Cannabis Use and Blood Pressure Levels: United States National Health Blood pressure was determined by an average of up to four .. Cannabis, Ischemic Stroke, and Transient Ischemic Attack: A Case-Control Study. The text will follow the three phases of anandamide on blood pressure, and we . extreme physical alterations (e.g. low pH value or high temperature) but also. 6 days ago The scientific debate has been going on for years whether marijuana has an effect on the cardiovascular system. Marijuana CBD and blood.
Lower Levels Pressure Cannabinoids Normal Blood to
Pulse pressure mmHg was calculated as the numeric difference between the systolic and diastolic blood pressure [ 17 ]. Subsequent models were controlled for ethnic self-identification ESI: Our first step involves assessing the distributions of the variables of interest and examining outliers. We ran linear regression models to estimate the differences in systolic and diastolic blood pressure mmHg by cannabis use status.
To further ensure that the association was parallel for subgroups, we performed subgroup analyses by ESI, education, BMI, alcohol and smoking categories. Standard errors were estimated using the Taylor series linearization method. Compared to never users, recently active cannabis users were younger, and more likely to be males, non-Hispanic Whites with income below the federal poverty threshold.
Recently active cannabis users also were more likely to be recently active tobacco and alcohol users Table 1. The main estimates of the study are presented in Table 2. We found no appreciable variations among subgroups of ESI, education, tobacco cigarette smoking, alcohol drinking, or BMI. There was no association between former cannabis use and systolic blood pressure levels. There was no association between cannabis use both recent and former and diastolic blood pressure.
Our results did not change when excluding those who reported current use of antihypertensive medications. Table 3 displays the association of cannabis use frequency and blood pressure levels. Number of days of cannabis use in the 30 days prior to the interview was associated with increased systolic blood pressure in the age-sex as well as the covariate-adjusted models.
There was no association between days of cannabis use and diastolic blood pressure levels. Table 4 presents the association of cannabis use and prehypertension, high pulse pressure, isolated systolic hypertension and hypertension. There was no association between cannabis use and hypertension or prehypertension. The main findings of this study may be summarized succinctly as follows. First, we detected a modest association between recent cannabis use and increased systolic blood pressure.
No association was detected between cannabis use and diastolic blood pressure levels. A statistically robust positive association between recent cannabis use and high pulse pressure was detected, whereas no association was detected between cannabis use and hypertension or prehypertension. No association was detected between lifetime history of cannabis use and blood pressure levels.
Before detailed discussion of these results, several of the more important study limitations merit attention, of most important is the cross sectional nature of NHANES which constrains causal or temporal inferences. Cannabis use was self-reported and was not ascertained by drug testing. The overall congruence between self-report and urinalysis was There were no data on the route of administration of cannabis smoking vs. To account for that we averaged blood pressure levels on up to four readings.
There was no data on the frequency of cannabis use beyond the 30 days prior to the interview and hence it is difficult to distinguish whether the association of cannabis use and blood pressure is of a short term or of a chronic nature. Despite limitations such as these, the study findings are of interest because of the NHANES standardized data collection approaches, and the ability to adjust for potential confounders.
The current study included a relatively larger nationally representative multiethnic sample of US adults which may enable us to detect differences. Cardiovascular disease is the leading cause of death both globally and in the US [ 19 ]. Previous studies have linked cannabis use to myocardial infarction, angina, and stroke [ 20 — 22 ]. However, the association between cannabis use and cardiovascular disease is not always consistent [ 6 ]. Although both systolic and diastolic blood pressure levels correlate significantly with cardiovascular morbidity and mortality, recent studies have suggested that systolic blood pressure is more strongly correlated than diastolic blood pressure [ 23 , 24 ].
The results of this study indicate a modest association between recently active cannabis use and increased systolic blood pressure which is consistent with pre-clinical studies indicating an acute increase in blood pressure after cannabis use [ 1 ].
The current study cannot elucidate if cannabis use is associated with chronic elevation in blood pressure. We did not detect an association between cannabis use and hypertension. There is a possibility that cannabis users who were diagnosed with hypertension were advised to stop cannabis use. However, lifetime history of cannabis use was not associated with hypertension in the current study.
The use of non-steroidal anti-inflammatory drugs NSAIDs is associated with increase in blood pressure [ 25 ]. In a sensitively analysis excluding those who reported NSAIDs use in the past 30 days, our results did not change. We detected a modest association between recent cannabis use and increased pulse pressure.
