Re: Alice - long

[Guest guest]

Alice,

I am sending you good thoughts they the docs can find a way to help you

feel a little better.

I found an article that I am pasting part of here that talks about the

metobolic relationship of cardiomyopthy and CHF in " normal " patients. I

found it interesting that most of it a lot of us mito patients already

take. It is long, but here goes.

Additional research demonstrates that some nutritional supplements help

to reduce cardiac enlargement and other symptoms of CHF. In addition to

its antiarrhythmic potential noted above, carnitine has also been shown

to reduce the ventricular dilation associated with cardiomyopathy.(18

http://www.wellnessreview.com/reports/cardiomyopathy#R18>) Another

supplement, Coenzyme Q10 (CoQ10)(22-26

http://www.wellnessreview.com/reports/cardiomyopathy#R22>), has been

shown to significantly strengthen myocardial contraction and possibly

reduce the frequency of arrhythmias. It is now recommended that CoQ10 be

added to the regimen of all cardiomyopathy patients.(22

http://www.wellnessreview.com/reports/cardiomyopathy#R22>) Long-term

survival has been shown to be more than three times as great in patients

taking CoQ10.(23

http://www.wellnessreview.com/reports/cardiomyopathy#R23>) Further,

patients who take CoQ10 feel significantly better and important

measurements of the heart often show substantial improvement within

months of initiating CoQ10 therapy.(22

http://www.wellnessreview.com/reports/cardiomyopathy#R22>) There is

also research indicating that taurine can, in some cases, help treat

cardiomyopathy as well as relieve symptoms of CHF.(27-28

http://www.wellnessreview.com/reports/cardiomyopathy#R27>)

Looking at nutritional supplements in a collective fashion, Sole et al

concluded that restoring adequate myocyte nutrition could be an

essential therapy for CHF patients. They documented several metabolic

deficiencies in the failing myocardium including unusually low levels of

L-carnitine, CoQ10, creatine, thiamin, taurine and other antioxidants.

They also described studies in which replenishment of these was

beneficial in both people and animals. Given the numerous deficiencies

associated with heart disease, they concluded that the best nutritional

approach is to supplement to control a wide array of deficiencies, not

just one or two.(29

http://www.wellnessreview.com/reports/cardiomyopathy#R29>)

Research supporting use of the nutritional supplements introduced above,

along with a few others, will now be presented.

Magnesium and Potassium

The membrane and action potential of cardiac cells, including formation

of tachyarrhythmias, is affected by the fluxes of sodium, potassium,

calcium and magnesium ions. Atrial and ventricular tachyarrhythmias

occur by (1) repetitive automatic or triggered impulses or (2) reentrant

circus movement which usually follows an ectopic automatic or triggered

premature beat.(4

http://www.wellnessreview.com/reports/cardiomyopathy#R4>) Reentrant

tachycardia can also begin from asynchronous propagation of an automatic

or a triggered impulse, whether single or multiple. Iseri et al reported

that a decrease in magnesium ions can induce triggered ectopic impulses,

and a decrease in potassium ions can delay conduction of these impulses

to set up reentrant tachycardia. Both magnesium and potassium have,

accordingly, proven useful in treating arrhythmias. Iseri et al also

noted that magnesium deficiency can induce coronary spasm and create an

ischemic environment for ionic balance. They cited four double-blind

randomized studies that have shown infusion of magnesium during the

first 24 hours after acute myocardial infarction reduced the development

of VT and ventrical fibrillation (VF). They questioned the use of

diuretics as the first-line treatment of hypertension and CHF since

diuretics are the most common cause of magnesium and potassium

depletion. In this same report, Iseri et al recommended 250 mg. or more

of elemental magnesium per day in humans, along with a diet rich in

magnesium.(6 http://www.wellnessreview.com/reports/cardiomyopathy#R6>)

In another review article, Iseri et al noted that in some cases when

magnesium was used to successfully abort the recurrence of VT and VF,

serum potassium levels decreased. When potassium was added to the

regimen, control of arrhythmias was made more effective.(4

http://www.wellnessreview.com/reports/cardiomyopathy#R4>) In a separate

report, Iseri noted several cases where serum potassium and/or sodium

levels fell precipitously during magnesium treatment.(7

http://www.wellnessreview.com/reports/cardiomyopathy#R7>) Potassium and

magnesium supplementation should be considered even if serum levels are

normal since serum magnesium and potassium levels do not necessarily

reflect the levels of these elements within the myocardium.

In 1990, Iseri reported on a study where eleven of 12 patients with VF

and/or VT converted to sinus or paced rhythm within 5 minutes of a 2 g

infusion of magnesium. Arrhythmias in the twelfth patient were also

successfully controlled, although they took longer to initially control.

In one case, despite intravenous administration of lidocaine and

phenytoin, the patient had 18 episodes of VF that required countershock

treatment. A dose of 12 g of magnesium raised serum magnesium to 3.9

mEq/liter and controlled VF. In another patient, after controlling

initial VT with intravenous magnesium, a combination of oral magnesium

chloride, 2 tablets 3 times daily, along with amiodarone, controlled VT

for 1 year. Iseri noted that patients with cardiopulmonary disease are

highly susceptible to magnesium deficiency, some of which may not be

revealed by low serum levels. In the absence of renal insufficiency,

magnesium infusion is safe and can be quite effective in controlling

intractable VT and VF whether or not the patient is hypomagnesemic.(8

http://www.wellnessreview.com/reports/cardiomyopathy#R8>)

Ceremuzynski et al reported in 2000 that intravenous magnesium sulphate

can be a safe and effective antiarrhythmic intervention which should be

considered more often in medical practice before resorting to

pharmacological antiarrhythmic medications. They found that intravenous

administration of magnesium caused a significant decrease in the number

of ventricular ectopic beats (P < 0.0001), couplets (P < 0.003) and

episodes of nonsustained VT (P < 0.01).(9

http://www.wellnessreview.com/reports/cardiomyopathy#R9>)

