Dietary and Nutritional Considerations

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Nutrition is considered an important nonpharmacologic component of heart failure management. Congestive heart failure is associated with inadequate intakes of macronutrients, micronutrients and vitamins. The majority of CHF patients are deficient in their intake of calories and protein resulting in muscle protein breakdown and reduced energy availability for physical activity.1 Nutritional impairment has been shown to be an independent predictor an overall worse health-related quality of life with increased clinical events, rehospitalization and early death.1-3

Nutritional Alterations in Patients with Heart Failure

A number of factors have been identified to be associated with poor nutritional status in patients with heart failure. A recent study by Lennie et al.4 sought to compare patients with heart failure to healthy elderly individuals with regards to the extent to which they perceived how appetite and hunger, emotional and social, and illness-related factors affected the amount of food they consumed. Table 1 shows the results of this study.

Factors affecting food intake

 Nutritional Support in Heart Failure

There is a growing recognition that nutrition may play a crucial role in the comprehensive management of patients with heart failure. In this section we will review what is known about nutrition and heart failure.

  • Dietary sodium restriction is considered by many health care practitioners to be the leading nonpharmacologic therapy for heart failure. Currently, there is no clear scientific evidence on which to base guidelines on how far dietary salt intake should be restricted in heart failure. The Heart Failure Society of America (HFSA) recommends that patients who have the clinical syndrome of heart failure and preserved or depressed left ventricular ejection fraction restrict daily sodium intake to no more than 2-3 grams. Further restriction may be necessary for individuals classified as having moderate to severe heart failure. Table 2 describes the five common levels of sodium-restricted diets prescribed by nutritionists.

 

Sodium Restricted Diets

A low salt diet is widely prescribed for patients with heart failure. Although most persons with heart failure have considerable difficulty in following such low-sodium diets, little is known about why heart failure patients fail to adhere to this diet. A variety of factors,  many of which are avoidable, are associated with a failure to comply with low-sodium  diets:

1.   The vast majority of patients with heart failure are unaware of recommended sodium restriction guidelines prior to referral to a heart failure specialty clinic.6
2.   Many patients lack the knowledge, or ability to sort foods into high- and low-sodium categories,6 especially when eating in restaurants.7
3.   Many patients are unaware of the sodium content or the “hidden salt” in many foods.8
4.   Salt restricted diets interfere with the ability of heart failure patients to participate in social events where food is served.8
5.   Limited food selection.7;8
6.   Food does not taste as good without salt.7
7.   Many patients state that following a low-sodium diet is difficult because they rarely cook and mainly eat already prepared meals (TV dinners, canned or boxed food).7
8.   Some patients state that poor concentration and poor memory are an ongoing problem. Several studies have shown that many heart failure patients could not recall any dietary instructions provided, while other patients recall incorrect information. These data suggest that reinforcement of dietary sodium recommendations should be repeated on a regular basis.7
9.   Some patients perceive no medical benefit to following the low-sodium diet.7
10. Some patients state that it is difficult to follow a low-sodium diet because other family members and friends do not eat the same low-salt foods.7

Careful attention to these factors through individual counseling and educational material provided by a nutritionist with reinforcement at each clinic visit may have a positive impact in maintaining dietary sodium compliance.

A recent study by Lennie et al.9 published in the Journal of Cardiac Failure suggests that the degree of sodium restriction required will differ greatly among heart failure patients depending on symptom severity (NYHA functional class). In this trial, patients in NYHA class III/IV with dietary sodium intake greater than 3 grams per day were approximately two and one-half times more likely to be hospitalized for cardiac problems or die over the median follow-up period of 12 months after controlling for a number of key variables. On the other hand, sodium intake less than 3 grams per day was associated with a higher risk for hospitalization and death in heart failure patients categorized as NYHA class I/II. The results of this study show that sodium restriction may not be effective for some less symptomatic patients with heart failure.

 

  • In addition to the usual factors (age, body size and composition, physiologic state, level of physical activity, etc.), an assessment of the energy needs of the heart failure patient must take into consideration the patient’s current weight, physical activity restrictions and severity of disease. Studies have shown that a significant number of non-obese, clinically stable and free living patients with heart failure have an inadequate intake of calories and protein. Aquilani et al.1 reported in the Journal of the American College of Cardiology that 54.4% of their non-obese patient population was malnourished, 15.8% were protein and calorie malnourished and that 38.5% had protein malnutrition with a normal body weight. The authors of this report recommend that clinically stable, heart failure patients with depleted muscle reserves should have a daily intake of at least 31.8 kcal/kg + 1.37 grams of protein/kg and normally nourished heart failure patients a daily intake of at least 28.1 kcal/kg + 1.12 grams of protein in order to preserve their actual body composition or counteract the effects of hypercatabolism.

