News on Health & Science

Plastic Bottles Behind Earlier Puberty in Girls?

Girls are beginning to grow breasts at an earlier age, and starting their periods sooner too, and scientists suspect chemicals in plastic   bottles may be behind this trend.

The findings back up recent studies that found earlier breast development in American girls over the past several years,
Lise Aksglaede of Rigshospitalet in Copenhagen, the lead researcher on the study, said. “At this point, we don’t know what is happening, and that is also what worries us.”

Aksglaede noted that she and her colleagues have seen an increasing number of girls with precocious puberty, meaning sexual maturation beginning before age eight.

To investigate whether this might represent a trend, or simply greater recognition of the problem by parents, the Denmark-based researchers looked at 1,100 girls who were studied in 1991-1993 and 995 examined between 2006-2008. The study participants ranged in age from 5.6 to 20 years old.

While the average age at which breast growth began was 10.88 years for the 1991 group, it was 9.86 for the 2006 group. Age at first menstruation was 13.42 for the 1991 group, and 13.13 for the 2006 group.

Most experts believe that the obesity epidemic may have something to do with earlier puberty in girls, Aksglaede noted, but she and her colleagues found no difference in the prevalence of overweight and obesity between the 1991 and 2006 groups.
There also were no differences in levels of several reproductive hormones between the two groups, although the 8- to 10-year-olds tested in 2006 actually had lower estrogen levels than girls of the same age tested in 1991.

Chemicals which can produce estrogen-like effects in the body may be responsible, Aksglaede said. However, she pointed out that the effects of such chemicals are extremely difficult to study, given that there are so many different chemicals out there, and that the levels girls are exposed are in constant flux.

Chemicals in plastics like the chemical bisphenol A (BPA) and phthalates have the potential to interfere with estrogen and other reproductive hormones.

While precocious puberty can have psychological consequences for girls, and may also stunt growth, the girls in the current study were still entering puberty at a relatively normal age.

“It is the first time we are seeing this in Europe,” the researcher said. “It might be happening in other countries, but it hasn’t been reported yet.”

Sources: The Times Of India

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Herbs & Plants

Indian Liquorice (Crab’s Eye)

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Botanical Name : Abrus precatorius
Family: Fabaceae
Genus: Abrus
Species: A. precatorius
Kingdom: Plantae
Order: Fabales

Synonyms : Abrus minor and A. pauciflorus Desv.

Common name: Rosary pea, crab’s eye, jequerite, precatory bean, weesboontje, paternoster bean, deadly crab’s eye, wild liquorice, ruti, jequirity bean, coral bean, prayerbead, Ma Liao Tou, Tento Muido, Indian liquorice, Gunja.

English names: Indian liquorice, Crab’s eye.

Sanskrit name: Krishna gunja.

Vernacular names: Asm : Latuwani; Ben: Rati, Kunch; Guj: Gumchi; Hin and Pun: Rati; Kan : Gurgunn, Gulaganji; Ori : Kaincha, Gunja; Mal: Kunnikkura; Tam: Kunthamani; Tel: Gumginja.

Trade names: Rati, Kunch.

Family:Fabaceae / Leguminosae.

Habitat : Occurring throughout greater parts of India, ascending the outer Himalaya up to 1200 m, occasionally planted in gardens.

Ecology and cultivation: Naturalised in tropical countries.

A small climbing tropical vine with alternately compound leaves, indigenous to Indonesia but also growing in Surinam.
The flowers are small, pale, violet to pink and arranged in clusters.


The fruit (a pod) is flat and truncate – shaped (1½ – 2″ long).
This seedpod curls back when it opens to reveal the seeds.

Click to  see....>..(01)....(1)…..…(2).……..(3)....…..(4)…..

Copiously branched climber with slender branches; leaves alternate, pinnately compound with numerous deciduous leaflets; flowers small, in dense racemes on axillary peduncles or short branches; pods 2.5-3.7 by 1.0-1.25 cm; seeds bright scarlet and black or whitish or black or mixed black and white, large like pea.

The small, hard, brilliant red seeds with a black spot are very toxic due to the phytochemical abrin (consisting of 5 glyco-proteins); a single seed if broken, can cause blindness or even death if ingested.
Abrin is a ribosome – inactivating protein (it blocks protein synthesis) and is one of the most deadly plant toxins known.
Fortunately, the toxin is only released if the seeds are broken (and swallowed) but this is unlikely since they have a hard seed coat!

