Sodium and Blood Pressure
It is often recommended for patients with hypertension to reduce their sodium intake. There is evidence that a diet restricted in salt can lower blood pressure in those with and without hypertension (Sacks et al., 2001). The rationale is in part derived from the understanding that sodium accumulation in the body, along with subsequent water retention, can increase blood pressure. However, the intake of sodium may not be the primary influence on its retention in the body. Another influence is potassium intake (R Curtis Morris Jr, Schmidlin, Frassetto, & Sebastian, 2006).
In patients with kidney disease, renal sodium excretion can be impaired, in which case salt restriction prevents excessive accumulation and subsequent rise in blood pressure (Krikken, Laverman, & Navis, 2009). In those without kidney disease, research suggests that adequate intake of potassium may be more effective than restricting dietary sodium (R Curtis Morris Jr et al., 2006). Potassium is obtained in the diet through intake of vegetables, fruit, milk, and other foods. Today’s relatively low intake of vegetables and fruits in many individuals may not be providing sufficient potassium for proper sodium excretion.
Potassium and Blood Pressure
This leads to the hypothesis that increased potassium intake without sodium restriction can normalize blood pressure. To answer this question, one study tested increased potassium intake on blood pressure in older patients with hypertension (S. R. Smith, Klotman, & Svetkey, 1992). They found that increased potassium through KCl supplementation increased sodium excretion and lowered blood pressure. However, in another study in hypertensive men, KCl supplementation did not reduce the need for antihypertensive medication, even on a sodium-restricted diet (Grimm et al., 1990).
In a study in young rats, potassium deficiency per se increased blood pressure and induced salt sensitivity (Ray, Suga, Liu, Huang, & Johnson, 2001). Salt sensitivity refers to the tendency for some individuals to react to a moderate elevation of salt intake with an elevation of blood pressure. Salt sensitivity has been shown to occur when dietary potassium is even marginally deficient, but this effect is reduced in a dose-dependent manner when potassium intake is increased to adequate levels (R C Morris Jr, Sebastian, Forman, Tanaka, & Schmidlin, 1999). This supports the recommendation to combat hypertension by first increasing dietary potassium and second by moderate reduction in sodium intake, if necessary.
Chloride and other Salts of Sodium
Other minerals may also influence blood pressure. Increased dietary intake of calcium and magnesium have also been shown to decrease blood pressure (Houston & Harper, 2008). Dietary sodium is obtained through added salt (NaCl). Sodium chloride has in fact been shown to increase calcium excretion compared to sodium bicarbonate, which did not (Luft, Zemel, Sowers, Fineberg, & Weinberger, 1990). This raises the question if chloride is partly responsible for salt’s effect on blood pressure. In one study, chloride loading raised blood pressure in rats due to its effects on sympathetic nervous activity (Miki et al., 1989). That chloride also increases blood pressure along with its potential effect on calcium excretion suggest that sodium obtained through other salts (eg. bicarbonate, acetate, etc.) may have different effects than sodium chloride, including blood pressure.
In a study unrelated to blood pressure, both sodium bicarbonate and acetate induced metabolic alkalosis and increased energy expenditure (G. I. Smith, Jeukendrup, & Ball, 2007). Sodium bicarbonate increased fatty acid oxidation, whereas sodium acetate did not. This was believed to be due to the increase in oxidation of acetate for energy. Excessive renal acid load has been speculated to negatively influence a range of health problems including bone demineralization and muscle retention (Remer, Dimitriou, & Manz, 2003). This raises the question if sodium obtained through salts other than chloride influence blood pressure in the same manner as sodium chloride.
Acetate has been shown to decrease peripheral arterial resistance, lowering blood pressure, while slightly increasing cardiac output and decreasing myocardial contractile force (Keshaviah, 1982; Kirkendol, Pearson, Bower, & Holbert, 1978; Schohn, Klein, Mitsuishi, & Jahn, 1981). This shows that sodium acetate can have a blood pressure lowering effect, which is contrary to sodium chloride’s effect. However, it appears that increased plasma acetate may lead to problems related to metabolic alkalosis and heart function. Nevertheless, sodium itself may not be as problematic as the form it’s obtained in.
In addition to the effects of acetate, acetic acid (5% in vinegar) has been investigated for its metabolic effects. When added to a bread meal, it lowers postprandial blood glucose and insulin response (Ostman, Granfeldt, Persson, & Björck, 2005). A similar effect was found when vinegar was added to a meal of potatoes (Leeman, Ostman, & Björck, 2005). The effect was not due to decreased gastric emptying. This raises the question if sodium acetate (the sodium salt of acetic acid) would have a similar beneficial effect on postprandial blood glucose control. In fact, acetate directly activates AMPK in the liver, also lowering glucose-6-phosphatase and genes involved in gluconeogenesis and lipogenesis, potentially leading to better blood glucose control (Sakakibara, Yamauchi, Oshima, Tsukamoto, & Kadowaki, 2006). However, when added to a meal, sodium acetate was not as effective as acetic acid (Brighenti et al., 1995). This suggests that the acidity is partly responsible for vinegar’s effect on postprandial glycemia.
Acid (dietary and endogenous) is neutralized in our small intestines with bicarbonate (Gropper, Smith, & Groff, 2009). When neutralized with bicarbonate, acetic acid produces sodium acetate. If all dietary acetic acid is neutralized upon entering the duodenum, it would not be expected to have a different effect than sodium acetate. This suggests that acid is incompletely neutralized in our small intestines, or that we have a limited capacity to neutralize acid.
To support this, patients with hyperchlorhydria as well as those with pancreatitis show lower duodenal pH than normal individuals (Gerber, Gerber, & Arendt, 1987). This decrease is potentially low enough to deactivate intestinal enzymes, including amylases and disaccharidases. Enzymes operate optimally within a specific pH range. Outside this range, enzyme activity is decreased, potentially completely. If in fact we have a limited capacity to neutralize acid, then dietary acid may decrease intestinal pH low enough for amylase and disaccharidase to be reduced, thus decreasing the rate of intestinal absorption of sugars and subsequent rise in blood sugar. In fact, fermented milk (containing lactic acid) was shown to reduce the glycemic response compared to nonfermented milk. This is similar to the beneficial effect of vinegar (acetic acid) in previously mentioned studies. Additionally, acetate was shown to have more anti-disaccharidase activity than other acids (succinic, lactic, and tartaric) (Ogawa et al., 2000).
Excess sodium chloride increases blood pressure. Potassium deficiency increases blood pressure. Adequate potassium intake increases salt tolerance. Sodium chloride has different metabolic effects compared to bicarbonate or acetate. Sodium acetate lowers blood pressure but may have negative effects with excessive intake. Dietary acid reduces postprandial glycemic response. Acetic acid has a greater effect on postprandial glycemia than sodium acetate.
Eat plants. Salt food to taste. Consider some vinegar or fermented foods (eg. yogurt, sauerkraut, pickles, etc.) to reduce postprandial glycemia. Don’t go crazy with dietary experiments.
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