Myasthenia: from the Greek words, myelos, meaning muscle, and astheneia, meaning weakness
Gravis: from the Latin word, gravidus, meaning heavy (serious)

Myasthenia gravis (MG) is an autoimmune disease that is characterized by impairment of motor nerve impulses causing episodic muscle weakness and fatigue, especially in the face, tongue, neck, and respiratory muscles. MG occurs at all ages, usually between the ages of 20 and 40, sometimes in association with a thymic tumor or thyrotoxicosis, as well as in rheumatoid arthritis and lupus erythematosus. It is most common in young women with HLA-DR3; if thymoma (tumor) is associated, older men are more commonly affected. Onset is usually insidious, but the disorder is sometimes unmasked by a coincidental infection that leads to exacerbation of symptoms. Exacerbations may also occur before the menstrual period and during or shortly after pregnancy.

Symptoms

Symptoms are due to a variable degree of neuromuscular transmission blockage caused by autoantibodies binding to acetylcholine receptors. These autoantibodies are found in most patients with the disease and have a primary role in reducing the number of functioning acetylcholine receptors. Additionally, cellular immune activity against the receptor is found. Clinically, this leads to weakness, and initially powerful movements fatigue readily. The external ocular muscles and certain other cranial muscles, including the masticatory, facial, and pharyngeal muscles, are especially likely to be affected, and the respiratory and limb muscles may also be involved. In the ocular variety, there is difficulty with movements of the lids and the eyeball itself. When the pharyngeal muscles are involved, difficulty in swallowing ensues.

Only voluntary (or striated) muscles are affected; involuntary heart muscle and smooth muscle of the gut, blood vessels, and uterus are not involved. Muscles of the limbs may also be affected in some MG patients. Asymmetrical weakness may occur, with one side of the body more affected than the other. Difficulty may be encountered with simple tasks such as combing one's hair, shaving, and putting on makeup. Climbing stairs or walking distances may cause the legs to easily tire. In 10% of the cases, people develop a weakness of the muscles needed for breathing, a condition known as myasthenia crisis. Hospitalization and mechanical breathing assistance may be necessary in such cases. The disease is painless but may become painful if the patient goes into spasm as a result of early fatigue. Skin sensation is preserved.

The effect of pregnancy on MG varies from patient to patient. Symptoms of the disease may disappear, worsen, or remain the same during the course of pregnancy. Obstetrical problems are usually not present because the smooth muscle of the uterus is unaffected by the disease. During second-stage labor, when voluntary striated abdominal muscles are used, weakness becomes noticeable. Pregnant women with MG may pass affected antibodies through the placenta to their unborn child. This results in temporary neonatal myasthenia, in which the infant has muscle weakness that disappears several days to a few weeks after birth.

Diagnosis

Doctors may suspect MG in anyone with generalized weakness that increases with the use of affected muscles and recovers with rest or in anyone presenting with weakness in the muscles of the eye and face. Since acetylcholine receptors are blocked in MG, drugs that increase the amount of acetylcholine--such as edrophonium--can be used as test drugs, administered intravenously, to see if muscle strength will temporarily improve. Blood testing for antibodies to acetylcholine as well as diagnostic measurement of nerve and muscle function may also be administered. In equivocal cases, electrophysiological studies testing nerve transmission and muscle reaction may be helpful. A computerized axial tomographic (CAT) scan of the chest may reveal an associated thymoma.

SHORT-TERM CONVENTIONAL TREATMENT

Short-term treatment for MG includes medications to counteract the symptoms of weakness and muscle fatigue. Anticholinesterases, such as neostigmine and pyridostigmine, which boost the levels of acetylcholine by blocking the enzyme which breaks acetylcholine down, can provide relief for a few hours. Some patients may show no response or even become weaker while taking the drug. Ephedrine sulfate may be used in conjunction with an anticholinesterase for added strength if patients are not bothered by possible side effects, such as nervousness and insomnia.

Plasmapheresis is an expensive short-term treatment in which several liters of blood are removed from the patient, centrifuged for removal of abnormal antibodies, and returned intravenously in artificial plasma. This treatment is considered when short-term improvement is crucial for the patient. However, the benefits of the procedure may last only weeks.