Phenology: Flowering: August and September; Fruiting : January to March (even up to May).

USDA zone 9 – 11.
Can be planted in the spring up to zone 7 as an annual.

These seeds germinate more consistantly if scarified; soak overnight in hot water or until they swell. Sow swollen seeds immediately in seeding mix. Don’t overwater or allow to dry out.

Full sun / partial shade, well – drained moist soil.
Plant in frost free spots.

Chemical contents: Root and Leaf: glycyrrhizin, isoflavanquinones, abrusquinone A, B & C; leaves taste sweet and roots less so; roots also contain precol, abrol, abrasine and precasine. Seed: poisonous, principal constituents being ‘abrin’; a fat-splitting enzyme, haemaagglutinin, urease; alkaloid (abrin), a glucoside (abralin) and a small quantity of fatty oil have also been isolated from seed. Pharmacologically,abrin is considered to be intensely poisonous. Besides abrin, a seed contains hypaphorine, two steroids­one oily and the other crystalline- β-sitosterol, stigmasterol, 5 B-cholanic acid, abricin, abridin, cholesterol, lectins and toxic proteins.

Medicinal Aplication & Uses:

In Traditional medicinal applications :Leaves, roots and seeds are used.
The seeds are used as a contraceptive, to treat diabetes and chronic nephritis.
The root is used to induce abortion against abdominal discomfort, gonorrhoea, jaundice and haemoglobinuric bile.Also traditionally used to treat tetanus and to prevent rabies.

Jequirity seeds have been used medicinally in the past as a contraceptive, abortifacient, and as a treatment for chronic conjunctivitis.  However, they are so poisonous that even external application is no longer justifiable.  Even small amounts brought into contact with an open wound can prove fatal.  The leaves and roots contain glycyrrhizin and can be substituted for licorice. The leaves have been used in the Ayurvedic tradition in the treatment of asthma, bronchitis, sore throats, dry coughs and other chest conditions.  They have been used in Chinese medicine to treat fever.  Externally the leaves are used for sciatica, hair loss, skin disease, leprosy, nervous debility and the seeds for paralysis.

Medicinal – not recommended due to extreme toxicity (Abortifacient, Ache(Head), Anodyne, Antidote, Aphrodisiac, Bilious, Bite(Snake,) Bladder, Blennorrhagia, Boil, Cancer, Chest, CNS-Sedative, Cold, Colic, Collyrium, Conjunctivitis, Consumption, Contraceptive, Convulsion, Cough, Diarrhea, Diuretic, Dysuria, Emetic, Emollient, Enteritis, Epithelioma, Expectorant, Expectorant, Eye Fatal, Fatality, Febrifuge, Fever, Fracture(Veterinary), Freckle, Gastritis, Gingivitis, Gonorrhea, Gravel, Heart, Hemostat, Hoarseness, Homicide, Hookworms, Insomnia, Jaundice, Kidney, Laxative, Loin, Malaria, Masticatory, Myalgia, Night-Blindness, Ophthalmia, Ordeal, Pectoral, Poison, Puerperium, Purgative, Refrigerant, Rheumatism, Sedative, Skin, Sprue, Stomach, Styptic, Throat, Trachoma, Urogenital, Venereal, Vermifuge), Sweetener, (like Liquorice),

