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Program HE
Heart Support
Breakfast
Organic oatmeal, milk, soymilk, or goat’s milk, 3 Tbsp. fresh ground flaxmeal
*
Hot brown rice cereal w/cinnamon and freshly ground almonds, green tea
*
Organic cottage cheese with flax oil, organic fruit or raw nuts (almonds, walnuts), green tea
*
1 cup cottage cheese or yogurt, 1 tablespoon flax oil, 1 Tbsp. natural preserves
*
Poached organic omega-3 eggs or three egg omelet, sweet potatoes w/rosemary, ½ cup black
beans
*
2 organic eggs any style, 1 slice whole grain toast, 3 Tbsp. freshly ground flaxmeal
Lunch and Dinner
Season sardines in water (green and white label), green salad
*
Swordfish steak, grilled onions, green salad with flax oil dressing
*
Flank steak, baked potato, green salad with flax oil dressing
*
Broiled red snapper, steamed broccoli, baked yams
*
Large mixed green salad w/ oil and lemon juice, small can of tuna, chopped yellow and sweet
red pepper
*
Broiled mackerel, steamed broccoli, green beans or other vegetable
*
Beef, lentil and vegetable soup, (celery, carrots, onion, cabbage)
*
Chicken salad made with sugar-free mayonnaise, roasted vegetables, spinach salad
*
Gourmet salmon salad made with 1 can salmon, 2 tsp. sliced scallions, 1 tsp. sliced radishes, 2
tsp. Rice vinegar, 1 tsp. flax oil, 1 tsp. soy sauce, and ¼ tsp. minced
ginger root, all placed atop a green salad
Snacks
Roasted garlic or almond butter on rice cake or celery, protein shakes with freshly ground
flaxseeds added, fresh green vegetable juice, handful of raw almonds, hazelnuts, walnuts,
brazil nuts, or sesame seeds, an organic apple, pear, or grapes, sugar-free yogurt, rice cakes
with nut butter, hard boiled egg.
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Program HE
Heart Support
Beverages
Green drinks: Green Magma, Kyogreen, or Green Kamut: 1 tsp. 1-3x day in water
Herbal Teas: Ginger, Cinnamon, Chamomile, Linden Tea (improves integrity of blood vessel
walls), Green Tea with Cinnamon Stick
Avoid
Cigarette smoke (even 2 hand), sugar, refined and processed foods, hydrogenated oils,
safflower, sunflower, corn oils, soft drinks, alcohol, processed meats, being overweight. Do
not consume large amounts of licorice as this can lower levels of magnesium and potassium.
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Suggestions and goals
The basic idea of this eating program is to increase consumption of omega 3 fats, fiber, and
whole natural foods. Eliminate sugar, refined or processed foods, and hydrogenated oils.
Drink plenty of pure water.
Supplements
Magnesium
Carnitine
CoQ10
Vitamin E
Taurine
EPA/DHA
B Complex
Vitamin C
Zinc
Lipoic Acid
Selenium
Creatine
500-1,000 mg (balance with potassium in diet)
500-4,000 mg (½ to 1 hour before breakfast and lunch)
100-400 mg
400-800 IUs
1-3 grams
500-2,000 mg
1-2 per day
1-3 grams
25-50 mg
100 mg
200-400 mcg
1 gram
Herbs:
Hawthorn (leaf, berry, and flower)
Cactus grandiflorus
Motherwort
Collinsonia (Stone Root)
1-4 ml per day
½-2 ml per day
1-3 ml dropper per day
1-2 ml dropper per day
For MVP Patients: Hypoglycemia is one of the components that so often accompanies
mitral valve prolapse (MVP), and it is important to balance blood sugar well if one is to
successfully treat this condition. Adequate protein, sugar avoidance, and all the other
recommendations for hypoglycemia should be followed by those with MVP. Hawthorn and
cactus grandiflorus are two wonderful heart strengthening herbs that are very useful in MVP.
