The diets of the average healthy Americans and Canadians were studied. The results show that the amount of potassium in the diet is lower than what is needed to sustain health... this sheds light on increase of hypertensive drugs, diabetes, cancer and other metabolic diseases that ravage the populations.
The average intake of potassium by adults:
Men 2.8 to 3.3 g (72 to 84 mmol)/day
2.2 to 2.4 g (56 to 61 mmol)/day
Because blacks on average have a relatively
low intake of potassium and a high prevalence of elevated
blood pressure and sodium sensitivity, this subgroup of the US population
would especially benefit from potassium supplementation.
Sodium bicarbonate deficiency is one substance demonstrated to increase acidosis in the body leading to an increase of cancer in the western diet. Potassium deficiency is directly linked to bicarbonate deficiency.
In raw foods, the conjugate anions (Since protons are positively charged and electrons are negatively charged, if there are more electrons than protons, the atom or molecule will be negatively charged. This is called an anion (pronounced; an-eye-on), of potassium
are mainly organic anions, such as citrate, that are converted in the
body to bicarbonate. Hence an inadequate intake of potassium is
also associated with reduced intake of bicarbonate precursors. Acting
as a buffer, bicarbonate neutralizes diet-derived noncarbonic acids, such as sulfuric acid generated from sulfur-containing amino
acids commonly found in meats and other high protein foods. In
the setting of an inadequate intake of bicarbonate precursors, buffers
in the bone matrix neutralize the excess diet-derived acid, and
in the process, bone becomes demineralized.
Excess acids in the body irritates bone calcium and leads to increased urinary calcium and reduced
urinary citrate excretion.
Calcium stone disease is attributable to super saturation of the urine with calcium and other salts, the presence of substances that promote crystallization and a deficiency of inhibitors of crystallization. Citrate is a potent inhibitor of calcium oxalate and calcium phosphate stone formation whose excretion is diminished in some patients with stone disease following the spontaneously or secondary factors such as bowel disease and use of diuretic.
Urine concentrations of calcium and citrate (Citrate is an intermediate in the (Krebs) Cycle ) are the most important factors in stone formation.
Studies using potassium citrate, which increases urinary citrate excretion, had therapeutic effects for patients with kidney stone disease and hypocitraturia refractory.
Considering the forgone information, the resultant adverse clinical consequences
are possibly increased bone demineralization and increased
risk of calcium-containing kidney stones. In processed
foods to which potassium has been added and in supplements, the
conjugate anion is typically sodium chloride, which does not act as a buffer.
Because the demonstrated effects of potassium often depend on
the accompanying anion and because it is difficult to separate the
effects of potassium from the effects of its accompanying anion,
studies indicate that supplementing with Potassium citrate instead of potassium chlorides.
Increasing potassium from foods naturally high in potassium such as fruits, vegetables,
and other potassium-rich foods, would help improve ones life.
In addition to its blood pressure-reducing effects, increased potassium
intake has independent vascular protective properties.
In a series of animal
models, including both stroke-prone spontaneously hypertensive
and Dahl salt-sensitive rats, the addition of either potassium
chloride or potassium citrate markedly reduced the mortality
from stroke, a reduction that was unrelated to any measured attenuation
of hypertension (Tobian, 1986; Tobian et al., 1984).
In a more
recent study with stroke-prone spontaneously hypertensive rats in which aortic blood pressure was
measured by continuous radiotelemetry, dietary potassium supplemented
as either potassium bicarbonate or potassium citrate attenuated
hypertension and prevented stroke (Tanaka et al., 1997).
However, supplemental potassium chloride exacerbated hypertension,
increased risk of stroke (Tanaka et al., 1997), and amplified renal
microangiopathy (Tanaka et al., 2001), in comparison with potassium
bicarbonate or citrate.
In several studies, an increased dietary intake of potassium has
been associated with a reduced risk of kidney stones.
Kidney stones in both sexes are directly related to the urinary
sodium:potassium ratio (Cirillo et al., 1994). In a pre-post,
uncontrolled study of children with idiopathic hypercalciuria, reducing
the dietary sodium:potassium ratio greatly reduced urinary
calcium excretion (Alon and Berenbom, 2000). Excessive urinary calcium excretion is
generally accepted as a major risk factor for calcium-containing kidney
stones (Coe et al., 1992). The incidence of kidney stones has
been shown to increase with an increased sodium:potassium ratio
(Stamler and Cirillo, 1997).
In a longitudinal study of 51,529 men conducted prospectively
over 4 years, the incidence of symptomatic kidney stones, while not
correlating with dietary sodium, did correlate strongly and negatively
with dietary potassium as measured by a food-frequency questionnaire
over a broad range of intake (2.9 to 4.0 g [74 to 102
mmol]/day) (Curhan et al., 1993) .
The absence of
a relationship between dietary sodium and kidney stones should be interpreted cautiously because the food-frequency questionnaire
used in these studies did not measure sodium intake either accurately
or precisely (Subar et al., 2001). In this study (Curhan et al.,
1993), the incidence of kidney stones correlated directly with meat
In a 12-year prospective study of an even larger number of
female nurses, the incidence of stone formation was inversely associated
with dietary potassium (2.0 to 4.7 g [52 to 119 mmol]/day)
(Curhan et al., 1997).
In a study conducted in Finland where the
dietary potassium intake is greater than in the United States, risk
for kidney stones appeared to decrease with an increased intake of
potassium (3.8 compared with 4.6 g [97 to 118 mmol]/day)
(Hirvonen et al., 1999). However, higher intakes of potassium did
not appear to further reduce risk, and the relationship between
potassium intake and kidney stones, overall, was nonsignificant.