Potassium protects the heart
Genetically salt-sensitive rats were fed a normal diet (0.3% sodium chloride)
or a high-salt diet (8% sodium chloride), with or without high potassium intake
(8% potassium chloride) for eight weeks. High salt intake significantly increased
blood pressure, impaired left ventricular relaxation, and increased the activity
of NADPH oxidase in cardiac tissue. High potassium intake improved left ventricular
relaxation and reversed the elevation of NADPH oxidase activity, even though
blood pressure remained high.
In other studies, dogs made potassium-deficient by means of a low-potassium
diet and administration thiazide diuretics showed impairments of both systolic
and diastolic heart function, with the most striking effect being a 49% reduction
in the peak rate of ventricular filling. In a study of healthy human volunteers,
potassium depletion resulted in a 14% reduction in the peak rate of ventricular
filling. In a randomized trial, elderly men who switched from regular salt
to potassium-enriched salt (49% potassium chloride, 49% sodium chloride, 2%
other additives) for 31 months had a 41% decrease in cardiovascular mortality.
Comment: Diastolic dysfunction (impaired left ventricular filling) is a common
and important, though under-appreciated, cause of heart failure. In one recent
study, of 556 unselected patients with heart failure, 55% had a normal left
ventricular ejection fraction, indicating that heart failure was almost certainly
due to diastolic dysfunction. Patients with diastolic heart failure have mortality
rates similar to those with systolic heart failure.
The studies reviewed above suggest that potassium deficiency can contribute
to diastolic dysfunction and possibly to systolic dysfunction as well. One
mechanism by which potassium might help prevent heart failure is by inhibiting
cardiac NADPH oxidase activity, thereby decreasing oxidative stress.
Most people do not consume enough fruits and vegetables (the main dietary sources
of potassium). Some diuretics used to treat heart failure may also promote
or exacerbate potassium deficiency. In addition, some of the pathophysiological
mechanisms underlying heart failure may lead to a loss of both potassium and
magnesium from myocardial cells. Magnesium is required for the intracellular
uptake of potassium, so potassium supplementation alone will not correct intracellular
potassium deficiency unless magnesium deficiency is also corrected. In patients
with renal failure (which is sometimes associated with heart failure), potassium
and magnesium should be administered with caution and monitored with appropriate
Matsui H, et al. Protective effect of potassium against the hypertensive cardiac
dysfunction: association with reactive oxygen species reduction. Hypertension.
Young DB. Potassium depletion and diastolic dysfunction. Hypertension. 2006;48:201-202.
Chang HY, et al. Effect of potassium-enriched salt on cardiovascular mortality
and medical expenses of elderly men. Am J Clin Nutr. 2006;83:1289-1296.
Improving cardiac risk factor with a nutritional supplement
Forty men with a history of myocardial infarction who had completed a cardiac
rehabilitation program (including supervised exercise training and lifestyle
and dietary recommendations) were randomly assigned to receive 500 ml/day
of a fortified dairy product (active-treatment group) or 500 ml/day of semi-skimmed
milk (control group). The fortified product provided the following nutrients
that were not present in the control drink (alpha-linolenic acid, 0.6 g/100
g of total fat; eicosapentaenoic acid, 2.1 g/100 g of fat; docosahexaenoic
acid, 1.2 g/100 g of fat; vitamin E, 15 IU/L; vitamin B6, 3 mg/L; and folic
acid, 300 mcg/L). The fortified product also contained larger amounts of
oleic acid than the control drink. The mean C-reactive protein concentration
decreased from 3.90 mg/L at baseline to 2.01 mg/L after 12 months in the
active-treatment group and from 3.64 mg/L to 3.23 mg/L in the control group
(p < 0.05 for the difference in the change between groups). The difference
between groups was also significant after six months.
Comment: C-reactive protein is a marker of inflammation. An elevated serum
C-reactive protein level is an independent risk factor for coronary heart disease.
The results of this study demonstrate that supplementation with modest doses
of fatty acids, vitamin E, and B vitamins can significantly reduce C-reactive
protein levels in patients with a history of myocardial infarction. Another
way to reduce C-reactive protein levels is to avoid heavily cooked foods (such
as well-done meat and pizza) and to emphasize raw or lightly cooked foods.
