Most Americans Do Not Get Enough Potassium
Modern human dietary requirements were encoded into our DNA during evolution starting with the Paleolithic diet, which contained about 35% meat and about 65% plant foods. The type of meat (more monounsaturated, less saturated fat) and of plant foods (more omega-3 fatty acids and far more fiber) eaten by early man was different as well.
One of the most important differences was that there was far more potassium (from fruits and vegetables) and much less acid-forming content (because of the increased ratio of plant to animal foods) in the early human diet. The change to a low potassium, high acid-forming content diet has had a profound impact on many aspects of wellness and healthy aging, including those listed above.
Nothing in biology makes sense except in the light of evolution.—Theodosius Dobzhansky
. . . modern DNA is a coded description of the environments in which ancestors survived. A survival manual is handed down the generations.—Richard Dawkins, A Genetic Book of the Dead
Much Higher Potassium Content in Paleolithic Diet
According to one study,1 “the Stone Age human potassium intake averaged 400 ± 125 mEq/d [about 15 grams per day!], which exceeds the NHANES III [Third National Health and Nutrition Examination Survey, 1988-1994] age-grouped averages (~60-85 mEq/d) [2.3–3.3 grams/d] by factors greater than 4.” This amount also “exceeds the 120 mEq/d set for adequate intake by the Food and Nutrition Board of the Institute of Medicine in 2004 and 2006 and the same value, 120 mEq/d recommended by the U.S. Department of Agriculture in 2005 [4.7 grams per day].”1 Note that the potassium content of the average American adult diet is only 50% to 70% of the amount recommended. This means that most American diets are officially deficient in potassium. Worse yet, we believe that the official RDA is too low.
Much Lower Sodium Content in Paleolithic Diet
The Paleolithic diet contained much lower levels of sodium than our modern diet, typically only a fraction of a gram per day. By comparison, our modern diet contains far more sodium, about 2.5 to 5 grams of sodium per day.10 This means that the ratio of potassium to sodium in our diet has changed from about 5 to about 0.7, a change toward less potassium and more sodium of 700%. Our kidneys are not evolved to deal with such a radically changed dietary ratio of potassium to sodium, and may be losing too much potassium and retaining too much sodium with potentially serious adverse health consequences, such as some cases of hypertension.
Much Lower Acid Formation from the Paleolithic Diet
The Institute of Medicine also reported that “. . . Fruits and vegetables, particularly leafy greens, vine fruit [aka, vegetable fruit, such as tomatoes, cucumbers, zucchini, eggplant, and pumpkin] and root vegetables, are good sources of potassium and bicarbonate precursors. Although meat, milk and cereal products contain potassium, they do not contain enough bicarbonate precursors to balance their acid-forming precursors, such as sulfur-containing amino acids.” The results of a high net-acid producing diet include1 increased urinary calcium excretion, increased bone resorption markers (indicative of bone loss), and increased urinary nitrogen excretion (negative nitrogen balance as occurs with loss of lean body mass).
Reduction of Stroke Risk by Potassium
One paper reported on the potassium dietary intake (estimated from a 24 hour recall of dietary foods) versus occurrence of stroke during a 12-year follow-up of 356 men and 503 women who were 50 to 79 years old at baseline and without pre-existing history of heart attack, heart failure, or stroke.2 The results showed that the relative risks of stroke-associated mortality in the lowest tertile of potassium intake, as compared with that in the top two tertiles combined, were 2.6 (p=0.16) in men and 4.8 (p=0.01) in women. The effect was partially independent of known cardiovascular risk factors, such as age, sex, blood pressure, blood cholesterol levels, obesity, fasting blood glucose levels, and cigarette smoking.
Another study3 of 5,600 men and women older than 65 years and who were free of strokes, followed for 4 to 8 years, reported that a lower serum potassium level was associated with an increased relative risk of stroke (RR:1.5, p<0.005); a lower serum potassium level in those taking diuretics (presumably for high blood pressure) was associated with an even greater increased risk of stroke (RR:2.5, p<0.0001). In fact, “for each SD [standard deviation] decrease in serum potassium in a diuretic user, there was a 38% increase in the RR for stroke. For each SD decrease in dietary potassium in a nondiuretic user, there was an 18% increase in the RR for stroke.”3
A Possible Mechanism for Increased Stroke Damage As a Result of a High Acid Diet
One interesting relationship between increased tissue acid level and stroke was reported in the Sept. 17, 2004 Cell.4 Researchers found that the acidosis (increase in tissue acid) that results from ischemia (reduced oxygen availability)-induced increase in anaerobic glycolysis (the production of energy via a non-oxygen requiring glucose pathway) worsens ischemic brain injury, such as in stroke. These scientists found that knocking out the ASICs (acid-sensing ion channels) that detect the acidosis provided neuroprotective effect against excitotoxic damage in knockout mouse neurons, as compared to neurons of wild-type mice. In fact, they found that the area of killed brain tissue (infarct) was about 60% less in strokes induced in the ASIC knockouts as compared to wild type mice.
