Cane sugar or SUCROSE is the most prominent substance currently used as homeopathic drug dispensing vehicles. It is used in the form of GLOBULES of different sizes, which are medicated by adding potentized homeopathic drugs.
I think a detailed study of SUCROSE is essential to decide whether it is an ideal dispensing vehicle. Theoretically, an ideal DISPENSING VEHICLE should be a substance with following properties:
1. IT SHOULD NOT A DRUG SUBSTANCE BY ITSELF,
2. IT SHOULD BE CHEMICALLY INERT,
3. IT SHOULD NOT INTERACT WITH DRUGS,
4. IT SHOULD BE INDIGESTIBLE,
6. SHOULD NOT BE ABSORBED INTO THE BODY,
7. IT SHOULD NOT HAVE LONG TERM OR SHORT TERM TOXIC EFFECTS,
8. IT SHOULD NOT HAVE NUTRITIONAL OR CALORIC VALUE
In this article, I am presenting some scientific facts related with CANE SUGAR, which I collected from various knowledge sources. I am also giving the complete MATERIA MEDICA of Cane sugar from Clarke’s Materia Medica. Please read these information carefully, and you decide yourself whether CANE SUGAR we regularly feed our patients is an ideal DISPENSING VEHICLE.
SOME SCIENTIFIC FACTS ABOUT CANE SUGAR:
Sucrose is common table sugar. It is a disaccharide, a molecule composed of the two monosaccharides, glucose and fructose. Sucrose is produced naturally in plants, from which table sugar is refined. It has the formula C12H22O11.
Sucrose we use in homeopathic pharmacy as dispensing vehicle is extracted, and refined from sugar cane plants. Sugar canes are crushed mills to produce raw sugar which is then refined into pure sucrose. The sugar refining process involves washing the raw sugar crystals before dissolving them into a sugar syrup which is filtered and then passed over carbon to remove any residual colour. clear sugar syrup is then concentrated by boiling under vacuum and crystallised as the final purification process to produce crystals of pure sucrose. These crystals are clear, odourless, and have a sweet taste.
In sucrose, the components glucose and fructose are linked via an ether bond between C1 on the glucosyl subunit and C2 on the fructosyl unit. The bond is called a glycosidic linkage. Glucose exists predominantly as two isomeric “pyranoses” (α and β), but only one of these forms links to the fructose.
Fructose itself exists as a mixture of “furanoses”, each of which having α and β isomers, but only one particular isomer links to the glucosyl unit. What is notable about sucrose is that, unlike most disaccharides, the glycosidic bond is formed between the reducing ends of both glucose and fructose, and not between the reducing end of one and the nonreducing end of the other. This linkage inhibits further bonding to other saccharide units. Since it contains no anomeric hydroxyl groups, it is classified as a non-reducing sugar.
The purity of sucrose is measured by polarimetry, through the rotation of plane-polarized light by a solution of sugar. The specific rotation at 20 °C using yellow “sodium-D” light (589 nm) is +66.47°. Commercial samples of sugar are assayed using this parameter. Sucrose does not deteriorate at ambient conditions.
Sucrose does not melt at high temperatures. Instead, it decomposes—at 186 °C (367 °F)—to form caramel. Like other carbohydrates, it combusts to carbon dioxide and water. Mixing sucrose with the oxidizer potassium nitrate produces the fuel known as rocket candy that is used to propel amateur rocket motors.
Sucrose burns with chloric acid, formed by the reaction of hydrochloric acid and potassium chlorate. Sucrose can be dehydrated with sulfuric acid to form a black, carbon-rich solid, as indicated in the following idealized equation:
Hydrolysis breaks the glycosidic bond converting sucrose into glucose and fructose. Hydrolysis is, however, so slow that solutions of sucrose can sit for years with negligible change. If the enzyme sucrase is added, however, the reaction will proceed rapidly. Hydrolysis can also be accelerated with acids, such as cream of tartar or lemon juice, both weak acids. Likewise, gastric acidity converts sucrose to glucose and fructose during digestion, the bond between them being an acetal bond which can be broken by an acid.
Fully refined sugar is 99.9% sucrose, thus providing only carbohydrate as dietary nutrient and 390 kilocalories per 100 g
There are no micronutrients of significance in fully refined sugar.
In humans and other mammals, sucrose is broken down into its constituent monosaccharides, glucose and fructose, by sucrase or isomaltase glycoside hydrolases, which are located in the membrane of the microvilli lining the duodenum. The resulting glucose and fructose molecules are then rapidly absorbed into the bloodstream. Sucrose is an easily assimilated macronutrient that provides a quick source of energy, provoking a rapid rise in blood glucose upon ingestion. Sucrose, as a pure carbohydrate, has an energy content of 3.94 kilocalories per gram.
