USE OF CORTISOL 30 IN MANAGING THE CONDITIONS ASSOCIATED WITH METABOLIC SYNDROME

Homeopathic drug CORTISOL 30 contains Molecular imprints of the hormone cortisol. CORTISOL 30 is a great remedy for many ailments that are associated with Metabolic Syndrome.

Cortisol, also known as “stress hormone”, is a very important hormone produced mainly by the zona fasciculata of the adrenal cortex in the adrenal gland. It is produced in other tissues also in smaller quantities. It is released with a diurnal cycle and its release is increased in response to stress and low blood-glucose concentration. It functions to increase blood sugar through gluconeogenesis, to suppress the immune system, and to aid in the metabolism of fat, protein, and carbohydrates. It also decreases bone formation.

In general, cortisol stimulates the synthesis of ‘new’ glucose from non-carbohydrate sources. This is known as gluconeogenesis, mainly in the liver, and also in the kidneys and small intestine under certain circumstances. The net effect of cortisol is an increase in the concentration of glucose in the blood, further complemented by a decrease in the sensitivity of peripheral tissue to insulin, thus preventing this tissue from taking the glucose from the blood. Moreover, cortisol has a permissive effect on the actions of hormones that increase glucose production, such as glucagon and adrenaline.

Cortisol also plays an important, but indirect, role in liver and muscle glycogenolysis, the breaking down of glycogen to glucose.

Elevated levels of cortisol, if prolonged, can lead to proteolysis or breakdown of proteins, and muscle wasting. The reason for proteolysis is to provide the relevant tissue with ‘building blocks’ for gluconeogenesis. The effects of cortisol on lipid metabolism are more complicated since lipogenesis is observed in patients with chronic, raised circulating cortisol levels, although an acute increase in circulating cortisol promotes lipolysis. The usual explanation to account for this apparent discrepancy is that the raised blood glucose concentration through the action of cortisol will stimulate insulin release. Insulin stimulates lipogenesis, so this is an indirect consequence of the raised cortisol concentration in the blood but it will only occur over a longer time scale.

Metabolic syndrome or MetS is a cluster of common abnormalities arising from persistent high levels of cortisol in the blood. This Syndrome includes hyperglycemia, abdominal obesity, reduced high-density lipoprotein cholesterol levels, and elevated triglyceride and blood pressure. The common characteristics of MetS and hypercortisolemic conditions such as Cushing’s syndrome suggest that the pathogenesis of MetS and central obesity might involve prolonged and excessive exposure to cortisol.

Metabolic Syndrome was originally described as “insulin resistance syndrome”. The components of Metabolic Syndrome are associated with endothelial dysfunction and atherosclerosis and increase the risk for type 2 diabetes mellitus as well as vascular morbidity and mortality. It is estimated that about one fourth of the world’s adult population has Metabolic Syndrome.

Despite the increasing prevalence of MetS worldwide, there is still a lack of uniformly accepted diagnostic criteria, and there is controversy regarding the pathogenesis of MetS. Different organizations have provided their own definitions of MetS. MetS is diagnosed when three or more of the following parameters are present: waist circumference greater than 102 cm in men and greater than 88 cm in women, TG of at least 150 mg/dl (≥1.7 mmol/liter), HDL-C less than 40 mg/dl (<1.04 mmol/liter) in men and less than 50 mg/dl (<1.29 mmol/liter) in women, BP of at least 130/85 mm Hg, and fasting glucose of at least 110 mg/dl (≥6.1 mmol/liter).

It is unclear whether a single primary abnormality triggers a cascade of diverse events that lead to the manifestation of the components of MetS. Because the diagnostic features of MetS are shared by Cushing’s syndrome (CS), which results from endogenous or exogenous hypercortisolism, it was proposed that cortisol contributes to the pathogenesis of both states although only mild hypercortisolism occurs in MetS in contrast with CS. It was also suggested that inhibiting cortisol action could provide a novel therapeutic approach for MetS. Indeed, preliminary data suggest that circulating cortisol concentrations are higher in patients with MetS compared with healthy subjects, both in basal conditions and during dynamic stimulation. This difference is more evident in patients with MetS and hypertension or impaired glucose tolerance. Furthermore, weight loss normalizes cortisol levels and improves insulin resistance. Despite the fact that cortisol levels are within the normal range, there is evidence of increased activity of cortisol in the periphery and dysregulation of the hypothalamic-pituitary-adrenal axis. Differences between CS and MetS also need to be emphasized; in CS, once the tumor is removed, symptoms improve; in the MetS, weight loss reverses both hypercortisolism and phenotypic abnormalities.

Cortisol appears to play a role in adiposity in Metabolic Syndrome. Elevated serum uric acid levels are shared by MetS and CS Syndome. Increased exposure to cortisol contributes to increased fat accumulation in visceral deposits of fat. Increased cortisol serum overnight levels are also associated with insulin resistance.

Some studies showed elevated cortisol levels in situations such as work stress and unemployment. Others reported that chronic life stress results in subtle hyperactivity of HPA axis leading to intraabdominal adiposity and development of Metabolic Syndrome. Patients with Metabolic Syndrome appear to have higher urinary excretion of cortisol metabolites compared with healthy subjects. In vitro, cortisol appears to increase lipoprotein lipase or fat-storing enzyme levels in adipose tissue and particularly in visceral fat.

