This study investigates the relationship between hypertension, glucose intolerance, and hyperinsulinemia in a large, representative sample of the adult Jewish population in Israel. The findings show a strong association between hypertension and glucose intolerance, with 83.4% of hypertensives being either glucose intolerant or obese. Hypertension was independently associated with hyperinsulinemia, even in mild untreated hypertensives. The study also found that hypertension, obesity, and glucose intolerance are associated with altered internal cation distribution, with 88.1% of individuals with all three conditions presenting at least one marker of internal cation imbalance. These results suggest that insulin resistance and/or hyperinsulinemia are common pathophysiological features of obesity, glucose intolerance, and hypertension, and may explain their widespread association. The study further proposes that tissue insulin resistance could alter internal sodium and potassium distribution, leading to increased peripheral vascular resistance, which is hypothesized to contribute to the pathogenesis of hypertension.This study investigates the relationship between hypertension, glucose intolerance, and hyperinsulinemia in a large, representative sample of the adult Jewish population in Israel. The findings show a strong association between hypertension and glucose intolerance, with 83.4% of hypertensives being either glucose intolerant or obese. Hypertension was independently associated with hyperinsulinemia, even in mild untreated hypertensives. The study also found that hypertension, obesity, and glucose intolerance are associated with altered internal cation distribution, with 88.1% of individuals with all three conditions presenting at least one marker of internal cation imbalance. These results suggest that insulin resistance and/or hyperinsulinemia are common pathophysiological features of obesity, glucose intolerance, and hypertension, and may explain their widespread association. The study further proposes that tissue insulin resistance could alter internal sodium and potassium distribution, leading to increased peripheral vascular resistance, which is hypothesized to contribute to the pathogenesis of hypertension.