Hawthorn

There is a lot of reference to hawthorn in older texts, and much of the indications are towards cardiac diseases and circulation. It was used in the past to treat conditions including tachycardia, hypertension, angina pectoris, and myocardial weakness. The berries were also used as an astringent for sore throats, and as a diuretic. ^{25Reference 25Bone et al. · 2013Principles and Practice of Phytotherapy}.

Traditionally the berry was mainly used, however more recent findings suggest the leaves to have a stronger action medicinally ^{25Reference 25Bone et al. · 2013Principles and Practice of Phytotherapy}.

Hawthorn has also been extensively used as a source of wood, and the berries as a flavouring of liquor. ^{25Reference 25Bone et al. · 2013Principles and Practice of Phytotherapy}.

The British herbal pharmacopoeia lists crataegus as cardiotonic, coronary vasodilator, and hypotensive specific for cardiac failure, myocardial weakness, hypertension, arteriosclerosis, Buerger’s disease, and paroxysmal tachycardia ^{27Reference 27British Herbal Medicine Association · 1983British Herbal Pharmacopoeia}.

In Chinese medicine, the fruit was often used to improve digestion, stimulate circulation, and treat blood stasis. ^{25Reference 25Bone et al. · 2013Principles and Practice of Phytotherapy}.

This is hawthorn’s largest evidence base and its most instructive one. A Cochrane systematic review of 14 double-blind RCTs (10 pooled, 855 patients, NYHA I-III) found that standardised leaf-and-flower extract, used mostly as an adjunct, improved maximal workload (+5.35 W), exercise tolerance, the pressure-heart-rate product, and symptoms of breathlessness and fatigue versus placebo ^{1,2Reference 1Pittler et al. · 2008Meta-analysisHawthorn extract for treating chronic heart failure — systematic review and meta-analysisView study →Reference 2Pittler et al. · 2003Meta-analysisHawthorn extract for treating chronic heart failure: meta-analysis of randomized trialsView study →}. But those trials largely predate or ran alongside older heart-failure regimens. When hawthorn was tested on top of contemporary therapy the story changed: the US HERB CHF RCT (n=120, patients already on ACE-inhibitors and beta-blockers) found no benefit on six-minute walk distance, quality of life, or functional capacity, and reported more adverse events in the hawthorn arm ^{4Reference 4Zick et al. · 2009RCTHawthorn Extract Randomized Blinded Chronic Heart Failure (HERB CHF) trial — randomised controlled trialView study →}. The large SPICE trial (n=2,681, WS 1442 900 mg/day for 24 months) missed its primary endpoint of time-to-first-cardiac-event, though it confirmed safety and hinted at reduced sudden cardiac death in the subgroup with less-impaired ejection fraction (LVEF ≥25%) ^{3Reference 3Holubarsch et al. · 2008RCTThe efficacy and safety of Crataegus extract WS 1442 in patients with heart failure: the SPICE trial — randomised controlled trialView study →}. A separate US trial by the same HERB CHF team reported that the extract increased early heart-failure progression ^{5Reference 5Zick et al. · 2008RCTThe effect of Crataegus oxycantha special extract WS 1442 on clinical progression in patients with mild to moderate heart failure — randomised controlled trialView study →}.

Gap: the symptomatic benefit was demonstrated mainly as add-on to pre-modern therapy; on today’s guideline-directed treatment the functional benefit is neutral-to-negative and there is no mortality benefit — the German Commission E approval (NYHA II) predates this evidence.

A 2024/2025 systematic review and meta-analysis of six randomised placebo-controlled trials (428 participants) found hawthorn produced a clinically meaningful reduction in systolic blood pressure (mean difference −6.65 mmHg) with a non-significant diastolic reduction, across treatment periods of 10 weeks to 6 months ^{6Reference 6Szikora et al. · 2025Meta-analysisHawthorn (Crataegus spp.) clinically significantly reduces blood pressure in hypertension: a meta-analysis of randomized placebo-controlled clinical trialsView study →}. The single best individual trial randomised 79 people with type 2 diabetes — most already taking antihypertensive and hypoglycaemic drugs — to 1,200 mg/day hawthorn extract or placebo for 16 weeks, and found a significant group difference in diastolic (but not systolic) reduction, with no herb-drug interaction detected ^{7Reference 7Walker et al. · 2006RCTHypotensive effects of hawthorn for patients with diabetes taking prescription drugs: a randomised controlled trialView study →}. An earlier pilot in mild essential hypertension (n=36, 500 mg/day) showed only non-significant trends ^{8Reference 8Walker et al. · 2002RCTPromising hypotensive effect of hawthorn extract: a randomized double-blind pilot study of mild, essential hypertensionView study →}.

Gap: the trials are small, heterogeneous, and used widely varying doses (250-1,200 mg/day); no large dedicated hypertension trial exists, and the effect size, while real, is modest.