Increased pulse pressure may be a strong predictor of cardiovascular disease [ 26 ]. A strong association between increased systolic blood pressure, increased pulse pressure, increased arterial stiffness and the prevalence of cardiovascular disease was detected [ 27 ]. Aging is a major risk factor for arterial stiffness and increased pulse pressure [ 23 ]. A variety of CBD and hemp oils, lotions, and balms are available to purchase online.
You should always purchase from a reputable supplier and check with a doctor first to ensure these products are safe for you to use. You should also check that the product is legal in your state. Products that contain only CBD are non-psychoactive. Those with THC may have psychoactive effects. Before obtaining or using marijuana for any purpose, people should check if it is legal in their state.
It is also best for an individual to ask a doctor's advice to ensure that they can safely use marijuana or any other complementary therapy or supplement. Medicinal marijuana is a complementary therapy. It is vital to follow the treatment regime for your condition alongside supplemental therapies and not to replace them.
There have been studies that showed how the whole plant was more effective than the single-molecule compounds of one CBD or another. There is some theory that the different parts of the plant work together to boost effectiveness, without increasing dose or side effects.
I think more research will come but, currently, the whole plant is still illegal in many places so using only one component of the plant might be your only legal choice. We picked linked items based on the quality of products, and list the pros and cons of each to help you determine which will work best for you. We partner with some of the companies that sell these products, which means Healthline UK and our partners may receive a portion of revenues if you make a purchase using a link s above.
Article last updated by Yvette Brazier on Thu 9 August Visit our Diabetes category page for the latest news on this subject, or sign up to our newsletter to receive the latest updates on Diabetes. All references are available in the References tab. Laws, fees, and possession limits. Cannabidiol CBD and its analogs: A review of their effects on inflammation [Abstract]. CBD compound in cannabis could treat diabetes, researchers suggest.
Diabetes Part IV — Treatment with cannabis. Neuroprotective and blood-retinal barrier-preserving effects of cannabidiol in experimental diabetes [Abstract]. The American Journal of Pathology, 1 , — Facts about diabetic eye disease. Fact sheet — Sativex. FDA approves first drug comprised of an active ingredient derived from marijuana to treat rare, severe forms of epilepsy [Press release].
Overcoming the bell-shaped dose response of cannabidiol by using Cannabis extract enriched in cannabidiol. Efficacy and safety of cannabidiol and tetrahydrocannabivarin on glycemic and lipid parameters in patients with type 2 diabetes: A randomized, double-blind, placebo-controlled, parallel group pilot study.
Diabetes Care, 39 10 , — Obesity and cannabis use: Results from 2 representative national surveys. American Journal of Epidemiology, 8 , — Metabolic effects of chronic cannabis smoking. Diabetes Care, 36 8 , — The impact of marijuana use on glucose, insulin, and insulin resistance among US adults. The American Journal of Medicine, 7 , — European Journal of Pain, 18 7 , 99— Efficacy of inhaled cannabis on painful diabetic neuropathy [Abstract].
The Journal of Pain, 16 7 , — Marijuana and the developing brain. What is medical marijuana? MNT is the registered trade mark of Healthline Media. Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a healthcare professional.
Privacy Terms Ad policy Careers. This page was printed from: The mechanism is poorly understood so far, but the involvement of CB 1 receptors was excluded. There is good evidence to suggest that there are peripheral and central components. CB 1 receptors leading to a direct negative inotropic effect and other mechanisms may contribute.
The reason why the cardiovascular effects in anaesthetized and conscious animals are described in separate sections is that there are very marked differences.
The most prominent effect in anaesthetized rodents is a prolonged hypotension, whereas in conscious rodents, a pressor response prevails. How can we explain this discrepancy? The most obvious reason is the direct influence of anaesthetic agents on components of the endocannabinoid system.
Thus, urethane, but not pentobarbitone, attenuates presynaptic CB 1 receptor function Kurz et al. On the other hand, pentobarbitone, but not urethane, inhibits the pressor effect of AEA Kwolek et al. In addition, anaesthesia per se affects the resting sympathetic tone, which is higher under the influence of urethane than in unstressed conscious rats Carruba et al. It has already been mentioned that phase III is related to the inhibition of the sympathetic tone.
Moreover, the complex haemodynamic effects of AEA, that is two hypotensive responses separated by a hypertensive one, causes that a factor that reduces the fall in BP e. An initial bradycardia, hypotension and hindquarters vasoconstriction were also observed in response to AEA, especially its higher doses phase I ; however, unlike in anaesthetized rats, none of the five cannabinoids led to a prolonged hypotension phase III.