High-dose intravenous human immunoglobulin (IVIg) has emerged as a conventional therapy for various neurologic diseases. It may be considered the opposite of plasmapheresis. Rather than expunging the blood of abnormal antibodies, IVIg floods the body with pooled gamma globulin antibodies from several donors. Although expensive, IVIg has become a first-line or adjunctive therapy in the treatment of diverse autoimmune diseases, including MG. IVIg therapy has received Food and Drug Administration approval for use as a maintenance treatment of patients with primary humoral (blood-based) immunodeficiencies, and as therapy for acute or chronic autoimmune thrombocytopenic purpura. In controlled clinical trials, IVIg has been effective in treating chronic inflammatory demyelinating polyneuropathy. IVIg also has produced improvement in some patients with MG, but has had a variable or unsubstantiated benefit in others.

LONG-TERM CONVENTIONAL TREATMENT

Long-term treatment may include removal of the thymus gland. About 15% of patients with MG are found to have a tumor of the thymus gland, known as a thymoma. Most thymomas are benign. Thymectomy has become a common treatment modality for patients without thymoma. If most of the thymus is removed, symptoms usually lessen and, in some individuals, disappear completely. However, the thymus gland is the master gland of immunity, and removing this gland severely weakens the body's ability to fight infections and cancer.

Another long-term treatment approach is the use of immunosuppressive drugs. This group of drugs is used to suppress the body's immune system, although it is not known how they work in MG. Prednisone, azathioprine, cyclophosphamide, and cyclosporine are all immunosuppressive drugs. While patients may show significant improvement or drug-dependent remission of symptoms, they must be monitored closely for undesirable or serious side effects.

NATURAL THERAPY

Etiology
As previously mentioned, MG has been shown to be an autoimmune disease. This means that the immune system attacks some of its own body proteins. Specifically, the transmission of signals from the nerve endings to the muscle receptors is partly blocked by antibodies. The messenger chemical or neurotransmitter released as a signal from nerve endings to muscles is acetylcholine. Acetylcholine molecules travel the short distance in the gap between nerve ending and muscle to find a receptor on the motor end plate. When a sufficient number of acetylcholine molecules are attached to muscle receptors, there is an electric discharge of the normal membrane potential and the muscle fiber can contract.

In MG most of the receptors are already occupied by antibodies; therefore, not enough acetylcholine molecules find receptors to trigger this discharge and subsequent muscle contraction. Normally, the acetylcholine is split by an enzyme (cholinesterase) and, with this, is removed from the receptor in a fraction of a second. Using anticholinesterases, drugs that hinder this enzyme, acetylcholine molecules have more time to find receptors with an increased chance of leading to a discharge. However, if too much of this enzyme antagonist is present, the cells remain discharged for too long and the muscles become paralyzed. This is a "cholinergic crisis" in which heart and breathing may stop.

To test the theory that antibodies clog up muscle receptors, serum from an MG patient was injected into mice and also into healthy human muscle, which promptly produced MG-like symptoms. This is as far as the conventional medical understanding of MG goes. The cause of the main event, the blocking of the muscle receptors by antibodies, is not known. There is no curative medical treatment available and there is also no attempt to overcome this disorder with nutritional therapy. However, there are indications that nutrition and chemicals are involved.

During World War II, MG was attributed to malnutrition developed in prisoners of war in Singapore. A high-vitamin, nutritious diet with plenty of yeast and liver soon restored these patients to normal (Denny-Brown 1947). Other MG cases have also been reported with more or less permanent remissions as long as a highly nutritious diet was used. One patient reportedly lost all symptoms of MG when she took vitamins in large doses (McGraw et al. 1975). There are various statements on the Internet to the effect that raw-food diets lead to gradual improvement with MG and may be curative after 6 to 12 months

MG may manifest after exposure to crop sprays with chemicals that have an antagonistic effect on acetylcholinesterase. Another report links the development of MG to general anesthesia and hepatitis B vaccination (Biron 1998). There is also a supposedly confirmed case of MG associated with chlorine exposure ( www.lindane.org/chemicals/chlorine.htm ).

Further implicated is the enzyme poison, fluoride. Fluoridated water may trigger an MG crisis or contribute to long-term deterioration with extreme exhaustion and muscle weakness (Waldbott 1998). Problems may also arise from commercial liquids, such as soft drinks, soymilk, or reconstituted 100% fruit juices, in countries where water fluoridation is practiced.

