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Substance Abuse with Self-Medicating Effects in ADHD

Substance Abuse with Self-Medicating Effects in ADHD

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Upon closer examination, some substance abuse turns out to be a form of self-medication.1 This does not alter the fact that the substance is being abused, nor does it affect whether such behavior is a criminal offense. Furthermore, the desired effect of normalization is not achieved, and significant unpleasant side effects arise. However, a tendency to prefer certain drugs can provide insight into the causes of substance abuse.

ADHD is characterized, among other things, by an increased number of DATs. One study reports a significant reduction in DATs among people with ADHD who were also users of dopaminergic drugs.2

1. Nicotine

Nicotine and methylphenidate are both stimulants. They have similar mechanisms of action.3 Both nicotine and methylphenidate reduce the number of dopamine transporters (DAT) in the medium term4 and—in part as a result—increase the availability of dopamine in the synaptic cleft.5
Empirical evidence shows that people with ADHD-HI who are not taking medication smoke significantly more often than people with ADHD-HI who are taking medication or people without the condition.6

The increased risk of ADHD due to maternal smoking during pregnancy (for more information, see ⇒ Maternal nicotine use during pregnancy In the article ⇒ Environmental Factors as a Cause of ADHD in the chapter ⇒ Development) is likely attributable, at least in part, to the increased likelihood of passing on the genetic predisposition that caused the mother herself to become a person with ADHD. Furthermore, the fact that a woman is unable to quit smoking despite being pregnant indicates, first, that she has a strong need for nicotine; second, a lack of self-control; and third, a lack of care for the child entrusted to her. Given that this occurs more frequently in lower socioeconomic classes than in more affluent ones, the question arises as to whether social class is a consequence of impaired self-regulation or vice versa. In any case, a low socioeconomic status correlates with an increased risk of ADHD.

  • Nicotine significantly increases adrenaline levels and tends to lower norepinephrine levels. As a result, nicotine improves test results and reaction times.789
  • In a double-blind study, nicotine patches were shown to have a positive effect on ADHD.101112
  • Nicotine and smoking are said to significantly increase the risk of depression and markedly worsen one’s mood.13 Psylex also cites a study that showed a clear causal link between smoking and depression, but not between depression and smoking. Unfortunately, this source could not be verified.
  • Smoking significantly reduces the number of dopamine transporters in the striatum. An increased number of dopamine transporters is said to be a typical feature of ADHD. A SPECT study of 31 adults with ADHD found a greater increase in DAT in people with ADHD-HI than in people with ADHD-I. However, DAT levels in people with ADHD-I were still elevated compared to levels in non-ADHD individuals. Smoking significantly reduced DAT levels in both subtypes.14
  • A study of smokers with ADHD found that people with mild ADHD showed reduced inhibition and increased impulsivity after a break from smoking, while, surprisingly, this was not the case for people with severe ADHD.15

2. Cannabis: THC, Cannabidiol

The misuse of hashish, cannabis, or marijuana is very common among people with ADHD.
A study found that 14.3% of all people with ADHD use cannabis, while only 4.3% of those without ADHD use cannabis. ADHD thus increases the likelihood of cannabis use by more than three times.16 In addition, those with hyperactivity began using cannabis significantly earlier than those with inattention alone.

The assumption that this is due to its relaxing or sedative effects is questionable, given its invigorating and stimulating effects on biomarkers. Nevertheless, cannabis appears to effectively relieve “internal pressure.”

The active ingredients it contains are primarily the psychoactive cannabinoids (such as THC = dronabinol) and the non-psychoactive cannabidiol (CBD).

2.1. Cannabinoids (THC)

2.1.1. Cannabinoids affect dopamine, serotonin, and acetylcholine in the PFC

Cannabinoids affect dopamine, serotonin, and acetylcholine in the PFC.17 Deficits in working memory, attention, and reversal learning associated with recreational THC use appear to be mediated by activation of the CB1 cannabinoid receptor.
The positive effects of THC as a medication or when used for microdosing (without producing a psychoactive high) could potentially be mediated through this mechanism. Further information on this is lacking.