It would be interesting to see whether, using the same model, potassium bicarbonate could produce a similar neuroprotective effect by reducing tissue acidosis itself, which should also reduce the activation of acid-sensing ion channels.
Alkaline Diets Favor Lean Tissue Mass in Older Adult Humans
Chronic metabolic acidosis can result from eating a diet whose metabolism yields acids (such as sulfuric acid) in excess of bases (e.g., bicarbonate). In fact, this type of diet is typically consumed by populations of industrially developed (Westernized) countries, where animal foods rich in acid precursors are consumed disproportionally to that of plant foods rich in base precursors.5 One result of chronic metabolic acidosis is an acceleration in the protein degradation of skeletal muscle; moreover, diet-dependent metabolic acidosis tends to increase in severity with age.5 One recent study6 reported that increased potassium urinary excretion (derived from alkaline potassium salts found in dietary fruits and vegetables) was associated with increased lean body mass in 384 men and women 65 or older who participated in a calcium and vitamin D versus placebo study of osteoporosis. The authors concluded that “. . . subjects with a potassium intake of 134 mmol/d [5.2 grams/d] can expect to have 1.64 kg more lean tissue mass than subjects with half that potassium intake.”5
In a separate paper,6 researchers studying the effect of an oral potassium bicarbonate supplement (60–120 mmol/day for 18 days) in 14 healthy postmenopausal women found that the supplements reduced urinary nitrogen excretion, an indicator of preserved lean body mass. The authors concluded that “[t]he magnitude of the KHCO3[potassium bicarbonate]-induced nitrogen sparing effect is potentially sufficient to both prevent continuing age-related loss of muscle mass and restore previously accrued deficits.” The amount of potassium bicarbonate supplement used in this study was 6 to 12 grams per day, which supplied 2.34 to 4.68 grams of potassium per day.
Decreased Calcium Excretion Helps Protect Bones
In another paper,7 the effect of potassium bicarbonate on calcium excretion in postmenopausal women was reported. The authors note that potassium bicarbonate has been shown to potently reduce urine calcium excretion in adult humans, including patients with hypertension or calcium urolithiasis, and postmenopausal women. As the authors note, “[t]he [Western] diet-induced low-grade metabolic acidosis that persists further contributes to the external losses of calcium by direct impairment of renal [kidney] calcium reabsorptive efficiency, a characteristic of metabolic acidosis.” They, therefore, studied the effect of 30, 60, or 90 mmol/d potassium bicarbonate treatment in 170 postmenopausal women for up to 36 months. (3, 6, or 9 grams per day of potassium bicarbonate supplying 1.17, 2.34, or 3.51 grams per day of potassium, respectively.)
All doses of potassium bicarbonate reduced urinary calcium excretion throughout the study. Interestingly, in the 28% of the subjects that had high baseline urinary calcium excretion, 60 mmol/day of potassium bicarbonate decreased the urinary calcium excretion by an amount that, over a 36 month period, would accumulate up to 55,845 mg of calcium or nearly 5% of bone calcium content.7
Potassium is Vasoactive, Increasing Blood Flow, Helping Regulate Blood Pressure
It has been reported that potassium depletion in normal humans increases blood pressure, as well as reducing the ability to deal with an acute sodium load and sodium retention.8 In borderline hypertensives (140/90), “a low-potassium diet (16 mmol/day) for 10 days increases systolic and diastolic pressures by 7 and 6 mmHg, respectively, relative to 10 days on a high-potassium diet (96 mmol/day).”8 Indeed, potassium supplementation lowers blood pressure in established hypertension.
“Potassium is vasoactive; when infused into the arterial supply of a vascular bed, blood flow increases.”8 Potassium release is regulated by the Na+-K+-ATPase [sodium-potassium-ATPase) enzyme in the plasma membrane. “Potassium increases the uptake of norepinephrine [aka noradrenaline] into the sympathetic nerve terminals, leaving less in the [synaptic] cleft. This also promotes relaxation of the vascular smooth muscle and increases blood flow.” In this way, potassium acts importantly to regulate the excitatory effects of norepinephrine. In one study,9 reduced dietary potassium reversibly enhanced vasopressor (vascular contraction, which induces increased blood pressure) response to stress in African Americans. As noted in the paper, the blood pressure of normotensive blacks is much more likely to be salt sensitive than that of normotensive whites. “In normotensive [but salt sensitive] blacks but not whites [normotensive and not salt sensitive], a marginally reduced dietary intake of potassium reversibly enhances adrenergically mediated vasopressor responsiveness to stress.”
How to Take Potassium Bicarbonate
You can easily eat more like a Caveman without having to become a hunter/gatherer by taking one or two capsules, each containing 1.35 grams of potassium bicarbonate (13.5 meq or 527 mg potassium) two to four times per day. Take with meals.11
If you are an adult eating a typical American diet, you would need approximately 3 to 4 capsules per day of potassium bicarbonate to increase your total potassium intake to the RDA.
WARNING: IF YOU ARE TAKING A POTASSIUM-SPARING DIURETIC PRESCRIPTION DRUG DO NOT TAKE SUPPLEMENTAL POTASSIUM!