Stress-Protective Nutrients
A wide variety of vitamins and minerals are involved in muscle activity, partly in energy production and partly in the synthesis of proteins and neurotransmitters. The main B vitamins are essential for energy production in the muscles, and some improvement in MG can be expected with B-complex supplementation so that, for instance, less of the enzyme-blocking drug may be required.

In addition to the general effect on energy production and protein synthesis, several vitamins (McGraw et al. 1980) are thought to have a specific relationship with MG.

Vitamin B1, working together with manganese, is the key vitamin for the synthesis of acetylcholine in the nerve endings. A lack of this vitamin, therefore, can cause a reduced signal from nerves to muscles and, with this, muscle weakness and other neurological complications. Vitamin B1 helps acetylcholine to bind to receptors. It also has a significant role in nerve excitation and potentiates the effects of acetylcholine. Furthermore, with low vitamin B1 levels, lactic acid accumulates in the muscles and causes fatigue; deficiency can also lead to nerve degeneration.

Vitamin B2 is important for tissue respiration, the storage of glycogen in muscles and liver, as well as for the metabolism of glycine, an amino acid linked with MG. A deficiency lowers the resistance to stress. Vitamin B6 is essential for the synthesis of neurotransmitters and receptors.

Pantothenic acid (vitamin B5) supplies the acetyl part in the synthesis of acetylcholine. It opposes the effects of substances that are known to block receptors. Pantothenic acid is the anti-stress vitamin, most important for healthy adrenal glands, which are especially weak with MG. The importance of the stress-protective vitamins can be seen in the observation that MG frequently develops during or after a period of intense stress.

Vitamin C is another anti-stress vitamin. It is essential for collagen synthesis. Collagen is the connective tissue between muscle cells, cementing them together. Vitamin C is involved with the use of glycogen in muscles, with muscle contractions and exercise tolerance. It affects muscle metabolism and the functioning of muscle membranes. Together with folic acid, it is involved with the synthesis of neurotransmitters and steroid hormones. It has a mild anticholinesterase activity and this enhances the action of the reduced amount of acetylcholine that finds a receptor.

Vitamin B12 and folic acid are required for the synthesis of choline before forming acetylcholine.

Vitamin A is needed for the immune system to produce steroid hormones and to protect the thymus and adrenal glands from the effects of stress. It can protect the thymus gland from involution during times of stress and even stimulates the thymus to regrow after premature stress-induced shrinking. In studies, vitamin A-deficient rats developed weakness of the head and leg muscles.

Vitamin E is important to protect cell membranes from damage through oxidation and peroxidation, while a deficiency causes changes in muscle protein with swelling and fragmentation of individual muscle fibers, leading to muscle weakness, dystrophy, and paralysis. Vitamin E is directly involved with the energy metabolism of muscles. A deficiency causes increased amounts of muscle protein to break down and be expelled with the urine as it happens in MG. The development and function of all endocrine glands depend on vitamin E. The pituitary gland has an exceptionally high content of vitamin E, 15 times higher than in other parts of the body, while in the adrenal glands it is almost 6 times higher.

The importance of vitamin E in MG can be seen in cases where the initial use of other vitamins improved the condition somewhat, but only after the addition of vitamin E did all symptoms of the disease disappear (Josephson 1961). Also, MG may resurface after a year or two and then vitamin E is no longer effective unless manganese is supplemented in addition.

In a study using rabbits with experimentally induced MG, more animals survived with high-dose vitamins B1, C, and E than in the unsupplemented group (Peeler et al. 1979). These same vitamins in megadoses were successfully used for MG patients as reported by Klenner (1973). However, while helpful, these vitamins alone are often not sufficient for a permanent cure.

While magnesium is an essential mineral and activates many enzymes, a large dose of a magnesium supplement acts as a muscle relaxant and may cause extreme weakness in MG.

Manganese and the Thymus Gland
While the nutrients discussed so far may be seen as co-factors, manganese and the thymus gland are the keys to the development and treatment of MG. Numerous enzymes are activated by manganese, and it is essential for the production of energy from glucose. It is equally important for the growth of bones, the development of the skeleton, and the formation of cartilage. It is essential for the development and functioning of nerves and muscles. Specifically it is involved with muscular contraction. When muscles are damaged, manganese leaches into the bloodstream and causes its level to rise.