Zehender et al reported in 1997 on a randomized, double-blind study with

232 patients experiencing frequent ventricular arrhythmias. Patients

were treated either with a combination of oral magnesium and potassium,

or with a placebo. Treatment involved a relatively small dose of

magnesium and potassium (only 50% above recommended minimum daily

dietary intake) yet still produced a moderate but significant

antiarrhythmic effect when compared to placebo. They concluded that in

light of its simplicity, cost-effectiveness, and safety, increasing the

daily intake of magnesium and potassium may provide another first-line

option for treating patients with frequent but not life-threatening

ventricular tachyarrhythmias.(5

http://www.wellnessreview.com/reports/cardiomyopathy#R5>)

Bean et al in 1994 speculated that hypomagnesemia, like hypokalemia, may

potentiate arrhythmias caused by catecholamine excess. They reported

that acute administration of magnesium in normal dogs increased the

arrhythmogenic threshold for epinephrine, further supporting the use of

magnesium as an antiarrhythmic agent.(3

http://www.wellnessreview.com/reports/cardiomyopathy#R3>)

Based upon the evidence presented above, magnesium supplementation can

clearly be useful in the treatment of arrhythmias. Unfortunately, some

forms of oral magnesium are associated with a high incidence of emesis,

diarrhea and soft stools. This rarely occurs, however, with use of

magnesium lactate, even in large doses. Magnesium lactate is

manufactured by Niche Pharmaceuticals in a 12-hour time release tablet

form (84 mg/tablet) known as Mag-Tab SR.

Robbins et al reported that magnesium lactate has many properties

suggesting that it is a good form of magnesium to use as a dietary

supplement. It is soluble at neutral pH, the anion is well absorbed and

well tolerated, and it is 10% magnesium by weight. This time-release

form of magnesium is easy on the stomach, and offers a much more

consistent serum level of magnesium when compared to enteric-coated

magnesium chloride tablets. When magnesium lactate was given to dogs,

the mean level of serum magnesium was found to rise quickly, peaked at

four hours, then dropped slowly over subsequent hours.(30

http://www.wellnessreview.com/reports/cardiomyopathy#R30>)

Selenium

In 1998, Tanguy et al reported on the use of selenium supplementation to

control VT and VF. Selenium was added to the diet of rats at the rate of

50 mcg selenium per kg of food. Selenium significantly affected the

incidence of reperfusion-induced VT (91% in controls vs. 36% in

selenium-supplemented rats, p=0.03; Chi2 test corrected for continuity

using the Yates' method.) While not statistically significant, the

incidence of total VF was also reduced in the selenium group (91% in

controls vs. 45% in selenium-supplemented rats, p=0.07, ns; Chi2 test

corrected for continuity using the Yates' method). The reduction was

much more pronounced for sustained VF, which was markedly and

significantly decreased in the selenium group (45% in controls vs. 0% in

selenium-supplemented rats, p=0.04; Chi2 test corrected for continuity

using the Yates' method). These findings confirmed that selenium

supplementation decreased the severity of reperfusion arrhythmias.

Tanguy et al also noted other studies that indicated a negative

relationship between plasma selenium levels and the incidence of

cardiovascular disease. Some of these studies further demonstrated that

plasma levels of selenium are significantly lower during the acute phase

of myocardial infarction.(10

http://www.wellnessreview.com/reports/cardiomyopathy#R10>)

In 1994, Lehr reported that a patient with several years of episodic

occurrence of disabling ventricular bigemini returned to unbroken normal

sinus rhythm one week after introduction of selenium supplementation.

While selenium supplementation was among a multiplicity of possible

reasons for this development, Lehr reported that it was the most

obvious, though only a tentative explanation. Selenium represented the

sole modification of otherwise reasonably standardized conditions of

antiarrhythmic therapy, lifestyle and diet.(11

http://www.wellnessreview.com/reports/cardiomyopathy#R11>)

Lehr also noted studies that indicated a high rate of cardiovascular

disease in the coastal plain of Georgia might have been caused by

selenium deficiency in the soil. Further, he described a study in which

a group of investigators showed that selenium deficiency in soil is one

of the principal factors responsible for a form of dilated

cardiomyopathy known as Keshan disease. Lehr also reported that a

negative selenium balance might be created if no attention is paid to

selenium intake in persons on hypocaloric diets, in paranteral

nutrition, and in the case of anorexia nervosa. Further, he noted that

6% of young women afflicted with anorexia nervosa, and without

underlying heart disease, die suddenly, usually with intractable VT. In

humans, up to 750 to 850 mcg of selenium can be ingested daily without

the development of selenosis. Nutritional sources of selenium include

grains, shrimp, as well as various meats and milk. In an effort to

forestall sudden cardiac death from intractable cardiac arrhythmias,

Lehr suggested close attention be paid to adequate selenium

supplementation based upon postulated influences of selenium on cardiac

function.(11 http://www.wellnessreview.com/reports/cardiomyopathy#R11>)

Fish Oil

Billman et al in 1999 reported on nine studies which demonstrated omega

3 polyunsaturated fatty acids (PUFAs) prevent fatal cardiac ventricular

ischemia-induced arrhythmias in animals, and another six studies which

demonstrated probable benefit in humans. In their own study, they

reported that a fish oil preparation helped prevent fatal VF in dogs.