When large amounts of refined food that contain high percentages of sucrose are consumed, beneficial nutrients can be displaced from the diet, which can contribute to an increased risk for chronic disease. The rapidity with which sucrose raises blood glucose can cause problems for people suffering from defective glucose metabolism, such as persons with hypoglycemia or diabetes mellitus.
Sucrose can contribute to the development of metabolic syndrome. In an experiment with rats that were fed a diet one-third of which was sucrose, the sucrose first elevated blood levels of triglycerides, which induced visceral fat and ultimately resulted in insulin resistance. Another study found that rats fed sucrose-rich diets developed high triglycerides, hyperglycemia, and insulin resistance. A 2004 study recommended that the consumption of sucrose-containing drinks should be limited due to the growing number of people with obesity and insulin resistance.
Studies have indicated potential links between consumption of free sugars, including sucrose which is particularly prevalent in processed foods, and health hazards, including obesity and tooth decay. It is also considered as causing endogenous glycation processes since it metabolises into glucose and fructose in the body.
Tooth decay (dental caries) has become a pronounced health hazard associated with the consumption of sugars, especially sucrose. Oral bacteria such as Streptococcus mutans live in dental plaque and metabolize any sugars (not just sucrose, but also glucose, lactose, fructose, into lactic acid. The resultant lactic acid lowers the pH of the tooth’s surface, stripping it of minerals in the process known as tooth decay.
All 6-carbon sugars and disaccharides based on 6-carbon sugars can be converted by dental plaque bacteria into acid that demineralizes teeth, but sucrose may be uniquely useful to Streptococcus sanguinis (formerly Streptococcus sanguis) and Streptococcus mutans. Sucrose is the only dietary sugar that can be converted to sticky glucans (dextran-like polysaccharides) by extracellular enzymes. These glucans allow the bacteria to adhere to the tooth surface and to build up thick layers of plaque. The anaerobic conditions deep in the plaque encourage the formation of acids, which leads to carious lesions. Thus, sucrose could enable S. mutans, S. sanguinis and many other species of bacteria to adhere strongly and resist natural removal, e.g. by flow of saliva, although they are easily removed by brushing. The glucans and levans (fructose polysaccharides) produced by the plaque bacteria also act as a reserve food supply for the bacteria. Such a special role of sucrose in the formation of tooth decay is much more significant in light of the almost universal use of sucrose as the most desirable sweetening agent.
Sucrose is a disaccharide made up of 50% glucose and 50% fructose and has a glycemic index of 65. Sucrose is digested rapidly, but has a relatively low glycemic index due to its content of fructose, which has a minimal effect on blood glucose.
As with other sugars, sucrose is digested into its components via the enzyme sucrase to glucose (blood sugar) and fructose. The glucose component is transported into the blood (90%) and excess glucose is converted to temporary storage in the liver – named glycogen. The fructose is either bonded to cellulose and transported out the GI tract or processed by the liver into citrates, aldehydes, and, for the most part, lipid droplets (fat).
As the glycemic index measures the speed at which glucose is released into the bloodstream a refined sugar containing glucose is considered high-glycemic. As with other sugars, over-consumption may cause an increase in blood sugar levels from a normal 90 mg/dL to up over 150 mg/dL. (5 mmol/l to over 8.3 mmol/l).
Authorities advise diabetics to avoid sugar-rich foods to prevent adverse reactions.
The occurrence of gout is connected with an excess production of uric acid. A diet rich in sucrose may lead to gout as it raises the level of insulin, which prevents excretion of uric acid from the body. As the concentration of uric acid in the body increases, so does the concentration of uric acid in the joint liquid and beyond a critical concentration, the uric acid begins to precipitate into crystals. Researchers have implicated sugary drinks high in fructose in a surge in cases of gout.
Sucrose intolerance, also called sucrase-isomaltase deficiency, congenital sucrase-isomaltase deficiency (CSID), genetic sucrase-isomaltase deficiency (GSID), is the condition in which sucrase-isomaltase, an enzyme needed for proper metabolism of sucrose (sugar) and starch (i.e., grains and rice), is not produced or the enzyme produced is either partially functional or non-functional in the small intestine. All GSID patients lack fully functional sucrase, while the isomaltase activity can vary from minimal functionality to almost normal activity. The presence of residual isomaltase activity may explain why some GSID patients are better able to tolerate starch in their diet than others with GSID. Signs and symptoms of GSID are, Abdominal cramps and bloating, Diarrhoea and constipation, Vomiting, Hypoglycemia and headaches, Poor weight gain and growth, Upper respiratory tract and viral diseases, Anxiety and heart palpitations, Excess gas production etc.
