by Malcolm Knox
What is going on inside the brain to produce such a cornucopia of emotions and responses? From Charlie Parker dipping asthma inhaler strips in his coffee to American and Japanese Second World War pilots, from Jack Kerouac and 1990s party kids all the way to Mohammed Kerbatieh losing any contact with reality and assaulting three girls, what was the common chemical event happening in the human brain?
When they enter the body, methamphetamine molecules head, via the bloodstream, to the central nervous system, kidney and liver. In the brain, they easily cross the blood-brain barrier and enter tiny ‘storage terminals’ in the nerves.
Nerve cells, or neurons, are asymmetrical. At one end is the axon, and the storage terminals are located in the end of each axon. One nerve cell’s axon is adjacent to the next cell’s dendrite—the part of the nerve cell that receives messages. When one nerve cell communicates with the next, it sends out neurotransmitters to cross the gap, or synapse, between the axon and the neighbouring dendrite. These neurotransmitters are held in the storage terminals.
Among the different types of neurotransmitters are the so-called ‘feel-good’ neurotransmitters, such as dopamine, serotonin and norepinephrine. Methamphetamine molecules are very similar in shape to dopamine molecules. What the methamphetamine molecules do, crucially, is force the neurotransmitters out of their storage terminals and across the synapses in large numbers. The normal role of these neurotransmitters is to respond to different kinds of signals. Sometimes those signals are pleasant, and the spread of neurotransmitters is, literally, what makes us feel good. At other times, neurotransmitters are released as a defence against pain; again, their role is to make us feel better. When something good happens, axons release neurotransmitters like dopamine across a synapse; when they lodge in the nearest dendrite, they pass on a message that says ‘be happy’.
But nature only intends for them to work in moderation. Methamphetamine, particularly in large doses, sets loose great multitudes of neurotransmitters—hence the observation of many users that meth is ‘a thousand times better than sex’. The pleasure effect, measured by the amount of dopamine and serotonin released, can literally be a thousand times greater than what would naturally occur during sex.
This would not be so bad for the brain if it was the only effect, and if, afterwards, the production of neurotransmitters could resume as per normal. But in the aftermath of neurotransmitter release, the methamphetamine is involved in other chemical reactions that damage the body’s capacity to make new neurotransmitters.
Normally, once they have carried their message across a synapse, neurotransmitters either die or are taken back by the axon they originated from. This process is called the ‘reuptake’ of the neurotransmitter. But methamphetamine inhibits the reuptake process. Dopamine and serotonin, instead of being replenished, are oxidised and damaged by the methamphetamine. They are left in the system for an unusually long time, thus extending the high, but they are unable to return to the axon. The payoff is that the half-life of methamphetamine can be ten to twenty hours, rather than the much shorter half-life of cocaine, for instance.
The downside is that once the released dopamine is gone, it is gone. Subjectively, this is the cause of the ‘crash’—the user feels awful because the brain is not producing or releasing neurotransmitters in sufficient numbers. It’s also one of the things that makes methamphetamine addictive. When it wears off, it leaves you feeling so terrible that the only solution is to take more. Unfortunately, the greater the dose, the more the damage, and the more the damage, the greater the dose needs to be to create the same effect. This squirrel-wheel inside the user’s chemistry is what we know as ‘tolerance’ to the drug. It’s also responsible for the particular pains of methamphetamine withdrawal. Whereas a withdrawing heroin user might experience symptoms similar to a bad flu, a withdrawing meth user can suffer from a depression lasting months. The risk of relapse is correspondingly higher, as the withdrawal symptoms last much longer.
Whether or not the brain recovers, and if so how much, has been a point of scientific contention for many years. It is now generally agreed that long-term use can cause permanent damage to the process of neurotransmitter production and secretion, so that mental health consequences such as chronic depression can have a lifetime effect even when the user has given up.
More disturbing still is recent research suggesting that methamphetamine catalyses a process called apoptosis, or a form of natural cell death. Apoptosis is very important to the body; cancer, for instance, can be a deficiency of apoptosis, in which cells are allowed to proliferate without the downward regulation of natural cell death. In embryos, apoptosis is what happens between the fingers and toes, killing off cells so that we have gaps between our digits rather than joined flesh.