*Note: Although BMI (body mass index) is an easy and cost effective measure of  nutritional status, with an unintentional loss of 10% in BMI being an indicator of malnutrition, its use in heart failure patients is subject to interpretation. Several studies  have reported BMI as being a major risk factor for the development of heart failure, in  which mortality was increased at the lowest and highest extremes and decreased in the  middle ranges. The prevalence of edema increases BMI on  the basis of fluid excess  rather than solid tissue mass.10 Determinations of lean body mass by anthropometric  measurements such as skinfold thickness and arm-muscle circumference may be more  reliable indicators of nutritional status.

  • Fluid retention, resulting in swollen ankles, legs and abdomen, is a central component in the pathophysiology of heart failure. Fluid restriction of 1.5 – 2.0 liters per day should be considered in all patients exhibiting fluid retention that is difficult to manage despite sodium restriction and high doses of diuretics. The least restriction that will achieve fluid balance should be used.

There are foods that are not consumed in a liquid form but must be counted as part of your total fluid intake since they are liquid at room temperature or contain a high percentage of liquid. Table 3 lists the fluid content of some commonly consumed foods. Table 4 list some common household equivalents. Too much fluid in your body can weaken your heart further if you have heart failure by forcing it to work harder to pump the blood through the body as well as exacerbate the symptoms of heart failure. Furthermore, excessive fluid intake negates the positive effects of diuretics. On the other hand, precautions must be taken in prescribing fluid restriction for the treatment of fluid retention to ensure that it does not result in salt depletion, electrolyte imbalance, and/or dehydration.11 To avoid these complications it is extremely important to follow the fluid intake guidelines prescribed by your doctor. To help you plan and count out your fluids for the day, try placing your allowed amount of water per day in an appropriate-sized container; consume your water from this container and pour out an amount equivalent to the fluids consumed from other sources.

Fluid Table 3 and 4

Tips that will help keep you from becoming thirsty throughout the day:

1.   Limit salty foods
2.   Eat frozen grapes or other fruits
3.   Eat ice chips
4.   Suck on a piece of hard candy or chew a piece of gum; this will activate the salivary glands to secrete saliva, preventing dry mouth
5.   Do not eep your house overly warm
6.   Use a humidifier to moisten the air; dry air increases thirst
7.   Avoid alcohol, tea, coffee and soft drinks; these beverages may cause further dehydration
8.   Rinse your mouth with mouthwash or water (do not swallow)
9.   Ask your doctor if “dry mouth” is a side effect of any of the medications you are taking

  • Thiamine (vitamin B1) serves as a coenzyme in many physiological functions including fat, protein and nucleic acid metabolism, it is critical component of key reactions in   carbohydrate energy metabolism. Malnutrition, advanced age, frequent hospitalization, prolonged use of loop diuretics, and alcoholism have all been demonstrated to increase the risk of thiamine deficiency.12
    The clinical manifestations of thiamine deficiency typically present in the nervous and cardiovascular systems as dry beriberi or wet beriberi, respectively. Dry beriberi is characterized by mental confusion and peripheral neuropathy with muscular wasting and loss of function or paralysis of the lower extremities. The symptoms of wet beriberi are similar to those of congestive heart failure. Therefore, thiamine deficiency may actually intensify underlying heart failure by interfering with the efficiency of cellular energy production. A study by Hanninen et al.13 published in the American College of Cardiology concluded that one-third of hospitalized congestive heart failure patients were thiamine deficient.

Thiamine supplementation trials in patients with heart failure have reported beneficial effects on cardiac function  as well as in thiamine status. A recent study  by Schoenenberger et al.14 conducted at the University of Bern in Bern, Switzerland  showed that thiamine repletion (300 mg/day) for 28 days was able to improve left  ventricular ejection fraction (LVEF). The study also demonstrated a trend towards an  improvement in functional status as measured by the 24 hour steps counter (pedometer).  See Table 5 (adapted from Ballister)15 and Table 6  (adapted from Ballister)15 for sources  of thiamine-rich fruits and vegetables, respectively.

