psychotherapy, change, and cocaine

In How People Change, Allen Wheelis describes two ways that change occurs in psychotherapy. There’s the easy way, which probably won’t happen for you:

Sometimes in therapy profound change occurs spontaneously, without effort or intention. It is a rare experience–any time, anywhere–to be known and understood without being judged, to be regarded with affection and respect, without being used. No therapist can feel this way about all his patients, though he must try. When he does genuinely so feel, he creates a nurturing context in which the patient may take in and make his own the therapist’s way of thinking about problems, a certain reflectiveness about suffering, a tendency to hold conflicting motives in suspension while looking for connections, meanings, significance.

Such identification leads to slight, subtle, often unnoticed changes in action and behavior, in one’s way of dealing with one’s self and others; and over a period of time these changed actions may achieve a change of being. One then feels one’s self to be profoundly different without knowing how or why. If one is asked, “Well, what did you learn? What was the main insight?” one may stumble about, fabricate some inadequate answer, yet may know certainly that one is a better person, more able to love.

This sort of change is rare. We can’t count on it, can’t make it happen; when it occurs it is great good fortune, a bonus. Usually change–when it occurs at all–follows long and arduous trying.

Then there’s the hard way;

Personality change follows change in behavior. Since we are what we do, if we want to change what we are we must begin by changing what we do, must undertake a new mode of action. Since the import of such action is change it will run afoul of existing entrenched forces which will protest and resist. The new mode will be experienced as difficult, unpleasant, forced, unnatural, anxiety-provoking. It may be undertaken lightly but can be sustained only be considerable effort of will. Change will occur only if such action is maintained over a long period of time.

Probably because of its effects on the mesolimbic dopamine system, cocaine can be helpful in providing the necessary energy, motivation, and self-confidence. Cat Marnell [<– read this] explains:

“Omigoddd, why am I friends with such freaks,” I whimper. “Why am I friends with such nightmares. I hate you guys.” I pull my hoodie over my head. I really do hate them all of the time. They are my only family and I love them, but I also fucking hate them.

Mint waits about ten seconds to make sure I’m done before he cranks up the music.

MAKE IT RAIN/ MAKE IT MAKE IT RAIN TRICK/ MAKE IT RAIN TRICK/ MAKE IT MAKE IT RAIN TRICK

That’s the stripper-singer. A coke headache hits me like a brick to the face.

What the fuck happened to me, I think. Why am I here. I just want to be normal.

I’MA MAKE IT RAIN BITCH/ I’MA MAKE IT RAUN/ UHH I’M THROW SOME 20S/ AINT GOT NO MUTHA FUCKING CHANGE BITCH

That’s whoever the rapper dude is. Travis Porter—whatever. The shit is blaring. I take a bag of coke out of my pocket, along with the straw I asked the bartender cut in half at the Shore Club, and snort a whole half gram right from the baggie until it’s empty so no one else can have any.

“You wanna see some ass?” the stripper-singer whines. “I wanna see some cash!”

And I lose it.

“I WANT TO GO BACK TO THE LOFT NOW!” I shriek. We are staying together in a loft in the Design District. “MY HEAD HURTS, WE’VE BEEN DOING THIS FOR TWO HOURS. YOU ARE DRUNK DRIVING HIDEOUSLY, MIKE MINT, AND I AM DONE.”

MAKE IT RAIN TRICK/ MAKE IT MAKE IT RAIN TRICK

“CAN YOU FUCKING TURN THAT DOWN?” I scream. And Serf does.

“I can’t do this anymore!” I wail to no one. “I need to make some changes. GOD.” I press my forehead against the car window.

The slums of Miami are sunrise-glowy all around. “I need to get a boyfriend. A non-graffiti writer boyfriend. Someone I can, like, watch TV shows with. I need to learn to cook. I need to start eating. I’m gonna find a boyfriend and I am going to cook with him—”

Mint turns the music back on. I rummage through my blue Balenciaga for another coke bag and my iPhone. Wu-Tang is on now, and the sun is not quite up.

I start reading my Twitter feed: An ocean is stained with blood in a Japanese port city. Madonna has said she is afraid of not being “in control” and might be launching a nail polish. There’s a new disease they’re calling “the AIDS of the Americas” that can cause victims’ hearts to explode. Media Takeout has accused Mariah Carey of being shaped like a chalkboard eraser; I want to disappear, and everyone in the car knows that the only thing anyone could ever imagine me romantically cooking with a man is a ton of crack.

Sigmund Freud recommends this practice with great enthusiasm because COCAINE FUCK YEAH!!!:

I will kiss you quite red and feed you till you are plump. And if you are forward you shall see who is the stronger, a little girl who doesn’t eat enough or a big strong man with cocaine in his body. In my last serious depression I took cocaine again and a small dose lifted me to the heights in a wonderful fashion. I am just now collecting the literature for a song of praise to this magical substance.

Sigmund Freud was on the right track. Lack of pleasure and motivation, or “anhedonia,” is a major part of depression, and it has to do with dopamine. The opposite of anhedonia is “being really high,” and drugs with this effect are said to have “abuse potential.” In the excerpt below, “bupropion” is the same as the antidepressant Wellbutrin or the anti-smoking drug Zyban:

In terms of pharmacological treatments, the exploration of tailored treatments for individuals experiencing motivational anhedonia using DA-active pharmacotherapies is recommended. This includes psychostimulants, DA [dopamine] agonists, and the NE/DA reuptake inhibitor bupropion. Of the current FDA approved antidepressant drugs with DA-acting properties, bupropion is the most widely used in clinical practice. However, the pharmacological profile of bupropion is complex, and its effects on reward processing in animals and humans may rely on a variety of mechanisms, some of which are still not entirely known.

