What Alloxan offers to Diabetes mellitus?

Dr Ambey Jha 

We often come across “health is wealth”. To be wealthy we need to be healthy first. In the  present era, due to so called sedentary life, we end up in lifestyle diseases. Diabetes mellitus is considered to be one among those lifestyle diseases, which once if corrupt our health, difficult to unhook it.

India has more diabetics than any other country in the world. India with an estimated 31 million diabetics in 2000 and 79 million by the year 2030, 1 million Indians die due to diabetes mellitus every year. According to the Indian Heart Association India is projected to be home to 109 million individuals with diabetes mellitus by 2035.1

Every system which is involved or has a view on health of an individual has its own way for the treatment of diabetes mellitus.

Homoeopathy also has its own remedies to control blood sugar level in cases of diabetes.

Alloxan is one among those marked remedies to have an action in reduction in the number of phosphates in the blood plasma, reduces blood glucose level in the blood, azotaemia. Reduction of sedimentation rate and glycosuria.3

Alloxan is an organic compound. It is classified as a derivative of pyramidine. It was originally obtained by oxidation of uric acid by nitric acid. It is prepared by oxidation of barbituric acid by chromium trioxide.

The toxicological action of Alloxan can be seen at the level of the pancreas, kidneys, the liver, the lungs, and in the blood.3

In animals, diabetes mellitus is provoked, or in other words, Alloxanic diabetes. There would be a rapid degeneration of the islet of beta cells responsible for the production of insulin.

Even though Alloxan has put on view a special action to reduce blood sugar level in literatures, a systematic homoeopathic study on the same is not yet conducted.

What is diabetes mellitus?

As per the WHO, diabetes mellitus is defined as a hetrogenous metabolic disorder characterized by common features of chronic hyperglycaemia with disturbance of carbohydrate, fat and protein metabolism.4

Current classification of DM based on etiology divides it into two broad categories – Type 1 and type 2.4

Type 1 DM: It constitutes about 10% cases of DM. It was previously termed as juvenile onset diabetes, due to its occurrence in younger age, and called insulin dependent diabetes mellitus. In new classification, neither age nor insulin dependence are considered as absolute criteria. Instead, based on underlying etiology, type 1 DM is further divided into 2 subtypes:

  1. Subtype 1A (immune mediated) DM characterized by autoimmune destruction of beta cells usually leads to insulin deficiency.
  2. Subtype 2B (idiopathic) DM characterized by insulin deficiency with tendency to develop ketosis but these patients are negative for autoimmune markers.

Type 2 DM-This type comprises about 80% cases of DM. It was previously called maturity-onset diabetes or non- insulin dependent diabetes mellitus of obese and non-obese type.

Although type 2 DM predominantly affects older individuals, it is now known that it also occurs in obese adolescent children. Moreover, many type 2 DM patients also require insulin therapy to control hyperglycaemia or to prevent ketosis and thus are not truly non- insulin dependent contrary to its older nomenclature.

Etiology for type I DM

  1. Genetic susceptibility
  2. Environmental event ordinarily initiates the process in genetically susceptible individuals.
  3. Insulitis 
  4. Activation of autoimmunity
  5. Immune attack on beta cells
  6. DM

Etiology for type II DM

  1. Obesity (BMI> 25 kg/msq)
  2. Family history of Type 2 Diabetes Mellitus
  3. Above 40 years of age
  4. Physical inactivity (sedentary lifestyle)
  5. Females with history of delivering a baby weighing more than 4kg or diagnosis of gestational DM.
  6. Previously impaired glucose tolerance.
  7. Westernized diet habits, red meat, high fats, more sugar etc.
  8. Ethnicity more common in non-Hispanics of Northern European descent
  9. Cigarette smoking decreases insulin sensitivity
  10. Hypertension >140/90 mm of Hg or on therapy of Hypertension.
  11. HDL cholesterol level <35 mg/dl or triglyceride level >250 mg/dl or both
  12. Female with PCOS
  13. Stress
  14. Genetic markers


In type I DM, most of the beta cells in the pancreas have been destroyed. The destructive process is almost certainly autoimmune in nature. Genetic susceptibility to the disease must be present then environmental event initiates the process.then the sequence of inflammatory response in pancreas called insulitis. The cells that infiltrate the islet are activated T lymphocytes. There is in an alteration or transformation of the surface of the beta cell such that is no longer recognized as self but is seen by the immune system as a foreign cell. Now islet is considered as foreign cell because of cytotoxic antibodies develop and act in concert with cell mediated immune mechanism. The end result is the destruction of the beta cell and appearance of DM.  