2.1.2. Increase in cortisol levels

One possible explanation could be that THC (in people who are not dependent on THC) increases cortisol levels in a dose-dependent manner.1819 This had previously been observed in animal studies.20 However, another study found no change in cortisol levels due to THC.21
In general, cannabinoids influence the activation of neurotransmitters such as GABA and glutamate, which regulate the stress axis; THC activates the HPA axis.22 When cortisol levels were measured 4 hours after THC administration, they were no longer elevated.23
Among drug users who had been abstinent for at least 2 weeks prior to the study, no increase in cortisol levels was observed in response to THC.24 This could possibly be the consequence of receptor downregulation.

2.1.3. HPA Axis Suppression Due to a THC-Mediated Increase in Cortisol?

We consider it theoretically possible that a (rarer and milder) THC high could potentially produce a relaxing effect by causing an increased release of cortisol, which effectively downregulates the HPA axis in people with ADHD-HI and ADHD-C. People with ADHD-HI and ADHD-C (with hyperactivity) have a blunted cortisol response to stress, whereas people with ADHD-I exhibit excessive cortisol release in response to acute stress. Since cortisol not only mediates stress symptoms but also (as the last stress hormone released by the HPA axis) serves to downregulate the HPA axis, (at least some) people with ADHD-HI and ADHD-C lack the regular deactivation of the HPA axis by cortisol.
However, this likely applies only to occasional users, not to chronic THC users, in whom receptor downregulation may prevent this effect.
This hypothesis would be consistent with the idea that THC is primarily consumed by people with ADHD-HI, while people with ADHD-I—who, due to their elevated cortisol response to stress, do not experience HPA axis shutdown—would consume THC less frequently. However, earlier indications of such consumption preferences have not been confirmed.
This hypothesis is further supported by reports from people with ADHD-HI that the sense of calm achieved after THC use lasts for about 2 to 3 days.

2.1.4. Reduced cortisol response to acute stressors

Among regular users who consume THC every day or almost every day, (likely due to downregulation or upregulation ⇒ downregulation / upregulation), the cortisol response to acute stressors is reduced.

In chronic users, THC can no longer trigger downregulation of the HPA axis via cortisol due to the lack of an increase in cortisol release.
The reduced cortisol response to acute stress in chronic THC users2526 could explain the hypothesis that THC causes high cortisol release and that people with a blunted cortisol response to stress have a particular affinity for THC.

People with schizophrenia who had previously used cannabis showed a lower morning cortisol rise upon waking (CAR) than people with schizophrenia who had not previously used cannabis, whose levels were comparable to those of people without the condition.27 This finding may also reflect the tendency of people with blunted cortisol responses to stress.

Regardless of this, THC has an anxiolytic (anxiety-reducing) effect at certain doses. At higher doses, however, it increases anxiety.28
Anxiety-relieving medications reduce the intensity of HPA axis activation by calming the amygdala.

2.1.5. Reduction in amygdala volume

There is evidence that long-term cannabis use reduces the volume of the amygdala and hippocampus.29
It is conceivable that reducing the size of the amygdala would also reduce its activity, and that such a reduction in amygdala activity would decrease the intensity of stress responses.
Unfortunately, this is not the only effect of cannabis.

The problem is that even infrequent use can lead to dependence, which is why treatment cannot be recommended even for those who use cannabis infrequently.
On the other hand, people with ADHD-HI (especially those with comorbid aggression disorders) report that even long-term use gives them a sense of inner calm that they cannot achieve in any other way.
Chronic cannabis users with ADHD are characterized by an increased rate of hospital admissions and a reduced use of medication and behavioral therapy.30

2.1.6. Cannabinoids alter the EEG: Alpha waves increase, beta waves decrease

Cannabis increases activity in the brain’s alpha band and decreases activity in the beta band as well as in the other EEG frequency bands.313233
The fact that cannabis, beyond its acute effects, increases alpha activity (which is necessary for concentration) while simultaneously reducing the activity of all other frequencies (including beta frequencies, which, when elevated, prevent proper relaxation—e.g., ruminating), could explain why many people with ADHD find cannabis pleasant. It is understandable that this effect is not beneficial in the long term in terms of overall health. It is also plausible that this effect provides short-term relief for people with ADHD.

