7 There are very few known effects of essential oils on the heart, except when taken in overdose. Cardiovascular consequences of human poisoning from various essential oils include irregular heartbeat (tansy), rapid heartbeat (wintergreen), cardiovascular collapse (eucalyptus) and congestive heart failure (wormwood) (Eimas 1938; Gurr & Scroggie 1965; Grieve 1978; Weisbord et al 1997). Damage to the heart has been seen after fatal doses of wintergreen and wormseed oils (Eimas 1938; Opdyke 1976 p. 713–715). Heart activity is dependent upon the movement of calcium ions into myocardial cells, and substances that inhibit this influx, the so-called calcium channel blockers, have a depressant effect on the heart. They act on slow calcium channels to reduce contractility and electrical conduction in the heart. They also act on vascular smooth muscle to reduce vascular tone (see Calcium channel blockade below). Bisabolol, carvacrol, β-caryophyllene oxide, eugenol, (+)-carvone, (−)-menthol, thymol and possibly (E)-anethole, block calcium channels in cardiovascular cell membranes (Schafer et al 1986; Teuscher et al 1989; Sidell et al 1990; Sensch et al 2000; Damiani et al 2004; Magyar et al 2004). The same effect has been observed with peppermint oil (Hills & Aaronson 1991). In addition, β-caryophyllene oxide strongly inhibited potassium ion fluxes, while eugenol exerted a smaller effect (Sensch et al 2000). Thujone had a depressant action on the isolated rabbit heart, affecting both systole and diastole. A preliminary fall in pressure was followed by a rise, and these were explained in terms of a direct action on heart muscle, and an action on the vasomotor center, respectively (Florey and Student, 1968). A depressant effect on dog heart has been observed following the iv administration of 1–2 mL per kg doses of a “saturated solution” of sage oil in 33° alcohol (equivalent to 18.9% v/v ethanol) (Caujolle & Franck 1945a). Geraniol, thymol and (−)-carvone all had a depressant action on frog heart function, when a 10% aqueous emulsion was injected into the femoral lymphatic sac, e.g., geraniol has an effect at 180 mg/kg or higher, but not at 90 mg/kg (Lysenko 1962). These findings imply that only high doses of these constituents affect the heart. Camphor produced a rise in heart rate in isolated rabbit heart, via a direct effect on heart muscle (Christensen and Lynch 1937). In humans, the predominant effect on the heart appears to be depressant. However, one report suggests that camphor can sensitize the heart to epinephrine (adrenaline) (Saratikov et al 1957). The only known negative effects from essential oils in moderate doses apply to menthol and peppermint. Mentholated cigarettes and peppermint confectionery have been linked to cardiac fibrillation in patients prone to the condition while being maintained on quinidine, a stabilizer of heart rhythm (Thomas JG 1962). This might be explained by an interaction between menthol and quinidine, but no precedent for this could be found. Bradycardia (slowing of heartbeat) has been reported in an individual addicted to menthol cigarettes (Luke 1962). Menthol-rich oils (cornmint and peppermint) should probably be avoided altogether in cases of cardiac fibrillation. There is an ongoing debate about the relationship between BP and cardiovascular disease. It is now thought that the risk of cardiovascular disease begins when systolic and diastolic pressures are 115 and 75 mmHg, respectively, and that this doubles with each increment of 20 and 10 mmHg, respectively. It has also been suggested that individuals with systolic and diastolic readings of 120–139 and/or 80–89 mmHg, respectively, should be classified as prehypertensive, and may need to adopt health-promoting lifestyle changes (Chobanian et al 2003). Any excessively elevated or prolonged increase in BP (hypertension) is undesirable because it increases the work of the heart and can lead to irreversible changes to organs including the blood vessels, heart, kidneys and brain. The most common form of hypertension (in 90–95% of cases) is known as ‘primary’ or ‘essential’ hypertension, where no single causal