Manganese deficiency causes defective growth, muscular weakness, lack of coordination and balance, reproductive abnormalities, and disorders of the central nervous system. Manganese is required for a healthy immune system, and it is also involved in the synthesis of acetylcholine.

While the thymus gland is best known for its importance in the development and functioning of the immune system, it also has other, less known functions.

The thymus is an endocrine gland situated behind the upper part of the breastbone. It increases in size until puberty and then gradually shrinks again. Severe stress, including infections, causes the thymus to shrink excessively and prematurely, especially if there are deficiencies of the anti-stress vitamins. The experimental removal of the thymus in some animal experiments resulted in a 60% reduction in the contractility of muscles, while the capacity to work was reduced by 42% (Josephson 1961).

In MG, the thymus is generally abnormal, usually much enlarged (hyperplasia), and not infrequently containing tumors (thymomas). Administration of high doses of manganese reportedly causes the thymus to shrink to its normal size in a very short time and thymomas and symptoms of MG to disappear.

This manganese therapy for MG was discovered and tested in the 1940s and 1950s in the United States by E. M. Josephson (A-albionic Research 1961). The report of his first MG case (below) with this new method is quite instructive.

A 43-year-old female developed the symptoms of MG in 1932. She had intermittent X-ray treatments for thymoma over many years. Drug treatment was started later but gave only a slight transient improvement, and after some months she completely failed to respond. Nutritional therapy was started in 1937 with high doses of vitamins A, B, and C, along with a high salt intake because of severe adrenal weakness, and glycine, an amino acid important for the muscles. Within 3 weeks the patient was much improved. The later substitution of part of the salt with potassium chloride caused acute glaucoma and had to be stopped.

After a year, the therapy started to become ineffective and the condition deteriorated again. Now vitamin E was added in the form of wheat germ oil. The condition rapidly improved and symptoms of MG disappeared except for occasional mild relapses. However, after 2 years, MG reappeared without relief from the treatment.

In 1942, manganese sulfate was added to the therapy. Within 1 week her muscle strength was better than at any time during previous treatments, and all symptoms of MG disappeared. The thymus tumor that had previously been unsuccessfully treated with X-rays disappeared as well. Until her death 10 years later from a heart attack, she had no more symptoms of MG.

In another case, a young woman developed rapidly progressing MG after her thyroid had been removed because of hyperthyroidism. Within 2 days of starting manganese therapy, she showed marked improvement. However, in this case it took 2 to 3 years until she was completely well. In the following years she had two relapses, which cleared up each time within a few weeks with manganese therapy. This included shrinking of the enlarged thymus during the initial therapy and the last relapse.

Another interesting case was an elderly male who first developed signs of systemic lupus erythematosus and after several years also signs of Parkinson's disease. Many years later MG appeared. Nutritional therapy including manganese soon removed the symptoms of all three diseases.

In his summary, Josephson (1961) states that generally, myasthenia cleared up within days to weeks rather than months. At the same time, hyperplasia of the thymus and thymomas "virtually melted away."

Josephson's book is still in print by A-albionic Research under the title Thymus, Manganese and Myasthenia Gravis (see www.msen.com or www.addall.com ). However, it is written as a scientific monograph and difficult for most readers to understand. Amazingly, there is no indication that this method has been tested in a clinical trial, despite Josephson having presented it before the American Association for Advancement of Science at the Harvard School of Public Health in 1946.

An MG patient was a female golf professional, who took manganese therapy on a raw-food diet, but only gradually. When she started taking manganese, she was back to playing golf within a few weeks. Initially she still had some double vision, which cleared up after one warm castor oil pack over the eyes. Another female patient started immediately with manganese and fully recovered within 2 weeks, except for a slight weakness in one eyelid.

It might be added that these patients also benefited from improved nutrition and suitable other supplements.

Complications
Removal of the thymus gland is widely practiced as long-term therapy for MG. Most patients improve for a period and some may continue improving, while others soon deteriorate again. Josephson reported the complete failure of nutritional and manganese therapy in MG patients who had their thymus removed.

Some researchers believe that the great variability of thymectomy outcomes is due to so-called accessory thymuses or pockets of thymus tissue that may be present in the neck area. These will often be sufficient to maintain a reasonable manganese metabolism and, with this, enable an eventual recovery. On the other hand, if all thymus tissue has been removed, then a full recovery may not be possible. However, there is cautious optimism that even then, a holistic approach can still lead to considerable improvement and to some regrowth of any remaining traces of thymus tissue.

