Morphology Description (Habit)
E.officinalis is a small or medium-sized deciduous tree with smooth, greenish grey, exfoliating bark. The leaves are feathery with small narrowly oblong, pinnately arranged leaflets. The fruits are depressed, globose, fleshy and obscurely 6-lobed, containing 6 trigonous seeds.

Principal Constituents
Amla is highly nutritious and is an important dietary source of Vitamin C, minerals and amino acids. The edible fruit tissue contains protein concentration 3-fold and ascorbic acid concentration 160-fold compared to that of the apple. The fruit also contains considerably higher concentration of most minerals and amino acids than apples. Glutamic acid, proline, aspartic acid, alanine, and lysine are 29.6, 14.6, 8.1, 5.4 and 5.3% respectively of the total amino acids. The pulpy portion of fruit, dried at 100- and freed from the nuts contains: gallic acid 1.32%, tannin, sugar 36.10%; gum 13.75%; albumin 13.08%; crude cellulose 17.08%; mineral matter 4.12% and moisture 3.83%. Amla fruit ash contains chromium, 2.5 ; zinc, 4; and copper, 3 ppm. Presence of chromium is of therapeutic value in diabetes. Fruit also contains phyllemblin and curcuminoides. The fruit contained 482.14 units of superoxide dismutase/g fresh weight, and exhibited antisenescent activity. The seed oil contains 64.8% linolenic acid and closely resembles linseed oil¹.

Pharmacology
Aqueous extracts of E. officinalis fruit and ascorbic acid equivalent to that in the fruit extract were fed to albino mice for 7 consecutive days, followed by intraperitoneal injection of Pb(NO3)2 or Al2(SO4)3.18H2O. The ability of the crude fruit extract and ascorbic acid to counteract the toxic effects induced by these metal salts in hepatic and renal tissues of the animals were studied. Histopathological observations revealed that both the fruit extract and ascorbic acid could prevent the toxic effects induced by both metals, but the extract was more effective than ascorbic acid alone². Feeding of Amla to the hypercholesterolemic rabbits for 12 weeks showed a two pronged effect, its feeding increased the lipid mobilization and catabolism and retarded the deposition of lipids in the extrahepatic tissues. Feeding of E. officinalis initially raised the plasma lipids and cholesterol levels but by the end of 12 weeks, their levels were reduced significantly below the levels in the control group. Lipid levels in the liver were also significantly lowered. Though lipid levels in the aorta increased during this period the increase was much less in Amla fed animals as compared to the control group. The degree of atherosclerosis at the end of 12 weeks of Amla feeding was much lower when compared to the control group³.

The relative effects of a crude aqueous extract from the fruit and an equivalent amount of synthetic ascorbic acid (vitamin C) in reducing the clastogenic action of cesium chloride (CsCl) in vivo on mice bone marrow cells were compared. CsCl-induced chromosomal aberrations were observed in the mice 24 hours after exposure in frequencies that were directly proportional to the dose administered even after treatment for seven days. On the other hand, oral administration of either ascorbic acid or E. officinalis extract for seven days prior to exposure to CsCl for 24 hours reduced the frequency of chromosomal aberrations. This protective action of orally-administered E. officinalis extract against damage induced by CsCl has been reported to be of considerable importance in view of the possible entry of Cs. into edible plants from soil and subsequently into the food chain following radioactive fallout⁴.

E. officinalis juice was administered at a dose of 5ml/kg body weight per rabbit per day for 60 days. Serum cholesterol, TG, phospholipid and LDL levels were lowered by 82 percent, 66 percent, 77 percent and 90 percent, respectively. Similarly, the tissue lipid levels showed a significant reduction following E. officinalis juice administration. Aortic plaques were regressed. E. officinalis juice treated rabbits excreted more cholesterol and phospholipids, suggesting that the mode of absorption was affected. E. officinalis juice is an effective hypolipidemic agent and can be used as a pharmaceutical tool in hyperlipidaemic subjects⁵.

Clinical Studies
Clinical studies were conducted to investigate the effect of Amalaki in amlapitta (gastritis syndrome). Amalaki churna was given in 20 cases in a dose of 3g., thrice a day for seven days. The drug was found effective in 85 per cent of cases. Cases of hyperchlorhydria with burning sensation in abdominal and cardiac regions and epigastric pain were benefited⁶.
The fruit was used successfully in the treatment of human scurvy in the Hissar famine of 1939-40⁷. The Therapeutic efficacy of Amalaki in cases of dyspepsia was evaluated and the results clearly indicate the efficacy of E.o. in relieving the dyspeptic symptoms as well as in promoting healing of ulcers⁸.

Indications
The fruit is acrid, cooling, refrigerant, diuretic and laxative. The dried fruit is useful in hemorrhage, diarrhea and dysentery. In combination with iron, it is used as a remedy for anemia, jaundice and dyspepsia. Amla fruits are anabolic, anti-bacterial and resistance building. They possess expectorant, cardiotonic, antipyretic, antioxidative, antiviral and anti-emetic activities. They are also used in the treatment of leukorrhea and atherosclerosis.

References

1. Chem Abstr , 1992, 116, 19982, 127273; 1993, 119, 103470; 1989, 110, 73906; Vohora, Indian Drugs, 1989, 26(10), 526; Janjua, Hamdard, 1991, 34(2), 104; Yaqeenudin et. al., Pakist J Sci Ind Res, 1990, 33, 268.
2. Roy, A.K. et. al., Int. J.of Pharmacog., 1991, v. 29(2), 117-126.
3. Mand, J.K. et. al., J. Res. Edu. in Ind.Med., 1991, v., 10(2), 1-7.
4. Ghosh, A. et. al., Int. J. of Pharmacog., 1993, v. 31(2), 116-120.
5. Mathur, R. et. al., J. of Ethnopharmacol., 1996, v., 50(2), 61-68.
6. Singh, B.N. and Sharma, P.V., J.Res. Ind. Med., 1971, 5, 223.
7. Ramaswamy, Minor Forest Products, Mysore, 1945,55; Damodaran & Nair, Biochem. J., 1936, 30, 1014; Giri, Indian J. med. Res., 1939, 27, 429; Mitra & Ghosh,Ann. biochem. exp. Med., 1942, 2, 205; Roy & Rudra, ibid., 1941, 1, 307; Srinivasan, loc. cit.
8. Chawla et. al., 1982, Indian J. Med. Res. 76 (Suppl.), 95-98.