The mechanisms by which OCD is transmitted from parent to child have not been identified, although they are likely to be both genetic and environmental, or due to the interaction between individual vulnerability factors (genetics) and environmental factors (e.g. acute and chronic stressors, maladaptive parenting). Identifying etiological influences on OCD is challenging, as OCD is a clinically and etiologically heterogeneous disorder (
9).
A complex segregation analysis provided evidence supporting major gene effects and other familial effects in OCD vulnerability, with respect to familial aggregation of OCD (
10).
A significant amount of research attests to the role of heredity in OCD, and in addition, a range of hypothesized biological factors (
8,
11), shared personality factors may account for the increased prevalence rates of OCD among first-degree relatives of OCD probands. Researchers have increasingly focused their attention on what is inherited. Phenotypic heterogeneity is increasingly recognized as a major impediment to the elucidation of the pathophysiology and etiology of neuropsychiatric disorders (
12). Although standard classification systems, such as the Fifth Edition Diagnostic and Statistical Manual of Mental Disorders and International Classification of Diseases-10, regard OCD as a unitary nosological entity, there is increasing evidence that this severe and potentially disabling condition is phenotypically heterogeneous (
6). However, comprising a new chapter on Obsessive-Compulsive and Related Disorders in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) reflects the increasing evidence of OCD relatedness to other disorders such as body dysmorphic disorder, trichotillomania, hoarding disorder and excoriation disorder (
13).
Using a family study design, with matched control subjects, and applying operational criteria for the assessment of OCD, McKeon and Murray (
14) found no increased familial risk of OCD, even though they did observe a greater rate of mental illness in the first-degree relatives of OCD probands. Bellodi et al. (
15), using no comparison group, found a low prevalence of OCD (3.4%) among first-degree relatives. In cases with an early onset (before age 14), prevalence reached 8.8%, which seems to indicate a biological vulnerability. Grabe et al. reported that Cox proportional hazard analyses revealed a 6.2-fold higher risk (hazard ratio) for relatives of all OCD cases, for definite OCD, and a 2.2-fold higher risk, for subclinical OCD, compared with relatives of comparison subjects (
16). Clinical features may correlate with course, prognosis and treatment responsiveness and it has been hypothesized that different clinical subgroups may result from different etiologies and pathogeneses (
17).
Regarding the reported case, this issue is whether counting can be a distinctive feature among inflicted and no inflicted individuals, such as hoarding. Another question is “what is really transferred?” Is it this vulnerability to disease, which is transferred among three generations, or the symptoms of counting itself are transferred by genes. This theory requires confirmation from genetic studies in this field.