Vascular smooth muscle cell apoptosis, macrophage and neutrophil infiltration, and upregulation of a range of inflammatory and oxidative stress markers. Histological evidence of aortic dissection was also demonstrated in 40% of the mice. While aneurysm induction was associated with hypertension, the rise in blood pressure induced was not correlated with the size or incidence of aneurysm development. Our study provides the first evidence in older men, who are most at risk of AAA, that, similar to rodents, salt intake is associated with AAA. Salt administration has also been used to induce cerebral aneurysm formation in rodents. The common feature of all these rodent model studies appears to be the administration of salt along with Ginsenoside-F2 activation of a part of the renin-angiotensin-aldosterone system. Raised blood pressure is another common feature of these models however lowering blood pressure does not necessarily inhibit aneurysm formation. These findings are in keeping with our observation that higher salt intake was associated with AAA independently of a history of hypertension or treatment for hypertension and measured mean blood pressure. High salt intake has been demonstrated to increase a range of neural, endocrine and renal 
changes which could promote cardiovascular disease including AAA. These changes promote aortic inflammation, angiogenesis, loss of aortic elasticity and oxidative stress, which are all implicated in AAA pathogenesis. A number of possible limitations of this study should be considered including measurement error, reverse causality and residual confounding. Firstly, our assessment of salt intake was limited to a simple questionnaire in which we asked whether salt was added to food never or rarely, sometimes, almost always or always. More sophisticated assessment methods, such as measured of 24-hour urinary sodium excretion, were not used. This approach may have introduced measurement error. It is however accepted that even biochemical methods of estimating salt intake are open to measurement error. Furthermore, self-reported Ginsenoside-F5 dietary intake of salt has been found to be reflective of 24 hour urinary sodium excretion, suggesting that self-report is a valid measure of salt intake. Secondly, this study was a cross-sectional human association study. It is not possible to conclude that the association between self-reported high salt intake and AAA is causative. The direct role of salt in AAA development could only be established by a randomized controlled trial of at risk individuals in which the effect of administering different amounts of salt was compared. Such a trial would require a large number of subjects and extended follow-up in order to assess the efficacy of salt restriction on AAA incidence. Thirdly, the mean aortic diameter differences between patients reporting different levels of salt intake were small and within the measurement error of aortic imaging. While we established the reproducibility of the ultrasound imaging during the course of the study it is possible, although we believe unlikely, that measure error may have confounded our findings. Fourthly, since we only studied men we can make no comment on how our findings relate to women. Finally we may have failed to adjust for some confounding factors. The current study included a large number of men and used adjustment for recognized confounding factors such as age, hypertension, high cholesterol, coronary heart disease and stroke.