For a study, researchers sought to look at the co-occurrence and family aggregation of Cannabis use disorder (CUD) and mood disorder subtypes.

Semistructured diagnostic interviews and family history records were used in this cross-sectional, community-based study in the Washington, DC, metropolitan region to assess lifetime DSM-IV disorders in probands and relatives. Mixed-effects models were used to assess familial aggregation and coaggregation of CUD with mood disorders while controlling for age, gender, recruitment source, concomitant mood, anxiety, and other drug use disorders. From May 2004 to August 2020, 586 adult probands (186 with bipolar disorder; 55 with CUD) and 698 first-degree relatives (91 with bipolar disorder; 68 with CUD) were recruited from a community screening in the greater Washington, DC, metropolitan region. Inclusion requirements included the capacity to communicate in English and the availability and agreement to contact at least two live first-degree relatives.

About 395 (67.4%) of the 586 probands were female; 437 (62.6%) of the 698 relatives were female. The mean (SD) age of the probands was 47.5 (15.2) years and 49.6 (18.0) years for relatives. In the proband group, 82 (14.0%) self-identified as African American or Black, 467 (79.7%) as White, and 37 (6.3%) as American Indian or Alaska Native, Asian, more than one race, another race or ethnicity, or declined to reply. In the related group, 53 (7.6%) self-identified as African American or Black, 594 (85.1%) as White, and 51 (7.3%) as American Indian or Alaska Native, Asian, more than one race, another race or ethnicity, or declined to reply. Because of their modest numbers, these groups were blended to safeguard privacy. CUD in probands (55 [9.4%]) was linked to an increase in CUD in relatives (aOR, 2.64; 95 % CI, 1.20-5.79; P=.02). Bipolar disorder II (BP-II) in probands was similarly related with an elevated risk of CUD in relatives (aOR, 2.57; 95% CI, 1.06-6.23; P=.04). However, among probands, bipolar disorder I (114 [19.5%]) and major depressive disorder (192 [32.8%]) were not substantially related to CUD in relatives. CUD was linked to BP-II (aOR, 4.50; 95% CI, 1.72-11.77; P=.002), major depressive disorder (aOR, 3.64; 95% CI, 1.78-7.45; P=.001), and mean (SD) age (42.7 [12.8] years with CUD vs. 50.3 [18.3] years without CUD; aOR, 0.98; 95 % CI, 0.96-1.00; P=.02. The addition of concomitant anxiety disorders reduced the familial coaggregation of BP-II with CUD. Furthermore, relatives with both a familial and individual history of BP-II had the highest rates of CUD (no familial or individual history of BP-II: 41 [7.2%]; familial history but no individual history of BP-II: 13 [19.1%]; individual history but no familial history of BP-II: 10 [22.2%]; familial and individual history of BP-II: 4 [28.6%]; Fisher exact test, In most cases, the start of mood disorder subtypes preceded the beginning of CUD in probands and families.

The data confirmed a familial CUD aggregation. The increased likelihood of CUD among relatives of BP-II probands implies that CUD and BP-II may have a shared underlying diathesis.

Reference: jamanetwork.com/journals/jamapsychiatry/article-abstract/2793123