Experimental studies with cortisol inhibitors further support the role cortisol in the pathogenesis of Metabolic Syndrome, and might provide novel therapeutic approaches in patients with metabolic syndrome or obesity.

The components of Metabolic Syndrome are associated with endothelial dysfunction and atherosclerosis, and increase the risk for type 2 diabetes mellitus as well as vascular morbidity and mortality.

It was also suggested that inhibiting cortisol action could provide a novel therapeutic approach for Metabolic Syndrome. Indeed, preliminary data suggest that circulating cortisol concentrations are higher in patients with Metabolic Syndrome compared with healthy subjects, both in basal conditions and during dynamic stimulation. It was also proved that
reduction of body weight normalizes cortisol levels and improves insulin resistance.

Emerging data suggest that patients with MetS show hyperactivity of the hypothalamic-pituitary-adrenal axis, which leads to a state of “functional hypercortisolism.” The cause for this activation of the HPA axis remains uncertain but may be associated with chronic stress, which is associated with increased circulating cortisol levels and greater responsiveness of the HPA axis. Increased exposure to cortisol contributes to increased fat accumulation in visceral depots. Increased enzyme activity in adipose tissue and liver might contribute to the development of several features of the MetS.

Central abdominal obesity is one of the main components of the MetS. Cortisol appears to play a role in adiposity in MetS. Increased urinary cortisone/cortisol ratio in women with increased abdominal fat compared with those with peripheral fat distribution was observed by researchers, suggesting an increase in the peripheral metabolism of cortisol. Interestingly, cortisol clearance seems to be inversely correlated with insulin sensitivity, and this correlation is independent of body fat. It is also well documented that glucocorticoids promote the differentiation and proliferation of human adipocytes and that their receptors are more abundant in visceral than in subcutaneous adipose tissue. They also redistribute adiposity from peripheral to central depots, increase the size and number of fat cells, and activate lipolysis and the release of free fatty acids into the circulation.

Increased cortisol levels are also associated with insulin resistance. Higher cortisol concentrations were related to a reduced insulin secretion.

Hypertension is one of the most distinguishing features of Metabolic Syndrome as well as hypercortisolism. Many studies reported an association between cortisol and systolic and diastolic BP levels. This correlation might be attributed to the effect of stress, which is associated with the activation of the HPA axis and sympathetic nervous system. Indeed, patients with Metabolic Syndrome and hypertension appear to have higher urine levels of both cortisol and catecholamine metabolites than healthy individuals. A possible mechanism by which cortisol elevate BP seems to be an increased responsiveness to vasoconstrictors along with a decreased vasodilator production.

Obesity , a common finding in both CS and MetS, is also associated with hypertension. The possible underlying mechanisms include volume expansion, increased cardiac output and systemic vascular resistance, increased sodium reabsorption, increased activity of the sympathetic nervous system and the renin-angiotensin-aldosterone system, high leptin levels and concurrent leptin resistance.

Patients with Metabolic Syndrome as well as hypercortisolism frequently have elevated blood glucose levels. In patients with MetS, serum cortisol levels are significantly associated with fasting glucose concentration. The relationship between fasting hyperglycemia and cortisol is due to the glucocorticoid effects on hepatic gluconeogenesis and insulin secretion.

Metabolic Syndrome is associated with endothelial dysfunction that significantly predisposes to an increased risk for cardiovascular diseases. Endothelial dysfunction is also observed in patients with hypercortisolism. Hypercoagulability of blood is also present in MetS. Indeed, elevated fibrinogen and homocysteine concentrations have been observed in MetS patients compared with healthy controls. Hyperfibrinogenemia and homocysteinemia seem to be independent risk factors for cardiovascular diseases and venous thrombosis.

Elevated serum uric acid levels are seen both in Metabolic Syndrome and Hypercortisolism. High uric acid levels are regarded as a predictor of cardiac and overall mortality in patients with cardiovascular diseases or stroke. Elevated uric acid is also associated with higher risk of stroke in patients with or without cardiovascular disease. It was demonstrated that statin atorvastatin therapy is associated with a reduction in uric acid levels, along with an increase in estimated glomerular filtration rate in CKD patients with MetS. This effect on renal function is perhaps due to an amelioration of endothelial function and renal blood flow. On the other hand, patients with CS may have higher SUA and urinary uric acid excretion than healthy subjects.

Adipose tissue is recognized as an important endocrine organ that secretes a variety of bioactive peptides, termed adipokines. These adipokines exert multiple effects and play a key role in glucose and lipid metabolism, insulin sensitivity, BP, and angiogenesis. The major components of this family of adipokines are adiponectin and leptin, which are mainly produced by adipose tissue. Both these proteins exert an insulin-sensitizing effect through fatty-acid oxidation and, in addition, adiponectin is associated with antiatherogenic, antidiabetic, and antiinflammatory properties. In obesity, insulin resistance has been linked to leptin resistance, elevated leptin, and low adiponectin levels, which are associated with higher cardiovascular risk. Resistin is expressed in abdominal fat and is also associated with increased risk of central obesity-related diabetes. However, resistin may not be an “adipokine” because in humans it is mainly produced by monocytes, and its link with central obesity is debated. Excess adiposity leads to dysregulation of adipokine production, which in turn promotes a state of low-level systemic chronic inflammation predisposing to atherosclerosis.