 

  • Potassium (K) is the major intracellular cation. Under normal physiological conditions, 98% of the body’s potassium is intracellular. The serum potassium concentration is tightly regulated between 3.5 and 5.0 mmol/L. Along with sodium and calcium, potassium regulates the contractility of smooth, skeletal, and cardiac muscle. It is also important in maintaining electrolyte and acid-base (pH) balance.16
    Disorders of potassium homeostasis are important because they can lead to life-threatening outcomes. In heart failure patients the risk of a disruption in potassium homeostasis is substantial. Potassium balance may be lost both as a result of the neurohormonal compensation mechanisms (stimulation of the renin-angiotensin-aldosterone system and sympathoadrenergic stimulation) associated with cardiovascular diseases and as a consequence of the drugs used in the treatment of heart failure (diuretics).16;17 The prevention of hypokalemia (plasma potassium concentration <3.5   mmol/L) and hyperkalemia (plasma potassium concentration >5.3 mmol/L) is of fundamental importance in the management of heart failure if electrolyte and cardiac rhythm disturbances are to be avoided. See Table 7 (adapted from Ballister)15 and Table 8 (adapted from Ballister)15 for sources of potassium-rich fruits and vegetables, respectively.

 

  • Magnesium (Mg) is the fourth most abundant cation in the human body (after calcium, potassium and sodium). Magnesium is important for more than 300 enzymatic reactions and plays a key role in a wide array of metabolic      pathways and physiological processes including18-20:

1.   energy metabolism
2.   glucose utilization via glycolysis, the Krebs cycle and the hexosemonophospate shunt pathway
3.   protein synthesis
4.   fatty acid synthesis and breakdown
5.   nucleic acid synthesis
6.   cardiac and smooth muscle contraction
7.   numerous hormonal reactions

Clinically relevant magnesium deficiency is associated with heart failure and is becoming more prevalent amongst the elderly in the United States and may be attributed to a very low dietary intake (<200-250 mg/day in adults) for prolonged periods of time (weeks). Magnesium deficiency may also be caused by low or normal dietary intake combined with urinary losses due to certain drugs used in the treatment of heart failure such as diuretics and digitalis.20

 

Hypokalemia (plasma potassium concentration <3.5 mmol/L) is a manifestation of magnesium depletion. Potassium depletion may be a contributing factor to the electrocardiological abnormalities and cardiac arrhythmias associated with magnesium deficiency. Magnesium deficiency has also been associated with reduced cardiac contractility and increased peripheral resistance. Attempts to reconstitute potassium levels with potassium therapy alone will not be fruitful without the simultaneous administration of magnesium.21;22  See Table 9 (adapted from Ballister)15 and Table 10 (adapted from Ballister)15 for sources of magnesium-rich fruits and vegetables, respectively.

 

Table 9. Fruit sources of magnesium (adapted from Ballister)15
Table 10. Vegetable sources of magnesium (adapted from Ballister)15
Table 10. Vegetable sources of magnesium (continued) (adapted from Ballister)15

  • Few foods contain naturally occurring vitamin D. The term vitamin D is used to refer to either of the previtamins, vitamin D2 or vitamin D3 (cholecalciferol). Vitamin D2 is formed from ergocalciferol which is found in plants. Vitamin D3 is formed from 7-dehydrocholesterol which is found in the epidermal layer of the skin. Both ergocalciferol and 7-dehydrocholesterol require UV irradiation for conversion to their previtamin forms. Because vitamin D can be synthesized in the skin as a result of adequate exposure to sunlight, many scientists consider vitamin D more of a hormone than a vitamin. Vitamin D from the skin and diet is further metabolized in the liver to 25-hydroxyvitamin D3 (calcidiol). The most active form of vitamin D, 1,25-dihydroxycholecalciferol D3 (calcitriol), is produced in the kidneys from the conversion of 25-hydroxyvitamin D3  by the enzyme 1-alpha hydroxylase.23

The most important biological function of vitamin D (in its most active form as calcitriol) is to regulate plasma calcium levels. Vitamin D performs this function in the following ways:

1.   by increasing the absorption of calcium in the intestine

2.   by stimulating the reabsorption of calcium and phosphorous in the distal renal tubule of the kidney