Sucrose intolerance can be caused by genetic mutations in which both parents must contain this gene for the child to carry the disease (so-called primary sucrose intolerance). Sucrose intolerance can also be caused by irritable bowel syndrome, aging, or small intestine disease (secondary sucrose intolerance). There are specific tests used to help determine if a person has sucrose intolerance. The most accurate test is the enzyme activity determination, which is done by biopsying the small intestine. This test is a diagnostic for GSID. A deficiency of sucrase may result in malabsorption of sugar, which can lead to potentially serious symptoms. Since sucrose-isomaltase is involved in the digestion of starches, some GSID patients may not be able to absorb starches as well. It is important for those with sucrose intolerance to minimize sucrose consumption as much as possible.
SOME FACTS ABOUT CANE SUGAR AS A DRUG SUBSTANCE:
CLARKE’S HOMEOPATHIC MATERA MEDICA OF CANE SUGAR OR SACCHARAM OFFICINALIS
Sugar. (Including Saccharum album, White Sugar.) Saccharose. C12H22O1l. Trituration. Solution.
Ascites. Cataract. Chlorosis. Cornea, opacity of. Diabetes. Dropsy. Dyspepsia. Hair, rapid growth of. Headache, periodic. Hoarseness. Liver, affections of. Ranula. Rheumatism. Rickets. Scurvy. Spleen, affections of. Tabes mesenterica.
Like so many other articles of diet, Sugar may be a poison and a medicine as well as a food. Sugar preserves food, as salt does; and both sugar and salt have produced scurvy. Cases of scurvy-rickets in bottle-fed children have been traced to excess of sugar in their food; and the exclusion of sugar from the dietary of the gouty, rheumatic, and the diabetic, shows the pathogenetic power it is credited with among practitioners of the present day. Acidity of the stomach and itching at the anus are common effects of taking too much Sugar. Lippe published “Fragmentary provings and clinical observations obtained principally from S. Bœnninghausen and S. E. Bute, who proved the 30th potency on himself” (Allen). To these symptoms have been added others observed by Swan on a patient who accidentally discovered, after twenty-five years of suffering, that the cause of his trouble was Sugar. All the symptoms disappeared when he abstained from sugar in food or drink, and only reappeared when he took it again by way of experiment. Then, from two to four days after taking sugar, the same train of symptoms invariably occurred in this order: (1) A burning at pit of stomach. A white coat on tongue, so thick
as to cause stiffness of it. Sharp burning pains run up from kidneys to shoulders, passing under scapulæ. Pains in bones from head to foot, causing a rigidity of the muscles so that it was impossible to rise from bed till he had been rubbed. Chill commencing in small of back and spreading up and down. Severe headache and occasional vomiting with the chill. Fever followed with headache, morbid hunger, and a hectic flush. Increased urine, strong odour, white sediment. Great pain in kidneys. Constipation. Sleeplessness. Œdema of feet and ankles. Weakness of legs, as if paralysed, causing staggering. Painful jactitation of feet and legs during the burning in the Stomach. Oppression, slight cough, profuse cream-like expectoration, very offensive, cold. Sac. a. 10m and 5m curedhim of some remaining symptoms, and the 41m enabled him to eat sugar with impunity. Swan also reports (Org. iii. 342) this case: Miss L. was continually eating candies, of which she was very fond, till her digestive organs were affected. A few doses of Sac. a. 30m changed her taste so that she ate no more, and could not even bear the sight of them. This case was also cured with Sac. off.: “Vomiting bile, < in night and at 1 a.m.; old-standing dyspepsia, milk, eggs, and bread being the only food tolerated; great longing for sugar, which > the symptoms.” Farrington traces a great similarity between Sac. off. and Calc. Sac. off. is indicated, he says, in children who are large-limbed, fat, and bloated, with a tendency to dropsy. It has produced opacity of the cornea, and ought to cure it. The children are dainty and capricious; care nothing for substantial food, but want little “nick-nacks”; always cross and whining, and, if old enough, are insolent, and do not care to occupy themselves in any way. Everything too much trouble. H. C. Allen relates (H. P., x. 478) a case of opacity of cornea cured with Sac. a.; and with the same remedy in 2m potency he cured swelling round the ankles following rheumatism. According to Lippe, black-and-tan terrier dogs that eat sugar go blind. The cataract and amblyopia of diabetics are well known. Here, again, Salt and Sugar meet: Burnett has shown in his Supersalinity of the Blood that excess of salt in food has been an important factor in the production of cataract. The symptoms are < in early morning. < From anger. > In erect position (dyspnœa).
