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ing effect on reward processing. Studies examining the neural response to rewarding stimuli in schizophrenia suggest that second generation antipsychotics are associated with intact response to reward outcomes in the ventral striatum. Since individuals with schizotypy and youth at clinical high risk for psychosis are much less likely to be prescribed antipsychotics, the apparent paradox may reflect medication effects that become evident with more severe pathology. Third, schizophrenia is associated with more severe cognitive impairment and poorer insight into clinical symptomatology than schizotypy or clinical high risk states. It is possible that impaired cognition and insight are paradoxically protective, causing schizophrenia patients to have less awareness of hedonic deficits that may actually exist. Those with schizotypy and clinical high risk youth may be better able to accurately report their hedonic state because of higher cognitive function and insight. Fourth, environmental and stress effects may have a greater impact on youth at clinical high risk for psychosis and those with schizotypy. Schizophrenia is associated with impoverished quality of life, which for many patients reflects an environment and daily routine with restricted social, cognitive and affective demands. For individuals with schizotypy and clinical high risk youth, environments and daily routines are generally more complex and stressful. It is possible that this stress attenuates reward system responsivity. Supporting this, individuals with schizotypy seem to enjoy solitary activities, yet report activities with others as being taxing, stressful and unenjoyable. Animal models and studies on humans support the notion of a “stress-induced anhedonia”; however, this phenomenon has yet to be directly investigated in the schizophrenia spectrum. The schizophrenia spectrum anhedonia paradox harkens back to the seminal writings of P. Meehl, who proposed that anhedonia is one of several polygenic potentiators that comprise the endophenotype for schizotaxia. Meehl distinguished between primary and secondary anhedonia. Primary anhedonia refers to one’s hedonic capacity. This capacity is polygenically determined and dependent on neurotransmitter function and neural circuitry responsible for reward responsivity. Capacity varies on a continuous dimension, but may be taxonic at the extreme end. It seems that only a small proportion of schizophrenia patients would fall at the extreme end of the continuum, whereas substantially more individuals with schizotypy and clinical high risk youth would display primary anhedonia. Primary anhedonia may be a risk factor for the development of many forms of psychopathology, with schizophrenia being a less common outcome than others. Meehl also proposed the existence of “secondary anhedonia”, which is measured via verbal report (through clinical interview or questionnaire) of one’s hedonic response. He proposed that such reports are influenced by “aversive drift”, which reflects heightened trait negative affect that becomes increasingly more prominent as the course of illness progresses. The aversive drift construct has yet to receive significant empirical attention; however, there is evidence from laboratory and ecological momentary assessment studies that those on the schizophrenia spectrum display elevated negative emotion that is contextually invariant. Thus, even in instances where the neural machinery for hedonic response is intact, co-activation of negative emotion may bleed over into potentially rewarding situations, lowering the overall net hedonic value of stimuli that would otherwise be rewarding. Whether secondary anhedonia worsens with illness progression has yet to be determined. However, a greater frequency of secondary anhedonia in the chronic phase of schizophrenia than in earlier phases of illness could be another viable explanation for the schizophrenia spectrum anhedonia paradox.