3.    by stimulating the mobilization of calcium and phosphorous from bone (an important reservoir of calcium)  when necessary to achieve a normal blood calcium concentration

Vitamin D deficiency is a common, global phenomenon, especially among elderly people. The incidence of vitamin D deficiency appears to be on the rise and is related to24-27:

1.     limited sun exposure

2.     advanced age

3.     reduced dietary intake

4.     reduced absorption

5.     increased body fat mass/obesity

6.     poor mobility

7.     living in northern latitude regions

8.     use of sunscreen with sun protection factor >15

9.     living in a nursing home or assisted care facility

10.    reduced vitamin D synthesis in the skin

11.    increased indoor lifestyles with efforts to minimize sun exposure

12.   smoking

13.   renal disease – impaired conversion to the more active form of vitamin D, calcitriol, in the kidney

 

There is growing evidence to support a possible association between low vitamin D levels and the development and progression of heart failure. Table 11 shows the various levels of vitamin D status and their associated symptoms.

 

Table 11. Vitamin D Status

 

 

 

  • The trace mineral selenium (Se)is an essential nutrient of critical importance to animals and humans. Selenium enters the food chain through incorporation into plant protein as the amino acids selenocysteine and selenomethionine.28 Selenium intake varies tremendously around the world mainly because of geographical variations in soil selenium concentration. Consequently, if the animal and human population consume predominantly food grown and produced locally, the selenium status of the population will reflect that geographical region’s selenium soil content.

   Because most plants do not require selenium for growth, plant materials may have a very low selenium content if the selenium concentration or availability of the soil is low. Conversely, plants will take up large amounts of selenium if the soil selenium concentration is high and available.28

   Throughout the world, there are regions where the selenium content of the soil is so poor that humans were formerly afflicted by diseases, such as Keshan disease (a cardiovascular disease associated with congestive heart failure)      in parts of China, that are now known to be due to selenium deficiency and are prevented by selenium supplementation.

   Selenium is of fundamental importance to health because it is incorporated into selenoproteins that play a key role in many physiological processes, including immune function, thyroid function, and protection against oxidative stress. Selenium deficiency may contribute to cardiovascular disease and other diseases such as cancer in which oxidative stress and inflammation are thought to be part of the pathophysiological process.

   A number of studies investigating selenium in the setting of heart failure have demonstrated that patients with heart failure tend to have a lower plasma concentration of selenium when compared with healthy individuals.29

   A recent study by Lymbury et al.30 in a rat model of heart failure demonstrated that increased dietary selenium intake was clearly associated with an increase in selenium-containing antioxidant enzyme activity and a corresponding  decrease in oxidative stress-mediated cardiac injury. Furthermore, providing selenium in the diet was shown to delay the onset of heart failure and decrease mortality.

   The current recommended dietary allowance in the United States for healthy men and women 51+ years of age is 55 μg/day. For heart failure patients, the recommended dietary allowance is probably higher than that recommended for healthy individuals. Based on the findings of Lorgeril et al.31 that the low blood levels of selenium in patients with chronic heart failure is due to a low consumption of selenium-rich foods, a selenium intake of approximately 80 μg/day is required to obtain a blood concentration of 70 μg/L.

 

  • Recommendations to restrict alcohol are common for patients with heart failure, even though strong scientific evidence on which to base these recommendations is lacking. The recommendation to avoid alcohol most likely stems from the  recognized association of alcohol abuse with cardiomyopathy, a well-known risk factor for heart failure. Current dietary advice is to limit intake of alcohol to no more than 1 to 2 glasses (6 to 8 ounces per glass) of wine per day. Patients with alcoholic cardiomyopathy should not consume alcohol in any amounts.32

 

  • Dietary Supplements

Coenzyme Q10 (CoQ10), also known as ubiquinone, is a vitamin-like, fat-soluble compound present in all tissues and cells. CoQ10 plays a critical role in energy transduction and antioxidant processes. Every cell in the body must    have a process for obtaining energy. Over time, cells have devised two basic metabolic processes to generate energy. Aerobic metabolism, which utilizes oxygen, serves as the predominant means of energy production in humans. In the total absence of oxygen, anaerobic metabolism provides energy for living organisms. Oxygen-based generation of energy takes place mainly in a highly specialized compartment of the cell known as the mitochondria.