But apoptosis, if out of control, means the devastation of cells, a premature old age. Some research has indicated that long-term methamphetamine use can ravage nerve cells in many regions of the brain, permanently. Imaging of meth users’ brains has shown apoptosis that is similar in appearance to the brains of Alzheimer’s and Parkinson’s disease sufferers. In the worst cases, heavy methamphetamine use can give the abuser every appearance of being a senior citizen decades before his or her time.
When someone takes methamphetamine, its peak presence in the bloodstream extends from one to three hours after ingestion. But there are faster effects. Blood pressure and pulse rates go up, the pupils dilate, and the sense of wellbeing and energy comes on fast. Sweating increases. Also, harking back to the original medicinal use of amphetamine, the lung passageways dilate, allowing for easier breathing—the rate of respiration also goes up.
In manageable doses, the subjective response is only pleasurable. One of the interesting things about the human brain is that many of the best feelings it produces are on the spectrum of many of the worst feelings. That is, the feeling of energy that methamphetamine induces is on the same continuum as hyperactivity. A greater dose pushes the user out towards the hyperactivity end. The teeth-grinding which overtakes even the most moderate methamphetamine users is a step out towards agitation and restlessness. Likewise, the opening of the bronchial pathways can lead to hyperventilation. The feeling of awareness and acuity is one step along the road towards confusion and paranoia. At its worst, this paranoia can mesh with hallucinations and delusions, where the user feels that someone is out to harm him. And it is that fear, and ‘hearing voices’, which in turn can lead to acts that are suicidal and homicidal.
For more than twenty years, scientists have identified an effect that is probably known to all meth users. The user’s pulse, blood pressure, breathing rate and eye dilation are all switched up so high that the user is unable to move, almost paralysed by an overflow of neurotransmitters. It is unlikely to result in death— methamphetamine rarely has the fatal overdose effect of opiates like heroin—but users have described a feeling of chest tightness in these ‘over-amped’ situations that may resemble a heart attack.
This description covers basic amphetamine effects, and within it lie the variations of methamphetamine and drugs like MDMA (commonly known as ecstasy) and MDA. The differences in the molecular structures of these drugs are responsible for the differences in the subjective experience. For instance, MDMA and MDA have more of a visual hallucinogenic effect than amphetamine.
When some unknown chemist on the Pacific Rim first synthesised a smokable crystal form of meth in the 1980s, the chemical secret lay in mirroring the drug’s molecular structure. Ice is dextro-isomer methamphetamine, what is called a ‘right-handed molecule’. Older forms of meth are the levo-isomer methamphetamine, or ‘left-handed molecule’. Whereas the l-isomer is more stimulating to the cardiovascular and respiratory systems, the d-isomer is much more stimulating to the brain.
Pseudoephedrine is a left-handed molecule which, when synthesised, makes the right-handed d-isomer methamphetamine molecule. It apes dopamine in a subtly different way, but users of the new version found that there was only one thin
g that mattered: it was better. And as it was sold in the smokable crystal form, it did something else. It gave users the rush or lift that was previously available only by injection.
But as far as the brain is concerned, it doesn’t end there. Chris Cruickshank is a PhD student at the University of Western Australia. When the heroin drought struck in that state, there was a rush towards methamphetamine like the Boxing Day sales. Everyone wanted to get onto meth. Cruickshank’s interest is in meth withdrawal—he interviews users on the sleeping problems, the anxiety, and the depression they experience in withdrawal.
But there’s also the guilt, in some cases. Users have to live with the memory of acting impulsively. They had sex with someone they shouldn’t have. They hit someone. They went into a screaming fit. They smashed up their parents’ home.
‘The aggression,’ says Cruickshank, ‘comes down to an impairment of cognition. With prolonged use of this drug, the sections of the brain that control impulses are impaired.’