2.1.7. Cannabis use is associated with ADHD symptoms, but not with cognitive problems

A large-scale study found a correlation between cannabis abuse and ADHD symptoms such as hyperactivity/impulsivity and inattention. Whether cannabis abuse was the cause/trigger or a consequence of the symptoms (self-medication) was not investigated. Furthermore, the study found no correlation between cannabis abuse and cognitive problems.34
Mood instability was associated with a 61% increased risk of ADHD and a 38% increased risk of depression.35

There is no evidence that cannabis abuse correlates with any specific presentation of ADHD. From a dimensional perspective, a correlation with inattention now appears to be better supported than one with hyperactivity-impulsivity. When assessed, conduct disorder (CD) is the significantly stronger predictor. The widely held view that “hyperactivity-impulsivity = onset, inattention = escalation” does not hold up to scrutiny.

 

Study Design, n Inattention ADHD-I Hyperactivity-Impulsivity ADHD-HI, ADHD-C Social Disorder
De Alwis 2014 (NESARC)36 Cross-sectional, 33,588 OR 1.49 (1.00–2.22) n.s. ADHD-HI: OR 2.43 (1.68–3.51); ADHD-C: 2.41 controlled for as a covariate
Brandt 2018 (NESARC, same dataset)16 Cross-sectional study Later age at first use Earlier age at first use Controlled for as a covariate
Elkins 2007 (MTFS)37 prospective, 1,512; ADHD diagnosis overall adj. OR 0.58 (0.28–1.20) = no effect adj. OR 0.91 (0.73–1.13) n.s. adj. OR 1.35 (1.07–1.68) adj. OR 5.51 (3.75–8.10)
Chang 2012 (CHAD)38 prospective, 2,960 adj. OR 0.94 n.s. adj. OR 1.10 n.s. adj. OR 1.14 n.s.
Molina & Pelham 200339 prospective clinical study, 242 β 0.25 / 0.23 (frequency / problems) β 0.01 / −0.14 n.s. β 0.10 / 0.18 n.s.; ADHD+CD OR 3.68
Bidwell 201440 Cross-sectional, 376 current B 0.35 / 0.64; Kindlich 0.47 current all n.s. (negative); childhood only: age at first use −0.97 r = 0.21–0.33 (externalization)
Petker 202041 Cross-sectional study, 1,008 significant significant, practically equally strong not reported
Kolla 2016 (CAMH)42 Cross-sectional study, 5,080 Women OR 1.13; Men 1.00 n.s. Men OR 1.08; Women n.s. OR 2.59–4.02, strongest predictor
Loflin 201443 Online survey, 2,811 43.4% of daily consumers 56.6% of daily consumers Not surveyed

Cannabis use by presentation type. ADHD-C and ADHD-HI correlated significantly with cannabis use, while ADHD-I did not. However, the group differences were not significant in the post hoc test, and in terms of dimensions, both dimensions were equivalent.36
Prospectively, the HI dimension predicted cannabis use disorders up to age 18, whereas inattention did not. The categorical ADHD-HI diagnosis did not predict anything at all, and the CD effect was four times as large as the HI effect. 37
Cannabis was combined with other drugs and inhalants into a binary variable, for which the adjusted result was consistently null. With only about 60 users, the study lacked sufficient statistical power for this analysis; the published effects pertain exclusively to tobacco and alcohol.38
For cannabis, no significant group differences were found in lifetime use, disorder diagnosis, problems, or age at first use; differences were found only in frequency of use. Within the ADHD group, only inattention in childhood predicted cannabis frequency and problems, and persistent ADHD without conduct disorder was not sufficient to account for increased use.39
Current inattention was associated with all cannabis measures, while current hyperactivity-impulsivity was not associated with any. The only HI finding (earlier age of first use) is due to a suppression effect, as the zero-order correlation is only r = −0.07.40
Inattention predicted problematic cannabis use only among women, while hyperactivity and impulsivity predicted it only among men. However, the domains were not adjusted for one another, the effects are minuscule (OR ≤ 1.13), and the mean age of the sample was 54 years.42
Among daily cannabis users, HI-containing subtypes were more prevalent (56.6% vs. 43.4%), whereas this was not the case among non-daily users. “Non-daily use” was defined as up to 29 days of use per month. The reported McNemar statistics are mislabeled proportion differences. Recruitment was conducted through a cannabis legalization organization.43