They then studied independently the various constituents of fish oil to

determine which may be responsible for its positive effect. They

demonstrated that the three most common dietary PUFAs of the omega 3

class are all potent antiarrhythmic agents when infused intravenously

just before exercise-plus-ischemia stress in dogs. While not immediately

antiarrhythmic in a dietary form, in the case of ischemia, severe

exertion, or major sympathetic adrenergic discharge, phospholipases and

lipases quickly liberate stored fatty acids, especially omega 3 PUFAs,

and these in their free form can prevent arrhythmias. If fish oil is

ingested on a regular basis, the PUFAs will be present in the stored

forms to be available when needed.(12

http://www.wellnessreview.com/reports/cardiomyopathy#R12>)

Sellmayer et al cited in 1995 two carefully controlled dietary trials

with omega 3 fatty acid enrichment that found improved survival after

acute myocardial infarction due to the potential antiarrhythmic effect

of omega 3 fatty acids. Also cited was a small Danish study with VT that

revealed a greater, though not statistically significant, reduction in

VPCs in the group treated with fish oil as compared to those treated

with corn oil. Sellmayer et al also reported on their own prospective,

double-blind and placebo-controlled study in which patients were advised

to take 15 ml of fish oil or placebo (sunflower oil) daily for the study

period of 16 weeks after which time tissue levels of omega 3 fatty acids

should have reached a steady state. During the trial, VPCs decreased by

48% after 16 weeks in the fish oil group, compared to only a 25%

reduction in the placebo group. Further, 44% of patients in the fish oil

group had reduction of VPCs greater than 70% while only 15% in the

placebo group had this same level of reduction. Fish oil exerted a

moderate antiarrhythmic effect when compared with group IC drugs

flecainide and encainide. The two drugs, however, adversely affected

survival in highly selected patients after myocardial infarction,

whereas, in two different trials, omega 3 fatty acids significantly

improved survival, even in unselected patients after myocardial

infarction. This benefit was credited to the antiarrhythmic effect of

fish oils. Among several thousand patients in controlled trials, no side

effects of omega 3 supplementation have been observed. It is thought

fish oil fatty acids may regulate calcium fluxes and suppress

intracellular calcium activity. Sellmayer et al cited three studies

which found increased intracellular calcium activity caused ventricular

electrical inhomogeneity and thus contributed to arrhythmias by phase 2

reentry or early afterdepolarizations.(13

http://www.wellnessreview.com/reports/cardiomyopathy#R13>)

In 1994 Isensee et al reported on their study in rats comparing the

effects of various oils, as well as a low-fat diet, on ischemia-induced

arrhythmias. They found that the incidence of VT was 60% in the low fat

group, 60% in the linseed oil group, 56% in the coconut oil group, 44%

in the corn oil group, and 0% in the fish oil group. Further, the

incidence of VF was 75% in the low fat group, 67% in the coconut oil

group, 44% in the corn oil group, 40% in the linseed oil group, and only

10% in the fish oil group. They also reported that the length of time

between coronary occlusion and the first occurrence of extrasystole was

shortest in the coconut oil group and longest in the fish oil group.

After trying the same experiment using aspirin to inhibit

cyclooxygenase, they found the protective effects of PUFAs were

completely abolished by cyclooxygenase inhibition. Elimination of all

the favorable effects of PUFAs by cyclooxygenase inhibition indicates

the prostaglandin system plays an essential role in the protection

offered by PUFAs from ventricular arrhythmias. (In contrast, the

antiarrhythmic effects of various forms of garlic, as described later in

this report, were only partially abolished by aspirin.)(14

http://www.wellnessreview.com/reports/cardiomyopathy#R14>)

Hock et al in 1990 reported on the influence of omega 3 fatty acids on

myocardial ischemia and reperfusion. Rats were fed a diet in which the

lipid was replaced with either corn oil or fish oil. Both the incidence

and severity of ventricular tachycardia and ventricular fibrillation

were significantly reduced during the ischemic and reperfusion periods

with fish oil feeding. The incidence of ventricular fibrillation was

only 14% in the fish oil group versus 91% in the corn oil group. When

the incidence, number, and duration of the arrhythmias were taken into

account using an arrhythmia scoring scale, the fish oil group had a

significantly lower arrhythmia score compared to the corn oil group (1.3

± 0.7 vs. 5.6 ± 0.8, P < 0.01). Survival after 24 hours of reperfusion

was 76% in the fish oil group and 41% in the corn oil group.(15

http://www.wellnessreview.com/reports/cardiomyopathy#R15>)

In 1989 McLennan et al reported on a study they did on the influence of

dietary fat in sudden cardiac death of rats. The study compared diets

enriched with sheep perirenal fat, sunflower oil or tuna fish oil.

During coronary artery occlusion the number of animals having episodes

of VT or VF was significantly diminished by the sunflower oil and fish

oil diets. Moreover, in the animals in which VT or VF did occur it was

less severe (shorter lasting) in the sunflower oil and fish oil groups.

While 70% of sheep fat supplemented animals suffered VF and 30% died,

only 12% of fish oil supplemented animals fibrillated and none died.(16

http://www.wellnessreview.com/reports/cardiomyopathy#R16>)

In 1980 Culp et al reported on a study they did exploring the effect of

fish oil on experimental myocardial infarction in dogs. In control

animals, the frequency of ectopic beats rose from less than 10% at the

beginning of the experiment to about 80% after 19 to 24 hours of

stimulation of the left circumflex coronary artery. In contrast, the

fish oil fed dogs maintained a more normal ECG pattern showing less than

30% ectopic beats after 19 hours, and less severe myocardial damage was

found in those with elevated omega 3 fatty acids.(17

http://www.wellnessreview.com/reports/cardiomyopathy#R17>)

L-carnitine

Rizos in 2000 reported on the three-year survival of patients treated

with L-carnitine at the rate of 2 g/day orally for CHF caused by dilated

cardiomyopathy. The study began with 80 patients, was double-blind and

placebo-controlled for the initial 3-month period, and then unblinded

for the remaining 33 months. The 3-year mortality rate was found to be

statistically significant in favor of the carnitine group with a

mortality rate of only 3% versus 18% in the placebo group (P < 0.04).