The authors concluded that either there is no TRPV1 receptor involvement in the cardiovascular actions of AEA, or that the dose of capsazepine was inadequate under the conditions of their experiment. Rimonabant slightly increased and prolonged the pressor effect of AEA Lake et al.
Another CB 1 receptor antagonist, AM, failed to affect the increase in BP and all vasoconstrictor responses induced by i. AEA injection Gardiner et al. The actions of WIN were also abolished by the ganglion blocking agent pentolinium pointing to sympathoexcitation as the underlying mechanism Gardiner et al. It has been also demonstrated that none of the cardiovascular effects of AEA was modified by the serotonin 5-HT 3 receptor antagonist azasetron Gardiner et al.
In contrast to the i. The depressor effects were connected with vasodilatation in the renal, mesenteric and hindquarters vascular beds Ho and Gardiner, Taken together, the data suggest that in conscious rodents phase I involves TRPV1 receptors although final proof is missing , phase II central CB 1 receptors this mechanism is agonist-specific and is not valid for AEA and phase III occurring in animals with an elevated blood pressure only peripheral CB 1 receptors.
In addition, non-CB 1 receptor-mediated mechanisms may be involved in the cardiovascular effects of AEA both in normotensive and in acutely hypertensive rats since CB 1 receptor antagonists failed to block cardiovascular effects of this agonist see above, Gardiner et al. Locations of the central CB 1 receptors leading to an increase in blood pressure have been examined in a series of studies in which cannabinoids have been administered topically to sites within the brain; these results will be discussed in the next few paragraphs.
Almost all experiments in which cannabinoids were applied centrally support the hypothesis that central mechanisms contribute to phase II Figure 3 , Table 1.
In the study by Niederhoffer and Szabo , cannabinoids have been administered into the cisterna magna i. Since the same pattern of changes has also been found in response to WIN in urethane-anaesthetized rats Pfitzer et al.
However, the above effects were accompanied by decreases in the respiratory rate and minute volume and all changes were sensitive to CB 1 receptor blockade. Thus, Pfitzer et al. A key centre in the CNS responsible for the tonical pressor activity of the sympathetic nerve fibres is the rostral ventrolateral medulla RVLM Figure 3.
The brief pressor response to AEA i. Sympathoexcitation can also result from the activation of the periaqueductal gray PAG Figure 3 , a mesencephalic region that has been proposed to play a role in specific cardiovascular changes associated with different emotional behaviours observed during the defense reaction. In anaesthetized rats Niederhoffer et al. It is suggested that an acute increase in BP leads to the activation of presynaptic CB 1 receptors that alter the release of GABA and hence prolong the baroreflex-related sympathoinhibition for detailed discussion, see Brozoski et al.
At the end of this section, two cannabinoids that have so far not been mentioned in this review will be discussed for their chemical structure, see Figure 1. By contrast, NADA i.
The mechanisms involved in the three phases have been disclosed only partially. No information is available with respect to the mechanism underlying the tachycardia in phase III. In summary, when comparing the data obtained on anaesthetized and conscious animals, phase I does not differ markedly. The reason why these receptors do not come into play in anaesthetized rats is so far unclear.
There is good evidence that this phase is unmasked only when the sympathetic tone is high; anaesthesia is a situation under which a high sympathetic tone occurs. Cannabinoids exhibit cardiovascular effects also in humans. Many components of the endocannabinoid system have also been shown in human tissues but only in few cases their function under in vitro conditions has been demonstrated Table 2.
It may be accompanied by a modest increase in BP particularly when supine and an increase in cardiac output. A review of almost articles describing almost different tests demonstrated that an increase in HR was the most consistent result, and almost all studies with the measurement of this parameter proved statistically significant.
Thus, an increase in HR is even believed to be a useful cannabinoid biomarker Zuurman et al. Tolerance to the acute cardiovascular effects of marijuana smoking develops over several days to a few weeks, but it is rapidly lost when cannabinoid administration is stopped Benowitz and Jones, In a study on male cannabis users, the tachycardia was markedly attenuated by orally administered rimonabant Huestis et al.
Additional studies suggest that the tachycardia may be related to an increased sympathetic activity connected with catecholamine release and decreased parasympathetic autonomic activity. However, the immediate tachycardia was not accompanied by an increase in noradrenaline levels, which increased 30 min after marijuana exposure only and remained elevated for at least 2 h Gash et al.