Byproducts formed during harsh cooking (advanced glycation end products) appear
to promote inflammation. For people who are overweight, weight loss also reduces
C-reactive protein levels.
Carrero JJ, et al. Intake of fish oil, oleic acid, folic acid, and
vitamins B-6 and E for 1 year decreases plasma C-reactive protein
and reduces coronary
heart disease risk factors in male patients in a cardiac rehabilitation program.
J Nutr. 2007;137:384-390.
Does vitamin D deficiency lead to heart failure?
This review article points out that the majority of patients with congestive
heart failure have vitamin D insufficiency (serum 25-hydroxyvitamin D < 50
nmol/L or < 20 ng/ml). Vitamin D deficiency in these patients is presumably
due in part to relatively low amounts of outdoor activity. Vitamin D deficiency
may contribute to the pathogenesis of heart failure, or may exacerbate heart
failure, by promoting the development of hypertension or by increasing parathyroid
hormone levels, which is believed to contribute to the development of cardiovascular
Comment: In recent years, evidence has accumulated that vitamin D deficiency
is very common and may contribute to the development of muscle weakness and
pain, some autoimmune diseases, osteoporosis, infections, and cancer. While
vitamin D deficiency has not been proven to cause or exacerbate heart failure,
it would be worthwhile to measure serum 25-hydroxyvitamin D levels in patients
with heart failure and to correct deficiencies either with supplementation
or sunlight exposure. The amount of oral vitamin D required to optimize 25-hydroxyvitamin
D levels might be higher in patients with heart failure than in healthy people,
because heart failure is often accompanied by bowel wall edema, which could
inhibit nutrient absorption.
Zittermann A, Schleithoff SS, Koerfer R. Vitamin D insufficiency in congestive
heart failure: why and what to do about it? Heart
Fail Rev. 2006;11:25-33.
forget thiamine for heart failure patients
The prevalence of thiamine deficiency (as determined by erythrocyte thiamine
pyrophosphate concentrations) was significantly higher in 100 patients with
congestive heart failure than in healthy controls (33% vs. 12%; p = 0.007).
Comment: Patients with congestive heart failure may be at increased risk for
thiamine deficiency as a result of diuretic-induced thiamine excretion, malnutrition,
and advanced age. Severe thiamine deficiency is a known cause of heart failure
(beri beri heart disease), and it is likely that even modest degrees of thiamine
deficiency would have an adverse effect on the course of heart failure. Routine
supplementation of heart failure patients with a high potency B-complex vitamin
would therefore be prudent.
Hanninen SA, Darling PB, Sole MJ, Barr A, Keith ME. The prevalence of thiamin
deficiency in hospitalized patients with congestive heart failure. J
Am Coll Cardiol. 2006;47:354-361.
Case report: parenteral magnesium for end-stage cardiomyopathy
A 57-year-old man came to see me from several hundred miles away with a 15-year
history of slowly progressive dilated cardiomyopathy. He was still functioning
relatively well, although he did experience shortness of breath after moderate
exertion. The patient was advised to take various nutrients that support
cardiovascular function, including coenzyme Q10, magnesium, and L-carnitine,
to continue seeing his cardiologist, and to check in with me periodically
by phone. He was also advised to take a series of weekly intramuscular magnesium
injections, but he was unable to find a practitioner in his town willing
to administer them.
Two years later, I received a call from the man's wife. Her husband was
in the final stage of his disease. He was in the hospital on a continuous dobutamine
drip, which was needed to him alive. The cardiologist's plan was to give
the patient time to get his affairs in order, and then to discontinue the dobutamine
and allow the patient to die. His wife asked if there was anything else that
could be done. I suggested that he be given one gram of magnesium sulfate intramuscularly,
daily for several days.
Within ten minutes of receiving the first injection, the patient converted
from atrial fibrillation to normal sinus rhythm, and he appeared to be improved
overall. He did revert to atrial fibrillation again shortly thereafter, but
the series of magnesium injections had a dramatic beneficial effect. He was
successfully weaned from the dobutamine drip and later discharged from the
He continued to receive magnesium injections at home every fourth day. If more
than four days elapsed between injections, his condition would deteriorate.
