09-06-2018, 02:14 PM
What is Good Nutrition AND How Does Sodium Impact The Health of a Dog With Signs of Heart Disease ?
Well IT SURE IS NOT AS SIMPLE AS FEEDING BARF !
The importance of nutrition in health and well-being has long been recognized in animal health and production. As small animal nutritional knowledge has expanded over the last 50 years, the ability to enhance our patients’ and pets’ “quality and quantity of life” obligates us to help promote optimal nutrition. The first steps in determining good nutrition are to provide regular nutritional assessments and appropriate dietary recommendations based on individual needs. Good nutrition is well recognized but often underutilized as a factor contributing to good health, disease resistance, and longevity in companion animals. Health and nutrition are largely composed of 3 key factors; genetics, environment and nutrition. Assuring a diet is complete and balanced for the species intended is indeed an important component of the nutritional assessment. However, determining it is the best option for a specific dog or cat requires a broader evaluation of animal-, diet-, and feeding-factors to determine nutrition risk. Animal factors include age, breed, reproductive status, altered physiology or disease, lifestyle, and activity levels. Disease risks associated with certain breed, age and gender may also be considered. Diet factors include both the nutritional adequacy of the food, nutritional balance, form of food (dry, canned), quality of the food, specific ingredients. It may include less factors such as the source of food and factors that may affect food safety (nutrient imbalances, spoilage, contamination, etc. Assuring the correct food is provided for a disease state is also important. For example, cat foods marketed for urinary tract health are often inappropriate for managing cats with chronic renal insufficiency due to the increased dietary acids and elevated sodium levels in some urinary diets . Owners may not differentiate between bladder health and kidney health when reading urinary tract health claims. Many owners are of the false belief that BARF is the answer to all canine or feline ailments, quite the contrary is factual but you try convincing Mrs Knowitall From Knowitall Road in Knowitall Nonsense Close – whose sole academic research is based on Fido down the street or social media sites such as BARF UK mostly ANECDOTAL! Sadly today with Google research that well known universal university has a lot of its membership that will argue blue is bright pink if the sheep like audience follow! Factors such as food amounts, feeding times, access to other foods, treats, foraging behaviour, food competition, and the like all contribute to the development of a nutritional overview. By preventing obesity, managing disease or altered physiology, optimizing growth or reproduction should help to meet the goals of improved quality and quantity of life which is of great importance , occasionally you get an insight into how owners feed their animals by looking at them, usually owners feed their animals as they eat and that can and does say an awful lot about general companion animal human relationships. Research is now beginning to show that dietary factors may be able to modulate canine cardiac disease, either by slowing the progression, minimizing the number of medications required, improving quality of life, or in rare cases, actually curing the disease. Veterinarians have extrapolated from the human literature since the 1960's in applying nutritional recommendations to dogs with cardiac disease. A prime example is sodium restriction. Healthy dogs can easily excrete excess dietary sodium in the urine but, even before clinical signs become apparent in dogs with cardiac disease, there is activation of the renin-angiotensin-aldosterone (RAA) system and abnormal excretion of sodium (Barger et al., 1955). Based on this pathophysiologic change, sodium restriction has been a mainstay of therapy for dogs with cardiac disease for nearly 50 years. However, very few studies have been conducted on dietary sodium in dogs with cardiac disease. Many questions remain on the specific intake of sodium recommended for dogs with different stages of disease, at what stage sodium restriction should be instituted, and if there are any detrimental effects of sodium restriction. Yet you will hear anecdotal evidence far and wide across sites using social media on ‘dogs shouldn’t have salt’ , they have absolutely no empirical evidence to support the ‘knowitall-sweeping statements’ – but sheep like followers will repeat it because one person happens to shout louder than the other , again all anecdotal – there is one significant issue here, the sufferer has no voice and many dogs die far earlier today than many did being fed foods high in salt some 40-60 years ago ! In fact quite the opposite has been empirically found :
Healthy dogs are relatively tolerant toward the sodium content of their diet.