The vascular-protective claim now rests on a specific, replicated mechanism rather than generic antioxidant assays. Standardised extract WS 1442 activates endothelial nitric-oxide synthase (eNOS) through phosphorylation at serine 1177, driving nitric-oxide-mediated vasorelaxation ^{11Reference 11Brixius et al. · 2006In vitroCrataegus special extract WS 1442 induces an endothelium-dependent, NO-mediated vasorelaxation via eNOS-phosphorylation at serine 1177 — in vitroView study →}; a follow-up showed this proceeds via redox-sensitive Src- and Akt-dependent eNOS activation rather than oestrogen-receptor signalling ^{12Reference 12Anselm et al. · 2009In vitroCrataegus special extract WS 1442 causes endothelium-dependent relaxation via a redox-sensitive Src- and Akt-dependent activation of endothelial NO synthase — in vitroView study →}. In aged animal/ex-vivo vessels the extract prevented aging-related endothelial dysfunction ^{13Reference 13Idris-Khodja et al. · 2012AnimalCrataegus special extract WS 1442 prevents aging-related endothelial dysfunction — animal modelView study →}. The classical claim that flavonoids strengthen the vessel wall by increasing collagen cross-linking traces to older herbal-pharmacology sources and has not been confirmed in humans.

Gap: the mechanism is well mapped preclinically but no human trial has shown an antioxidant clinical outcome — HERB CHF specifically measured oxidative-stress and inflammation markers and found no difference from placebo ^{4Reference 4Zick et al. · 2009RCTHawthorn Extract Randomized Blinded Chronic Heart Failure (HERB CHF) trial — randomised controlled trialView study →}.

Hawthorn’s cardiotonic reputation has a plausible, non-glycoside mechanism. Flavonoids inhibit cardiac cyclic-AMP phosphodiesterase in rat heart tissue ^{15Reference 15Petkov et al. · 1981AnimalInhibitory effect of some flavonoids and flavonoid mixtures on cyclic AMP phosphodiesterase activity of rat heart — animalView study →}, and hawthorn extract increased contraction amplitude and energy turnover in isolated rat cardiomyocytes ^{16Reference 16Pöpping et al. · 1995AnimalEffect of a hawthorn extract on contraction and energy turnover of isolated rat cardiomyocytes — animalView study →}; flavonoids from Crataegus produced measurable myocardial effects in isolated preparations ^{17Reference 17Schüssler et al. · 1995Myocardial effects of flavonoids from Crataegus species — animalView study →}. Unlike cardiac glycosides, the effect is described as improving the availability and utilisation of energy in the myocardium rather than acting directly on contractile fibres. The active constituents implicated include vitexin-2″-O-rhamnoside, ursolic acid, and crataegolic acid.

Gap: entirely animal and in-vitro; there is no isolated human study of hawthorn’s inotropic effect, and it is inferred within the broader heart-failure trials rather than measured directly.

Oligomeric procyanidins from Crataegus evoke endothelium-dependent vasorelaxation in isolated rat aorta ^{14Reference 14Kim et al. · 2000AnimalProcyanidins in crataegus extract evoke endothelium-dependent vasorelaxation in rat aorta — animalView study →}, consistent with the eNOS mechanism above, and older work reported improved coronary blood flow after oral dosing in dogs. The effect is attributed to the procyanidins together with flavonoids and triterpene acids acting on nitric-oxide release and, in some assays, angiotensin-converting-enzyme inhibition.

Gap: the coronary-flow data are animal and decades old; no human coronary imaging or flow-reserve study has tested hawthorn.

Preclinical models support an antiarrhythmic effect: Crataegus oxyacantha extract protected against reperfusion arrhythmias after global no-flow ischaemia in isolated rat heart ^{19Reference 19Al Makdessi et al. · 1999AnimalProtective effect of Crataegus oxyacantha against reperfusion arrhythmias after global no-flow ischemia in the rat heart — animalView study →}, and the contractile/energy effects on cardiomyocytes are consistent with a stabilising influence on the ischaemic myocardium ^{16Reference 16Pöpping et al. · 1995AnimalEffect of a hawthorn extract on contraction and energy turnover of isolated rat cardiomyocytes — animalView study →}. The only human hint is the SPICE subgroup in which sudden cardiac death trended lower with WS 1442 in patients with LVEF ≥25% — a secondary, non-primary finding ^{3Reference 3Holubarsch et al. · 2008RCTThe efficacy and safety of Crataegus extract WS 1442 in patients with heart failure: the SPICE trial — randomised controlled trialView study →}.

Gap: no dedicated human antiarrhythmic trial exists; the mechanism is rat-model and the human signal is a post-hoc subgroup.

