Excess dietary salt is notorious for increasing blood pressure – blood volume increases, placing more stress on blood vessel walls. This forces the heart to pump harder against the pressure, and also structural changes that harden the vessel wall (this hardening is called stenosis) occur in response to these high pressures.
About one-third of all American adults and over 50% of those over the age of 55 have hypertension, and hypertension carries significant risks. Elevated blood pressure accounts for 62% of strokes and 49% of coronary heart disease.  Notably, the risk for heart attack and stroke begins climbing with systolic pressures (first number in the blood pressure reading) above 115 mm Hg – considered “normal” by most standards. Also, dietary salt is not only dangerous to the cardiovascular system, but also contributes to kidney disease, osteoporosis , ulcers, and stomach cancer. 
There is new evidence that excess dietary sodium intake promotes atherosclerotic plaque development and heart disease, even in those without elevated blood pressure.
In the 1990s, it was found that the relationship between salt intake and stroke mortality was stronger than the relationship between blood pressure and stroke mortality; this suggested that salt may have deleterious effects on the cardiovascular system that are not related to blood pressure. Excess sodium in the diet affects sodium concentrations in the blood, which affects the cells of the blood vessel wall and blood volume, even if blood pressure itself does not change. The eventual results are long-term changes in vessel wall structure, including thickening of the vessel wall and arterial stiffening. Excess dietary sodium prompts changes in hormonal systems and also gene expression in endothelial cells (the cells that make up the inner lining of blood vessels). These changes in turn promote excessive growth of vascular smooth muscle cells, which contributes to thickening of vessel wall, and altered production of structural proteins, such as collagen, elastin, and fibronectin, which contributes to arterial stiffening. Dietary salt has also been associated with endothelial dysfunction (the inability of endothelial cells to properly regulate blood pressure), which is one of the initiating events of atherosclerotic plaque formation. [5-8]
The study population consisted of overweight and obese individuals withoutelevated blood pressure. Their sodium intake was evaluated by measuring the amount of sodium excreted in the urine. The authors found that higher urinary sodium (indicating higher sodium intake) was associated with greater carotid artery intima-media thickness – a predictor of future cardiovascular events. Intima-media thickness (IMT) is an indicator of atherosclerotic plaque development and is established in the medical literature as an accurate predictor of future cardiovascular risk. IMT testing is a non-invasive ultrasound technique for imaging any abnormal thickening in the intima (inner lining) and media (smooth muscle layer) layers of the carotid artery. Thickening indicates atherosclerotic plaque formation, and therefore increased risk of heart attack or stroke.  I use this test to assess cardiovascular risk and track patients’ progress in my medical practice.
Reducing dietary salt is not only important for those who already have elevated blood pressure – limiting added salt is essential for all of us to keep our cardiovascular systems in proper working order. On top of consuming the vast majority of our calories from phytochemical-rich, unrefined plant foods, salt avoidance adds another layer of protection against heart attack and stroke. It is also important to remember that a low fat, flexitarian or vegan diet plus a low cholesterol level does not protect you from developing high blood pressure later in life from years of using too much salt; it also does not protect you against the risk of later life hemorrhagic stroke, as long as you overly salt your food.
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2. Lewington, S., et al., Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet, 2002. 360(9349): p. 1903-13.
3. Tsugane, S. and S. Sasazuki, Diet and the risk of gastric cancer: review of epidemiological evidence. Gastric Cancer, 2007. 10(2): p. 75-83.
4. Perry, I.J. and D.G. Beevers, Salt intake and stroke: a possible direct effect. J Hum Hypertens, 1992. 6(1): p. 23-5.
5. Simon, G., Experimental evidence for blood pressure-independent vascular effects of high sodium diet. Am J Hypertens, 2003. 16(12): p. 1074-8.
6. Sanders, P.W., Vascular consequences of dietary salt intake. Am J Physiol Renal Physiol, 2009. 297(2): p. F237-43.
7. Safar, M.E., et al., Pressure-independent contribution of sodium to large artery structure and function in hypertension. Cardiovasc Res, 2000. 46(2): p. 269-76.
8. Dickinson, K.M., J.B. Keogh, and P.M. Clifton, Effects of a low-salt diet on flow-mediated dilatation in humans. Am J Clin Nutr, 2009. 89(2): p. 485-90.
9. Lorenz, M.W., et al., Prediction of clinical cardiovascular events with carotid intima-media thickness: a systematic review and meta-analysis. Circulation, 2007. 115(4): p. 459-67.