An assessment of the effect Of cannabis on symptoms found reduced mental frustration (OR 2.39) and impulsivity (OR 1.69), but impaired attention (OR 0.59). If cannabis reduces impulsivity and impairs attention, self-medication would be more likely for hyperactivity/impulsivity and less likely for ADHD-I.44

In the ADxS.org symptom test (an online survey only, with no adjustment for covariates), n = 353 participants reported having used cannabis more frequently. This group of participants showed significantly increased impulsivity and restlessness in adulthood, as well as significantly increased hyperactivity during their school years, while inattention and distractibility did not differ from those of people with ADHD who did not use cannabis. This finding contradicts the existing body of research.

2.2. Cannabidiol (CBD)

Cannabidiol (CBD) is not psychoactive and, along with the cannabinoids (THC), is another important component of cannabis.

Cannabidiol reduces anxiety after a stress test, but not before or during it.45

A comparison of different dosages showed that cannabidiol reduced anxiety during and after a stress test only at a low dose (300 mg), but not at doses of 600 mg or 900 mg.46 Another study, which compared the effects of 600 mg of cannabidiol to a placebo in people with social anxiety disorder, found an anxiety-reducing effect during the stress test, although participants still reported higher levels of anxiety than people without ADHD.47

People with anxiety told us that taking CBD hemp oil allowed them to significantly reduce their use of anti-anxiety medications.
No effects of CBD on ADHD have been reported.

2.3. THC-Based Medications for ADHD

THC-based medications (which, due to their dosage, do not cause intoxication but are rather designed to provide a consistent, long-lasting effect) can have a positive effect on ADHD symptoms.

  • THC is a drug of choice for people with ADHD. They value its relaxing effect, which some describe as lasting for 2 to 3 days after use. This long-lasting effect could (in occasional users, not chronic users) possibly be the result of downregulation of the HPA axis caused by THC-induced cortisol release.
  • THC stimulates the brain’s reward/reinforcement center. This is precisely where one of the key neurological issues in ADHD lies: low dopamine levels in the striatum.
  • It is unclear whether THC actually increases dopamine release in the brain’s reward center, the striatum. Some studies suggest it does,4849 while others suggest it does not.50 In summary, according to Pertwee.51 Since dopaminergic recreational drugs work by increasing dopamine levels in the brain’s reward center, and a “high” is based on a massive, short-term dopamine surge, an increase in dopamine levels caused by THC would be plausible. Aside from the fact that recreational use causes a rapid rise in dopamine levels beyond the functional level, whereas medications cause a slow rise to a constant (functional) level, the short-term effect also changes, at the latest with chronic use: In THC-dependent individuals, dopamine levels in the striatum are reduced.52 This raises the question of whether this is a consequence of the addiction (which would be logical, since a persistently elevated dopamine level causes downregulation of dopamine transporters, leading to increased presynaptic reuptake of dopamine, resulting in less dopamine being available in the synaptic cleft at the postsynaptic site), or whether it is a consequence of elevated dopamine levels in the PFC, since this leads to reduced dopamine levels in the striatum. Persistently low dopamine levels in the striatum are likely to trigger an increase in DAT as a counter-regulatory response. It is also conceivable that the reduced dopamine levels in the striatum are the reason THC once became appealing to addicts. Heinz addresses this for alcohol-dependent individuals by suggesting a “both-and” scenario, although the relationships are infinitely more complex.53
    It should be noted, however, that cannabinoids are dopaminergic drugs and that people with ADHD also have a far above-average affinity for nicotine and alcohol, which also have dopaminergic effects.
  • THC is an established treatment for Tourette syndrome.54 Tourette syndrome is a very common comorbidity of ADHD.
  • Some people with ADHD report that “regular” low-level THC use significantly reduces their risk of migraines. Migraines are a common comorbidity associated with ADHD.