factor can be identified. Rather, a number of predisposing or risk factors are likely to be present, including smoking, excessive drinking of alcohol, a stressful life, poor diet and lack of exercise. Some people have a genetic predisposition to hypertension (Coy 2005; Imumorin et al 2005). Temporary fluctuations in BP are normal and harmless in a healthy individual. They may be due to a variety of factors such as psychosocial demands or changes in physical activity. It should be stressed that psychological factors can play a role in raising or lowering BP (Whyte 1983; Linden & Moseley 2006). Substance use can also lead to the elevation of BP, salt and caffeine being two examples. In a hypertensive individual, though small fluctuations may not be harmful, regular, moderate increases can be damaging. The essential oils most commonly cited in aromatherapy texts as being contraindicated in hypertension are hyssop, thyme, rosemary and sage (Table 7.1). Similar advice is repeated in other books and on many websites, but very little supporting evidence could be found in the scientific literature. The original source for this information appears to be Valnet (1990), first published in French in 1964. In this text, the four essential oils are claimed to be hypertensive, and in each case two references are given. One is Caujolle & Franck (1944b), but this is a mistake since this paper concerns lavender, lavandin and spike lavender oils only. The other reference is a thesis by R. Cazal, published in 1944. We were not able to locate a copy of this. Data on these and other essential oils are outlined below. Table 7.1 Essential oils reputed to raise blood pressure in aromatherapy texts Valnet 1964 p. 220, 260, 272, 288; Tisserand 1977 p. 201–204; Franchomme & Pénöel 1990 p. 374; Battaglia 1997 p. 295; Davis P 1999 p. 153; Pitman 2004 p. 343. There is a complex relationship between convulsants and BP (Freeman 2006). Intracranial hypertension can lower the seizure threshold, and for example in eclampsia, both hypertension and seizures are seen. In a report of nine distressed neonates whose BP was continuously recorded, three had generalized seizures, during which mean aortic pressure increased dramatically (Lou & Friis-Hansen 1979). However, a sudden drop in BP can also precipitate seizures (Agrawal & Durity 2006). When injected iv in convulsant doses, both wormwood oil and hyssop oil produce a sudden drop, then rise in BP, the convulsions coinciding with BP elevation. After apparently extensive testing in cats, Coombs & Pike (1931) concluded that ‘oil of absinthe’ (wormwood oil) produced a hypotension that initiated the seizures, and that the muscular contraction of the seizures caused the spike in hypertension. BP dropped below baseline after a seizure, and did not rise until the next seizure took place. In some instances, doses below the convulsive threshold caused a fall in BP that was so precipitous it was fatal. The type of wormwood oil used in this study is not stated, but the commercially available oil was the β-thujone CT (Parry 1922 p. 288; Guenther 1949–1952 vol 5 p. 494; Arctander 1960 p. 661–663). The wormwood oil was diluted to 5% v/v in 95% ethanol, and the minimum convulsive dose was 0.08 mL/kg bw of the solution, so 0.004 mL/kg (3.6 mg/kg) for the oil. Clonic convulsions were produced, with tonic limb extension appearing at just under a lethal dose (Pike et al 1929). Similarly, injecting dogs iv with 1–2 mL of a ‘saturated solution’ of hyssop oil in 33° alcohol resulted in an initial fall in BP, followed by a rise, accompanied by clonic convulsions, both lasting 3–4 minutes (Caujolle & Franck 1945b). The convulsant constituents of wormwood oil and hyssop oil are the thujones and pinocamphones, respectively. In cats, camphor caused an initial fall in BP lasting 2–10 minutes, followed by a rise of 8–30 mmHg above normal and lasting for up to 30 minutes, when given intravenously at only 5 mg/kg (Christensen & Lynch 1937). Considering that this was a sub-convulsant dose, the longer hypertensive phase is interesting. However, whether camphor is hypotensive or hypertensive has been debated