Atrial fibrillation developed in 7 patients in the placebo group. In

contrast, only one patient in the carnitine group was unable to maintain

sinus rhythm for the entire follow-up period. Electrical stability of

the carnitine group may explain mortality risk reduction as evidenced by

improved sinus rhythm scores in that group.(19

http://www.wellnessreview.com/reports/cardiomyopathy#R19>)

In 2000 Helton et al conducted a multicenter retrospective study to

investigate the outcome of patients treated with carnitine. They found

carnitine useful in treating cardiomyopathy based upon its role of

shuttling fatty acids across the mitochondrial membrane of the heart,

delivering them for beta-oxidation and the production of energy. They

found carnitine patients tended to have lower mortality from

cardiomyopathy as the primary diagnosis than controls (6.8% vs. 17.9%),

and that there was less transplantation among carnitine-treated patients

than control patients (9.6% vs. 15.0%). Their analysis of the

association between concomitant medications and clinical outcome

unexpectedly revealed that the population of patients who received ACE

inhibitors had significantly poorer survival. Significant improvement in

survival was observed both for carnitine-treated patients who did not

receive ACE inhibitors versus control patients (P = 0.46) as well as for

control patients who did not receive ACE inhibitors compared to controls

who did (P=.0001). The incidence density in the ACE inhibitor-treated

group was approximately 4.4 times higher than the non-ACE

inhibitor-treated group in both the carnitine-treated and control

groups, indicating many more events per person per day of follow-up

among ACE inhibitor-treated patients. Helton et al suggested that while

there could be short to intermediate term improvements in myocardial

function with ACE inhibitors, the data of their study suggested

uncertainty for improvements in long-term mortality through ACE

inhibitor use.(2 http://www.wellnessreview.com/reports/cardiomyopathy#R2>)

In 1998 Signh et al reviewed several studies on the administration of

carnitine in coronary artery disease and cardiomyopathy. They made note

of a randomized, double-blind and placebo-controlled trial in which it

was found that after 2 g/day of L-carnitine administration,

carnitine-treated patients showed a significant reduction in mean

infarct size compared to the placebo group. Further,

electrocardiographic QRS-score was significantly less in the carnitine

group compared to placebo while serum glutamic oxalaspartate

transaminase and lactate dehydrogenase and lipid peroxides showed

significant reduction in the carnitine group. In another study noted by

Signh et al, of 146 acute myocardial infarction (AMI) patients (97 in

the control and 49 in the treatment group) those treated with carnitine

had no deaths, while those in the control group had 18 deaths. The dose

of L-carnitine was 9 g/day IV for 3 days followed by 4 g/day oral for 21

days. In another study, 100 randomly selected angina pectoris patients

were administered L-carnitine (2 g/day) for six months. There was a

significant decrease in VPCs at rest, increased tolerance to exercise,

and other positive cardiac effects. In yet another reviewed study 81 AMI

patients were selected to receive 4 g/day of L-carnitine for one year,

and were compared to 79 controls. Carnitine caused significant reduction

in heart rate, angina pectoris, and most notably a reduction of deaths

(1.2% vs. 12.5%, p < 0.05) in the intervention group compared to the

control group. In a more recent study involving 472 first AMI patients,

treatment with carnitine was associated with a significant attenuation

of left ventricular dilation in the first year after treatment compared

to placebo. The combined incidence of death and CHF after discharge was

6% in the carnitine group versus 9.6% in the placebo group (P=NS). Singh

et al also reported that carnitine supplementation in patients with

cardiomyopathy is usually associated with rapid beneficial effects

characterized by improvement in cardiac function. In one 5.5 year old

boy, left ventricular ejection fraction was increased from 39% to 75%

after only one month of treatment. Clinical benefits from carnitine may

be reduction in heart size and heart failure and reduction in the

amplitude of T-waves recorded in precordial leads.(18

http://www.wellnessreview.com/reports/cardiomyopathy#R18>)

Red meat, milk and milk products are rich sources of carnitine. Adverse

reactions that have been observed in carnitine therapy consist of mild

gastrointestinal complaints such as nausea, vomiting, diarrhea and

abdominal cramps. These effects usually resolve with a reduction of

carnitine dosage.(18

http://www.wellnessreview.com/reports/cardiomyopathy#R18>)

Carnitine-Related Amino Acids and Cofactors

According to the PDR for Nutritional Supplements, only 20% of a

supplement containing 2 g of L-carnitine is absorbed following

ingestion.(31

http://www.wellnessreview.com/reports/cardiomyopathy#R31>) As such, it

may be useful to supplement with other amino acids that have been found

to aid in the absorption and synthesis of carnitine. Singh et al noted

that L-lysine and L-methionine are important for the biosynthesis of

carnitine, and foods rich in these amino acids may help increase

absorption of carnitine.(18

http://www.wellnessreview.com/reports/cardiomyopathy#R18>)

In 1993 Pierrefiche et al reported that potentiation of carnitine is

increased threefold when given with an equimolar dose of L-lysine. As

such, they suggested that an equivalent effect can be obtained with

lower doses of carnitine when combined with lysine. The potentiation of

carnitine resulted from lysine increasing availability of carnitine in

the target organs caused by endogenous synthesis of carnitine from

lysine. Lysine also reduced plasma peaks of carnitine, diminished

urinary loss of carnitine, and improved the uptake and utilization of

carnitine by the target organs. Various proportions of the

carnitine/lysine combination were studied, and under the experimental

conditions used, the optimum ratio was found to be 1:1 to 1:2. In other

experiments, no potentiation of carnitine was observed with concomitant

administration of arginine, ornithine or aspartic acid; only lysine was

effective. Further, the L-isomer form of carnitine was found to be much

more effective than the D,L form.(32

http://www.wellnessreview.com/reports/cardiomyopathy#R32>) Various

reports recommend against supplementing with the D,L form of carnitine.