Traditional use: SANTAL(Indian Tribals): (i) grind the roots, make small pills, encase the pills in molasses and eat the same to treat night-blindedness; (ii) make a plaster by grinding the roots of white-fruited variety and apply the plaster on the painful part of inflammated sections of the gum; (iii) to treat white-coloured urine they drink a mixture made by grinding roots of the following: (a) white-fruited A. precatorius, (b) Indigofera pulchella, (c) Panicum repens and (d) Spatholobus roxburghii; (iv) to treat gravel they drink a mixture made of the following: (a) roots of A. precatorius, (b) the refuse of molasses, (c) exudation from a sapling of Diospyros tomentosa, (d) exudation from Acacia catechu, (e) little saltpeter, and (f) pinch of sulphur; (v) to treat the variety of childbed complaints (usually caused by anaemia) characterized by profuse diarrhoea, roots of A. precatorius are used in preparing two different varieties of mixtures; the ingredients of the mixtures are given below: (a) first variety: roots of A. precatorius, Elaeodendron roxburghii, Coix lachryma-jobi, Piper longum, Ruellia suffruticosa, white onion, rhizome of Zingiber officinale; (b) second variety: roots of A. precatorius, Coix lachryma-jobi, Embelia robusta, Piper longum, bark of Casearea tomentosa, Elaeodendron roxburghii, Gmelina arborea, Emblica officinalis, white onion, leaves of Ocimum sanctum, rhizome of Curcuma angustifolia and Zingiber officinale – all these are ground together, boiled and mixed with the refuse of molasses; (vi)roots as abortifacient and in paralysis; (vii) apply leaf-paste with lime-water (2:1) on swelling of glands; (viii) grind the leaves of white-flowered A. precatorius, warm slightly and plaster on the loins to kill pain there; (ix) grind leaves of A. precatorius along with leaves of Lawsonia alba and Tamarindus indica (1:1:1), add a little salt, boil a little and apply the plaster on the whole body to get relief from muscular pain caused by over­exhaustion; (x) make a paste of leaves of A. precatorius along with roots of Carissa carandas and Gossypium arboreum, warm the paste slightly and plaster the same over the whole body of the patient suffering from stealth convulsions; (xi) leaf-paste in leucoderma; (xii) seed-paste in skin diseases; (xiii) seeds after some processing as contraceptive. MUNDA: Root-paste in gonorrhoea. ORAON: dried root-powder as mild purgative.

AGNI PURANA: (i) husks of A. precatorius along with the same of Vitis vinifera and the decoction of Polyalthia longifolia, Moringa pterigosperma, payomuca and tripha/a (fruits of Terminalia belerica, Terminalia chebula and Emblica officinalis) destroys all intestinal worms; (ii) the mixture of powder of A. precatorius, marine salt and pathya in warm water removes all fevers; (iii) consumption of the seeds of A. precatorius along with the fruits of Melia azadiracta, Holarrhena antidysenterica (leaves). Acorus calamus (young leaves) and Glycyrrhiza glabra (powder of stem) causes vomiting; (iv) regular drinking of A. precatorius along with Acorus calamus, G/oriosa superba, vasa, nisagada, Zingiber officinalis, Glycyrrhiza glabra and marine salt daily in the morning enhances memory of young boys; (v) A. precatorius can enhance the span of a man’s life, if it is eaten with marine salt and some other plants (Tinospora cordifolia, pathya, citraka, dried rhizome of Zingiber officinalis).

Modern use: Roots: emetic and alexiteric; Decoction of roots and leaves: for cough, cold and colic; Seeds: purgative, emetic, tonic, aphrodisiac, used in nervous disorder and cattle poisoning; Poultice of seeds: as suppository to bring about abortion; Paste of seeds: applied locally in sciatica, stiffness of shoulder joints and in paralysis.

In certain parts of India, the boiled seeds are eaten; cooking seems to destroys the poison.The small seeds are used in jewelry (necklaces) and have a uniform weight of 1/10th of a gram.

Click to learn more about->Indian Liquorice  and Some Medical Plants of India

The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider


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News on Health & Science

Strength Training Relieves Neck Pain

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A new study has found that specific strength training exercises lead to significant prolonged relief of neck muscle pain, while general fitness training results in only a small amount of pain reduction.


Women are more likely than men to suffer from persistent neck pain, particularly those who engage in repetitive tasks such as working at a computer keyboard.

The team, led by Gisela Sjøgaard and Lars L. Andersen of the National Research Centre for the Working Environment in Copenhagen, Denmark, therefore conducted the study on women.

They conducted a randomised controlled trial for which they recruited 94 women from seven workplaces.

The work tasks performed by the women consisted of assembly line work and office work, with 79 per cent reported using a keyboard for more than 75 per cent of their working time.

The study participants first filled out a questionnaire about their pain and then underwent a clinical exam to confirm a diagnosis of trapezius myalgia, muscle pain in the trapezius muscle, which extends along the back of the neck.

They were assigned to three intervention groups: those who did supervised specific strength training (SST) exercises for the neck and shoulder muscles, those who did high-intensity general fitness training (GFT) on a bicycle ergometer, and a control group that received health counselling but no physical training. Both exercise groups worked out for 20 minutes three times a week for 10 weeks.

The researchers found that while the GFT group showed a small decrease in neck muscle pain only immediately after exercise, the SST group showed a marked decrease in pain over a prolonged training period and with a lasting effect after the training ended.