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Program HE
Heart Support
Research Review
Antioxidants
Cardiomyopathies are the group of diseases affecting the cardiac muscle. Although they have never been
related to oxidative stress diseases, an analysis of the causes of these pathologies reveals the presence of a prooxidative agent or that the intracardiocytic balance between oxidation and antioxidation has been broken. In
support of this hypothesis, we analyze the pro-oxidative factors which co-operate with other factors or by
themselves to promote the development of this group of pathologies. We show also data demonstrating that
the tissue and cellular damages are characteristic of an oxidative stress situation. Finally, we present evidence
that in some cases of particular cardiomyopathies, the use of antioxidative strategies greatly improves the
health of the patients. Therefore, we suggest that the use of antioxidants can be an alternative or
complementary therapy in this group of diseases.1
Magnesium
Reduced tissue magnesium stores may represent a significant risk factor for arrhythmias.2
These results suggest that intravenous magnesium sulfate may be effective in the acute management of
cardiac arrhythmias in patients with a low serum iMg2+ level.3
The intricate role of magnesium on a biochemical and cellular level in cardiac cells is crucial in maintaining
stable cardiovascular hemodynamics and electrophysiologic function. In patients with congestive heart failure,
the presence of adequate total-body magnesium stores serve as an important prognostic indicator because of
an amelioration of arrhythmias, digitalis toxicity, and hemodynamic abnormalities.4
Magnesium and Potassium
The interactions of Mg and K in cardiovascular disease are diverse and complex. However, Mg deficiency and
loss from the heart and arteries, caused e.g. by dietary deficiency or imbalance, or by diseases and their
treatment, can contribute to cardiovascular damage, and to functional abnormalities. Although Mg deficiency
interferes with K retention, it is seldom measured in routine clinical practice, and the need to correct low Mg
levels, in order to replete K, is rarely considered. The heart, with its high metabolic activity, is particularly
vulnerable to Mg deficiency or loss because of the importance of Mg in mitochondrial structure and
enzymatic function. The need for Mg to activate Na/K ATPase has long been known. Mg has also been
shown to be structurally part of the enzyme in cardiac mitochondria. Additionally, Na/K exchange occurs in
association with phosphorylation and dephosphorylation, reactions that are also Mg- dependent. The
demonstration that Mg modulates K+/proton (H+) exchange, and that cation selectivity in Na+ and K+
exchange for H+ is highly dependent on the concentration of Mg++, provides new insights into how Mg
protects against K loss. The loss of myocardial K that results from Mg deficiency contributes to
electrophysiologic changes, as can the Ca shifts of Mg loss. A high Ca/Mg ratio also predisposes to arterial
spasms, and increases catecholamine release. Thus the arrhythmogenic potential of Mg deficiency can be
related to imbalances between Mg and K or between Mg and Ca, or both. Electrical or K-induced
catecholamine release is increased by a low Mg/Ca ratio, as are increased fatty acids and lipids and
intravascular hypercoagulability. K or Ca loading of the patient with undiagnosed Mg inadequacy is not only
often unsuccessful, but it may carry inherent risks. It can intensify the Mg depletion, the arterial contractility,
and ECG abnormality. In the patient receiving digitalis, Mg deficiency can increase drug toxicity. In the case
of myocardial infarction, Mg deficiency can increase the risk of malignant ventricular arrhythmias and sudden
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Program HE
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cardiac death. In the absence of alcoholism or gastrointestinal disease, the use of loop diuretic therapy for
congestive heart failure, especially in elderly patients, is the most common cause of Mg depletion. A high
concurrence of hypomagnesemia with hypokalemia, from whatever cause, has been documented. However,
systemic Mg deficiency can exist despite normal Mg serum levels. Methodological difficulties hamper direct
