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Marijuana use triples risk of death from hypertension
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<blockquote data-quote="Nelson Vergel" data-source="post: 81525" data-attributes="member: 3"><p>Background :</p><p></p><p><span style="color: #000000">Acute cannabis administration has been shown to increase resting heart rate and blood pressure, and induce orthostatic hypotension (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R15" target="_blank">Jones, 2002</a>). Increased heart rate following acute cannabis exposure has been shown to be dose-related (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R13" target="_blank">Heishman et al., 1989</a>). Peak effects on heart rate appear to occur 10 to 15 minutes after smoking and result in an increase of 20 to 30 beats per minute, but mean increases as high as 43.5 beats per minute have been reported (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R8" target="_blank">Chait and Zacny, 1992</a>; <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R11" target="_blank">Galanter et al., 1972</a>; <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R13" target="_blank">Heishman et al., 1989</a>; <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R14" target="_blank">Ilan et al., 2005</a>). </span></p><p><span style="color: #000000"></span></p><p><span style="color: #000000">There are few studies in which the effects of smoked cannabis administration on blood pressure are reported. Supine blood pressure has been shown to increase following cannabis exposure (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R18" target="_blank">Mathew et al., 1993</a>), but blood pressure has also been shown to drop when participants move from a supine to standing position (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R19" target="_blank">Renault et al., 1974</a>). Insufficient published data are available to confidently report on the time course or typical magnitude of these effects, and it appears that orthostatic hypotension is reliably observed whereas an increase in supine blood pressure is not. Epidemiological studies and case reports have linked acute cannabis intoxication to myocardial infarction, angina, arrhythmias, transient ischemic attacks, and stroke (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R17" target="_blank">Karch, 2006</a>). However, associations between cannabis use and these cardiovascular events are not always consistent, case reports of these types of occurrences are rare, and controlled studies are generally lacking.</span></p><p><span style="color: #000000"></span></p><p><span style="color: #000000">Tolerance to the acute cardiovascular effects of cannabis develops rapidly with repeated exposure. In laboratory studies, the acute cardiovascular effects of delta-9-tetrahydrocannabinol (THC; the primary psychoactive component of cannabis) are attenuated with repeated administration, and have even been shown to result in a reduction of heart rate and blood pressure relative to baseline levels (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R3" target="_blank">Benowitz and Jones, 1975</a>; <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R2" target="_blank">Benowitz and Jones, 1981</a>). However, Jones (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R15" target="_blank">Jones, 2002</a>) recently pointed out that understanding of the cardiovascular effects of chronic cannabis use is limited by the fact that most human research has been of short duration, used relatively low doses of smoked cannabis or oral THC, and has largely excluded participants who are female, older, or exhibit symptoms of cardiovascular disease.</span></p><p><span style="color: #000000"></span></p><p><span style="color: #000000"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/" target="_blank">Source</a></span></p></blockquote><p></p>
[QUOTE="Nelson Vergel, post: 81525, member: 3"] Background : [COLOR=#000000][FONT='inherit']Acute cannabis administration has been shown to increase resting heart rate and blood pressure, and induce orthostatic hypotension ([URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R15"]Jones, 2002[/URL]). Increased heart rate following acute cannabis exposure has been shown to be dose-related ([URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R13"]Heishman et al., 1989[/URL]). Peak effects on heart rate appear to occur 10 to 15 minutes after smoking and result in an increase of 20 to 30 beats per minute, but mean increases as high as 43.5 beats per minute have been reported ([URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R8"]Chait and Zacny, 1992[/URL]; [URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R11"]Galanter et al., 1972[/URL]; [URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R13"]Heishman et al., 1989[/URL]; [URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R14"]Ilan et al., 2005[/URL]). There are few studies in which the effects of smoked cannabis administration on blood pressure are reported. Supine blood pressure has been shown to increase following cannabis exposure ([URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R18"]Mathew et al., 1993[/URL]), but blood pressure has also been shown to drop when participants move from a supine to standing position ([URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R19"]Renault et al., 1974[/URL]). Insufficient published data are available to confidently report on the time course or typical magnitude of these effects, and it appears that orthostatic hypotension is reliably observed whereas an increase in supine blood pressure is not. Epidemiological studies and case reports have linked acute cannabis intoxication to myocardial infarction, angina, arrhythmias, transient ischemic attacks, and stroke ([URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R17"]Karch, 2006[/URL]). However, associations between cannabis use and these cardiovascular events are not always consistent, case reports of these types of occurrences are rare, and controlled studies are generally lacking. [/FONT][/COLOR] [COLOR=#000000][FONT='inherit']Tolerance to the acute cardiovascular effects of cannabis develops rapidly with repeated exposure. In laboratory studies, the acute cardiovascular effects of delta-9-tetrahydrocannabinol (THC; the primary psychoactive component of cannabis) are attenuated with repeated administration, and have even been shown to result in a reduction of heart rate and blood pressure relative to baseline levels ([URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R3"]Benowitz and Jones, 1975[/URL]; [URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R2"]Benowitz and Jones, 1981[/URL]). However, Jones ([URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/#R15"]Jones, 2002[/URL]) recently pointed out that understanding of the cardiovascular effects of chronic cannabis use is limited by the fact that most human research has been of short duration, used relatively low doses of smoked cannabis or oral THC, and has largely excluded participants who are female, older, or exhibit symptoms of cardiovascular disease. [URL="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045206/"]Source[/URL][/FONT][/COLOR] [/QUOTE]
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Marijuana use triples risk of death from hypertension
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