“Thus specific strength training locally of the neck and shoulder muscles is the most beneficial treatment in women with chronic neck muscle pain,” the authors said.

It was also found that the reduction in pain occurred gradually in the SST group, with trapezius muscle pain gradually decreasing as muscle strength increased.

The researchers said that the marked reduction in pain in the SST group is of major clinical importance.

“Based on the present results, supervised high-intensity dynamic strength training of the painful muscle 3 times a week for 20 minutes should be recommended in the treatment of trapezius myalgia,” they said.

Sources: The Times Of India

Ailmemts & Remedies

Cirrhosis of the Liver

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Cirrhosis is a consequence of chronic liver disease characterized by replacement of liver tissue by fibrotic scar tissue as well as regenerative nodules, leading to progressive loss of liver function. Cirrhosis is most commonly caused by alcoholism and hepatitis C, but has many other possible causes.


Cirrhosis leading to hepatocellular carcinoma (autopsy specimen)
Liver cirrhosis as seen on an axial CT of the abdomen.

Ascites (fluid retention in the abdominal cavity) is the most common complication of cirrhosis and is associated with a poor quality of life, increased risk of infection, and a poor long-term outcome. Other potentially life-threatening complications are hepatic encephalopathy (confusion and coma) and bleeding from esophageal varices. Cirrhosis is generally irreversible once it occurs, and treatment generally focuses on preventing progression and complications. In advanced stages of cirrhosis the only option is a liver transplant.

The liver, the largest organ in the body, is essential in keeping the body functioning properly. It removes or neutralizes poisons from the blood, produces immune agents to control infection, and removes germs and bacteria from the blood. It makes proteins that regulate blood clotting and produces bile to help absorb fats and fat-soluble vitamins. You cannot live without a functioning liver.

The word “cirrhosis” is a neologism that derives from Greek kirrhos, meaning “tawny” (the orange-yellow colour of the diseased liver). While the clinical entity was known before, it was René Laennec who gave it the name “cirrhosis” in his 1819 work in which he also describes the stethoscope.

Symptoms and signs

The following signs and symptoms may occur in the presence of cirrhosis or as a result of the complications of cirrhosis. Many are nonspecific and may occur in other diseases and do not necessarily point to cirrhosis. Likewise, the absence of any does not rule out the possibility of cirrhosis.

  • Spider angiomata or spider nevi. Vascular lesions consisting of central arteriole surrounded by many smaller vessels due to an increase in estradiol. These occur in about 33% of cases.
  • Palmar erythema. Exaggerations of normal speckled mottling of the palm, due to altered sex hormone metabolism.
  • Nail changes.
    • Muehrcke’s nails – paired horizontal bands separated by normal color due to hypoalbuminemia (low production of albumin).
    • Terry’s nails – proximal two thirds of the nail plate appears white with distal one-third red, also due to hypoalbuminemia
    • Clubbing — Angle between the nail plate and proximal nail fold > 180 degrees
  • Hypertrophic osteoarthropathy. Chronic proliferative periostitis of the long bones that can cause considerable pain.
  • Dupuytren’s contracture. Thickening and shortening of palmar fascia that leads to flexion deformities of the fingers. Thought to be due to fibroblastic proliferation and disorderly collagen deposition. It is relatively common (33% of patients).
  • Gynecomastia. Benign proliferation of glandular tissue of male breasts presenting with a rubbery or firm mass extending concentrically from the nipples. This is due to increased estradiol and can occur up to 66% of patients.
  • Hypogonadism. Manifested as impotence, infertility, loss of sexual drive, and testicular atrophy due to primary gonadal injury or suppression of hypothalamic or pituitary function.
  • Liver size. Can be enlarged , normal, or shrunken.
  • Splenomegaly. Due to congestion of the red pulp as a result of portal hypertension.
  • Ascites. Accumulation of fluid in the peritoneal cavity giving rise to flank dullness (needs about 1500 mL to detect flank dullness).
  • Caput medusa. In portal hypertension, the umbilical vein may open. Blood from the portal venous system may be shunted through the periumbilical veins into the umbilical vein and ultimately to the abdominal wall veins, manifesting as caput medusa.
  • Cruveilhier-Baumgarten murmur. Venous hum heard in epigastric region due to collateral connections between portal system and the remnant of the umbilical vein in portal hypertension.
  • Fetor hepaticus. Sweet pungent smell in breath due to increased dimethyl sulfide due to severe portal-systemic shunting.
  • Jaundice. Yellow discoloring of the skin, eye, and mucus membranes due to increased bilirubin (at least 2-3 mg/dL or 30 mmol/L). Urine may also appear dark.
  • Asterixis. Bilateral asynchronous flapping of outstretched, dorsiflexed hands seen in patients with hepatic encephalopathy.
  • Many people with cirrhosis have no symptoms in the early stages of the disease. However, as scar tissue replaces healthy cells, liver function starts to fail and a person may experience the following symptoms: Weakness, fatigue, anorexia, weight loss, loss of appetite and abdominal pain.As the disease progresses, complications may develop. In some people, these may be the first signs of the disease.