An early study in 1964 showed no significant changes in extracellular water, sodium, or chloride in normal dogs fed a low sodium diet (Pensinger, 1964). This study also showed that healthy dogs were able to maintain sodium and potassium balance on both low and high sodium diets.Two other studies found that normal dogs fed a low sodium diet had no changes in plasma sodium, chloride, or extracellular fluid volume compared to those fed a high sodium diet (Hamlin et al., 1964; Morris et al., 1976). In 1994, a study examined the effects of a low sodium diet and furosemide in healthy dogs with or without captopril (Roudebush et al., 1994). Although there were no within-group changes in electrolytes in this study, 3 of 6 dogs became hyperkalemic while receiving a low sodium diet plus furosemide and 2 of 6 became hyperkalemic while receiving a low sodium diet plus furosemide and captopril (Roudebush et al., 1994). The effects of the low sodium diet alone were not reported.In normal dogs, low sodium diets caused an increase in plasma renin activity (PRA) and plasma aldosterone concentration compared to a high sodium diet, although plasma concentrations of ACE, atrial natriuretic peptide (ANP), arginine vasopressin (AVP), and endothelin-1 (ET-1) remained unchanged (Pedersen et al., 1994a, Pedersen et al., 1994b). Normal dogs receiving enalapril while eating a low-sodium diet, however, had an exaggerated increase in PRA and a larger decrease in ACE and ANP compared to a dogs eating a high sodium diet (Koch et al., 1994). These investigators also found an inverse correlation between PRA and sodium content of the diet (Koch et al., 1994).
The biggest gap in the issue of sodium restriction is for dogs with early cardiac disease [Stage I or II: (International Small Animal Cardiac Health Council (ISACHC), 2001). Based on the pathogenesis of sodium retention, authors in the 1960's recommended institution of low-sodium diets for dogs when a heart murmur was first detected, even before clinical signs were present (Morris, 1976). Only recently have the benefits and potential problems been questioned. One of the earliest and major compensatory responses in cardiac disease is activation of the renin-angiotensin-aldosterone (RAA) system. Sodium restriction can further activate the RAA system (Pedersen et al., 1994a-1994b; Koch et al., 1994. In the 1960's for dogs with CHF were to restrict protein intake to "reduce the metabolic load on congested, aging, and diseased kidneys and liver" (Pensinger, 1964). Restricting protein can actually be detrimental in terms of lean body mass loss and malnutrition. Dogs with CHF should not be protein restricted, unless they have concurrent advanced renal disease. Some of the diets designed for dogs with cardiac disease are low in protein (3.6 - 4.2 g/100 kcal). In addition, some veterinarians recommend protein-restricted renal diets for dogs with cardiac disease because these diets often (but not always) are also moderately sodium restricted.Unless severe renal dysfunction is present (i.e., serum creatinine >3.0 mg/dL), high-quality protein should be fed to meet canine AAFCO minimums for adult maintenance requirements (5.1 g/100 kcal; Association of American Feed Control Officials (AAFCO), 2005). In one study, daily protein intake of dogs with cardiac disease ranged from 2.3 - 18.8 g/100 kcal so some dogs with cardiac disease are clearly not eating sufficient dietary protein (Freeman et al., 2003b).
Another misconception that impacts cardiac disease is the still widespread belief that dietary protein should be restricted in early renal disease . Although the majority of dogs treated with ACE inhibitors do not develop azotemia, some dogs receiving ACE inhibitors can develop azotemia (COVE Study Group, 1995). Azotemia occurs more frequently when ACE inhibitors are used in conjunction with diuretics although, in a small number of dogs, azotemia can develop from ACE inhibitors alone. When concurrent ACE inhibitor and diuretic use causes azotemia, reduction of the furosemide dose is indicated to reduce azotemia. A protein-restricted diet is not necessary in this situation unless medication changes do not correct the problem and the renal disease progresses.
Much attention has been given to antioxidants for their potential role in the prevention and treatment of human cardiac diseases. Reactive oxygen species are a by-product of oxygen metabolism for which the body normally compensates through the production of endogenous antioxidants. An imbalance between oxidant production and antioxidant protection (e.g., oxidative stress), however, could increase the risk for cardiac disease . Antioxidants are produced endogenously but also can be supplied exogenously. The major antioxidants include enzymatic antioxidants (e.g., superoxide dismutase, catalase, glutathione peroxidase) and oxidant quenchers (e.g., vitamin C, vitamin E, glutathione, and β-carotene) Oxidative stress has been implicated in the development of a number of cardiac diseases. Increased oxidative stress has been demonstrated in people with CHF (Belch et al., 1991; Keith et al., 1998). In dogs with heart failure, regardless of the underlying cause, there are increased levels of biomarkers of oxidative stress and a reduction in certain antioxidants, particularly vitamin E (Freeman et al., 1999; Freeman et al., 2005). These alterations suggest an imbalance between oxidant stress and antioxidant protection in dogs with CHF.