In 1984 Bamji reported that in adult human volunteers, plasma carnitine

showed a significant increase 3 to 6 hours after administration of oral

lysine. In that report, the phenomenon was found to be specific for

lysine and not observed when other amino acids such as tryptophan and

threonine were administered. Bamji also reported that carnitine

deficiency may arise in the case of dietary deficiency of either of the

precursor amino acids (lysine and methionine) or any of the cofactors

(iron, ascorbic acid, vitamin B6 and niacin) required by the enzymes of

the lysine-carnitine pathway. In a different study noted by Bamji,

supplementation with threonine along with lysine also produced

improvement in cardiac carnitine levels.(33

http://www.wellnessreview.com/reports/cardiomyopathy#R33>) It may,

therefore, be prudent in the case of cardiomyopathy or CHF to supplement

with lysine, methionine, iron, ascorbic acid, vitamin B6, niacin and

threonine, along with carnitine. Adverse effects have been noted from

L-methionine supplementation, so it may be best to obtain methionine

strictly from food sources.(31

http://www.wellnessreview.com/reports/cardiomyopathy#R31>)

In 1996 Dodson et al reported that choline supplementation causes

significantly more supplemented carnitine to be retained in muscle

tissues with less being excreted in urine. They also noted a study that

indicated choline may be needed to aid in the transport of carnitine

into cells.(34

http://www.wellnessreview.com/reports/cardiomyopathy#R34>) Accordingly,

it may be beneficial to supplement with choline to help increase the

efficacy of carnitine therapy.

Niacin

In addition to the fact that niacin, as a cofactor, may bolster the

effectiveness of carnitine supplementation, several studies have shown

that niacin on its own may exhibit certain cardioprotective effects.

Niacin comes in three forms, nicotinic acid, niacinamide and inositol,

each with very different effects on the body. Nicotinic acid (NA) is the

form most often shown to have significant effects on the myocardium. NA

in very high doses lowers the serum level of low-density lipoprotein

cholesterol (LDL-C), however, at these doses, it can also cause severe

adverse reactions including hepatic toxicity.(31

http://www.wellnessreview.com/reports/cardiomyopathy#R31>) Research

indicates that NA may also offer other cardioprotective benefits, even

at safe, nutritional levels.

In 2000 Trueblood et al reported that NA has been shown to decrease

myocyte injury. They found NA significantly improved functional and

metabolic parameters providing rationale for its use as a therapeutic

agent in patients with ischemic heart disease.(35

http://www.wellnessreview.com/reports/cardiomyopathy#R35>)

In 1984 Talesnik et al reported that NA may be of significance as an

adjuvant in the treatment of coronary insufficiencies. They noted

studies indicating NA to be one of the most active anti-lipolytic agents

in adipose tissue and that it also inhibits the lipolytic effect of

isoproterenol in cardiac muscle. This is of particular relevance since

the increased cardiac contractility induced by tachycardia has been

shown to produce endogenous triglyceride lipolysis. They also noted a

study in 1947 by Calder on rabbits which demonstrated that NA restored

rhythm, tension development and coronary flow in failing hearts.(36

http://www.wellnessreview.com/reports/cardiomyopathy#R36>)

In 1975 Rowe et al reported that when a nicotinic-acid analogue (NAA)

was given within 5 hours of the onset of myocardial infarction, the

incidence of R-on-apex T ventricular premature beats and beats in which

the ectopic R wave interrupted the apex of the T wave of a previous

ventricular premature beat were reduced.(37

http://www.wellnessreview.com/reports/cardiomyopathy#R37>)

Garlic

In 1993 Isensee et al reported on a study evaluating the

cardioprotective actions of garlic (Allium sativum). In their

experiments using rat hearts, a marked cardioprotection during ischemia

and reperfusion was found, especially with respect to the development of

fatal irreversible VF. The diet of evaluated rats was enriched with 1%

garlic powder. The powder was standardized to an allicin content of 1.3%

with a capacity for liberation of allicin of 0.6%. When compared to

controls, the hearts of the garlic group beat significantly longer in

normal sinus rhythm. While 35.5% of control hearts developed VT, none of

the garlic hearts developed VT. The incidence of VF was 88% in the

control group, and significantly reduced in the garlic group at 50%. The

ischemic areas of the hearts of the garlic group were significantly

smaller (31.7 ± 2.4%) than those of the control group (40.9% ± 2.3%). In

the case of reperfusion-induced arrhythmias, 90% of hearts developed VF

in the control group (of which 20% were reversible) while only 30% in

the garlic group developed VF (of which 80% were reversible). Further,

the incidence of VT was halved by the garlic diet. The study did not

confirm what component of garlic exhibited a protective effect, although

allicin is the component of garlic most often thought to be

cardioprotective.(20

http://www.wellnessreview.com/reports/cardiomyopathy#R20>)

In another study, Rietz et al reported on the cardioprotective actions

of wild garlic (Allium ursinum). In that study, rat diets were enriched

with 2% pulverized dried leaves of wild garlic. The time until

occurrence of extrasystole was increased significantly from 3.4 minutes

in the control group to 7.1 minutes in the wild garlic group. Although

the time until occurrence of VT was likewise prolonged, there was no

significant difference in the incidence of VT. The most notable finding

was that the incidence of VF was reduced from 88% in the control group

to 20% in the wild garlic group. The ischemic zones of the hearts of the

wild garlic group were significantly smaller than those of the control

hearts (33.6% versus 40.9% of total cardiac tissue). In the case of

reperfusion-induced arrhythmias, rats fed the diet containing wild

garlic powder showed a significant reduction in both the incidence of VT

(70% vs. 100%) and VF (50% vs. 90%). It was also reported that the

antiarrhythmic effects of wild garlic were not related to the fatty acid

composition of the heart.(21

http://www.wellnessreview.com/reports/cardiomyopathy#R21>)