Since molecular imprints of cortisol contained in cortisol 30 can act as artificial binding pockets for cortisol, it can antidote the adverse biological effects of excess cortisol circulated in the body. As such, cortisol 30 will be a powerful ingredient of Homeopathic Prescriptions in the management of all complaints associated with Metabolic Syndrome.

Author: Chandran Nambiar K C

I started practicing homeopathy in 1970, when I was 20 years old and studying for final year of BSc (Zoology) course. My interest in homeopathy happened very accidentally, through a constant relationship with a local practitioner who happened to be father of my classmate. I was a regular visitor in his clinic, where from I started reading BOERICKE MATERIA MEDICA and other homeopathic books, which helped me to cure myself my troublesome asthma that have been haunting me since my childhood days. I became a voracious reader of homeopathy. I was also deeply involved in studying marxism and dialectical materialism during my college days, which attracted me to political activities. MARXISM and HOMEOPATHY became two essential parts of my intellectual and practical life, which still continues so. Even though I joined DHMS course in a karnataka homeopathic college, I could not continue it due to my intense involvement in revolutionary political activities that resulted in jail life and a lot of criminal cases. Once that phase was over, I took a diploma in veterinary science and became a livestock inspector in animal husbandry department under govt of kerala. I have been continuing my study and practice of homeopathy all through these years. Since CCH act came into force only in 1976, and it contained provisions allowing existing practitioners to continue, my homeopathic practice went smoothly in parallel with my government job. In 1987, co-operating with some local homeopaths and social activists, I started Kannur District Homeopathic Hospital Sociey, which established a chain of hospitals and homeopathic clinics in different parts of Kannur district. After a few years I had to leave the society for some political reasons, and I established a 100 bedded well equipped homeopathic hospital in Taliparamba, employing a number of prominent homeopaths. That was ended up as a financial disaster for me due to many reasons, including my lack of skills as a money manager, and I was compelled to close down my dream project with in a short period. I lost huge money I invested, lost my reputation, and it pulled me into a debt trap. I learned a lot of valuabl lessons from this failure- about life, human psychology, relationships, and above all, about myself. I realized failure is the greatest teacher, if you are prepared learn from it. I learned how will power and determination to win will help us come back into life as a phoenix from our own ashes. I learned, one does not fail unless he stops fighting and accepts failure. My failure and the hardships that followed has moulded my personality in such a way that I can now withstand any disaster and fight back. I tell you, you will not know what life really is, unless you miserably fail at least once in your life. By this time, I left my government job also, and settled as a full time homeopathic practitioner. By this practice, I could repair my earlier financial losses, and establish well in life. It was during this period that I felt the need of developing a simple and user-friendly homeopathic software, that resulted in the evolution of SIMILIMUM, which was later upgraded into SIMILIMUM ULTRA. Similimum Ultra was well accepted by the profession, and it collected good revenues which continues even today. I stopped my practice a few years back , and concentrated in the study and research activities to evolve scientifically viable explanations to the so-called riddles of homeopathy. This unrelenting study resulted in MIT or Molecular Imprints Therapeutics, which provides a scientific and rational explanation for homeopathy. I started a homeopathic discussion group on facebook called HOMEOPATHY FOR TOTAL CURE, which has more than 35000 homeopaths as members. By this work on facebook, I could establish close relationship with many homeopaths around the world. It goes on. I could successfully convert facebook as my office and work place, from where I propagate my MIT ideas, co-ordinate my works for homeopathic community, and sell my Similimum Ultra Software. My years of hardwork in search of HOW HOMEOPATHY WORKS ultimately resulted in the publication of a book titled REDEFINING HOMEOPATHY (3000 pages, 3 volumes, hard bound, Rs 6000), in which I have compiled my articles regarding my scientific explanations of basic principles of homeopathy. These ideas are called MIT or MOLECULAR IMPRINTS THERAPEUTICS. MIT is now included in the syllabus of MD (HOM) course of prestigious DY PATIL DEEMED UNIVERSITY, PUNE, INDIA. Research department of SARADA KRISHNA HOMEOPATHIC COLLEGE, Kulashekharam, Tamilnadu, India, the only NAC accredited homeopathy college in India, has recently taken up certain reserch projects for proving the scientific explanations proposed by MIT. Based on MIT perspective of homeopathy, I had developed an MIT PROTOCOL for scientific homeopathy, and initiated a project for establishing a chain of MIT NETWORK CLINICS all over India, where MIT PROTOCOL will be practiced. More over, I have developed a whole range of 351 MIT FORMULATIONS, which are disease-specific combinations of post-avogadro diluted homeopathy drugs. NOW I AM IN 71st YEAR OF MY LIFE, AND STILL LOOKING FOR NEW HORRIZONS!

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