The use of recreational amphetamine, popularly known as 'speed', 'ice', and 'ecstasy', may hasten the biological ageing of the heart, suggests Australian research. The effects were seen in both men and women, and irrespective of other potential risk factors for heart disease and stroke, the findings indicate.
Amphetamine is a stimulant, which sends the sympathetic nervous system and production of the "fight or flight "hormone adrenaline into overdrive. It is associated with cardiovascular system effects, including speeding up the heart rate, sharply increasing blood pressure, and boosting the risk of stroke, heart attack, and aneurysm rupture.
Prolonged stimulant use is reflected in premature ageing of the skin, and the researchers led by Albert Stuart Reece, at the School of Psychiatry and Clinical Neurosciences, University of Western Australia, wanted to know if amphetamine use might also prematurely age the heart.
They therefore measured the flow of blood through the brachial artery in the upper arm and the radial artery in the forearm of 713 people in their 30s and 40s, attending a clinic for substance misuse between 2006 and 2011. They did this to assess the degree of arterial stiffening; arteries harden as the body ages.
They used a normal blood pressure cuff for the upper arm and a non-invasive monitoring system, called the SphygmoCor, for the forearm. SphygomoCor’s software calculates the biological vascular age of an individual by matching the extent of arterial stiffening with chronological age, sex, and height.
Each patient was asked about their drug use, and placed into one of four groups: non-smokers (483); smokers (107); amphetamine users (55); and methadone (heroin substitute) users (68). Most (94%) of those in the amphetamine group had used within the previous week and nearly half had used just the day before, on the 66 occasions they were monitored with the SphygmoCor.
The results showed that of all four groups, the cardiovascular system of amphetamine users seemed to be ageing much faster than that of smokers and methadone users, both in terms of pure chronological age, and over time. These findings held true even after taking account of other known cardiovascular risk factors, such as weight, cholesterol levels, and an indicator of inflammation, C reactive protein.
This suggests that the heart itself is ageing faster than expected, say the researchers, who point out that amphetamine use is often protracted, repeated, and long term.
Many physiological processes in the body start to fail over the course of the lifespan as part of the normal ageing process, say the researchers. But on the basis of their findings, stimulant abuse seems to compound and accelerate this process, they suggest.
By way of a possible explanation for their findings, they point to previous research which has shown that amphetamines interfere with stem cell functioning – the cells involved in tissue repair and renewal – and normal cell division.
This is an observational study, so no firm conclusions can be drawn about cause and effect, added to which the number of amphetamine users was small, and there was no information on ‘dose.’
But the researchers conclude: “The implication from the present work is that recurrent habitual amphetamine abuse ages the cardiovasculature, and likely the whole organism generally. It is therefore conceivable that stimulant abusers do physiological and cardiovascular harm.”
It’s not clear if this damage is reversible either, they add, suggesting that their findings add even greater impetus to the need to tackle the “global stimulant epidemic.”
Abstract
Background: Amphetamine abuse is becoming more widespread internationally. The possibility that its many cardiovascular complications are associated with a prematurely aged cardiovascular system, and indeed biological organism systemically, has not been addressed.
Methods: Radial arterial pulse tonometry was performed using the SphygmoCor system (Sydney). 55 amphetamine exposed patients were compared with 107 tobacco smokers, 483 non-smokers and 68 methadone patients (total=713 patients) from 2006 to 2011. A cardiovascular-biological age (VA) was determined.
Results: The age of the patient groups was 30.03 ±0.51–40.45±1.15 years. This was controlled for with linear regression. The sex ratio was the same in all groups. 94% of amphetamine exposed patients had used amphetamine in the previous week. When the (log) VA was regressed against the chronological age (CA) and a substance-type group in both cross-sectional and longitudinal models, models quadratic in CA were superior to linear models (both p<0.02). When log VA/CA was regressed in a mixed effects model against time, body mass index, CA and drug type, the cubic model was superior to the linear model (p=0.001). Interactions between CA, (CA) and (CA) on the one hand and exposure type were significant from p=0.0120. The effects of amphetamine exposure persisted after adjustment for all known cardiovascular risk factors (p<0.0001).
Conclusions
These results show that subacute exposure to amphetamines is associated with an advancement of cardiovascular-organismal age both over age and over time, and is robust to adjustment. That this is associated with power functions of age implies a feed-forward positively reinforcing exacerbation of the underlying ageing process.
Authors
Albert Stuart Reece, Amanda Norman, Gary Kenneth Hulse
[link url="http://www.bmj.com/company/newsroom/amphetamine-heart/"]BMJ material[/link]
[link url="http://heartasia.bmj.com/content/heartasia/9/1/30.full.pdf"]Heart Asia abstract[/link]