Coenzyme Q10

CoQ10 appears to be the first therapy that significantly improves the

strength of myocardial contraction and maintains this improvement over

months to years. No conventional cardiac drugs can biochemically

substitute for CoQ10 because of their different organic structure.(24

http://www.wellnessreview.com/reports/cardiomyopathy#R24>)

Langsjoen et al reported in 1997 on their treatment of patients with

hypertrophic cardiomyopathy using CoQ10. Patients were treated with an

average of 200 mg/day of CoQ10. All patients noted improvement in

symptoms of fatigue and dyspnea with no side effects. One patient even

noted complete resolution of her frequent and severe chest pain. After

three months of treatment with CoQ10, the mean intraventricular septal

thickness improved significantly from 1.51 ± 0.17 cm to 1.14 ± 0.13 cm,

a 24% reduction (P < 0.002). The mean posterior wall thickness improved

significantly from 1.37 ± 0.13 cm to 1.01 ± 0.15 cm, a 26% reduction (P

< 0.005). The one patient in the study with subaortic obstruction also

showed an improvement in resting pressure gradient after CoQ10 (70 mmHg

to 30 mmHg). These clinical and echocardiographic improvements were

sustained for up to 48 months (range 3 - 48 months with a mean of

21-months follow-up to the date the report was published). They went on

to note several previous studies indicating consistent improvement in

both left ventricular wall thickness and diastolic function in

hypertensive heart disease treated with CoQ10.(22

http://www.wellnessreview.com/reports/cardiomyopathy#R22>)

In a separate report in 1990, Langsjoen et al found a pronounced

increase of survival of patients with cardiomyopathy when treated with

CoQ10 along with conventional therapy. In that study, 137 patients were

treated with CoQ10, of which 43 had ejection fractions (EF) below 40%.

The survival rate for all 137 patients treated with CoQ10 including the

43 with EF below 40% was 75% after 46 months. This survival rate was of

extraordinary significance because 182 patients with EF below 46% on

conventional therapy, without CoQ10, had a survival rate of only 25%

after a shorter period of 36 months. The use of CoQ10 demonstrated a

three-fold increase in long term survival when compared to conventional

therapy. The dose of CoQ10 used in this study was 33.3 mg three times

per day, encased with soybean oil. Langsjoen et al noted several other

studies that also demonstrated extraordinary clinical improvement after

CoQ10 therapy and went on to state, " CoQ10 is so effective for patients

with advanced cardiomyopathy who are dying that it seems unethical to

extend the blind trial with placebo when an effective treatment is

available. " (23 http://www.wellnessreview.com/reports/cardiomyopathy#R23>)

Also in 1990, Langsjoen et al reported on a six-year clinical study

using CoQ10 to treat cardiomyopathy in 143 patients with chronic,

stable, non-secondary, non-hypertrophic cardiomyopathy, 98% of which

were in NYHA Classes III and IV. Each patient was given 100 mg/day CoQ10

orally, divided into three doses, in addition to their conventional

medical program in an open-label long-term study. Mean EF of 44%

measured by systolic time interval analysis rose to 60% within 6 months

and stabilized at that level with 84% of patients showing statistically

significant improvement. 85% of patients improved by one or two NYHA

classes. The survival rate was also encouraging with only 11.1%

mortality in 12 months. (Other studies show a mortality rate as high as

66% in 12 months when CoQ10 was not included in the regimen.) There was

only 17.8% mortality in 24 months which also compared favorably with

reports in the literature. CoQ10 treated patients lived as much as five

times longer, or more, when compared to those on conventional therapy

alone. There was no evidence of toxicity or intolerance in a total of

368.9 patient-years of exposure.(25

http://www.wellnessreview.com/reports/cardiomyopathy#R25>)

In 1988 Langsjoen et al reported on yet another trial of CoQ10 in 88

patients. 75% to 85% of patients showed statistically significant

increases in two monitored cardiac parameters. Patients with the lowest

ejection fractions (approximately 10% - 30%) showed the highest

increases (115% - 210%) and those with higher ejection fractions (50% -

80%) showed increases of approximately 10% - 25%. By functional

classification, 17/21 in class IV, 52/62 in class III, and 4/5 in class

II improved to lower classes. Clinical responses appeared maximal with

blood levels of approximately 2.5 µg CoQ10/ml and higher during therapy.

The dosage was 100 mg of CoQ10 in soybean oil daily for each patient.(24

http://www.wellnessreview.com/reports/cardiomyopathy#R24>)

Sacher et al in 1997 reported on their study of 19 congestive

cardiomyopathy patients treated with CoQ10. After four months of CoQ10

therapy, functional class improved 20% (3.0 ± 0.4 to 2.4 ± 0.6, p <

0.001) and there was a 27% improvement in mean CHF score (2.8 ± 0.4 to

2.2 ± 0.4, p < 0.001). Therapy with CoQ10 was associated with a mean

25.4% increase in exercise duration and a 14.3% increase in workload.

Patients received 30 mg CoQ10 three times per day for 16 weeks. They

noted other studies which reported that 75% of patients usually respond

to CoQ10 within 90 days and that this is probably based on the time

required for CoQ10 apoenzyme biosynthesis. They concluded that CoQ10

therapy is associated with significant functional, clinical, and

hemodynamic improvements within the context of an extremely favorable

benefit-to-risk ratio. CoQ10 was found to enhance cardiac output by

exerting a positive inotropic effect upon the myocardium as well as mild

vasodilation. They also noted that in some studies CoQ10 was also shown

to exhibit an antiarrhythmic effect.(26

http://www.wellnessreview.com/reports/cardiomyopathy#R26>)