detection of cellular Mg deficiency, but patients can be indirectly evaluated by use of Mg-loading tests, which
may be of combined diagnostic and therapeutic value.5
Selenium
A case of selenium-deficiency myopathy, secondary to total parenteral nutrition, is presented. The literature
on selenium-deficiency myopathy and cardiomyopathy is reviewed in the context of the literature concerning
selenium status in numerous diseases. 6
Carnitine
To evaluate the therapeutic efficacy of l-carnitine in heart failure, the myocardial carnitine levels and the
therapeutic efficacy of l- carnitine were studied in cardiomyopathic BIO 14.6 hamsters and in patients with
chronic congestive heart failure and ischemic heart disease. Oral administration of l-carnitine for 12 weeks
significantly improved the exercise tolerance of patients with effort angina. In 9 patients with chronic
congestive heart failure, 5 patients (55%) moved to a lower NYHA class and the overall condition was
improved in 6 patients (66%) after treatment with l-carnitine. L-carnitine is capable of reversing the inhibition
of adenine nucleotide translocase and thus can restore the fatty acid oxidation mechanism which constitutes
the main energy source for the myocardium. Therefore, these results indicate that l-carnitine is a useful
therapeutic agent for the treatment of congestive heart failure in combination with traditional
pharmacological therapy.7
CoQ10
Over an eight year period (1985-1993), we treated 424 patients with various forms of cardiovascular disease
by adding coenzyme Q10 (CoQ10) to their medical regimens. Doses of CoQ10 ranged from 75 to 600
mg/day by mouth (average 242 mg). Treatment was primarily guided by the patient's clinical response. In
many instances, CoQ10 levels were employed with the aim of producing a whole blood level greater than or
equal to 2.10 micrograms/ml (average 2.92 micrograms/ml, n = 297). Patients were followed for an average
of 17.8 months, with a total accumulation of 632 patient years. Patients were divided into six diagnostic
categories: ischemic cardiomyopathy (ICM), dilated cardiomyopathy (DCM), primary diastolic dysfunction
(PDD), hypertension (HTN), mitral valve prolapse (MVP) and valvular heart disease (VHD). For the entire
group and for each diagnostic category, we evaluated clinical response according to the New York Heart
Association (NYHA) functional scale, and found significant improvement. Of 424 patients, 58 per cent
improved by one NYHA class, 28% by two classes and 1.2% by three classes. A statistically significant
improvement in myocardial function was documented using the following echocardiographic parameters: left
ventricular wall thickness, mitral valve inflow slope and fractional shortening. Before treatment with CoQ10,
most patients were taking from one to five cardiac medications. During this study, overall medication
requirements dropped considerably: 43% stopped between one and three drugs. Only 6% of the patients
required the addition of one drug. No apparent side effects from CoQ10 treatment were noted other than a
single case of transient nausea. In conclusion, CoQ10 is a safe and effective adjunctive treatment for a broad
range of cardiovascular diseases, producing gratifying clinical responses while easing the medical and financial
burden of multidrug therapy.8
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Program HE
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Hypertrophic cardiomyopathy (HCM) is manifested by severe thickening of the left ventricle with significant
diastolic dysfunction. Previous observations on the improvement in diastolic function and left ventricular wall
thickness through the therapeutic administration of coenzyme Q10 (CoQ10) in patients with hypertensive
heart disease prompted the investigation of its utility in HCM. Seven patients with HCM, six non-obstructive
and one obstructive, were treated with an average of 200 mg/day of CoQ10 with mean treatment whole
blood CoQ10 level of 2.9 micrograms/ml. Echocardiograms were obtained in all seven patients at baseline
and again 3 or more months post-treatment. All patients noted improvement in symptoms of fatigue and
dyspnea with no side effects noted. The mean interventricular 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). Mitral valve
inflow slope by pulsed wave Doppler (EF slope) showed a non-significant trend towards improvement, 1.55