It is well established that bupropion has little direct effect on 5HT function (Stahl et al., 2004). Several studies exploring bupropion occupancy of DAT at clinical doses have reported occupancy rates ranging from 14%–26% in the striatum (Kugaya et al., 2003; Learned-Coughlin et al., 2003; Meyer et al., 2002), which are relatively low as compared to standard SERT occupancy rates of SSRIs (80%) or DAT occupancy of reinforcing psychostimulants (>50%) (Volkow et al., 1995; Volkow et al., 1997; Volkow et al., 1998). These findings suggest that bupropion’s direct ability to increase synaptic DA levels through blockade of DAT may account for only some of its antidepressant effects. However, more recent work has also shown that bupropion increases the activity of the intracellular vesicular monoamine transporter 2 (VMAT2) protein, which may enhance extracellular DA by increasing available DA in presynaptic pools (Rau et al., 2005). Bupropion may also exert regionally-specific influence over DA function through its action as an inhibitor of the norepinephrine transporter (NET), which is the primary transporter of DA in prefrontal regions. Finally, more recent work has suggested that bupropion decreases the activity of nicotinic acetylcholine receptors, which play a role in the effects of bupropion on psychomotor symptoms in MDD (See Dwoskin et al., 2006 for a review).

Preclinical studies have suggested that bupropion may be a superior treatment for symptoms of motivational anhedonia. Rats treated with bupropion demonstrate decreased immobility time during the forced swim test and tail suspension tests (Cryan et al., 2001; Cryan et al., 2004) and showed greater willingness to work for food rewards during a progressive ratio task (Bruijnzeel and Markou, 2003). Moreover, the influence of bupropion was blocked via administration of both D1-like and D2-like receptor antagonists, suggesting that effects of bupropion were partially mediated through DAergic mechanisms (Paterson and Markou, 2007). Additionally, rats treated with either chronic or acute doses of bupropion show a reduced threshold for intracranial self-stimulation of the posterior lateral hypothalamus (Paterson, 2009; Paterson et al., 2007). Similarly, bupropion enhanced responding to a conditioned reinforcer (Palmatier et al., 2009), although a separate study reported a bupropion-induced decrease in responding for sucrose (Reichel et al., 2008). The latter result is contrary to what would be expected, given the findings of (Bruijnzeel and Markou, 2003) and highlights the complex effects of the bupropion on reward processing. Interestingly, bupropion-mediated enhancement of conditioned reinforcers in the study by Palmatier et al. was ameliorated by Prazosin, an α2-NE receptor antagonist, suggesting that bupropion’s effects on reinforcement may also rely on noradrenergic mechanisms.

In addition to bupropion, psychostimulants, including dexamphetamine, methylphenidate and modafinil, have also been explored as both monotherapy and adjunctive treatment options for MDD. Results from these studies have not been encouraging (particularly in the case of monotherapy), although the majority of studies using psychostimulants were conducted several decades ago, before either DSM criteria or the Feighner criteria were in place (for reviews, see (Orr and Taylor, 2007) and (Candy et al., 2008)), and fail to meet current methodological standards for clinical trials. More recently, however, interest has reemerged in the utility of psychostimulants as an adjunctive therapy for specialized populations.

What’s interesting is that caffeine is another minor stimulant that people agree helps with life, which indirectly affects dopamine. If you’re a mouse, caffeine can make you less of a socially avoidant, joyless person after getting dominated:

Mice experienced chronic social defeat stress for 10 days. Caffeine was administered intraperitoneally before, during and after social defeat stress. The time spent in interaction zone, social interaction ratio and sucrose preference test was used to measure the social avoidance and anhedonia in mice. The results showed that chronic pretreatment with caffeine for 14 days and for 10 days during stress reversed the avoidance of social behavior and anhedonia induced by social defeat stress in mice, suggesting the enhancement of the resilience to social defeat stress induced by caffeine. However, neither the treatment with caffeine only during the social defeat stress for 10 days nor the treatment with acute caffeine after defeat stress altered the resilience to stress. Furthermore, chronic caffeine treatment did not affect the normal locomotor activity and the desperate behavior in naïve mice. Moreover, the antagonism of dopamine D1 receptor and not D2 receptor reversed the effect of caffeine on the social avoidance and depressive-like behavior. Finally, pretreatment with higher doses of caffeine did not affect the behavioral response to social defeat stress. Taken together, our findings provide new insight into the effects of caffeine on social avoidance and anhedonia in mice

You could say that “drugs of abuse” are psychiatric medications with “they take over your life” as a side effect. The point of long-term antidepressant treatment is to become physically dependent on the drug, in a sense. How does “you need to take drugs and be high all the time” compare to the “substantial risk for developing diabetes” that goes with clozapine, a widely-prescribed antipsychotic drug? Diabetes can have very serious consequences, and it’s in addition to the risk for tardive dyskinesia (permanent motor dysfunction). Heroin addiction and diabetes can both entail daily self-administered injections, for that matter.

A stressed out, vulnerable person might turn to food or drugs to self-medicate for the same underlying issues. Both choices can result in a need for self-injection. Blood levels of insulin or opiates have to be consciously regulated. Mistakes can have serious or fatal medical consequences. Obese people use more resources, by definition, which is socially undesirable. Addictive behaviors have undesirable social consequences. There are health-care costs associated with both. What’s the difference?

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