for more than a century. Topically applied camphor is likely to cause local vasodilation (Futami 1984). Sage oil, which can cause convulsions, contains varying amounts of camphor and 1,8-cineole though camphor usually predominates. When ~ 1 g/kg of alcohol saturated with sage oil was given iv to dogs there was no increase in BP, and in some cases a slight fall was observed (Caujolle & Franck 1945a). An intravenously administered aqueous-alcoholic extract of sage caused a moderate but prolonged hypotensive effect in cats (Todorov et al 1984). In early 20th century reports, benzyl alcohol apparently caused hypotension and convulsions in experimental animals (MMWR 1982). In low birth weight infants exposed to benzyl alcohol, toxic symptoms included respiratory distress and hypotension (Benda et al 1986; Sreenan et al 2001). Many infants also had central neural depression or seizures (Anon 1982). One proven way of lowering BP is to reduce the flow of calcium ions into heart and vascular muscle using calcium channel blockers. Apart from relaxing the heart, these drugs also reduce the tone of the arteries and arterioles, thereby decreasing the resistance to blood being pumped by the heart. Peppermint oil and its major constituent (–)-menthol both have calcium channel blocking actions. This explains why (–)-menthol dilates systemic blood vessels after iv administration, and why peppermint oil reduces smooth muscle spasm in the gut (Rakieten & Rakieten 1957; Grigoleit & Grigoleit 2005b; Hawthorn et al 1988; Hills & Aaronson 1991). A hypotensive action has been reported for thyme oil in a Russian paper (Kulieva 1980). This is consistent with the calcium channel blocking actions of its major constituents thymol and carvacrol (Magyar et al 2004), and the hypotensive action of carvacrol (Aydin et al 2007) and of topically applied thymol (Futami 1984). We could find no information on peppermint oil and BP, but topically applied menthol reduces blood pressure for a short time through an effect on local tissues (Futami 1984; Ragan et al 2004), and the calcium channel blocking effect of both peppermint oil and menthol (cited above, under The heart) makes a hypertensive action unlikely. In mice, cinnamon bark oil caused variable changes in BP after ip dosing at 100 mg/kg (Powers et al 1961). Cinnamaldehyde was hypotensive when administered to anesthetized dogs at 5–10 mg/kg iv. In guinea pigs, a lower dose of 1 mg/kg iv caused a small fall in BP. The authors inferred that this action was mainly due to peripheral vasodilation mediated by calcium channel blockade, similar to that caused by papaverine (Harada & Yano 1975). In a recent study, a range of 1 μM to 1 mM of cinnamaldehyde dose-dependently relaxed prostaglandin F2α, norepinephrine and KCl-stimulated rat aorta. It was suggested that a combination of endothelium-dependent and -independent effects were responsible. One of the latter mechanisms is thought to involve the blocking of calcium channels (Yanaga et al 2006). Other essential oil constituents with hypotensive actions caused by direct vasodilation include, in order of decreasing potency, linalool, citronellol, nerol, geraniol, α-terpineol and 1,8-cineole. These compounds caused a 25% fall in systolic pressure, in doses from 9.2–26.3 mg/kg, when administered iv to dogs in an emulsion (Northover & Verghese 1962). Intravenous 1,8-cineole was dose-dependently hypotensive in normotensive rats at 0.3–10 mg/kg, and decreased heart rate at the highest dose (Lahlou et al 2002a). Soares MC et al (2005) reported that 1,8-cineole probably has a calcium channel blocking action. Spike lavender oil (28.0–34.9% 1,8-cineole) injected iv in dogs resulted in a slight reduction in BP, followed by a rapid return to normal (Caujolle & Franck 1944b). The essential oil of Hyptis fruticosa was hypotensive in normotensive rats at 5–40 mg/kg iv, and caused concentration-dependent relaxation of phenylephrine-stimulated isolated rat superior mesenteric artery at 1–1000 μg/mL (Santos et al 2007). Although this oil is not commercially available, it is interesting to note that it contains 16.8% 1,8-cineole, as well as 