In other words, the meth user is dealing with a brain chemistry double-whammy. At the same time that he or she is feeling invulnerable, full of self-confidence, bursting with energy and ideas, or maybe exploding with fear and paranoia, he or she is also least able to say no to acting upon those impulses. The motivation to do something rash is at its highest, and the ability to stop it is at its lowest. And the worst of it is, both of these mechanisms—the impulse and the means to control it—move further apart over time.
‘The neurotoxicity of methamphetamine is cumulative,’ Cruickshank says. ‘The sections of the brain that inhibit impulses get progressively worse with use of the drug, so the person acts out their physical impulses more and more.’
In America, stories of the results—shocking, almost unbelievable violence—had been around for years. A causal link between amphetamines and violence had been investigated as early as the 1970s. Australia, in 2001, was about to get its wake-up call.
Among inner South Sydney’s stacked-up Legoland of housing department units, few blocks had a worse reputation than Northcott Flats in Surry Hills. Inspired, along with other similar public-housing experiments, by the post-war ideal of social improvement through architecture, Northcott had by the end of the century degenerated into a 24-hour crime scene, a second home for many South Sydney police. Although surrounded by lush grounds and a fast-gentrifying urban neighbourhood, Northcott’s tiny flats were a hotbed of poverty, petty crime, drug dealing, violence and sexual abuse.
Residents of the flats have in recent years banded together successfully to establish a more functional community. North-cott’s turnaround was a reaction to a series of watershed moments showing just how bad things were, including two of the most horrible murders imaginable. Ice played a pivotal role in both.
By 2001, Damien Peters was 32 years old and still living in Flat B9/15 Northcott Flats with his lover, Andre Akai, as they had been since 1998.
Since Akai had confessed he had AIDS, Peters was often upset, and his anger, which had resulted in many broken friendships and lost jobs before, sometimes got the better of him. Akai’s health worsened, and even though Peters hated him for giving him the infection, he nursed him at home. Peters had nowhere else to go. Even when Akai maltreated their pet dog and accused Peters of being first to have contracted the virus, Peters remained loyal. The relationship was abusive yet dependant; their days were filled with fighting and reconciliation. The make-up sessions usually took place with the help of a new score of heroin, cannabis or speed.
Neighbours would often hear Peters and Akai screaming and throwing things at each other, but in the late summer of 2000–01, the fights stopped overnight. Peters told neighbours and other acquaintances that Akai had decided to go away for a while; they needed time apart.
Akai’s disability pension was still going into his bank account, however, and Peters was using Akai’s ATM card to make cash withdrawals. He told a friend, Jillian Nash, that he and Akai had a ‘gentlemen’s agreement’: if Peters looked after the flat and the dog, Akai would allow him to use his money to pay the rent and other bills.
But in August 2001, Peters told Nash that the ATM card had been stolen and he needed her to go to a bank, taking with her a letter he had written, to withdraw money on his behalf.
Nash suspected something was amiss. She quizzed Peters about Akai’s whereabouts, and he broke down, confessing that he had killed Akai six months earlier, had cut up his body and put it down the toilet and into the rubbish, and had undertaken other measures to prevent the parts being identified: he had cut off Akai’s fingertips, knocked out his teeth, and burnt his hair.
Shocked, Nash went to the police, who executed a search warrant on Flat B9/15 Northcott Flats. Peters had cleared out. The flat had been ransacked; there were blood smears throughout and a smashed window.
The police found Peters in rehab at the Langton Clinic. In subsequent interviews, he repeated his story about the ‘gentlemen’s agreement’ and said he was ‘tearing my hair out’ worrying where Akai had gone. He admitted ransacking the flat, but said he had done so out of anger at Akai. He’d cut his hand in the course of doing so, he said, and the blood in the flat was his own.
During the next week, at the beginning of September 2001, police tapped phone calls between Peters and Nash. He repeatedly expressed his fear that he would be arrested for killing Akai.
What the police didn’t know yet was that Peters hadn’t been living in Flat B9/15 for six months. He had moved in with another older gay man in Northcott, Bevan James Frost, who lived in Flat A3/1. The pattern of the relationship had been much the same as with Akai: Peters had sought a protector, but had found only abuse. Frost had promised Peters protection, but had turned into a nasty, jealous, abusive bully.