Cirrhosis has many causes. In the United States, chronic alcoholism and hepatitis C are the most common ones.

Alcoholic liver disease (ALD). Alcoholic cirrhosis develops in 15% of individuals who drink heavily for more than a decade. There is great variability in the amount of alcohol needed to cause cirrhosis (as little as 3-4 drinks a day in some men and 2-3 in some women). Alcohol seems to injure the liver by blocking the normal metabolism of protein, fats, and carbohydrates. Patients may also have concurrent alcoholic hepatitis with fever, hepatomegaly, jaundice, and anorexia. AST and ALT are both elevated but less than 300 IU/L with a AST:ALT ratio > 2.0, a value rarely seen in other liver diseases. Liver biopsy may show hepatocyte necrosis, Mallory bodies, neutrophilic infiltration with perivenular inflammation.

Chronic hepatitis C. Infection with this virus causes inflammation of and low grade damage to the liver that over several decades can lead to cirrhosis. Can be diagnosed with serologic assays that detect hepatitis C antibody or viral RNA. The enzyme immunoassay, EIA-2, is the most commonly used screening test in the US.

Chronic hepatitis B. The hepatitis B virus is probably the most common cause of cirrhosis worldwide, especially South-East Asia, but it is less common in the United States and the Western world. Hepatitis B causes liver inflammation and injury that over several decades can lead to cirrhosis. Hepatitis D is dependent on the presence of hepatitis B, but accelerates cirrhosis in co-infection. Chronic hepatitis B can be diagnosed with detection of HBsAG > 6 months after initial infection. HBeAG and HBV DNA are determined to assess whether patient will need antiviral therapy.

Non-alcoholic steatohepatitis (NASH). In NASH, fat builds up in the liver and eventually causes scar tissue. This type of hepatitis appears to be associated with diabetes, protein malnutrition, obesity, coronary artery disease, and treatment with corticosteroid medications. This disorder is similar to that of alcoholic liver disease but patient does not have an alcohol history. Biopsy is needed for diagnosis.

Primary biliary cirrhosis. May be asymptomatic or complain of fatigue, pruritus, and non-jaundice skin hyperpigmentation with hepatomegaly. There is prominent alkaline phosphatase elevation as well as elevations in cholesterol and bilirubin. Gold standard diagnosis is antimitochondrial antibodies with liver biopsy as confirmation if showing florid bile duct lesions. It is more common in women.

Primary sclerosing cholangitis. PSC is a progressive cholestatic disorder presenting with pruritus, steatorrhea, fat soluble vitamin deficiencies, and metabolic bone disease. There is a strong association with inflammatory bowel disease (IBD), especially ulcerative colitis. Diagnosis is best with contrast cholangiography showing diffuse, multifocal strictures and focal dilation of bile ducts, leading to a beaded appearance. Non-specific serum immunoglobulins may also be elevated.

Autoimmune hepatitis. This disease is caused by the immunologic damage to the liver causing inflammation and eventually scarring and cirrhosis. Findings include elevations in serum globulins, especially gamma globulins. Therapy with prednisone +/- azathioprine is beneficial. Cirrhosis due to autoimmune hepatitis still has 10-year survival of 90%+. There is no specific tool to diagnose autoimmune but it can be beneficial to initiate a trial of corticosteroids.

Hereditary hemochromatosis. Usually presents with family history of cirrhosis, skin hyperpigmentation, diabetes mellitus, pseudogout, and/or cardiomyopathy, all due to signs of iron overload. Labs will show fasting transferrin saturation of > 60% and ferritin > 300 ng/mL. Genetic testing may be used to identify HFE mutations. If these are present, biopsy may not need to be performed. Treatment is with phlebotomy to lower total body iron levels.