Under such conditions, the tachycardia might be related to the CB 1 receptor-mediated inhibition of acetylcholine release from the parasympathetic nerves innervating the heart Figure 3. A second cardiovascular effect associated with marijuana smoking is orthostatic hypotension. The hypotension was greater and longer lasting in hypertensive compared with normotensive volunteers Crawford and Merritt, It may occur as a result of decreased vascular resistance e. Jones, ; Sidney, ; Mathew et al.
Chronic use of cannabis may elicit a long-lasting decrease in HR and BP. However, unlike in humans, both phenomena occurred in combination. Severe acute cardiovascular events may be associated with marijuana as described by some clinical reports. Thus, a decrease in the exercise time to angina, cardiac arrhythmias, ventricular tachycardia, palpitations or atrial fibrillation have been noticed Caldicott et al. Moreover, it caused a 4.
Marijuana use was also associated with a threefold greater mortality after myocardial infarction Mukamal et al. However, the exact aetiopathology of these changes still remains to be established. The following mechanisms are proposed: Transient vasospasm is suggested as a cause for stroke Caldicott et al.
The well-known reduction in cerebral blood flow may contribute as well. They frequently lead to a tachycardia sometimes associated with a modest increase in blood pressure. Rarely, they lead to decrease in blood pressure. There are two major differences with respect to animals. First, the two alterations do not occur in combination. Second, the stimulation of the cardiovascular system primarily involves an increase in heart rate rather than in blood pressure.
There are, however, also remarkable similarities to the situation in conscious animals. In some instances, presynaptic inhibitory CB 1 receptors on the parasympathetic nerve fibres supplying the heart decelerator nerves may be involved. Like in animals, this phase is more marked under hypertension. National Center for Biotechnology Information , U. Journal List Br J Pharmacol v. Author information Article notes Copyright and License information Disclaimer.
This article has been cited by other articles in PMC. Abstract The cannabinoids comprise three major classes of substances, including compounds derived from the cannabis plant e. Introduction Cannabis preparations have been used for recreational and therapeutic purposes for thousands of years, but details of the mechanisms of action have been disclosed during the recent 20 years only.
Open in a separate window. Influence of cannabinoids on cardiovascular parameters in anaesthetized animals In rats anaesthetized with urethane Varga et al. Table 1 Influence of cannabinoids on selected parameters of the animal cardiovascular system. Phase I The first phase of cardiovascular changes induced by AEA in anaesthetized rodents is mainly a short-lasting bradycardia and hypotension. Table 2 Occurrence of components of the endocannabinoid system in human cardiovascular tissues 1.
Aortic smooth muscle and umbilical vein endothelial cells Sugiura et al. Left ventricular myocardium Weis et al. Hepatic artery Liu et al. Coronary artery smooth muscle cells Rajesh et al. Cerebromicrovascular endothelial cells Golech et al. Influence of cannabinoids on cardiovascular parameters in conscious animals The reason why the cardiovascular effects in anaesthetized and conscious animals are described in separate sections is that there are very marked differences.
Influence of cannabinoids on cardiovascular parameters in humans Cannabinoids exhibit cardiovascular effects also in humans. Conflicts of interest None.
J Pharmacol Exp Ther. Cannabidiol injected into the bed nucleus of the stria terminalis modulates baroreflex activity through 5-HT 1A receptors. Marijuana as a trigger of cardiovascular events: Endocannabinoids and cardiac contractile function: Endocannabinoids acting at cannabinoid-1 receptors regulate cardiovascular function in hypertension. Cardiovascular and metabolic considerations in prolonged cannabinoid administration in man.
Pharmacological evidence for anandamide amidase in human cardiac and vascular tissues. Cannabinoids acting on CB 1 receptors decrease contractile performance in human atrial muscle. Differential endocannabinoid regulation of baroreflex-evked sympathoinhibition in normotensive versus hypertensive rats. Keep off the grass:
Can marijuana help people with diabetes?
Does cannabis lower blood pressure? Anecdotally, many people report that cannabis helps them maintain healthy blood pressure levels, an. Many need to know can marijuana lower blood pressure. Heart rate will come back to normal in the minutes after the stimulus; Need to Pass a Drug Test?. Cannabinoids exert different effects on blood pressure depending on the United Kingdom, and colleagues randomly assigned 9 healthy men.