Muscle tissues, especially skeletal and cardiac, have especially high concentrations of CoQ10 in their mitochondria due to the high energy requirements of this cell type. Considering that the normal heart beats continuously, it is not surprising that its energy requirements are high. Thus, adequate amounts of CoQ10 are necessary for optimal energy production.

CoQ10 is also part of a network of antioxidants that function to delay or prevent the oxidation of cell membranes and lipoproteins.33 As a result, this endogenous antioxidant has bright prospects for use in prevention and treatment of cardiovascular disease, especially hypertension, ischemic heart disease, hypertrophic cardiomyopathy and heart failure.34 Clinical studies have also demonstrated the benefit of CoQ10 in the cardiothoracic surgical setting where patients undergoing coronary bypass graft surgery treated 7-10 days preoperatively with 150-180 mg/day of CoQ10 experienced significantly fewer reperfusion arrhythmias and shorter hospitalization compared with the control group.35

Based on food frequency questionnaire studies, a typical Western diet provides an estimated 3.8 mg per day for women and 5.4 mg per day for men of CoQ10, primarily derived from meat, fish, nuts and some oils (see Table 12).36

 

Table 12. Food sources of Coenzyme Q10 (adapted from Higdon and Drake)37

The finding that myocardial CoQ10 levels are reduced by up to 50% in both animal and human models of congestive heart failure has provided the rationale for clinical trials of CoQ10 supplementation in heart failure patients.38 A number of small randomized, controlled studies that administered supplemental CoQ10 (60 – 300 mg/day for four to twelve weeks) to either patients with ischemic heart  disease or patients with congestive heart failure, in conjunction with conventional medical therapy, have demonstrated that CoQ10 may have beneficial effect as an adjunctive therapy on some cardiac function measures.39-43 The biochemical and physiologic benefits attributed to CoQ10 supplementation in heart failure patients include:

1.      improved endothelial function in patients with ischemic left ventricular systolic dysfunction43

2.      improved endothelium-dependent vasodilation42

3.      improved left ventricular contractility41

4.      decreased level of inflammatory markers40

5.      reduced blood viscosity39

6.      reduced systolic and diastolic blood pressure in hypertensive patients44

7.      improved ejection fraction, stroke volume, and cardiac out45;46

8.      supports intracellular anti-oxidative defense mechanisms47

Although CoQ10 is synthesized in most human tissues, and can be obtained from dietary   sources, the amount produced may not be sufficient in certain clinical situations where the need for CoQ10 surpasses the body’s ability to synthesize it or consume it as part of the diet. Blood and tissue levels of CoQ10 are reduced as a result of advancing age and cardiovascular disease.46 CoQ10 deficiency is most often observed in the cells and organs with high energy requirements, such as the heart, brain, immune system, liver, kidney and gastric mucosa. The highest concentrations of CoQ10 in the human heart are reached in the first 20 years of life, followed by a decrease of over 50% by 80 years of age.48

HMG-CoA reductase is an enzyme that plays an important role in the regulation of cholesterol synthesis as well as CoQ10 synthesis. HMG-CoA reductase inhibitors, also known as statins, are widely used and effective cholesterol-  lowering medications that may also block CoQ10 biosynthesis due to the partially shared biosynthetic pathway of CoQ10 and cholesterol.

The clinical use of statins, including simvaststin (Zocor), pravastatin (Pravachol),   lovaststin (Mevacor), rosuvaststin (Crestor) and atorvaststin (Lipitor), has been shown to significantly decrease CoQ10 blood and/or tissue levels, particularly when statins are taken at higher doses, most notably in the elderly and in settings of pre-existing CoQ10 deficiency such as heart failure.

Statin-induced CoQ10 deficiency has clinically important consequences that must be taken into consideration by all physicians when prescribing statin drugs. The depletion of plasma and/or tissue CoQ10 has been associated with several observed detrimental clinical changes49:

1.      mitochondrial dysfunction

2.      increased oxidation of LDL cholesterol

3.      reduced ejection fraction

4.      subclinical cardiomyopathy in diabetic patients

Deficiency of CoQ10 in tissues is associated with the degenerative changes of aging. Supplemental CoQ10 has been demonstrated to prevent or reverse the biochemical and physiological deficiency symptoms associated with satin therapy.

The necessity of CoQ10 for cellular energy production and its importance in heart muscle function is well established. A deficiency of CoQ10 is associated with a  deterioration of clinical status in congestive heart failure patients and is an independent predictor of mortality in the same population.50

 

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