Additional research is required to evaluate the effect, but antioxidant supplementation may hold promise in the future for the therapy of animals with cardiac disease. Low doses of furosemide were shown to cause increased urinary loss of thiamine in healthy people and in rats (Rieck et al., 1999; Lubetsky et al., 1999). Although B vitamin status has not been reported for dogs with CHF, they may have higher dietary B vitamin requirements. Most commercial cardiac diets contain increased levels of water soluble vitamins to offset urinary losses so supplementation usually is not required.
L-Carnitine
L-Carnitine is a quaternary amine whose major role is in long-chain fatty acid metabolism and energy production. Carnitine deficiency syndromes in people have been associated with primary myocardial disease and, based on this and its high concentrations in cardiac muscle, its role in canine DCM also has been of interest.
[img=100x53]file:///C:/Users/User/AppData/Local/Packages/oice_16_974fa576_32c1d314_2db8/AC/Temp/msohtmlclip1/01/clip_image001.jpg[/img]
Carnitine molecule. Discovered in 1905, L-carnitine is synthetized in dogs from lysine and methionine, if vitamin C and pyridoxine (vit B6) are present. It is a quaternary amine that acts as a water soluble vitamin. Carnitine can be synthetized in D or L forms, but L-carnitine is the only one of relevance for dogs with cardiac disease. L-carnitine deficiency was reported in a family of Boxers in 1991 (Keene et al., 1991). Since that time, L-carnitine supplementation has been used in some dogs with DCM but no blinded prospective studies have been done so a causative role has not been established. In human DCM patients, most studies of L-carnitine have not been well-controlled. However, one randomized, double-blind, placebo-controlled study showed improved three-year survival in human DCM patients receiving 2 mg/day L-carnitine (Rizos, 2000).
One of the difficult aspects of studying L-carnitine in DCM is that one must measure myocardial concentrations since plasma concentrations are often normal even in the face of myocardial deficiency. Therefore, the advancement of knowledge of the role of this nutrient in DCM has been slow. It is not yet clear whether the carnitine deficiency seen in some dogs with DCM is the cause of the disease or merely secondary to the development of CHF. One study of dogs with heart failure induced by rapid pacing showed that myocardial concentrations decreased in normal dogs after the onset of CHF (Pierpont et al., 1993). However, even if L-carnitine deficiency is not the inciting cause of DCM, supplementation may still provide benefits by improving myocardial energy production. The minimum or optimal dose of L-carnitine necessary to replete a dog with low myocardial carnitine concentrations is not known, but the currently recommended dose is 50 - 100 mg/kg PO q 8 hours.L-carnitine supplementation has few side effects but it is expensive and this may be a significant deterrent for some owners. The authors offer the option of L-carnitine supplementation to owners of dogs with DCM, especially Boxers and Cocker spaniels, but do not consider it essential. The minimum or optimal dose of L-carnitine necessary to replete a dog with low myocardial carnitine concentrations is not known, but the currently recommended dose is 50 - 100 mg/kg PO q 8 hours.
Coenzyme Q10
Coenzyme Q10 is a cofactor required for energy production and has antioxidant properties. There are a number of mechanisms by which coenzyme Q10 might play a role in cardiac disease. Some investigators have proposed coenzyme Q10 deficiency as a possible cause for DCM but this has not been proven. Even in dogs with experimentally-induced CHF, serum coenzyme Q10 levels were not reduced (Harker-Murray et al., 2000).
The most enthusiasm for coenzyme Q10 has been as a dietary supplement in the treatment of people or dogs with DCM. Coenzyme Q10 supplementation has anecdotally been reported to be beneficial but most of the human studies of coenzyme Q10 supplementation have not been well-controlled and results are conflicting. However, some encouraging results have been found (Langsjoen et al., 1994; Sacher et al., 1997; Munkholm et al., 1999). In one study of dogs with experimentally-induced CHF, coenzyme Q10 supplementation increased serum, but not myocardial, concentrations (Harker-Murray et al., 2000). The bioavailability of coenzyme Q10 varies in different tissues and also depends upon the degree of tissue deficiency in that tissue.
The current recommended dose in canine patients is 30 mg PO BID, although up to 90 mg PO BID has been recommended for large dogs. The purported benefits of supplementation include correction of a deficiency, improved myocardial metabolic efficiency, and increased antioxidant protection. Controlled prospective studies will be necessary to accurately judge the efficacy of this supplement.
