BURN YOUR CHOLESTROL WITH THE FIRE OF HOMOEOPATHY
Non communicable diseases are chronic diseases with slow progression and continued to evolve slowly with morbidity until it is intervened. Hyperlipidemia is a modifiable risk factor of cardio vascular disease. Its prevalence increasing in many developing countries due to dietary imbalance, sedentary habit, obesity, hypothyroidism etc. Well selected homoeopathic remedies can help to overcome such cases
Keywords: Hyperlipidemia, homoeopathy
Lipoproteins are complexes of lipids and proteins that are essential for the transport of cholesterol, triglycerides and fat soluble vitamins. The metabolic consequences associated with diet and life style have increased the number of hyperlipidemic individuals.
Lipoproteins contain a core of hydrophobic lipids surrounded by hydrophilic lipids and proteins that interact with body fluids. The plasma lipoproteins are divided into five major classes based on their relative densities; chylomicrons, very low density lipoproteins (VLDL), intermediate density lipoproteins (IDL), low density lipoproteins (LDL), and high density lipoproteins (HDL). Each lipoprotein class comprises a family of particles that vary slightly in density, size, and migration during electrophoresis, and protein composition. HDL is the smallest and most dense lipoprotein, where as chylomicrons and VLDL are the largest and least dense lipoprotein particles. Most triglycerides are transported in chylomicrons or VLDL, and most cholesterol is carried as cholesteryl esters in LDL and HDL.
Dietary triglycerides are hydrolysed by pancreatic lipases within the intestinal lumen and are emulsified with bile acids to form micelles. Dietary cholesterol and triglycerides are esterified in the enterocyte to form cholesteryl esters, retinyl esters respectively.
The endogenous pathway of lipoprotein metabolism refers to the hepatic secretion and metabolism of VLDL to IDL and LDL.
Disorders of lipoprotein metabolism:
1) Primary disorder of ApoB-containing lipoprotein biosynthesis causing low plasma cholesterol level.
a) Abetalipoproteinemia: characterises defect in absorption and transport of fat soluble vitamins, deficient in vitamin A,E,K
b) Familial hypobetalipoprotenemia: it is autosomal codominent in inheritance Pattern.
2) Primary disorders of ApoB: containing lipoprotein catabolism causing elevated cholesterol levels
a) Type1 hyperlipoproteinemia (familial chylomicronemia syndrome) : due to lipoprotein lipase and ApoC- II deficiency. Usually present in childhood with recurrent episodes of severe abdominal pain
b) Type III hyperlipoproteinemia (familial dysbetalipoproteinemia FDBL): characterized by a mixed hyperlipidemia due to the accumulation of remnant lipoprotein particles. The most common precipitating factors are a high caloric, high fat diet, diabetes mellitus, obesity, hypothyroidism, renal diseases, estrogen deficiency, alcohol use, or the presence of another genetic form of hyperlipidemia, most commonly familial combined hyperlipidemia (FCHL), or familial hypercholesterolemia (FH). Patients with FDBL usually present in adulthood with xanthoma, premature coronary and peripheral vascular disease. The diseases seldom presents in women before menopause. Xanthomas begin as clusters of small papules on the elbows, knees, or buttocks and can grow, to the size of small grapes. Palmar xanthomas are orange yellow discolouration of the creases in the palms. In FDBL plasma cholesterol and triglycerides are elevated to a relatively similar degree until the triglycerides reach 500mg/dl, and then the triglycerides tend to be greater than cholesterol.
c) Familial hypercholesterolemia (FH): it is autosomal codominant disorders characterised by elevated plasma LDL-C with normal triglycerides, tendon xanthomas, and premature coronary atherosclerosis. FH is caused by >750 mutations in the LDL receptor gene. The diagnosis can be done by obtaining a skin biopsy and measuring LDL receptor activity in cultured skin
3) Secondary disorders of lipoprotein metabolism:
a) Obesity: obesity is frequently, though variably, accompanied by hyperlipidemia,. The increase in adipocyte mass and accompanying decrease in insulin sensitivity associated with obesity have multiple effect on lipid metabolism. More free fatty acids are delivered from the expanded adipose tissue to the liver where they are re-esterified in hepatocytes to form triglycerides, which are packaged in to VLDL for secretion into the circulation. High dietary intake of simple carbohydrates also drives hepatic production of VLDL, leading to increase in production of LDL and /or VLDL in some obese individuals. Plasma HDL tends to be low in obesity
b) Diabetes mellitus: Patients with Type I diabetes mellitus arte generally not hyperlipidemic if they are under good glycemic control. Di9abetic keto acidosis is frequently accompanied by hypertriglyceridemia due to increased hepatic influx of free fatty acids from adipose tissue. The hypertriglyceridemia responds dramatically to administration of insulin in insulinopenic diabetes.