We are aware of several people with ADHD who have been able to largely alleviate severe ADHD symptoms accompanied by significant comorbid disorders (including bipolar disorder) through cannabinoid-based medications (medical cannabis)—at least more effectively than with stimulants and other medications. (Private prescription not covered by health insurance; €130 per month; as of fall 2017).
Meanwhile, more and more doctors are becoming aware of the medical benefits of prescribing THC to people with ADHD for whom other medications have not been effective, and are willing to prescribe it.

For more information on THC-containing medications for ADHD, see*⇒* Medical Cannabis for ADHD in the section ⇒ Appropriate Medications for ADHD in the chapter ⇒ Treatment and Therapy.

2.4. Improvement in ADHD Symptoms Through Microdosing

One argument against the theory outlined above—that THC-induced massive stress-related increases in cortisol shut down the HPA axis (at least as the sole mechanism of action)—is that people with ADHD (including those with the ADHD-I subtype) report a significant improvement in symptoms through microdosing of THC or cannabidiol.

Microdosing refers to a dose so small that (cumulatively)

  • there is no sensation of intoxication whatsoever
  • short-term memory is not impaired
  • there is no decline in performance or fatigue.

Several people with ADHD who have tried it report that microdosing cannabinoids or cannabidiol—usually using a vaporizer—significantly improves their focus. If short-term memory is impaired as a result, they report that an even lower dose can help improve it.
It is further reported that the optimal ratio of cannabinoids to cannabidiol varies from person to person and that the degree of symptom improvement is influenced by the individual adjustment of this ratio. A very low proportion of cannabidiol has been reported to be beneficial.

These notes are not a recommendation to self-medicate!
Under Sections 29 et seq. of the German Narcotics Act (BtMG), the unauthorized cultivation, production, trade, import, export, distribution, sale, other forms of placing on the market, acquisition, and possession of any part of the cannabis plant are criminal offenses in Germany.

The basic principle of microdosing can be viewed scientifically as the difference between a drug (high doses produce a euphoric effect) and a medication (low doses treat a deficiency). This principle is precisely what is known to distinguish amphetamine as a drug from its use as a medication (e.g., for ADHD).
However, amphetamine-based medications or amphetamine-related drugs, such as those widely used to treat ADHD, are subject to medical approval processes that involve multiple reviews and very precise dosing. This is not possible with natural substances, so there is always a risk of incorrect dosing.
For this reason—and regardless of any legal issues that may arise—self-medication is generally not recommended.

It should also be noted that the alleged medical use sometimes serves merely as a pretext to conceal drug abuse.

If the standard medications for ADHD (amphetamine-based medications, methylphenidate, guanfacine, atomoxetine, bupropion, nicotine) do not provide sufficient relief, a doctor may prescribe medical cannabis. It is well known that, in some cases, this is the most effective treatment for ADHD.
Medical cannabis has a defined active ingredient content (which is measured and verified for each batch) and can therefore be dosed precisely.
In this context, the explanation of microdosing is insightful.

42% of cannabis users with ADHD reported using it to manage their ADHD symptoms. People with ADHD who used cannabis daily reported reduced mental frustration (OR = 2.39) and impulsivity (OR = 1.69), as well as reduced attention (OR = 0.59), compared to non-daily cannabis users. Among people with ADHD who used cannabis, 156 reported reduced anxiety and 34 reported increased anxiety.44

3. Amphetamines / Methamphetamines

Amphetamine-based drugs can significantly reduce stress levels. However, the abuse of amphetamine-based drugs leads to an increased stress response in the long term.55
Meprobromate, a sedative from the 1960s (which is no longer approved due to its addictive potential), reduces the surge in adrenaline during times of stress.56
“Crystal meth” is a form of methamphetamine, and its effects are very similar to those of amphetamine, which is used as a medication for ADHD.57
It has been reported that the use of illegal substances such as cocaine and amphetamines can have a positive effect on concentration deficits (“self-medication”).58
It goes without saying that this cannot serve as a legal justification. However, it must be taken into account when determining the degree of culpability, which may not prevent a penalty but could potentially mitigate it.

