All posts by Dr Deepan

Dr DEEPAN P SHAH MD(HOMOEOPATHY) SPECIALISED HOMEOPATHIC PHYSICIAN AND SURGEON

RICKETS

Rickets is a childhood disease mainly occuring due to vitamin D deficiency. The bones become weak and soft and are more prone to fracture and deformities.
Osteomalacia is similar condition occuring in adults.

Types of Rickets

• Hypocalcemic Rickets  – This occurs due to impaired metabolism of vitamin D and calcium resulting into vitamin D deficiency and Calcium deficiency.
•Hypophosphatemic Rickets – This occurs due to low serum phosphate levels.

Causes

•Vitamin D Deficiency
-decreaed sun exposure
-malabsorption disease
•Chronic liver disease
•Renal tubular disease
•Neonatal hepatitis
•Limited breast feeding
•Improper diet
•Certain medications

•Certain Genetic anomalies

For Pathophysiology Also Refer This link VITAMIN D DEFICIENCY

Genes Related to Rickets-

•The most common form of disease is X-lined hypophosphatemic rickets (XLH).
•It is an autosomal form of disease.
•XLH rickets occur due to inactiving mutations in PHEX gene.
•PHEX(Phosphate regulating neutral endopeptidase) gene is expressed in bones , teeth and in mineralization and renal phosphate reabsorption.
•PHEX is involved in suppressing the response of FGF23
•FGF23(Fibroblast growth factor 23) gene signals the kidney to stop reabsorption of phosphate in to bloodstream.
•PHEX mutations lowers the tubular reabsorption of phosphate and vit D.
This contribute to bone diseases.

Signs and Symptoms –

•Muscle weakness
•Bone tenderness and retarded growth
•Delayed closure of anterior frontalle
•Delayed eruption of teeth and enamel defect
•Enlargement of long bones
•Anterior curving of legs,bow legs
•Green stick fracture
•Seizures and tetany
•Improper gait, bone pain

Diagnosis –

•Blood tests – Serum calcium and serum phosphate show low level along with changes in shape and structure of bone’s.
•Bone biopsy for confirmation.

Homoeopathic Medicine for Rickets-

•Thyroidinum – Thyroid producing anaemia, muscular weakness, nervous tremor, rheumatoid arthritis. Infantile wasting rickets. Delayed union of bones, nocturnal enuresis. Oedema of legs.

•Phosphorus – Dullnes of head, obstinate vertigo. Caries in teeth, drawing and tearing toothache, bleeding and grinding of teeth, gums separated from teeth. Weakness in all limbs, swelling of hand and feets, joint stiff.

•Calcaria Phosphorica – Wewakness of bones,large open frontalle, headache, skull soft. Slow dentition, tearing boring pain in gums, fever during dentition,pain in molars. Rheumatic pain in shoulder and arms, paralysis of joints.

•Baryta Carbonica – Suited to old people, dwarfs, scrofulous children inclined to grow fat. Glandular swelling. Chronic enlargement of tonsils. Abdomen distended and hard.

•Thuja occidentalis – Scalp sensitive to touch and painful, weakness in head. Caries of teeth, crown of teeth remains sound, gums swollen. Trembling of hands and feets, cracking of joints, frozen limbs.

•Silicea terra – Stiffness of nape,caries of clavicle, swelling of gland in nape,coccyx painful, tearing and shooting pain in back.Weakness of joints,cramps of arms and legs,jerk in limbs.

•Kalium Iodatum – Glands swollen or atrophied. Gouty daithesis. Swelling of bones, contraction of muscles and tendons, pain after long injury.its is also very well indicated in Dropsy accompanying Rickets basically due to renal complaints impairing calcium resoption.

Conservative management for Rickets-

  • Exposure to Ultraviolet B rays
  • Increasing dietary intake of calcium
  • Phosphate and vitamin D
  • Cod liver oil
  • Halibut liver oil
  • Vit D fortified milk
  • Vit D supplements

VITAMIN D DEFICIENCY HYPOVITAMINOSIS D

CALCIUM DEFICIENCY

OSTEOPOROSIS

IBD INFLAMATORY BOWEL DISEASE

IBD Inflammatory Bowel Disease is a functional Gastrointestinal disease that mainly affects the bowel-large or small intestine.
It is the chronic relapsing inflammation of intestine.
Certain genetic and environmental factors are known to be associated with IBD.
The disturbances of immune system and impaired action of microbes leads to development of IBD.
Chrons disease and ulcerative colitis are two different entities of IBD.

