) research is notable: CBD has consistently demonstrated cardioprotective effects in IR models — reducing infarct size, arrhythmia incidence, myocardial oxidative stress, and inflammatory cardiomyocyte injury following experimentally-induced cardiac ischemia. The proposed mechanisms include CB2-mediated suppression of neutrophil/macrophage-driven reperfusion inflammatory injury, antioxidant protection of myocardium during reperfusion oxidative burst, and CB1 modulation at cardiac sympathetic terminals reducing post-ischemic arrhythmic risk. These preclinical findings are mechanistically compelling but have not been tested in human post-MI populations. In the context of cardiac rehabilitation, what CBD's established mechanisms offer: anxiety and autonomic dysregulation are common after cardiac events, and CBD's anxiolytic and parasympathetic-supportive effects (GABA-A potentiation, 5-HT1A agonism) may support the psychological recovery and HRV restoration that are themselves markers of cardiovascular recovery; sleep disruption is also common post-MI, and CBD+CBN+melatonin's sleep support is directly relevant to the nocturnal BP dipping and sympathovagal balance that cardiac rehabilitation targets. The non-negotiable caution: post-cardiac event patients are typically on multiple medications with narrow therapeutic windows (antiplatelet agents, anticoagulants, antiarrhythmics, ACE inhibitors/ARBs, beta-blockers, statins) — CBD's CYP drug interactions in this polypharmacy context require cardiologist review before any CBD supplementation. This is not a consumer decision to make independently.

How long do CBD gummies take to support cardiovascular health?

The timeline for CBD gummies to produce measurable cardiovascular effects depends on the mechanism and what markers are being tracked. For acute blood pressure effects — the most directly documented cardiovascular CBD effect — changes are measurable within 1–2 hours of dosing at pharmacological doses; whether standard supplement doses produce acute blood pressure changes is less established. For HPA normalization and sustained cortisol reduction — the strongest standard-dose cardiovascular pathway — cumulative benefit develops over 2–6 weeks of consistent daily dosing. For inflammatory marker reduction (hsCRP, IL-6) — relevant to cardiovascular risk assessment — consistent daily CBD and elderberry supplementation over 4–8 weeks is the minimum intervention period that preclinical anti-inflammatory data would support for human effect detection. For heart rate variability (HRV) improvement — a functional cardiovascular autonomic marker trackable with consumer wearables — anxiety reduction and sympathetic tone normalization from CBD's autonomic mechanisms might be detectable over 4–6 weeks of daily use. Practical tracking: individuals interested in monitoring CBD's cardiovascular effects can use a home blood pressure cuff (daily morning measurements, 3-reading average, tracked over 4–8 weeks), a wearable device for resting heart rate and HRV trends, and physician-ordered hsCRP and lipid panels at 3–6 month intervals. The honest framing: CBD's cardiovascular support is a long-horizon strategy operating primarily through the stress-inflammation-endothelial pathway. It compounds gradually alongside diet, exercise, stress management, and sleep — and the most measurable early signal for most users is blood pressure and resting heart rate reduction from the autonomic and cortisol mechanisms, which begin developing within weeks of consistent supplementation.

References

Blessing EM, et al. Cannabidiol as a Potential Treatment for Anxiety Disorders. Neurotherapeutics. 2015;12(4):825–836. PMID: 26341731
Shannon S, et al. Cannabidiol in Anxiety and Sleep: A Large Case Series. Perm J. 2019;23:18–041. PMID: 30624194
Russo EB. Cannabinoids in the management of difficult to treat pain. Ther Clin Risk Manag. 2016;4(1):245–259. PMID: 28861491
Crippa JA, et al. Neural basis of anxiolytic effects of cannabidiol (CBD) in generalized social anxiety disorder. J Psychopharmacol. 2011;25(1):121–130. PMID: 20829306
Corroon J, Phillips JA. A Cross-Sectional Study of Cannabidiol Users. Cannabis Cannabinoid Res. 2018;3(1):152–161. PMID: 30014049
Capano A, et al. Evaluation of the effects of CBD hemp extract on opioid use and quality of life indicators in chronic pain patients. Postgrad Med. 2020;132(1):56–61. PMID: 31711352

Medical Disclaimer

This article is for informational and educational purposes only and does not constitute medical advice. CBD gummies are dietary supplements; these statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure, or prevent any disease or medical condition, including hypertension, atherosclerosis, coronary artery disease, heart failure, cardiac arrhythmia, myocardial infarction, or any cardiovascular disorder. Cardiovascular disease is a serious medical condition requiring diagnosis and management by a qualified cardiologist or physician. CBD inhibits CYP3A4, CYP2C9, CYP2C19, and CYP2D6 and has clinically significant interactions with many cardiovascular medications including statins, warfarin, beta-blockers, calcium channel blockers, antiarrhythmics, antiplatelet agents, and digoxin — physician review of your complete medication list is essential before beginning CBD supplementation. CBD is not a substitute for prescribed cardiovascular medications, blood pressure management, or physician-supervised cardiac care. If you are experiencing chest pain, palpitations, shortness of breath, or any cardiac symptoms, seek immediate medical attention.