Well IT SURE IS NOT AS SIMPLE AS FEEDING BARF !
The importance of nutrition in health and well-being has long been recognized in animal health and production. As small animal nutritional knowledge has expanded over the last 50 years, the ability to enhance our patients’ and pets’ “quality and quantity of life” obligates us to help promote optimal nutrition. The first steps in determining good nutrition are to provide regular nutritional assessments and appropriate dietary recommendations based on individual needs. Good nutrition is well recognized but often underutilized as a factor contributing to good health, disease resistance, and longevity in companion animals. Health and nutrition are largely composed of 3 key factors; genetics, environment and nutrition. Assuring a diet is complete and balanced for the species intended is indeed an important component of the nutritional assessment. However, determining it is the best option for a specific dog or cat requires a broader evaluation of animal-, diet-, and feeding-factors to determine nutrition risk. Animal factors include age, breed, reproductive status, altered physiology or disease, lifestyle, and activity levels. Disease risks associated with certain breed, age and gender may also be considered. Diet factors include both the nutritional adequacy of the food, nutritional balance, form of food (dry, canned), quality of the food, specific ingredients. It may include less factors such as the source of food and factors that may affect food safety (nutrient imbalances, spoilage, contamination, etc. Assuring the correct food is provided for a disease state is also important. For example, cat foods marketed for urinary tract health are often inappropriate for managing cats with chronic renal insufficiency due to the increased dietary acids and elevated sodium levels in some urinary diets . Owners may not differentiate between bladder health and kidney health when reading urinary tract health claims. Many owners are of the false belief that BARF is the answer to all canine or feline ailments, quite the contrary is factual but you try convincing Mrs Knowitall From Knowitall Road in Knowitall Nonsense Close – whose sole academic research is based on Fido down the street or social media sites such as BARF UK mostly ANECDOTAL! Sadly today with Google research that well known universal university has a lot of its membership that will argue blue is bright pink if the sheep like audience follow! Factors such as food amounts, feeding times, access to other foods, treats, foraging behaviour, food competition, and the like all contribute to the development of a nutritional overview. By preventing obesity, managing disease or altered physiology, optimizing growth or reproduction should help to meet the goals of improved quality and quantity of life which is of great importance , occasionally you get an insight into how owners feed their animals by looking at them, usually owners feed their animals as they eat and that can and does say an awful lot about general companion animal human relationships. Research is now beginning to show that dietary factors may be able to modulate canine cardiac disease, either by slowing the progression, minimizing the number of medications required, improving quality of life, or in rare cases, actually curing the disease. Veterinarians have extrapolated from the human literature since the 1960's in applying nutritional recommendations to dogs with cardiac disease. A prime example is sodium restriction. Healthy dogs can easily excrete excess dietary sodium in the urine but, even before clinical signs become apparent in dogs with cardiac disease, there is activation of the renin-angiotensin-aldosterone (RAA) system and abnormal excretion of sodium (Barger et al., 1955). Based on this pathophysiologic change, sodium restriction has been a mainstay of therapy for dogs with cardiac disease for nearly 50 years. However, very few studies have been conducted on dietary sodium in dogs with cardiac disease. Many questions remain on the specific intake of sodium recommended for dogs with different stages of disease, at what stage sodium restriction should be instituted, and if there are any detrimental effects of sodium restriction. Yet you will hear anecdotal evidence far and wide across sites using social media on ‘dogs shouldn’t have salt’ , they have absolutely no empirical evidence to support the ‘knowitall-sweeping statements’ – but sheep like followers will repeat it because one person happens to shout louder than the other , again all anecdotal – there is one significant issue here, the sufferer has no voice and many dogs die far earlier today than many did being fed foods high in salt some 40-60 years ago ! In fact quite the opposite has been empirically found :
Healthy dogs are relatively tolerant toward the sodium content of their diet.