Patients with Type II diabetes are usually hyperlipidemic, even if under relatively good glycemic control. The high levels of insulin and insulin resistance associated with type2 diabetes have multiple effects on fat metabolism. Patients with type2 diabetes has several lipid abnormalities, includi9ng elevated plasma triglycerides, elevated dense LDL, and decreased HDL-C. In some diabetic patients especially those with a genetic defect in lipid metabolism, the triglycerides can be extremely elevated. Elevated LDL –C levels are usually not a feature of diabetes mellitus and suggest the presence of underlying lipoprotein abnormality or may indicate the development of diabetic nephopathy. Patients with lipodystrophy, who have profound insulin resistance, have markedly elevated VLDL and chylomicrons.
c) Thyroid diseases: hypothyroidism is associated with elevated plasma LDL-C due primarily to a reduction in hepatic LDL receptor function and delayed clearance of LDL. Conversely, plasma LDL-C is often reduced in the hyperthyroid patient. Hypothyroid patient may have increased circulating LDL, and some are mildly triglyceridemic, because hypothyroidism is easily overlooked , all patients presenting with elevated plasma LDL-C or IDL should screened for hypothyroidism
d) Renal disorders: nephrotic syndrome associated with hyper lipoproteinemia. The hyperlididemia of NS appears to be due to combination of increased hepatic production and decreased clearance of VLDL, with increased LDL production.
e) Liver disorder: because the liver is the principal site of formation and clearance of lipoprotein , it is not surprising that liver diseases can profoundly affect plasma lipid levels in a variety of ways. Cholestasis is associated with hypercholesterolemia, which sometimes can be very severe, cholestatsis blocks the critical excretory pathway, plantar and eruptive xanthomas can also be seen in patients with cholestasis.
f) Alcohol: the most common effect if the alcohol is to increase plasma triglyceride level and LDL-C .regular alcohol use is also associated with a mild to moderate increase in plasma levels of HDL-C.
g) Estrogen: estrogen administration is associated with the increased VLDL and HDL synthesis resulting ion elevated plasma triglycerides and HDL-C. Use of low dose of estrogen preparation or the estrogen patch can minimize the effect of exogenous on lipids.
h) Glycogen storage disease: other rarer causes of secondary hyperlipidemias include glycogen storage diseases. The inability to mobilize hepatic glucose during fasting results in hypoinsulinemia and increased release of free fatty acids from adipose tissue. Hepatic fatty acids synthesis also increased , resulting in fat accumulation in the liver and increased VLDL secretion.
i) Drugs: many drugs have a significant impact on lipid metabolism and can result in significant alterations in lipoprotein profile(eg: thiazides, cyclosporine, tegretol, glucocortocoids, betablockers, retinoic acid, HIV protease enzymes etc.)
Hyperlipidemia can include under sycotic miasm in majority of the part.
Therapeutics (some specifics)
Allium sativa: adapted to fleshy subjects with dyspepsia and catarrhal affections. Patients who eats a deal more, especially meat, than they drink. And weight is gained. Arterial hypotension begins usually in 30-45 minutes after 20-40 drops of tincture.
Baryta mur: Arteriosclerosis with a high systolic pressure and comparatively low diastolic tension is attended by cerebral and cardiac symptoms. Narrowing of the cardiac orifice with pain.
Cholestrinum: it is almost specific for gall stones. Obstinate hepatic engorgements. Carcinoma and other liver diseases.
Thuja: sycotic remedy, anxious palpitation on walking in the morning , suited to hydrogenoid constitution. Strumous and sycotic pains. Diabetes mellitus, cysts and warts, rapid exhaustion and emaciation. Flatulace and distension, as if something alive without pain.
1. Harrisons’s principles of internal medicine- vol.2
2. Lotus materia medica- Robin Murphy
3. New manual of homoeopathic materia medica- W.Boericke