HJBR May/Jun 2022

DRUG ADDICTION 26 MAY / JUN 2022 I  HEALTHCARE JOURNAL OF BATON ROUGE   interview and trained interviewers, the Col- laborative Studies on Genetics of Alcohol- ism examined the likelihood that an indi- vidual diagnosed with a lifetime history of substance dependence would retain this classification after 5 years. This is obviously a diagnosis that, once met, by definition cannot truly remit. Lifetime alco- hol dependence was indeed stable in indi- viduals recruited from addiction treatment units, ~90% for women, and 95% for men. In contrast, in a community- based sample similar to that used in the NESARC [27], sta- bility was only ~30% and 65% for women and men, respectively. The most important characteristic that determined diagnostic stability was severity. Diagnosis was sta- ble in severe, treatment-seeking cases, but not in general population cases of alcohol dependence. These data suggest that commonly used diagnostic criteria alone are simply over- inclusive for a reliable, clinically meaning- ful diagnosis of addiction. They do identify a core group of treatment seeking individuals with a reliable diagnosis, but, if applied to nonclinical populations, also flag as “cases” a considerable halo of individuals for whom the diagnostic categorization is unreliable. Any meaningful discussion of remission rates needs to take this into account, and specify which of these two populations that is being discussed. Unfortunately, the DSM-5 has not made this task easier. With only 2 out of 11 symptoms being sufficient for a diagnosis of SUD, it captures under a single diagnostic label individuals in a “mild” category, whose diagnosis is likely to have very low test–retest reliability, and who are unlikely to exhibit a chronic relapsing course, together with people at the severe end of the spectrum, whose diagnosis is reliable, many of whom do show a chronic relapsing course. The NESARC data nevertheless show that close to 10%of people in the general popula- tion who are diagnosed with alcohol addic- tion (here equated with DSM-IV “depen- dence” used in the NESARC study) never remitted throughout their participation in the survey. The base life-time prevalence of alcohol dependence in NESARC was 12.5% [32]. Thus, the data cited against the concept of addiction as a chronic relapsing disease in fact indicate that over 1% of the US pop- ulation develops an alcohol-related condi- tion that is associated with high morbidity and mortality, and whose chronic and/or relapsing nature cannot be disputed, since it does not remit. Secondly, the analysis of NESARC data [4, 27] omits opioid addiction, which, together with alcohol and tobacco, is the largest addiction-related public health problem in the US [33]. This is probably the addic- tive condition where an analysis of cumu- lative evidence most strikingly supports the notion of a chronic disorder with frequent relapses in a large proportion of people affected [34]. Of course, a large number of people with opioid addiction are unable to express the chronic, relapsing course of their disease, because over the long term, their mortality rate is about 15 times greater than that of the general population [35]. However, even among those who remain alive, the prevalence of stable abstinence from opioid use after 10–30 years of obser- vation is <30%. Remission may not always require abstinence, for instance in the case of alcohol addiction, but is a reasonable proxy for remission with opioids, where return to controlled use is rare. Embedded in these data is a message of literally vital importance: when opioid addiction is diag- nosed and treated as a chronic relapsing disease, outcomes are markedly improved, and retention in treatment is associated with a greater likelihood of abstinence. The fact that significant numbers of individu- als exhibit a chronic relapsing course does not negate that even larger numbers of indi- viduals with SUD according to current diag- nostic criteria do not. For instance, in many countries, the highest prevalence of sub- stance use problems is found among young adults, aged 18–25 [36], and a majority of these ‘age out’ of excessive substance use [37]. It is also well documented that many individuals with SUD achieve longstanding remission, in many cases without any for- mal treatment (see e.g., [27, 30, 38]). Collectively, the data show that the course of SUD, as defined by current diagnostic cri- teria, is highly heterogeneous. Accordingly, we do not maintain that a chronic relaps- ing course is a defining feature of SUD. When present in a patient, however, such as course is of clinical significance, because it identifies a need for long-term disease man- agement [2], rather than expectations of a recovery that may not be within the individ- ual’s reach [39]. From a conceptual stand- point, however, a chronic relapsing course is neither necessary nor implied in a view that addiction is a brain disease. This view also does not mean that it is irreversible and hopeless. Human neuroscience documents restoration of functioning after abstinence [40, 41] and reveals predictors of clinical success [42]. If anything, this evidence sug- gests a need to increase efforts devoted to neuroscientific research on addiction recov- ery [40, 43]. Lessons from genetics For alcohol addiction, meta-analysis of twin and adoption studies has estimated heritability at ~50%, while estimates for opioid addiction are even higher [44, 45]. Genetic risk factors are to a large extent shared across substances [46]. It has been argued that a genetic contribution can- not support a disease view of a behavior, because most behavioral traits, including religious and political inclinations, have a genetic contribution [4]. This statement, while correct in pointing out broad herita- bility of behavioral traits, misses a funda- mental point. Genetic architecture is much like organ structure. The fact that normal anatomy shapes healthy organ function does not negate that an altered structure can contribute to pathophysiology of disease. The structure of the genetic landscape is no different. Critics further state that a “genetic predisposition is not a recipe for compul- sion”, but no neuroscientist or geneticist would claim that genetic risk is “a recipe for compulsion”. Genetic risk is probabilistic,