An early study in 1964 showed no significant changes in extracellular water, sodium, or chloride in normal dogs fed a low sodium diet (Pensinger, 1964). This study also showed that healthy dogs were able to maintain sodium and potassium balance on both low and high sodium diets.Two other studies found that normal dogs fed a low sodium diet had no changes in plasma sodium, chloride, or extracellular fluid volume compared to those fed a high sodium diet (Hamlin et al., 1964; Morris et al., 1976). In 1994, a study examined the effects of a low sodium diet and furosemide in healthy dogs with or without captopril (Roudebush et al., 1994). Although there were no within-group changes in electrolytes in this study, 3 of 6 dogs became hyperkalemic while receiving a low sodium diet plus furosemide and 2 of 6 became hyperkalemic while receiving a low sodium diet plus furosemide and captopril (Roudebush et al., 1994). The effects of the low sodium diet alone were not reported.In normal dogs, low sodium diets caused an increase in plasma renin activity (PRA) and plasma aldosterone concentration compared to a high sodium diet, although plasma concentrations of ACE, atrial natriuretic peptide (ANP), arginine vasopressin (AVP), and endothelin-1 (ET-1) remained unchanged (Pedersen et al., 1994a, Pedersen et al., 1994b). Normal dogs receiving enalapril while eating a low-sodium diet, however, had an exaggerated increase in PRA and a larger decrease in ACE and ANP compared to a dogs eating a high sodium diet (Koch et al., 1994). These investigators also found an inverse correlation between PRA and sodium content of the diet (Koch et al., 1994).
The biggest gap in the issue of sodium restriction is for dogs with early cardiac disease [Stage I or II: (International Small Animal Cardiac Health Council (ISACHC), 2001). Based on the pathogenesis of sodium retention, authors in the 1960's recommended institution of low-sodium diets for dogs when a heart murmur was first detected, even before clinical signs were present (Morris, 1976). Only recently have the benefits and potential problems been questioned. One of the earliest and major compensatory responses in cardiac disease is activation of the renin-angiotensin-aldosterone (RAA) system. Sodium restriction can further activate the RAA system (Pedersen et al., 1994a-1994b; Koch et al., 1994. In the 1960's for dogs with CHF were to restrict protein intake to "reduce the metabolic load on congested, aging, and diseased kidneys and liver" (Pensinger, 1964). Restricting protein can actually be detrimental in terms of lean body mass loss and malnutrition. Dogs with CHF should not be protein restricted, unless they have concurrent advanced renal disease. Some of the diets designed for dogs with cardiac disease are low in protein (3.6 - 4.2 g/100 kcal). In addition, some veterinarians recommend protein-restricted renal diets for dogs with cardiac disease because these diets often (but not always) are also moderately sodium restricted.Unless severe renal dysfunction is present (i.e., serum creatinine >3.0 mg/dL), high-quality protein should be fed to meet canine AAFCO minimums for adult maintenance requirements (5.1 g/100 kcal; Association of American Feed Control Officials (AAFCO), 2005). In one study, daily protein intake of dogs with cardiac disease ranged from 2.3 - 18.8 g/100 kcal so some dogs with cardiac disease are clearly not eating sufficient dietary protein (Freeman et al., 2003b).
Another misconception that impacts cardiac disease is the still widespread belief that dietary protein should be restricted in early renal disease . Although the majority of dogs treated with ACE inhibitors do not develop azotemia, some dogs receiving ACE inhibitors can develop azotemia (COVE Study Group, 1995). Azotemia occurs more frequently when ACE inhibitors are used in conjunction with diuretics although, in a small number of dogs, azotemia can develop from ACE inhibitors alone. When concurrent ACE inhibitor and diuretic use causes azotemia, reduction of the furosemide dose is indicated to reduce azotemia. A protein-restricted diet is not necessary in this situation unless medication changes do not correct the problem and the renal disease progresses.
Much attention has been given to antioxidants for their potential role in the prevention and treatment of human cardiac diseases. Reactive oxygen species are a by-product of oxygen metabolism for which the body normally compensates through the production of endogenous antioxidants. An imbalance between oxidant production and antioxidant protection (e.g., oxidative stress), however, could increase the risk for cardiac disease . Antioxidants are produced endogenously but also can be supplied exogenously. The major antioxidants include enzymatic antioxidants (e.g., superoxide dismutase, catalase, glutathione peroxidase) and oxidant quenchers (e.g., vitamin C, vitamin E, glutathione, and β-carotene) Oxidative stress has been implicated in the development of a number of cardiac diseases. Increased oxidative stress has been demonstrated in people with CHF (Belch et al., 1991; Keith et al., 1998). In dogs with heart failure, regardless of the underlying cause, there are increased levels of biomarkers of oxidative stress and a reduction in certain antioxidants, particularly vitamin E (Freeman et al., 1999; Freeman et al., 2005). These alterations suggest an imbalance between oxidant stress and antioxidant protection in dogs with CHF.