Taurine

Schaffer et al in 1999 reviewed various studies demonstrating that

taurine supplementation may lead to improvements in patients being

treated for cardiomyopathy and CHF. They described a study that found

when taurine is substantially decreased in the feline myocardium through

dietary changes, the animal develops cardiomyopathy. They also noted a

study that found the mortality rate of rabbits with experimental heart

failure was significantly reduced in animals maintained on a diet

containing 100 mg/kg taurine. Another reviewed study found that a daily

oral dose of 4 g taurine caused improvement in symptoms among people

with CHF. Schaffer et al described three theories as to why taurine may

have beneficial effects on the heart. First, taurine may help reduce

salt and fluid load. Second, it may improve contractile function thereby

lessening congestive symptoms. Third, it may inhibit the actions of

angiotensin II, thereby mimicking the actions of ACE inhibitors.(27

http://www.wellnessreview.com/reports/cardiomyopathy#R27>)

In 2003, Singh et al studied the combined use of taurine and CoQ10 in 51

patients with AMI or unstable angina. Patients were randomized to

receive a combination of 6 g taurine and 120 mg CoQ10 daily (each

divided into three doses), or placebo. The mean infarct size was

significantly smaller in the intervention group compared to the placebo

group. Also, the sum of Q or R waves, the site anterior or inferior to

the necrosis, the amplitude and changes in the curves during

surveillance were all significantly lower in the intervention group.

Further, total complications were shown to be significantly lower in the

intervention group than the control group (6 vs. 21, p < 0.05). They

reported that combined treatment with taurine and CoQ10 can provide

cardioprotective benefits in patients with AMI.(28

http://www.wellnessreview.com/reports/cardiomyopathy#R28>)

Combined Supplementation

Sole et al reported in 2002 that specific metabolic deficiencies are

observed in the failing myocardium including deficiencies of carnitine,

CoQ10, thiamin, creatine, taurine and antioxidant vitamins. They

described how studies of supplementation with single nutrients in a

pharmacological fashion have yielded mixed results and concluded that

replacement of just one nutrient is unlikely to completely correct the

cascade of interconnected abnormalities found in the failing myocardium.

Rather, they recommended supplementation with a wide array of nutrients

that could be lacking in the case of CHF. In order to test their theory,

Sole et al compared a placebo diet with one enriched with taurine,

CoQ10, carnitine, thiamin, creatine, vitamin E, vitamin C and selenium,

and fed to cardiomyopathyic hamsters in late stages of the disease.

Supplementation for 3 months markedly improved myocyte sarcomeric

ultrastructure, developed pressure, +dp/dt and -dp/dt measured in a

Langendorff apparatus. Further, they reported on a double-blind,

placebo-controlled trial containing these same nutrients given to human

patients with ischemic cardiomyopathy. The supplemented group had

myocardial levels of taurine, CoQ10 and carnitine restored resulting in

a significant decrease in left ventricular end-diastolic volume.(29

http://www.wellnessreview.com/reports/cardiomyopathy#R29>)

Conclusion

Based upon the numerous studies indicating significant improvement after

nutritional supplementation, it seems most treatment protocols for

cardiomyopathy, CHF and/or arrhythmias in humans as well as animals

would benefit from the inclusion of at least some, if not several, of

the nutrients detailed in this report. A proposed nutritional protocol

is presented below. While the supplements presented in this protocol

have not yet been scientifically tested together for use in cardiac

patients, the recommended nutrients are all common in foods and are not

known to have toxic effects when given at the doses presented.

It is possible that nutritional supplementation could lessen or

eliminate the need for some conventional pharmacological treatments, as

has already been documented in some cases with magnesium. Since this is

new ground, any reduction of conventional medications should only be

done with careful and consistent monitoring by a healthcare professional.

Complex relationships exist between some of the nutrients reported on

here and further study is needed to determine ideal doses and

combinations of nutritional supplements, both with and without

conventional medications, when used to treat diseases of the myocardium.

Proposed Nutritional Protocol Based Upon Current Research

1. Magnesium lactate 12-hour time release (Mag-Tab SR by Niche

Pharmaceuticals). 12 - 18 mg/kg/day divide into two or three

doses. (Use with caution in cases of renal insufficiency.)

2. Several servings per day of foods containing large amounts of

potassium such as bananas, beet greens, vegetable juice (with no

added sodium) and baked potatoes.

3. Coenzyme Q10. 3 - 4 mg/kg/day divided into three doses. (Oil-based

softgels provide best results.)

4. Fish Oil. 1 to 2 teaspoons per 10 kg/day. (Warning: Some forms of

fish oil contain such high levels of Vitamins A and D that they

become toxic at high doses. Select fish oil products that do not

contain Vitamins A or D, and that are also certified to not

contain excessive levels of contaminants such as organochlorines

or PCBs.)

5. Reduce as much as possible intake of salt as well as saturated

fats from meat products.

6. Selenium. 10 mcg/kg/day divided into two or three doses.

7. L-carnitine. 40 - 60 mg/kg/day divided into three doses.

8. Raw garlic, garlic powder and/or garlic supplements.

9. Nicotinic acid. 1 - 2 mg/kg/day divided into two doses. (Warning:

High doses of nicotinic acid can have dangerous side effects.

Supervision by a healthcare professional is advised for any dose

beyond this level.)

10. L-lysine. 40 - 60 mg/kg/day divided into three doses, administered

with L-carnitine.

11. Food products containing high doses of methionine (e.g. oatmeal).

12. Iron (1 mg/4 kg/day); L-threonine (8 mg/kg/day); Creatine (25

mg/kg/day); Vitamin B1 (2 - 3 mg/kg/day); Vitamin B6 (1 - 2

mg/kg/day); Vitamin C (15 mg/kg/day).

13. Choline. 15 - 20 mg/kg/day divided into three doses, administered

with L-carnitine.

14. Taurine. 100 mg/kg/day divided into three doses.

Formula to convert pounds to kilograms: Weight in Kilograms = Weight in

Pounds x 0.4536

Warning: A few supplements, particularly at higher doses, may cause

adverse reactions when combined with some conventional medications. A

healthcare professional should review and monitor any nutritional protocol.

