Anonymous #10 said:

Anonymous #11 said:

Link please to scientific proof showing heroin doing direct harm to a human other than overdose?

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Researchers have found that young heroin users suffer a level of brain damage similar to that seen in the early stages of Alzheimer's disease.

The research team from the University of Edinburgh studied the autopsied brains of 34 drug users with a history of opiate abuse - mainly heroin and methadone. Most had died of a drug overdose, but all were HIV negative and had no history of head injuries.

They also looked at the autopsied brains of 16 people who had no history of drug abuse or neurological impairment.

The average age in both groups was 26 and drug abusers as young as 17 were included.

The study found that young drug abusers were up to three times more likely to suffer brain damage, than those who did not use drugs. The drug abusers meanwhile sustained a level of brain damage normally only seen in much older people and similar to the early stages of Alzheimer's.

"Our study shows evidence of an increased risk of brain damage associated with heroin and methadone use, which may be highest in the young, when individuals are most likely to acquire the habit", said lead researcher, Professor Jeanne Bell.

Professor Bell said that in a previous study, the research team found that drug abuse causes low grade inflammation in the brain. Taken together, she explained, the two studies suggest that intravenous opiate abuse may be linked to premature ageing of the brain.

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http://www.irishhealth.com/article.html?id=7759

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Abstract  Approximately 3.7 million individuals have used heroin and other opiate substances in their lifetime. Despite increasing knowledge of the effects of heroin, it remains the most abused opiate and use among adults has recently increased. The empirical literature examining the neurocognitive effects of acute and chronic opioid use remains limited; however, findings to date suggest that the use of opiates has both acute and long-term effects on cognitive performance. Neuropsychological data indicate deficits in attention, concentration, recall, visuospatial skills and psychomotor speed with both acute and chronic opioid use. The long-term effects of opiate use appear to have the greatest impact on executive functions, including the ability to shift cognitive set and inhibit inappropriate response tendencies. Factors that contribute to addiction and recovery are also discussed, as it is difficult to disentangle the effects of opiate use on cognitive performance from other factors that may affect neurobehavioral measures.

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a study by Carlin (1986) found lower scores for opiate abusers than normal control subjects on measures of visuospatial and visuomotor function. A more recent study by Pakesch et al. (1992) compared opiate abusers to normal controls and found that opiate abusers scored significantly below control subjects on a visual memory recall test (Benton Visual Retention Test). Later, Ornstein and colleagues (Ornstein et al. 2000) found that chronic heroin use impaired performance on sequence generation tasks, spatial working memory and visual pattern recognition memory. In a Hong Kong based study by Lee and Pau (2002), investigators reported that individuals classified as �ex-heroin addicts� who had been abstinent from use for three to 18 months performed more poorly on a test of impulse control (qualitative score of the Porteus Maze Test) than control subjects. The authors state that the former heroin users were more reckless, ignored the rules of the test, and lacked an overall plan for solving the task relative to control subjects. Limited subject information was available, such as medication use, enrollment in a maintenance program, or poly-substance abuse diagnoses. Absence of these details make study results somewhat difficult to interpret.

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http://www.springerlink.com/content/t84q0303w7717wx0/

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Cortical function has been suggested to be highly compromised by repeated heroin self-administration. We have previously shown that street heroin induces apoptosis in neuronal-like PC12 cells. Thus, we analysed the apoptotic pathways involved in street heroin neurotoxicity using primary cultures of rat cortical neurons. Our street heroin sample was shown to be mainly composed by heroin, 6-monoacetylmorphine and morphine. Exposure of cortical neurons to street heroin induced a slight decrease in metabolic viability, without loss of neuronal integrity. Early activation of caspases involved in the mitochondrial apoptotic pathway was observed, culminating in caspase 3 activation, Poly-ADP Ribose Polymerase (PARP) cleavage and DNA fragmentation. Apoptotic morphology was completely prevented by the non-selective caspase inhibitor z-VAD-fmk, indicating an important role for caspases in neurodegeneration induced by street heroin. Ionotropic glutamate receptors, opioid receptors and oxidative stress were not involved in caspase 3 activation. Interestingly, street heroin cytotoxicity was shown to be independent of a functional mitochondrial respiratory chain, as determined using NT-2 rho(0) cells. Nonetheless, in street heroin-treated cortical neurons, cytochrome c was released, accompanied by a decrease in mitochondrial potential and Bcl-2/Bax. Pure heroin hydrochloride similarly decreased metabolic viability but only slightly activated caspase 3. Altogether, our data suggest an important role for mitochondria in mediating street heroin neurotoxic effects.

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http://www.biomedexperts.com/Abstract.bme/17250679/Street_heroin_induces_mitochondrial_dysfunction_and_apoptosis_in_rat_cortical_neurons

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Our findings indicate that chronic heroin did not interfere with mice performance in a battery of sensorimotor tests. On the other hand, cognitive ability in the Morris water maze and cognitive flexibility-related performance were strongly impaired by chronic heroin. These effects were associated with up-regulation of pro-apoptotic proteins such as Fas, FasL and Bad, in the cortex and hippocampus, indicating the activation of both the death receptor and the mitochondrial apoptotic pathways. Another indicator of apoptosis was the presence of TUNEL (TdT-mediated dUTP nick-end labeling) positive cells scattered throughout the brain.

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http://linkinghub.elsevier.com/retrieve/pii/S0028390807003735

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