Additional research is required to evaluate the effect, but antioxidant supplementation may hold promise in the future for the therapy of animals with cardiac disease. Low doses of furosemide were shown to cause increased urinary loss of thiamine in healthy people and in rats (Rieck et al., 1999; Lubetsky et al., 1999). Although B vitamin status has not been reported for dogs with CHF, they may have higher dietary B vitamin requirements. Most commercial cardiac diets contain increased levels of water soluble vitamins to offset urinary losses so supplementation usually is not required.
L-Carnitine
L-Carnitine is a quaternary amine whose major role is in long-chain fatty acid metabolism and energy production. Carnitine deficiency syndromes in people have been associated with primary myocardial disease and, based on this and its high concentrations in cardiac muscle, its role in canine DCM also has been of interest.
[img=100x53]file:///C:/Users/User/AppData/Local/Packages/oice_16_974fa576_32c1d314_2db8/AC/Temp/msohtmlclip1/01/clip_image001.jpg[/img]
Carnitine molecule. Discovered in 1905, L-carnitine is synthetized in dogs from lysine and methionine, if vitamin C and pyridoxine (vit B6) are present. It is a quaternary amine that acts as a water soluble vitamin. Carnitine can be synthetized in D or L forms, but L-carnitine is the only one of relevance for dogs with cardiac disease. L-carnitine deficiency was reported in a family of Boxers in 1991 (Keene et al., 1991). Since that time, L-carnitine supplementation has been used in some dogs with DCM but no blinded prospective studies have been done so a causative role has not been established. In human DCM patients, most studies of L-carnitine have not been well-controlled. However, one randomized, double-blind, placebo-controlled study showed improved three-year survival in human DCM patients receiving 2 mg/day L-carnitine (Rizos, 2000).
One of the difficult aspects of studying L-carnitine in DCM is that one must measure myocardial concentrations since plasma concentrations are often normal even in the face of myocardial deficiency. Therefore, the advancement of knowledge of the role of this nutrient in DCM has been slow. It is not yet clear whether the carnitine deficiency seen in some dogs with DCM is the cause of the disease or merely secondary to the development of CHF. One study of dogs with heart failure induced by rapid pacing showed that myocardial concentrations decreased in normal dogs after the onset of CHF (Pierpont et al., 1993). However, even if L-carnitine deficiency is not the inciting cause of DCM, supplementation may still provide benefits by improving myocardial energy production. The minimum or optimal dose of L-carnitine necessary to replete a dog with low myocardial carnitine concentrations is not known, but the currently recommended dose is 50 - 100 mg/kg PO q 8 hours.L-carnitine supplementation has few side effects but it is expensive and this may be a significant deterrent for some owners. The authors offer the option of L-carnitine supplementation to owners of dogs with DCM, especially Boxers and Cocker spaniels, but do not consider it essential. The minimum or optimal dose of L-carnitine necessary to replete a dog with low myocardial carnitine concentrations is not known, but the currently recommended dose is 50 - 100 mg/kg PO q 8 hours.
Coenzyme Q10
Coenzyme Q10 is a cofactor required for energy production and has antioxidant properties. There are a number of mechanisms by which coenzyme Q10 might play a role in cardiac disease. Some investigators have proposed coenzyme Q10 deficiency as a possible cause for DCM but this has not been proven. Even in dogs with experimentally-induced CHF, serum coenzyme Q10 levels were not reduced (Harker-Murray et al., 2000).
The most enthusiasm for coenzyme Q10 has been as a dietary supplement in the treatment of people or dogs with DCM. Coenzyme Q10 supplementation has anecdotally been reported to be beneficial but most of the human studies of coenzyme Q10 supplementation have not been well-controlled and results are conflicting. However, some encouraging results have been found (Langsjoen et al., 1994; Sacher et al., 1997; Munkholm et al., 1999). In one study of dogs with experimentally-induced CHF, coenzyme Q10 supplementation increased serum, but not myocardial, concentrations (Harker-Murray et al., 2000). The bioavailability of coenzyme Q10 varies in different tissues and also depends upon the degree of tissue deficiency in that tissue.
The current recommended dose in canine patients is 30 mg PO BID, although up to 90 mg PO BID has been recommended for large dogs. The purported benefits of supplementation include correction of a deficiency, improved myocardial metabolic efficiency, and increased antioxidant protection. Controlled prospective studies will be necessary to accurately judge the efficacy of this supplement.