+/- 0.49 m/sec2 to 2.58 +/- 1.18 m/sec2 (P 0.08). The one patient with subaortic obstruction showed an
improvement in resting pressure gradient after CoQ10 treatment (70 mmHg to 30 mmHg).9
Taurine
We compared the effect of oral administration of taurine (3 g/day) and coenzyme Q10 (CoQ10) (30 mg/day)
in 17 patients with congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy, whose
ejection fraction assessed by echocardiography was less than 50%. The changes in echocardiographic
parameters produced by 6 weeks of treatment were evaluated in a double-blind fashion. In the taurine- treated
group significant treatment effect was observed on systolic left ventricular function after 6 weeks. Such an
effect was not observed in the CoQ10-treated group.10
Omega 3 Fats and Arrhythmias
Interest in the potential cardiovascular benefits of omega-3 long chain polyunsaturated fatty acids has been
largely focused on possible antiatherothrombotic effects. In addition, however, definitive antiarrhythmic
effects of these dietary omega-3 fatty acids have been reported by Charnock & McLennan. Our studies
commenced with the observation that two of these fatty acids, eicosapentaenoic (C20:5n-3, EPA) and
docosahexaenoic acid (C22:6n-3, DHA) prevented contracture and fibrillation of isolated neonatal cardiac
myocytes when exposed to toxic levels of ouabain (0.1 mM). This protection was associated with prevention
of excessively high intracellular calcium concentrations in the myocyte. Further, it was shown that these fatty
acids modulate calcium currents through L-type calcium channels and that the effect occurs within a few
minutes of adding EPA or DHA to the medium perfusing the cultured cardiac myocytes. Infusing an
emulsion of the omega-3 fatty acids intravenously just prior to compression of a coronary artery in a
conscious, prepared dog will prevent the expected subsequent ischemia-induced ventricular fibrillation.11
Hawthorn
Hawthorn (crataegus) has been used since antiquity for medicinal purposes. More recent research suggests it
to be useful in congestive heart failure. Rigorous clinical trials show benefit concerning objective signs and
subjective symptoms of congestive heart failure stage NYHA-II. No adverse drug reactions have been
reported. It is therefore concluded that crataegus is an effective and safe therapeutic alternative for this
indication.12
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Program HE
Heart Support
1. Romero-Alvira D, Roche E, Placer L. Cardiomyopathies and oxidative stress. Med Hypotheses
1996;47(2):137-44.
2. Haigney MC, Berger R, Schulman S, et al. Tissue magnesium levels and the arrhythmic substrate in
humans. J Cardiovasc Electrophysiol 1997;8(9):980-6.
3. Kasaoka S, Tsuruta R, Nakashima K, et al. Effect of intravenous magnesium sulfate on cardiac arrhythmias
in critically ill patients with low serum ionized magnesium [published erratum appears in Jpn Circ J
1997 Oct;61(10):886]. Jpn Circ J 1996;60(11):871-5.
4. Douban S, Brodsky MA, Whang DD, Whang R. Significance of magnesium in congestive heart failure. Am
Heart J 1996;132(3):664-71.
5. Sheehan JP, Seelig MS. Interactions of magnesium and potassium in the pathogenesis of cardiovascular
disease. Magnesium 1984;3(4-6):301-14.
6. Marcus RW. Myopathy and cardiomyopathy associated with selenium deficiency: case report, literature
review, and hypothesis. Md Med J 1993;42(7):669-74.
7. Kobayashi A, Masumura Y, Yamazaki N. L-carnitine treatment for congestive heart failure--experimental
and clinical study. Jpn Circ J 1992;56(1):86-94.
8. Langsjoen H, Langsjoen P, Willis R, Folkers K. Usefulness of coenzyme Q10 in clinical cardiology: a longterm study. Mol Aspects Med 1994;15(Suppl):s165-75.
9. Langsjoen PH, Langsjoen A, Willis R, Folkers K. Treatment of hypertrophic cardiomyopathy with
coenzyme Q10. Mol Aspects Med 1997;18(Suppl):S145-51.
10. Azuma J, Sawamura A, Awata N. Usefulness of taurine in chronic congestive heart failure and its
prospective application. Jpn Circ J 1992;56(1):95-9.
11. Leaf A. Omega-3 fatty acids and prevention of ventricular fibrillation. Prostaglandins Leukot Essent Fatty
Acids 1995;52(2-3):197-8.
12. Weihmayr T, Ernst E. [Therapeutic effectiveness of Crataegus]. Fortschr Med 1996;114(1-2):27-9.
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