Also, the removal of the thyroid makes a cure more difficult, as one of Josephson's case histories shows. In addition to enlargement and tumors of the thymus, MG patients frequently have problems with other endocrine glands such as the thyroid, pituitary, and adrenal glands. There is a close relationship between the thymus and the thyroid in that hyperthyroidism generally leads to myasthenia gravis or muscular debility, as well as to hyperplasia of the thymus. As the disease progresses, most or all of the endocrine glands, organs, and metabolic functions tend to deteriorate. This, then, requires in addition to manganese therapy individualized support with a wide range of nutrients and remedies as well as a diet of highest quality.

Another set of problems may arise if the disease is due to chemical poisoning. This happened to Simon Kelly (as reported on his Website www.myasthenia.co.uk ). He had developed MG once before, apparently due to extensively working with oil paints in a confined space. Six years later he had another stressful period during which he painted his house and burned off old paint. Not only did he develop MG a second time, but his blood became very alkaline and his red blood cells "looked like sea urchins," shriveled, black, and full of spikes. He also believes that a high consumption of soymilk contributed to his condition by causing intestinal inflammation and diarrhea. After an odyssey of orthodox and alternative treatments, he had his first real improvement during a short period on manganese supplements, and then continued to improve further with Buteyko-type breathing to reduce the alkalinity of his blood. He also used some wheat grass juice. However, his best improvement came after several months of stagnation when he tried a second lot of manganese. His eyes were better than they had been for many years, and the strength of his legs improved tremendously.

It is now believed that in this case the poisoning of the energy-producing mitochondria caused an acute deficiency of metabolic acids, especially citric acid, in addition to the leaching of potassium from the poisoned cells. This is like developing chronic fatigue syndrome in addition to MG and may have contributed as much to his weakness as the MG itself. In such cases, clearly the highest quality of support is required.

A THEORY OF MYASTHENIA

From the various known facts and indications, we can now come to an understanding of the likely cause of MG.

The decisive experiment, in which antibodies from a MG patient attacked receptors in healthy muscles, shows that the basic problem is with the antibody production and not the muscle receptors of the myasthenics. This means that the muscle receptors are basically healthy and the antibodies are produced against something else and attack the muscle receptors only as innocent bystanders. The real target may actually be in the thymus itself, as it has been shown that the thymus contains muscle-type cells with acetylcholine receptors.

As the thymus is obviously diseased, at least in all advanced cases of MG, this suggests that the antibodies may actually be formed against faulty receptors in the thymus itself. After all, the thymus develops antibodies against many other conditions, but does not normally become diseased itself as it does in MG. The conclusion is that thymus receptors become faulty and susceptible to attack due to manganese deficiency. Otherwise the autoimmune attack would not stop and patients would start rapidly improving within days of manganese supplementation.

However, there may be additional factors to trigger an attack. A relevant observation is the presence of acetylcholine receptors in various bacteria, especially in Escherichia coli, the most common type of bacteria in the large intestine. If the intestinal wall is weak, bacterial proteins or endotoxins can pass from the intestines into the bloodstream and cause antibodies to develop against any bacterial receptors. These antibodies, originally formed against E. coli receptors, may in turn initiate the attack on thymus receptors in the presence of manganese deficiency. A surplus of antibodies spills over into the bloodstream and will then attack healthy muscle receptors.

The thymus, attacking itself, is unable to obtain sufficient manganese from a diet with marginal manganese levels, even after the invasion of E. coli endotoxins has stopped. Therefore, symptoms of MG persist until a sufficiently high manganese intake allows the thymus receptors to restructure and the attack by its own antibodies to stop.

The most common causes for a weak intestinal wall that allows endotoxins to invade the bloodstream are inflammatory conditions due to gluten sensitivity, food allergy, and Candida overgrowth. It may also be due to general dysbiosis of the intestinal tract as caused by prolonged or repeated antibiotic treatment. Commonly this is combined with a malfunctioning ileocecal valve, which normally prevents bacteria from the large intestine from invading the small intestine. It is possible that the same inflammatory changes that allow bacterial toxins to pass through the intestinal wall also reduce the absorption of manganese.