Most of the nutrients outlined above are found in a wide variety of food

products. It may be possible to obtain adequate amounts of some of these

through proper food choices. Below are links to Web pages provided by

the U.S. Department of Agriculture which can display detailed nutrient

content for most common food products.

USDA Nutrient Database: www.nal.usda.gov/fnic/cgi-bin/nut_search.pl

http://www.nal.usda.gov/fnic/cgi-bin/nut_search.pl>

View the nutrient content of most common food products using this online

database.

Nutrient Lists:

www.nal.usda.gov/fnic/foodcomp/Data/SR15/wtrank/wt_rank.html

http://www.nal.usda.gov/fnic/foodcomp/Data/SR15/wtrank/wt_rank.html>

View detailed reports listing foods rich in nutrients such as magnesium

or potassium.

References

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2. Helton E, Darragh R, Francis P, Fricker FJ, Jue K, Koch G, Mair D,

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H. Antiarrhythmic effects of increasing the daily intake of

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Investigators. J Am Coll Cardiol. 1997 Apr;29(5):1028-34.

6. Iseri LT, BJ, Ginkel ML, Brodsky MA. Ionic biology and ionic

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10. Tanguy S, Boucher F, Besse S, Ducros V, Favier A, de Leiris J.

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in rats limits reperfusion-induced arrhythmias. J Trace Elem Med

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11. Lehr D. A possible beneficial effect of selenium administration in

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15. Hock CE, Beck LD, Bodine RC, Reibel DK. Influence of dietary n-3

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16. McLennan PL, Abeywardena MY, Charnock JS. The influence of age and

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Copyright © 2003 World Environmental Organization. All rights reserved.

Alice wrote:

>I'm still crashing and very hard and in the process of testing. Heart testing

last week and one doctor said I have congestive heart failiure while my PCP

believes its Cardiomyopathy. Waiting for test results on that now.

>

>

>

>

[Guest guest]

Oh my.. Thank you for putting all this together . Unfortunately, I can't

read anything long and detailed. Everything looks like mexican jumping beans

and I can't focus much on the computer or in print. If I could hear, someone

could read it to me but at the moment, I can compare myself to being somewhat

deaf/blind and mobility impaired. I'm not able to easily handle self care and

had to board Stella for as long as I could afford to because I really can't care

for her.

I'm afraid this is much worse than I have led you to believe. I'm having to

limit computer time out of necessity. It actually feels better to try not to

look at things. Short messages I can handle but nothing more.

Alice

[Guest guest]

Alice,

Take care and THANK YOU for your previous response to my bruising

problem.

The email that put together is very good, in that it explains

all of the supplements which might work together to treat heart

related problems. If you can, you might want to print it out and

save until you're up to reading a portion at a time.

I hope after resting that you start to feel better.

Maggie

> Oh my.. Thank you for putting all this together .

Unfortunately, I can't read anything long and detailed. Everything

looks like mexican jumping beans and I can't focus much on the

computer or in print. If I could hear, someone could read it to me

but at the moment, I can compare myself to being somewhat deaf/blind

and mobility impaired. I'm not able to easily handle self care and

had to board Stella for as long as I could afford to because I

really can't care for her.

>

> I'm afraid this is much worse than I have led you to believe. I'm

having to limit computer time out of necessity. It actually feels

better to try not to look at things. Short messages I can handle

but nothing more.

>

> Alice

>

>

[Guest guest]

Alice

Don't worry about being on the computer. I know that it is important to you,

but let us take over. I wish I could come and help you.

laurie

>

> Reply-To:

> Date: Sun, 2 May 2004 10:31:02 -0600

> To: >

> Subject: Re: Alice - long

>

> Oh my.. Thank you for putting all this together . Unfortunately, I

> can't read anything long and detailed. Everything looks like mexican jumping

> beans and I can't focus much on the computer or in print. If I could hear,

> someone could read it to me but at the moment, I can compare myself to being

> somewhat deaf/blind and mobility impaired. I'm not able to easily handle self

> care and had to board Stella for as long as I could afford to because I really

> can't care for her.

>

> I'm afraid this is much worse than I have led you to believe. I'm having to

> limit computer time out of necessity. It actually feels better to try not to

> look at things. Short messages I can handle but nothing more.

>

> Alice

>

>

[Guest guest]

Oh Alice, I am so terribly sorry you are going through all this. I just

can't imagine having to face all of this on a daily basis. My prayers are

with you.

Love and smiles,

Re: Alice - long

> Oh my.. Thank you for putting all this together . Unfortunately, I

can't read anything long and detailed. Everything looks like mexican

jumping beans and I can't focus much on the computer or in print. If I

could hear, someone could read it to me but at the moment, I can compare

myself to being somewhat deaf/blind and mobility impaired. I'm not able to

easily handle self care and had to board Stella for as long as I could

afford to because I really can't care for her.

>

> I'm afraid this is much worse than I have led you to believe. I'm having

to limit computer time out of necessity. It actually feels better to try

not to look at things. Short messages I can handle but nothing more.

>

> Alice

>

>

[Guest guest]

God Bless you Alice you are in my prayers and thoughts. Warm hugs. Vivian

[Guest guest]

Hang in there Alice, and please get some rest. I had to sleep a

whole week, except for potty breaks every 12 hours, after working 80

hours one week.

Take care,

RH

> Oh my.. Thank you for putting all this together .

Unfortunately, I can't read anything long and detailed. Everything

looks like mexican jumping beans and I can't focus much on the

computer or in print. If I could hear, someone could read it to me

but at the moment, I can compare myself to being somewhat deaf/blind

and mobility impaired. I'm not able to easily handle self care and

had to board Stella for as long as I could afford to because I really

can't care for her.

>

> I'm afraid this is much worse than I have led you to believe. I'm

having to limit computer time out of necessity. It actually feels

better to try not to look at things. Short messages I can handle but

nothing more.

>

> Alice

>

>