Wilson’s disease. Autosomal recessive disorder characterized by low serum ceruloplasmin and increased hepatic copper content on liver biopsy. May also have Kayser-Fleischer rings in the cornea and altered mental status.

Alpha 1-antitrypsin deficiency (AAT). Autosomal recessive disorder. Patients may also have COPD, especially if they have a history of tobacco smoking. Serum AAT levels are low. Recombinant AAT is used to prevent lung disease due to AAT deficiency.
Cardiac cirrhosis. Due to chronic right sided heart failure which leads to liver congestion.


Glycogen storage disease type IV

Cystic fibrosis

Drugs or toxins

Certain parasitic infections (such as schistosomiasis)

The doctor may diagnose cirrhosis on the basis of symptoms, laboratory tests, the medical history, and a physical examination. For example, during a physical examination, the doctor may notice that the liver feels harder or larger than usual and order blood tests that can show whether liver disease is present.

If looking at the liver is necessary to check for signs of disease, the doctor might order a computerized axial tomography (CAT) scan, ultrasound, magnetic resonance imaging (MRI), or a scan of the liver using a radioisotope (a harmless radioactive substance that highlights the liver). Or the doctor might look at the liver using a laparoscope, an instrument that is inserted through the abdomen and relays pictures back to a computer screen.

A liver biopsy will confirm the diagnosis. For a biopsy, the doctor uses a needle to take a tiny sample of liver tissue, then examines it under the microscope for scarring or other signs of disease.

Treatment :
Liver damage from cirrhosis cannot be reversed, but treatment can stop or delay further progression and reduce complications. Treatment depends on the cause of cirrhosis and any complications a person is experiencing. For example, cirrhosis caused by alcohol abuse is treated by abstaining from alcohol. Treatment for hepatitis-related cirrhosis involves medications used to treat the different types of hepatitis, such as interferon for viral hepatitis and corticosteroids for autoimmune hepatitis. Cirrhosis caused by Wilson disease, in which copper builds up in organs, is treated with medications to remove the copper. These are just a few examples—treatment for cirrhosis resulting from other diseases depends on the underlying cause. In all cases, regardless of the cause, following a healthy diet and avoiding alcohol are essential because the body needs all the nutrients it can get, and alcohol will only lead to more liver damage. Light physical activity can help stop or delay cirrhosis as well.

Treatment will also include remedies for complications. For example, for ascites and edema, the doctor may recommend a low-sodium diet or the use of diuretics, which are drugs that remove fluid from the body. Antibiotics will be prescribed for infections, and various medications can help with itching. Protein causes toxins to form in the digestive tract, so eating less protein will help decrease the buildup of toxins in the blood and brain. The doctor may also prescribe laxatives to help absorb the toxins and remove them from the intestines.

For portal hypertension, the doctor may prescribe a blood pressure medication such as a beta-blocker. If varices bleed, the doctor may either inject them with a clotting agent or perform a so-called rubber-band ligation, which uses a special device to compress the varices and stop the bleeding.

When complications cannot be controlled or when the liver becomes so damaged from scarring that it completely stops functioning, a liver transplant is necessary. In liver transplantation surgery, a diseased liver is removed and replaced with a healthy one from an organ donor. About 80 to 90 percent of patients survive liver transplantation. Survival rates have improved over the past several years because of drugs such as cyclosporine and tacrolimus, which suppress the immune system and keep it from attacking and damaging the new liver.

Click for Herbal & Ayurvedic Relief………………………(A)..(B)...(C)…..(D)……(E)

Homeopathic treatment for Liver Disease………………..(A).….(B)……...(C)……(D)

Chiropetric View on the Treatment of Cirrhosis

For More Information:

American Liver Foundation (ALF)
75 Maiden Lane, Suite 603
New York, NY 10038–4810
Phone: 1–800–GO–LIVER (465–4837),
1–888–4HEP–USA (443–7872),
or 212–668–1000
Fax: 212–483–8179

Hepatitis Foundation International
504 Blick Drive
Silver Spring, MD 20904–2901
Phone: 1–800–891–0707 or 301–622–4200
Fax: 301–622–4702

United Network for Organ Sharing
P.O. Box 2484
Richmond, VA 23218
Phone: 1–888–894–6361 or 804–782–4800

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.