Compare: Sacch. l. In rickets, acidity, fat children, Calc. Craving for sweets, Arg. n., Sul. Rickets, Sil. Diabetes; swelled ankles, Arg. n. Kidney-ache, Santal.
Violent temper; irritable; quarrelsome.-Bilious, sanguineous temperament.-Increased modesty of women.-Melancholic mood with the chilliness.-Dainty, capricious; cross and whining; indolent.-Low-spirited, hypochondriacal mood; peevish.-Indifference; as from homesickness.-Disinclined to talk; want of interest.-Stupid.
Giddiness from indigestion.-Severe headache with the chill.-Headache every week the same day.-Hair grows; rapidly.
Eyes closed by swelling (and inflammation) of lids.-Varicose distension of vessels of eyes.-Ophthalmia.-Sight dim.-Cataract.
Discharge of pus from ears.
Sneezing; dry coryza.
Changed expression.-Face: pale; deathlike; bloated; œdematous.-Twitching of muscles of r. cheek over malar bone.
Dulness of teeth (with sour vomiting).-A white coat on tongue, so thick as to cause stiffness in it.-Rhagades, cracks on the tongue.-Ranula.-Inflammation of salivary glands of lining membrane of mouth.-Aphthæ of children.
Ulcers in throat.
Morbid hunger with the fever.-Nausea early in morning.-Violent retching.-Vomiting of white, viscid, tough mucus.-Periodical vomiting.-Vomiting: of blood; acid, making teeth dull; occasional, with the chill.-Stomach bloated.-Stomach overloaded with sour mucus.-Disordered stomach.-Digestion: impaired; weak, with acidity.-Burning at pit of stomach.-Heat in stomach.-Coldness of stomach.-Pressure in stomach, morning, fasting.-Painful constriction of stomach.-Painful sensitiveness of pit of stomach.-Pain in stomach with hypochondriacal persons.
Liver: swollen; indurated.-Bile increased.-Spleen swollen.-Pain in liver and spleen.-Abdomen: swollen; dropsical; hard as a stone (in children).-Tabes mesenterica.-Swelling and induration of mesenteric glands.
13. Stool and Anus
Congested and painful hæmorrhoids.-Itching at the anus.-Diarrhœa, stools watery and debilitating; of mucus and blood; bilious.-Constipation alternating with mucous diarrhœa.-Constipation; stools difficult.
14. Urinary Organs
Sharp burning pains run from kidneys to shoulders, passing under scapulæ.-Great pains in kidneys.-Increased urination; strong odour; white sediment.-Urine diminished.
15. Male Sexual Organs
Enormous swelling of scrotum; r. genitals.-Increased desire.-Frequent involuntary emissions.
16. Female Sexual Organs
Menses diminished.-Menstrual blood pale.-Suppressed leucorrhœa.
17. Respiratory Organs
Irritation of larynx, causing a slight hacking cough, with yellow, saltish sputa, which floats on water.-Dry rawness in larynx.-Hoarse, catarrhal voice.-Hoarseness from reading a short time.-Dry cough.-Cough with children.-Expectoration very offensive.-Breathing oppressed, cold expectoration.-Suffocative attacks, must be bolstered up.
Chest muscles wasted.-Pneumonia.-Swelling of lower part of sternum.-Fulness > by expectorating.-Stitches in l. chest.
Rheumatic pain in heart region.-Pulse weak and irregular.
Tingling in limbs.-Emaciation of hands and thighs.
22. Upper Limbs
Œdema of arms.
23. Lower Limbs
Œdema of lower limbs; hard as stones.-Paralytic weakness of legs.-Painful jactitation of legs during burning in stomach.-Cramps in calves.
Emaciation with great appetite.-Chlorosis: with dropsy; after anger.-Plethora.-Fainting attacks.-Scurvy rickets in children.-Pains in bones from head to foot.
Dry skin; perspiration suppressed.-Scurvy.-Pale and red blotches over body.-Panaritium.-Proud flesh in the ulcers.-Old herpes.
Sleeplessness.-Starts in sleep.
Chilliness from 10 a.m. till evening with melancholic mood.-Chill commencing in small of back, spreading up and down; severe headache and occasional vomiting; fever, followed by headache, morbid hunger, and hectic flush in cheeks; no sweats except when weakened by repeated attacks; before and during the paroxysm burning in stomach and back was simply intolerable; no thirst.-Chilliness alternates with perspiration.-Cold in the head.-Intermittent fever every one, two, or three days, irregular in its type.-Chill followed by profuse sweat.-Sweat on head (neck and shoulders).