The reactivity hypothesis implicates exaggerated cardiovascular reactions to acute psychological stress in the development of hypertension and other cardiovascular disease outcomes. However, cardiovascular reactivity has also been suggested as a mediator between a variety of psychosocial and behavioural risk factors and cardiovascular disease. Data from various analyses of the West of Scotland Twenty-07 study are discussed together, and caution against over-stretching the original reactivity hypothesis. Blood pressure and heart rate were assessed at rest and during an acute mental arithmetic stress task. First, depression, though a putative risk factor for cardiovascular disease, does not appear to confer this risk via exaggerated reactivity, as it was negatively related to reactivity. Second, obesity, another risk factor, was also associated with blunted rather than heightened reactivity. Finally, lower reactivity was related to poorer self-reported health. Similar associations emerged from both cross-sectional and prospective analyses. These seemingly paradoxical results are discussed in terms of implications for the reactivity hypothesis.