Although he was not able to do much more than walk slowly around the house,
magnesium injections extended his life by about two years.
Comment: One can only guess how much more the magnesium injections might have
helped this man if they had been started earlier in the course of his disease.
"Fever of unknown origin" caused
by food allergy
Between the ages of 21 and 30 months, a girl was seen by 16 doctors for fever
of unknown origin and C-reactive protein concentrations of 100-200 150 mg/L
(normal, less than 5 mg/L). Elimination of dairy products and subsequent
challenge demonstrated that the fever was due to cow's milk allergy. On a
diet, the C-reactive protein level normalized within one week, and no further
Comment: Fever has been mentioned repeatedly over the years as a potential
manifestation of food allergy. As early as 1937, one practitioner described
three patients with constant fever for long periods of time (up to eight
years in one case) that resolved after identification and avoidance of
allergenic foods. Despite these reports, allergy is not mentioned as a
of "fever of unknown origin" in standard texts.
Hozyasz KK, et al. Fever and high C-reactive protein level as the sole manifestation
of allergy to cow milk. Explore. 2006;2:520-521.
Folic acid prevents age-related hearing loss
Seven hundred twenty-eight older men and women (mean age, 60 years) residing
in the Netherlands who had plasma total homocysteine concentrations of 13
micromol/L or greater, serum vitamin B12 concentrations of 200 pmol/L or
greater, and no pathologic ear conditions were randomly assigned to receive,
in double-blind fashion, 800 mcg/day of folic acid or placebo for three years.
After three years, the mean threshold for hearing of low frequencies increased
by 1.0 dB in the folic acid group and by 1.7 dB in the placebo group (p =
0.02 for the difference in the change between groups). Folic acid supplementation
did not affect the decline in hearing of high frequencies.
Comment: Low folate status has been associated with poor hearing. In the new
study, folic acid supplementation slowed age-related decline in hearing of
the speech frequencies. The study was conducted in a country in which food
is not fortified with folic acid, so it is not clear whether similar results
would be seen in the United States, where grains are fortified with folic acid.
Nor is it clear whether people with normal homocysteine levels would obtain
the same benefit from folic acid. Folic acid supplementation should be combined
with vitamin B12, because these nutrients work together in the body and administering
a large dose of one might promote a deficiency of the other.
Durga J, et al. Effects of folic acid supplementation on hearing in older adults:
a randomized, controlled trial. Ann Intern Med. 2007;146:1-9.
Eggs are a good source of lutein and zeaxanthin
Twenty-four female volunteers (aged 24-59 years) were assigned to consume six
eggs per week or a placebo pill, while continuing their normal diet, for
12 weeks. The eggs were obtained either from a local supermarket (EGG 1)
or from an organic farm (EGG 2). The lutein and zeaxanthin content of the
eggs varied considerably, but the means were higher in EGG 2 than in EGG
1 (964 vs. 331 mcg of lutein + zeaxanthin per yolk). Serum zeaxanthin, but
not serum lutein, increased in both the EGG 1 (p = 0.04) and EGG 2 (p = 0.01)
groups. Macular pigment optical density increased in both the EGG 1 (p =
0.001) and EGG 2 (p < 0.05) groups. The higher-carotenoid eggs were not
more effective at increasing macular pigment optical density than the lower-carotenoid
Comment: The macular pigment, which consists
largely of the carotenoids lutein and zeaxanthin, appears to protect against
the development of age-related macular
degeneration, apparently by filtering the phototoxic blue-light portion of
the spectrum. Previous studies have shown that people with a thicker macular
pigment (as measured by macular pigment optical density) have a lower risk
of developing macular degeneration. Although the content of lutein + zeaxanthin
in eggs is relatively modest relative to other sources such as spinach, their
bioavailability to the retina appears to be high, as demonstrated in this study
by an increase in the macular pigment optical density.
Wenzel AJ, et al. A 12-wk egg intervention increases serum zeaxanthin and macular
pigment optical density in women. J Nutr. 2006;136:2568-2573.
R. Gaby, MD