An alternative or additional model of MG may be based on the observation that MG frequently starts during or following a prolonged period of intense stress. Commonly, this is emotional stress but may also be due to malnutrition, chemical exposure, or food sensitivity. This tends to lead to weakness or exhaustion of the adrenal glands, which manifests as an unusual sensitivity of myasthenics to stress.

The adrenal glands have a direct influence on the thymus in that a high level of adrenocortical steroids leads to its atrophy, while adrenal exhaustion, as in Addison's disease, tends to retard or prevent the normal involution of the thymus after puberty. With MG, this adrenal weakness may either prevent the thymus from utilizing manganese or it may be combined with manganese deficiency to produce faulty thymus receptors. This, then, leads to the formation of antibodies that attack healthy muscle receptors as an unintended side effect.

Manganese deficiency may also be due to a diet high in refined food--white bread, for instance, has only 5% of the manganese content of whole meal bread. Produce grown organically in mineral-rich soil can have more than a hundred times the manganese content of that grown commercially with synthetic fertilizers. The highest and lowest values for manganese found in lettuce were 169 ppm and 1 ppm, respectively.

Furthermore, a lack of gastric acid leads to reduced mineral absorption, while inorganic (ferric) iron makes manganese unavailable and destroys vitamin E. Also prolonged use of antibiotics can cause manganese deficiency. Finally, even manganese-rich whole meal bread may not be of much help, because the high phytate content of whole meal binds and makes manganese and other minerals unavailable. Minerals only become readily available after phytates break down. This happens when seeds are sprouted or properly fermented as in sourdough bread.

Several factors may come together to upset the utilization of manganese by the thymus, such as a marginal intake or malabsorption, a low level of antistress vitamins during a stressful period, infection, food allergy, and exposure to toxic chemicals.

Sometimes, especially in milder conditions, the symptoms of MG may disappear even without additional manganese when high-level antistress vitamins are supplied, as these may reduce inflammatory conditions and improve the efficiency of the thymus in utilizing manganese. Similarly, a high-quality low-allergy or raw-food diet may have the same beneficial effect. It supplies increased amounts of manganese and may at the same time correct intestinal conditions. With a normalized manganese metabolism in the thymus, the faulty acetylcholine receptors can be quickly repaired and the production of receptor antibodies stops.

The remaining question is why the thymus becomes enlarged. Josephson suggested that the thymus reacts to manganese deficiency in a way similar to how the thyroid gland reacts to iodine deficiency. Both react with hypertrophy. He saw the proof for this assumption in the observed rapid shrinking of the enlarged thymus with manganese supplements, in the same way as the enlarged thyroid shrinks with iodine supplements.

THE DIET

Raw-food diets have generally been shown to improve and possibly cure MG. Therefore it is advisable to use a high percentage of food raw and in easily digestible form, such as freshly pressed vegetable juice. This may require a dedicated helper. Grass juice grown in mineral-rich soil is high in manganese. The best juice is made from mixed wheat and barley grass together with red beet. Add other vegetables as available; possibly flavor with apple, ginger root, and bee pollen. Preferably use a slow-turning single auger or twin gear juicer (see www.buyjuicers.com ). Drink a glass very slowly before most meals. If you can make juice only once a day or every second day, you may refrigerate or freeze some of the juice for later use.

Another excellent food is sprouted seeds. They are high in enzymes and their minerals can easily be absorbed. Easy to sprout are mung beans, brown lentils, and fenugreek. If chewing is difficult, these may be juiced as well or pureed, or even cooked. If chewing is not a problem, then use sprouted seeds as part of a vegetable salad prepared with gelatin and finely grated root vegetables such as red beet, carrot, and turnip. As salad dressing use lemon juice, extra-virgin olive oil, herbs, spices, and possibly the yolk of a free-range egg.

As cooked food use mainly fresh vegetables, arrowroot, sago, tapioca, rice, and lentils. Buckwheat flour may be used for binding instead of gluten flour. Instead of cow's milk use rice milk or almond milk; also yogurt, cheese, or cottage cheese from goat's milk. Tea leaves and walnuts are high in manganese (15 mg/100 g). Use fruits cautiously before or between meals.

Frequently use beef broth, which can also be used for flavoring salads. While beef is often beneficial for muscle strength, it should be in an easily digestible form, such as steamed or boiled minced meat. In addition, simmer fish heads for several hours with the addition of vinegar or lemon juice in a non-metal pot. Blend and strain the broth as a source of gelatin and minerals. Steamed fish or sea