Fretting over his police interview only drove Peters into a more erratic state. On 9 September, Frost lay face-down on his bed and asked Peters to give him his regular back massage.
Instead, as Frost lay on the bed, Peters began stabbing him in the back and the neck with a 32-centimetre carving knife he had got from the kitchen. Then he decapitated Frost and put the corpse in the bathtub. For the next two days Peters stayed in the flat, periodically erupting in fear and anger, overturning furniture and smashing windows. When the police arrived on 11 September, it might have come as a relief to Peters. Certainly he went quietly, admitting to murdering Frost and telling the police he had hidden the weapon under the carpet near the front door.
Arrested and taken into custody, Peters confessed to killing Akai as well. He said Andre had repeatedly called him stupid, and Peters had got ‘revved up’, taking a knife from the kitchen and stabbing Akai. He detailed the six hours he had spent dismembering Akai—flushing his teeth and liver down the toilet, burning his hair, slashing the fingerpads off his hands, all very calmly and in full knowledge of what he was doing. He had been engaged in doing the same with Frost’s body, and had cut out a number of internal organs, but had grown sickened by the task and hadn’t been able to complete it.
Peters had cut off his victims’ genitals, pointing to what he said was one of his motives: he was ‘sick of being used for sex’. There was no doubt that his sexual relationships were disturbing and dysfunctional, and a key subjective motive for the murders. Frost, he said, would ‘fist’ him against his will, a practice that sounds painful enough when performed with consent, let alone without it. When police asked him why he didn’t just leave the relationships, Peters said he had nowhere else to go and had to keep looking after the pet dog.
Yet if the killings were instances of domestic violence, they were unusual in their ferocity. Why, when Peters lost his temper, did he go all the way and kill his lovers? Why did he stab them repeatedly, in a merciless frenzy? How had he then had the presence of mind to dismember them over a period of several hours, with the clear purpose of rendering them unidentifiable? What explained this coexistence of uncontrollable, homicidal fury and cool, clear-headed cover-up?
The answer, found
in subsequent examinations of Peters, lay in his pharmacological history.
At the time of his arrest, Peters had a veritable chemist’s shop in his bloodstream: apart from cannabis, amphetamines, cocaine, heroin and methadone, Peters had been prescribed or been given a number of antidepressants, anticonvulsants, tranquillisers and body-building drugs, including Valium, Zoloft, Prozac, testosterone, Xanax, Dilantin and Mogadon. It doesn’t take much to imagine what the pure toxicity of his drug use alone did to Peters’s mental state, but none of this provided a clear key to his murderous eruptions. That key was provided by Peters himself, in his admissions to medical examiners.
Speed, as noted earlier, had been Peters’s principal drug of choice for more than a decade. Yet he had no record of violence, only one minor assault in 1998. He had exhibited no behaviour as frenzied, excessive and paradoxically cool-headed as that which followed in 2001.
Peters, as an inner-city polydrug user, embodied why Rebecca McKetin and the NDARC researchers viewed such people as a sentinel group for the advent of new drugs. When ice hit the streets, as noticed by NDARC in the late 1990s, Peters was one of the population who would first notice it. It’s not known exactly when Peters bought highly purified methamphetamine rather than the low-grade speed he’d been taking since his late teens, but it most likely happened in 1999–2000, when he was living with Andre Akai. By early 2001, Peters was a frequent and often daily user of ice. Significantly, when he told medical examiners of his mood leading up to Akai’s murder, it was his methamphetamine intake, out of all the other drugs he was using, that he blamed. He said he was ‘depressed from speed’ when he killed Akai.
That depression had a sharp edge. Spread over the two days leading up to Akai’s murder, Peters injected himself with half a gram of ice. In the two days leading up to Frost’s murder, he was still injecting ice, about the same amount. When describing his state of mind, although much of what had happened was a blur Peters could remember the severe depression he was suffering as he was coming down from ice highs. This was a man who had been taking amphetamine, and suffering its crashes, for perhaps thirteen years. But the ice crash was so terrible that he lost his sense of where to stop lashing out.