In a rat model of prolonged coronary ischaemia and reperfusion, WS 1442 improved cardiac function and reduced infarct size ^{18Reference 18Veveris et al. · 2004AnimalCrataegus special extract WS 1442 improves cardiac function and reduces infarct size in a rat model of prolonged coronary ischemia and reperfusion — animal modelView study →}, and a related model showed protection against reperfusion arrhythmias ^{19Reference 19Al Makdessi et al. · 1999AnimalProtective effect of Crataegus oxyacantha against reperfusion arrhythmias after global no-flow ischemia in the rat heart — animalView study →}. These findings underpin the traditional use of hawthorn after myocardial injury but have not moved into humans.

Gap: rodent ischaemia–reperfusion models only; no human infarct or post-MI outcome data.

The human lipid evidence is weak. A randomised, double-blind trial in 49 diabetic patients with chronic coronary disease already on statins found that Crataegus laevigata (400 mg three times daily for 6 months) lowered LDL and non-HDL cholesterol within the treatment group and reduced neutrophil elastase, but the between-group differences did not reach significance ^{20Reference 20Dalli et al. · 2011RCTCrataegus laevigata decreases neutrophil elastase and has hypolipidemic effect: a randomized, double-blind, placebo-controlled trialView study →}. A 2024 RCT reported reductions in body fat and triglycerides — but with a Crataegus-plus-Citrus combination product, not a hawthorn monopreparation ^{22Reference 22Song et al. · 2024RCTEfficacy of a Crataegus extract mixture on body fat and lipid profiles in overweight adults: a 12-week randomized, double-blind, placebo-controlled trialView study →}.

Gap: the monopreparation effect is a non-significant within-group trend; the clearer result comes from a combination product and cannot be attributed to hawthorn alone.

Hawthorn appears in anxiety trials only as one ingredient in fixed combinations. A double-blind RCT of 264 patients with mild-to-moderate generalised anxiety found a preparation of Crataegus oxyacantha plus Eschscholtzia californica (californian poppy) and magnesium outperformed placebo on the Hamilton anxiety scale ^{21Reference 21Hanus et al. · 2004RCTDouble-blind, randomised, placebo-controlled study of a fixed combination of Crataegus oxyacantha and Eschscholtzia californica with magnesium in mild-to-moderate anxiety disordersView study →}, and the hawthorn hypertension pilot noted an incidental trend toward reduced anxiety ^{8Reference 8Walker et al. · 2002RCTPromising hypotensive effect of hawthorn extract: a randomized double-blind pilot study of mild, essential hypertensionView study →}.

Gap: every positive result is a combination product; no trial has tested hawthorn alone for anxiety, so the effect cannot be attributed to the herb.

Hawthorn is well tolerated: a systematic review of 24 clinical studies (5,577 patients evaluated) found adverse events were generally mild and transient — most commonly dizziness/vertigo, gastrointestinal complaints, headache and palpitations — with only a small number of severe events, all in trials of the LI 132 extract ^{9Reference 9Daniele et al. · 2006Systematic reviewAdverse-event profile of Crataegus spp.: a systematic reviewView study →}. The most important caution is in heart failure: while older adjunctive trials showed symptomatic benefit, a controlled trial in patients on modern therapy found no functional benefit and more adverse events in the hawthorn arm, and a separate trial from the same team reported increased early heart-failure progression ^{4,5Reference 4Zick et al. · 2009RCTHawthorn Extract Randomized Blinded Chronic Heart Failure (HERB CHF) trial — randomised controlled trialView study →Reference 5Zick et al. · 2008RCTThe effect of Crataegus oxycantha special extract WS 1442 on clinical progression in patients with mild to moderate heart failure — randomised controlled trialView study →} — so hawthorn should not be self-prescribed as a substitute for guideline-directed heart-failure treatment. A dedicated pharmacokinetic RCT found hawthorn (WS 1442 450 mg twice daily) did not significantly alter digoxin levels, suggesting the two can be co-administered without a major interaction, though monitoring remains prudent given hawthorn’s own cardioactivity ^{10Reference 10Tankanow et al. · 2003RCTInteraction study between digoxin and a preparation of hawthorn (Crataegus oxyacantha) — randomised controlled trialView study →}. Additive effects with cardiac glycosides, antihypertensives and other cardiovascular drugs are theoretically plausible and warrant supervision.

Scope note: a dedicated RCT assessed the digoxin pharmacokinetic interaction ^{10Reference 10Tankanow et al. · 2003RCTInteraction study between digoxin and a preparation of hawthorn (Crataegus oxyacantha) — randomised controlled trialView study →}; additive pharmacodynamic effects with cardiac glycosides, beta-blockers and antihypertensives are plausible but have not been formally quantified, and no CYP450 interaction study was identified. Pregnancy and lactation have not been assessed (see below).