The severity of clinical symptoms of polyuria and polydipsia is directly related to the degree of hyper-glycaemia. In asymptomatic cases when there is persistently elevated fasting plasma glucose level, diagnosis again poses no difficulty. The problem arises in asymptomatic patients who have diabetes on other grounds and are thus subjected to oral glucose tolerance test.5

Blood glucose is normally maintained in a very narrow range of 70-120 mg/dl. According to the ADA and WHO, diagnostic criteria for DM.5

  1. A fasting plasma glucose glucose =or > 126 mg/dl
  2. A random plasma glucose > or =200 mg/dl
  3. 2 hour plasma glucose > or = 200mg/dl during an oral glucose tolerance test(OGTT) with loading dose of 75 mg, and
  4. (HbA1c) level > or = 6.5%

Impaired glucose tolerance (pre-diabetic) is defined as:5

  1. A fasting plasma glucose  between 100 and 125 mg/dl
  2. 2 hour plasma glucose between 140 and 199 mg/dl following a 75gm glucose OGTT
  3. A glycated haemoglobin (HbA1c) level between 5.7% and6.4%

As many as one fourth of individuals with impaired glucose tolerance will develop overt diabetes over 5 years, with additional factors such as obesity and family history compounding the risk.

The complications are mainly acute or chronic. Acute being hypo-glycaemia, keto-acidosis. Chronic being chronic renal failure, cardiovascular disease, retinal damage, nerve damage, micro-vascular damage.6


Chemical formula- C4H2N2O3

Molecular wt. – 142.07

Source: Synthetic source

Kingdom: Chemical

Uses: Diabetes and related symptoms.

Description: Alloxan or Meoxalylurea was discovered accidently by Dum and his collaborators in 1943. It takes the form of rhomboid crystals. Odor disagreeable, freely soluble in water, soluble in acetone, alcohol, methanol, glacial acetic acid slightly soluble in chloroform petroleum ether and insoluble in ether. Pink at 230 degree Celsius and decompose at 256 degree Celsius. The anhydrous crystals are dark yellow in color, and the hydrogenised crystals are colourless.3

Sphere of action: The toxicological action can be seen at the level of the pancreas, the kidneys, the liver, the lungs and in the blood.3

Pathogenesis: In animals, diabetes mellitus is provoked, or in other words, alloxanic diabetes. There would be rapid degeneration of the islet of beta cells responsible for the production of insulin. This attack would follow the inhibition either the enzymatic process (proteins in thiol group, SH) or of the chelation ability of the molecule with regard to positively-charged ions, notably zinc, which has a role in the intra-cellular fixation of insulin.3

Homoeopathic experiment : The Hahnemannian proving was undertaken by W.L.Templeton on two occasions: in 1949 on six provers, when the potencies 6c and 30c were tried out and in 1951 on 9 provers and seven controls.3,7

Biological characteristics: Reduction in the number of phosphates in blood plasma, reduces blood glucose level in blood, azotaemia, reduction of sedimentation rate, glycosuria.3

Preparation: Trituration 1x for 1kg

           Alloxan in course powder -100g

           Sugar of milk- 900g

           For 2x 100g of 1x and add 900g of sugar of milk and triturate.8

Clinical indications: diabetes mellitus type I and type II, diabetes insipidus , phosphoglucidic renal diabetes, glycosuria without hyperglycemia, lowering down of the phosphoremia and increase of sanguine phosphates, beard’s disease, lasegue’s disease,aphthaes, glossitis cortico-gastric dystonia aerophagia, dysentery,etc.

Guiding symptoms 

Constitutions: The subjects are often phosphoric and very weak. Subjects nervous, uneasy, anxious. want of heat and vital reaction.

Neuro-endocrine-psychic system:  great forgetfulness. Forget places, names, things just done, just heard. loss of short-term memory. Spelling mistakes. Need for solitude, general indifference. Irritable with people, talking, loud voices, Quarrelsome and impatient. Want to dash about, wants to do everything quickly. sadness and tearfulness improved by solitude. Weeping better when alone. Keeps washing hands. alcoholic poly neuritis with mental troubles. sensation of constriction and of heat in the head which is cold to touch. headache and heaviness of head when waking up with the impression of having the hairs drawn, worse in evening. Forehead painful. sensation of separation of body.

Sleep: disturb.nightmares. dreams of accidents, being chased by horse,resurrection,death of friends, dreams of bsndits, robber.

Eyes: conjunctivitis . eyelids red burning and itching.  Weak sight with patches.

Mouth-tongue-pharynx: cracks in the corner of the lips. Lips dry, cracked. Lower jaw painful.toothache aggravated by sweets. Tip of the tongue painful. Small ulcerations,superficial of the mouth and of the palate. bitter taste , sweet of the lips, dry mouth. Breath smells like apples.salty taste on lips. Corners of of lips cracked.

Stomach-intestine-Abdomen :feeling hungry, quickly sated. Hypoglycemia, desire for cold drinks,refreshing things.excessive thirst and feeling of dryness of mouth<cold drinks>warm drinks. abdominal distension with profuse rumbling. Toxic diabetes. Ileocecal pain,aggravated by bending forwards and by movement. Sensation of a band around abdomen. Thirst increase. Unsatisfactory stool. Flatulence. Aversion to salt.

Liver: pain in liver on breathing , after eating , better pressure.pulsating and bubbling in liver.

Cardio-hemo-vascular system: reduction in the number of phosphates in the blood plasma, normal presence of glucose in the blood, azotemia. Reduction of sedimentation rate. Pain as if from a dagger in the precordial region.crampoid retrosternal pain< walking.