4. Cocaine

Cocaine inhibits the reuptake transporters for dopamine, norepinephrine, and serotonin.

5. Alcohol

  • Alcohol increases dopamine levels
    • in the PFC59
    • in the striatum59
  • Alcohol significantly increases adrenaline levels for at least 12 hours after consuming moderate amounts of alcohol (1.43 g/kg of body weight). Norepinephrine levels are significantly elevated, particularly during the first 6 hours, and tend to remain elevated thereafter.60
  • Excessive alcohol consumption can raise adrenaline and norepinephrine levels for up to a week. Elevated levels of 17-hydroxycorticosteroid were also found. 0.5 g of chloromethiazol reduced catecholamine levels.61

6. LSD

Microdoses of LSD (100 nanograms per kilogram or less) appear to increase serotonin levels, while even slightly higher doses cause a decrease in serotonin.62

An online survey found that microdosing with psychedelic substances such as LSD had a significantly higher subjective effect size than conventional treatment for mental and physical conditions, particularly in cases of63

  • ADHD
  • Anxiety Disorders
  • Autism spectrum disorders (ASD) (though not significant in this case)
  • Personality disorders (though not significant in this case).

In contrast, higher doses that regularly produce psychedelic effects were rated more highly than microdosing in

  • Depression
  • Anxiety.

No significant difference was found in

  • physiological disorders.

One review found that the subjectively reported effect size was as high as that of stimulants for ADHD; however, this was not confirmed by experimental studies.64

Another study reported fewer side effects with LSD microdosing (10 micrograms of LSD every third day was tested on more than 1,000 participants with a wide range of disorders over a period of 18 months) compared to conventional treatment.65
An RCT study found no side effects associated with repeated microdosing of LSD (20 μg, twice weekly for four weeks), but also found no improvement in ADHD symptoms compared to placebo.66

7. Psilocybin

Adults with severe ADHD symptoms reported, based on their own accounts, that microdoses of psychedelics (primarily psilocybin) led to improvements in emotional regulation, empathy, and ADHD symptoms similar to those experienced by people taking conventional ADHD medications.67

8. Medications and Drugs—The Difference

Dopaminergic drugs (THC, cocaine, amphetamines, alcohol, nicotine) work by causing dopamine levels in the striatum to rise very rapidly, reach very high levels, and then drop very rapidly again.68 The rapid, sharp rise in dopamine triggers the euphoric effect, while the rapid decline triggers craving. With prolonged drug use (even with regular tobacco smoking or alcohol consumption), the persistently elevated dopamine levels lead to downregulation of dopamine receptors and upregulation of dopamine transporters. When the dopamine-increasing drug is discontinued, the dopamine levels—which have returned to normal—are insufficient to maintain the dopaminergic brain functions due to the insufficient number of receptors and the excessive number of transporters. The result is withdrawal symptoms, which subside within a few days or weeks once the dopamine receptors and transporters have regenerated.

Dopaminergic ADHD medications, on the other hand, do not act as intoxicants because they cause dopamine levels to rise very slowly, remain constant for a long time, and decline slowly. Medications merely compensate for the existing dopamine deficiency; they do not lead to an excess of dopamine. Since no excess of dopamine is produced, neither a state of euphoria nor a dysregulation of dopamine receptors or transporters can result from this.

When methylphenidate is taken orally, it causes a slow rise in dopamine levels that does not result in a euphoric effect. In contrast, intravenous administration of MPH causes a more rapid rise in dopamine levels, which is associated with euphoric states.69

While drugs can induce a state of euphoria due to a rapid rise in dopamine levels (which saturate the majority of dopamine receptors), and the subsequent rapid drop can lead to cravings, this possibility does not apply to the medicinal use of stimulants (methylphenidate and amphetamine-based medications) because they are taken orally, resulting in a slow rise to a low level.
To put it figuratively and simply: A deep pothole in the road can really throw you off course. Medications merely fill in the pothole—they correct the deficiency, but nothing more. Drugs, on the other hand, are like a truckload of asphalt. Instead of the pothole, a crater now forms, which is harmful in a different way than the pothole.

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