Chrons disease

It is a type of IBD that may affect the GI tract from mouth to anus.
Most probably it involves sharply demarcated single or multiple areas of large intestine, terminal ileum or ileocecal region.

Risk factors and cause

Age- chrons disease can occur at any age but most commonly develops at young age.
Hereditary-About 15%of patients with chrons disease have one or more family members either with chrons disease or ulcerative colitis.
Cigratte smoking-smokers are most likely to develop chrons disease than non smokers.
Diet-high intake of refined sugars and low intake of fibre can mainly contribute to chrons disease.
Certain medications like NSAID’s.

Pathogenesis

Chrons disease is believed to be result of an imbalance between proinflammatory and anti-inflammatory cells.
There are some mutations in NOD2 gene that disrupts the mucosal defence mechanism.
NOD2 earlier known as CARD15 helps protect body against foreign Invader like bacteria and viruses through immune system cells like macrophages, monocyte and dendritic cells.
When triggered by some bacteria they become active and regulate activity of multiple genes that controls inflammatory response.
ATG16L1 is also involved in pathogenesis.it provides information for making a protein that is required for autophagy (destruction of cells in body).
It’s mutations impaires autophagy process and allows worn our cells to persist in body.
Depressed defence mechanism can stimulate microbial proliferation in body.
Under microscope biopsies of affected colon shows mucosal inflammation characteristed by inflitration of neutrophilis.
Neutrophils along with mono nuclear cells infiltrate crypt’s leading to inflammation and abscess.

Signs and symptoms

Intestinal manifestation-
-Ileum- abdominal pain and cramps
Diarrhoea
Obstructive symptoms
Mass in right iliac fossa
Acute ileitis
-colon- rectal bleeding
Intestinal stenosis
Perianal disease
-rectum-proctitis
Extraintestinal manifestation-
Eyes-it causes uveitis causing blurred vision and eye pain.Photophobia
Oral cavity-it causes apthous stomatitis, geographic tongue,chelitis granulomatosa.
Skin-erythema nodusum, ulcerative nodules.
Chrons disease can also cause osteoporosis and thinning of bones
Clubbing of fingers
Deep vein thrombosis
Fatigue

Diagnosis

Blood test-Anaemia is noted in PT with chrons disease.there are low blood cell count.

Stool test-For presence of any occult blood.

Colonoscopy-it is more accurate test that detects the ulcers and areas of inflammation.It can also be used to take biopsies.

Ultrasonography can be useful in patients with palpable abdominal mass and in order to differentiate from abscess

CT scan-this test is used to diagnose entire bowel as well as tissue outside the bowel.it has replaced barium x-rays.

MRI is useful for investigating complex perianal disease

Upper GI endoscopy- A flexible tube containing a camera is inserted in stomach and upper part of small intestine.it can also be done using a capsule.

GASTRITIS

Gastritis is a condition in which mucosa(stomach lining)is inflammed or swollen.
The mucousa consists of gastric glands that secrete digestive juices.
They are covered by layer of columnar epithelial tissues.
It produces acid and pepsin that helps in breakdown of food and digestion of protein
When stomach lining is inflammed it produces less acid and enzymes.

Types

Acute Gastritis -starts suddenly and appears with noticeable symptoms that resolves without treatment within few days.
Chronic Gastritis -It is long lasting and stays in body unnoticeable and can cause complications.
Other classification-
Atrophic/autoimmune
Non atrophic mainly caused due to H pylori
Multifocal atrophic caused due to H pylori and environmental causes
Radiation-caused due to radiation injury.
Non inflammatory granulomatous

Gastritis can also be classified as

Erosive Gastritis -The acids residing with in stomach erode and wear away the stomach lining causing ulcers and deep sores.
Non Erosive Gastritis – It causes inflammation of stomach lining.it does not cause erosion or ulcers.