12.3% bicyclogermacrene and 11.3% α-pinene (Menezes et al 2007). The action of eucalyptus oil will undoubtedly reflect that of 1,8-cineole. Single iv injections of eugenol (1–10 mg/kg) elicited immediate and dose-dependent hypotension in rats (Lahlou et al 2004), and similar results were found for eugenol-rich Ocimum gratissimum leaf oil when given to hypertensive rats (Interaminense et al 2005). Intravenous administration of either 1–20 mg/kg of Alpinia zerumbet leaf oil (~ 40% terpinen-4-ol) or 1–10 mg/kg of terpinen-4-ol, elicited dose-dependent decreases in mean aortic pressure in rats (Lahlou et al 2002b). The hypotension induced by 1,8-cineole, eugenol or tepinen-4-ol appears to be due to direct vascular relaxation, rather than by affecting sympathetic tone. Northover & Verghese (1962) reached the same conclusion. Both geranium and lavender oils lowered BP in dogs when administered iv in a ‘saturated alcoholic solution’ at 1–2 g/kg (Clerc et al 1934). Similarly, an aqueous suspension of carrot seed oil, injected iv into dogs, produced dose-dependent falls in BP (Bhargava et al 1967). Taget oil was hypotensive in dogs, reducing BP by up to 50% for 45 minutes after an iv dose of 50 mg/kg (Chandhoke & Ghatak 1969). Essential oils of angelica (type unspecified), calamus, zedoary and tomar seed each caused a transient fall in BP and heart rate when injected iv into dogs at 0.01–0.05 mL/kg (Chopra et al 1954). Intravenous doses of 0.2–1.6 mg/kg black seed oil dose-dependently decreased arterial BP in rats (El Tahir et al 1993). This action is in part due to the main constituent, thymoquinone, which counteracted induced increases in systolic BP in rats when given orally at 0.5 or 1 mg/kg/day (Khattab & Nagi 2007). In cats, β-eudesmol at 10 mg/kg iv precipitated a hypotensive response of 50–69% that lasted for 5–6 hours, but at a dose of 5 mg/kg iv, there was no effect (Arora et al 1967). (+)-Limonene, which constitutes 16.4–24.4% of black pepper oil and 44.2% of white camphor oil, lowered monocrotaline-induced pulmonary hypertension in rats, when given orally at 400 mg/animal/day for up to 21 days (Touvay et al 1995). The farnesyltransferase inhibitory activity of limonene was suggested as being linked to this action. In a clinical study, 14 of 15 hypertensive patients who ingested 0.45 mL/day of geranium oil for two months showed significant improvement in their condition. They also showed a reduction in cortisol levels (Nozaki 2001). Two small-scale controlled trials showed preliminary clinical evidence for garlic oil having a hypotensive action. When taken in capsules at 18 mg/day for four weeks by normotensive volunteers, the oil reduced mean (presumably systolic) pressure from 94 mmHg to 88 mmHg, compared with a 2.3 mmHg mean reduction in the placebo group in a two period, cross-over trial with 10 volunteers per group. However, this ‘garlic oil’ was cold-pressed from fresh garlic (Barrie et al 1987). A second randomized-controlled trial in 27 normotensive trained male runners noted a mean drop of 4.5 mmHg in systolic pressure following daily ingestion of 2.3 mg steam-distilled garlic oil in capsules for 16 weeks (Zhang et al 2001). Temporary hypertension has been recorded following the inhalation of certain of essential oils. Grapefruit, fennel, black pepper or tarragon oil caused a slight increase of systolic BP in humans after being inhaled for either three or seven minutes (Haze et al 2002). It is feasible that these effects may have been due to psychological factors. Human inhalation of ylang-ylang oil caused a significant reduction in BP, which was thought to be psychologically mediated (Hongratanaworakit & Buchbauer 2004). After 10 minutes of inhaling cedrol, both systolic and diastolic pressures were reduced in healthy male and female Japanese volunteers due to a reduction in sympathetic and an increase in parasympathetic activity (Dayawansa et al 2003). Conversely, inhalation of grapefruit oil for 10 minutes raised BP in rats, due to the enhancement of sympathetic and the suppression of parasympathetic activity (Shen et al 2005, Tanida et al 2005). This appears to indicate a