Respiratory system: acute catarrh of nasal mucus membrane with streaming, sometimes from the right side, sometimesfrom the left.sensation of heat in nose on inspiration. Smell in nose as of musty books.acute and chronic laryngitis.>warm drinks, expectoration , talking and singing. breathing <after meal

Uro-genital organ: pain in left kidney during micturation. Foamy urine, burning during passage in the urethra. Feeling of fullness in the bladder. Incontinence on hurrying to get up, on sneezing. Bedwetting. Glycosuria  frequent urination by day. Waking from sleep to urinate, morbid desire, sudden urging, can’t hold urine for long. dysuria.

Female: Inflammation of the vulva and vagina. Feeling of swelling in the vagina,< standing.

Modalities: <4-7pm, while waking, sweets, noise,mental and physical exertion

                 >hot weather,eating rest closing eyes.

Relationships: compare- uranium nit: excessive thirst, morbid hunger, emaciation. Polyuria. phosphoric acid: apathy, indifference, weakness,headaches,diarrhea, abundant urine, seminal discharges, weakness. Need for solitude, general indifference. Argentums nitricum: weakness of leg, apprehension, sadness, urinary incontinence day and night, desire for sweets.

Dosage: Potencies orally from 4c to 30c.3


  1. Piyush Gupta, Textbook of Preventive and Social medicine, 3rd edition. CBS Publisher and Distributors.
  2. Rao CR, Kamath VG, Shetty A, Kamath A. A study on the prevalence of the type 2 diabetes in coastal Karnataka. International journal of diabetes in developing countries.2010 apr; 30(2); 80.
  3. O.A Julian, Virginia Munday (Translator), Materia Medica of new homoeopathic remedies, 3rd edition, pg. 36-41.
  4. Mohan Harsh. Textbook of Pathology.6th ed. Chandigarh: Jaypee Brothers Medical Publishers (p) ltd; 2005.p.842-854.
  5. Robbins & Cotran, Pathologic Basis of Disease, South Asia edition, volume 2, 4th edition, p.1105-1120.
  6. Shlomelmed, Kenneth Polonsky, P. Reed Larsen, Henry kronenberg Williams, Textbook of Endocrinology, 12th edition.
  7. Templeton WL. A third proving of Alloxan. British Homeopathic Journal. 1951 Jul; 41(03):111-9.
  8. Homoeopathic pharmacopoeia of India (H.P.I), Volume 7, 1999, p. 9.
  9. Kumar S, Nayak C. Ultra Dynamised and Undynamised Dilutions of Alloxan at Micro-doses Influence Selective Pancreatic Beta Cell and Hormonal Profile: An Experimental Approach. Indian Journal of Research in Homoeopathy. 2008 Oct 1; 2(4):10.
  10. Brunschwig A, Allen J.G, Owens F.M, Thornton T.F. Alloxan in the treatment of insulin producing islet cell carcinoma of pancreas. Journal of the American Medical Association. 1944 Jan 22; 124(4):212-6.
  11. Kollerstrom J. Basic scientific research into the “low-dose effect”. British Homeopathic Journal. 1982 Apr; 71(02):41-7.
  12. Patel R, Panchal C, Jadav K, Mashru R. Tautopathy: wonder for antidoting to side effect of allopathic drugs. World journal of pharmaceutical research.2018 June 24.
  13. E. Van Woensel, Radar Keynotes, version 4, characteristics and peculiarities-A Compiled Materia Medica.
  14. R. Murphy, Homoeopathic Remedy Guide, RADAR Homoeopathic software. Robin Murphy, ND, Lotus Materia Medica, 3rd edition p.61-63.
  15. Dr. P.N Verma and Dr. Indu Vaid, Encyclopedia of Homoeopathic Pharmacopoeia and Drug Index, 3rd edition. B. Jain Publisher. Updated edition 2007.p.59.
  16. K.Park, Textbook of Preventive and Social Medicine, 23rd edition, 2015, Publisher India: Bhanot.
  17. Cier A, Boiron J, Vingert M. Experimental diabetes treated with Infinitesimal doses of Alloxan. British Homoeopathic Journal. 1967 Ja; 56(01):51-7.
  18. Templeton WL. Provings of Alloxan. British Homeopathic Journal. 1949 Oct; 39(04):246-81.
  19. Jacobs HR. Hypoglycemic action of alloxan. Proceedings of the Society for Experimental Biology and Medicine. 1937 Nov; 37(2):407-9.
  20. Lenzen S, Panten U. Alloxan: history and mechanism of action. Diabetologia. 1988 Jun 1-31(6):337-42.

Dr.Ambey Jha
PG Scholar In Dpt Of Homoeopathic Pharmacy
Fathe Rmuller Homoeopathic Medical college And Hospital
Phone No. 8208605053
EMAIL- jhaambey@gmail.com


  1. hope for best ,plz let me know how the clinical indication and guiding symptoms could be differ from each other .

  2. is it’s can taken as under :
    First Day– Arnica 1 m 2 drop
    Second Day– Rust Tux 1 m 2 Drops.
    third day — Alloxa 30 ch 4 pills 3 times.
    Again same type reaps.

Leave a Reply

Your email address will not be published.