Risk factors –

Helicopter pylori-The bacteria that resides in mucosa.
Alcohol consumption – excessive alcohol consumption can cause irritation of the mucosal lining.
Stress-stress due to major surgery or injury can lead to gastritis.
Age– older adult people are more prone to this Condition due to thinning of mucosal lining and they are more likely to have Helicobacter Pylori infections.
Bile reflux– regurgitation of bile into stomach from bile tract.
Certain medications.

Pathology

Chronic Gastritis – it can be divided into two

  • Autoimmune Atrophic Gastritis
  • H Pylori Associated Gastritis

Autoimmune Atrophic Gastritis –

It is a chronic condition that results in replacement of parietal cell by metaplastic mucosa.
The interaction of autoantibodies against parietal cell proton pump leads to destruction of parietal cells.
It in turn causes imparied absorption of vitamin B12 and pernicious anaemia.

H. Pylori Associated Gastritis

H Pylori Bacteria enters the body and resides in stomach
It attacks the Lining of the stomach that protects it from acid that digest the food.
Once bacteria damage the lining acid can enter through the lining easily causing ulcers.
H pylori produces its virulence through motility,urease activity and association with mucosal cells.
Urease activity create ammonia that neutralizes the activity of acid
Motility allows the bacteria to penetrate the mucus layer and promote association of bacteria and epithelial cells.

Symptoms-

Pain in upper abdomen.
Feeling of fullness in upper abdomen.
Belching and heartburn.
Hiccups
Indigestion
Nausea
Vomitting
Faltulence
Weight loss
Early satiety

Diagnosis-

Breath test – for H. Pylori
Blood test– pernicious anemia and H pylori infections can be ruled out with blood test.
Stool test-For presence of blood in stools.
Endoscopy-for stomach lining inflammation and erosion
Stomach biopsy
Liver, kidney and pancreas function test.

HOMOEOPATHIC MEDICINES

ARSENICUM ALBUM

Intense burning and heat in stomach and pit of stomach.violent burning pain. Vomiting after eating and drinking.

NUX VOMICA

Spasmodic pain in abdomen. Colickly pain with urge to stool and urinate. Cutting Pains causing patient to bend. Reversed peristalsis.

ARGENTUM NITRICUM

Belching, vomiting, nausea. Ulcerative pain in Left side.gastritis especially of drunkards. Trembling and throbbing pain In stomach.enormous distension.

KALIUM BICHROMICUM

Cutting pain in abdomen soon after eating.dilatation in stomach, round ulcer of stomach, cannot digest meat, vomiting of bright yellow water.painful retraction, burning.

ARGENTUM NITRICUM

Abdominal colic with flatulent distension.stitchy ulcerative pain in left side of abdomen.nausea, retching vomitting of mucus.great craving for sweets.painful spot over stomach that radiates to all over abdomen.

DIABETES MELLITUS

Diabetes Mellitus is a complex condition in which the blood sugar levels are raised for a long period of time either because of inadequacy of insulin production or lack of body cell responses to insulin

Causes of Diabetes

Weight-Weight is the important risk factor in type 2 diabetes.
The more the weight the more the body becomes resistant to insulin.
Age-Risk of Diabetes increases after 45 years of age.
Family history-Those having family history of Diabetes have greater risk of acquiring diabetes.
Diet-Diet high in fats, calories and cholesterol and deficient in fibre increases risk of diabetes.
Lack of exercise and sedentary lifestyle.
Hormonal imbalances.

Types of Diabetes Mellitus

1- Diabetes Mellitus (Type 1)-Also known as insulin dependent diabetes mellitus or juvenile diabetes as it is usually diagnosed in childhood.
In this type the insulin production is not enough or very less.
They require insulin on daily basis to survive
2- Diabetes Mellitus (Type 2) -In this type the body is incapable of responding to insulin.
The body becomes insulin resistant.
It is most common type of Diabetes due to sedentary lifestyle and increased obesity.
3- Gestational Diabetes -It occurs in cases where there are high blood sugar level during pregnancy.
Occurs in women who previously delivered baby weighing more than 4.5kg(10lbs).