physiological effect. Inhalation of lavender oil by rats resulted in a fall in mean arterial BP, which is consistent with iv data cited above. The effect was thought to be autonomically mediated, and was eliminated following induced anosmia (Tanida et al 2006). However, 30 minutes of lavender oil inhalation by 30 healthy young men had no effect on BP, though other effects were seen (Shiina et al 2008). In the summary of an article published in Korean, once daily inhalation of a mixture of lavender, bergamot and ylang-ylang oils for four weeks was said to lower BP in patients with essential hypertension (Hwang 2006). Both psychological and pharmacological processes were determined to be responsible for increases in BP in humans following 30 minutes inhalation of (+)-limonene (systolic), (–)-limonene (systolic), (+)-carvone (diastolic), or (–)-carvone (systolic and diastolic) (Heuberger et al 2001). For example, fragrance-induced subjective ratings of increased alertness correlated significantly with increases in BP. However, these same compounds, when not administered by inhalation, may be hypotensive. In a human study that prevented inhalation, 1 mL of 20% sandalwood oil or α-santalol in peanut oil was applied to the abdominal skin of volunteers, resulting in a small but significant reduction in both systolic and diastolic pressures compared to control subjects. This was presumably due to a physiological effect resulting from transdermal absorption (Hongratanaworakit et al 2004). Intravenous administration leads to a direct action on the vascular system, which is primarily due to calcium channel antagonism (Lahlou et al 2005). In inhalation studies, the effects are autonomically mediated, and in humans, psychological factors may come into play. In both rats and humans, elevations of BP were seen in conditions that reflect those of intentional and fairly intensive essential oil inhalation. Since soft tissue massage reduces BP, the only potential risks seem to be either from overdoses of certain convulsant essential oils, and from intensive (as distinct from incidental) inhalation. Oral garlic oil is possibly the most likely to reliably reduce high BP, but there is no evidence that this would exacerbate an already established hypotension. The action of garlic oil is clearly not due to psychological factors nor, presumably, are the effects seen for other essential oils in animal studies. However, in those involving human inhalation, psychological factors are likely to play a part, and the effects are autonomically mediated. In contrast, iv administration leads to a direct action on the vascular system, which is primarily due to calcium channel antagonism (Lahlou et al 2005). A formulation containing fenugreek oil inhibited angiotensin-converting enzyme (ACE) in plasma and kidney when fed to male alloxan-diabetic rats. ACE inhibitors are now commonly used in the treatment of hypertension (Hamden et al 2011). The mode of administration can play a significant role in the resulting effect. For example, hypertension and convulsions can both be caused by acute methyl salicylate poisoning. However, topically applied methyl salicylate lowers BP through local effects (Futami 1984; Ichiyama et al 2002; Dawson et al 2004). We have already seen that in rats, (+)-limonene lowered BP on iv injection, but raised it on inhalation. Since different effects on BP seem to be possible from different methods of administration, those from inhalation or dermal absorption should not be assumed to reflect those of iv administration. There is no research that shows whether the use of single or blended essential oils can lead to a significant increase in BP during an aromatherapy massage, but this seems unlikely since soft tissue massage itself tends to reduce both systolic and diastolic pressure (Holland & Pokorny 2001; McNamara et al 2003; Aourell et al 2005).
The cardiovascular system
The heart
Heart rate and rhythm
Blood pressure
Animal and ex vivo studies
Convulsants
Calcium channel blockade
Undefined mechanisms
Human oral studies
Inhalation effects
Discussion
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