Pathogenesis

Type1 diabetes mellitus
Type 1 diabetes is considered to be an autoimmune disorder
In autoimmune disorder body attacks it’s own tissues and organs.
T1 DM results from destruction of insulin producing pancreatic beta cells.
Beta cell autoantigen, macrophages,B and T lymphocytes are involved in pathogenesis of T1 DM.
Activated macrophages,CD4+Tcells and beta cytotoxic CD8+Tcells destroy beta cells
Insulin antibodies, Islet antigen (IA 2) antibody, glutamic acid carboxylase also paly a major role in autoimmunity.
The Human leucocyte antigen (HLA) encoding the major histocompatibility complex proteins is known to be associated with increased susceptibility to T1 DM.
The HLA complex helps the immune system to distinguish body proteins from proteins made by viruses and bacteria.
Due to insulin deficiency there is excessive secretion of glucagon.
The excess glucagon secretion and insulin deficiency imparies the expression of genes for target tissue to respond normally to insulin resulting in T1 DM.

Type 2 Diabetes Mellitus

Inability of insulin to produce it’s desired effect on circulating glucose levels.
Destruction of pancreatic beta cells along with insulin resistance is associated with T2 DM.
Muscle fats and level cells fail to respond to insulin.
The main mechanism involves increased breakdown of lipids with in fat cells,lack of incretin,high glucagon levels.
Inability of insulin to suppress lipolysis results in increase plasma levels of fatty acids that in turn stimulates glucose production in liver.
The elevated free fatty acids also produces low grade inflammation which is also associated with T2 DM.
Genetic factors include insulin receptor and insulin receptor substrate gene polymorphisms that affects insulin signal.
Polymorphisms of beta3 adrenergic receptor gene associated with visceral obesity promote insulin resistance.
Adipokines are also seen to be involved in insulin resistance.
Other gene associated are ABCC8,CAPN10,GLUT2,TCF7L2.

Signs and Symptoms

  • High blood level of glucose
  • Frequent and painful urination
  • More thirsty and hungry
  • Feeling tired and dizzy
  • Lethargic feeling
  • Fatigue
  • Itching skin
  • Dry mouth
  • Blurred vision
  • Nausea
  • Vomitting
  • Smell of acetone in breathe
  • Increased susceptibility to Infections
  • Weight gain or loss
  • Slow healing if wounds, cuts and sores
  • High blood pressure

Diabetic Ketoacidosis

Diabetic ketoacidosis is complex disorder characterized by hyperglycaemia, acidosis and ketonaemia.
It occurs due to insulin deficiency that causes increase in counter regulatory hormones.
Insulin deficiency along with counter regulatory hormones leads to excessive production and accumulation of glucose in the body.
Insulin deficiency causes release of fatty acids and glycerol.
Glucagon stimulates liver to oxidize fatty acids into ketone bodies.
Ketone dissociates into anion and hydrogen ions.
Acidosis develops as body tries to maintain extracellular pH by binding hydrogen ions with bicarbonate ions.
Ketonaemia develops as the ability of tissue to utilize ketone bodies exceeds.
Kidney excrete large amount of ketone and glucose into urine that causes dehydration, ischemia that further worsen acidosis.

Diagnosis

  • Random blood sugar – By this test the level of glucose can be measured at any time irrelevant of diet.
    Blood glucose level of 200mg/DL or more indicates Diabetes.
  • Fasting blood sugar test-Blood sugar level of 126mg/DL indicates Diabetes.
  • Sugar level between range of 100-125mg/DL indicates prediabetes.
    Normal range is below 100 mg/DL.
  • Oral glucose tolerance test-Blood sugar level of 200 mg/DL indicates diabetes.
  • Sugar level with in range 140-200 mg/DL indicates prediabetes.
    Below 140 mg/DL indicates normal range.

Homoeopathic Medicines For Diabetes Mellitus

  • Syzygium Jambolanum
  • Cephalandra Indica
  • Rhus Aromatica
  • Acidum Phosphoricum
  • Gymnema Sylvestre
  • Uranium Nitricum
  • Helonias
  • Abroma Augusta
  • Iodium

OSTEOPOROSIS

Osteoporosis is a disorder of bone where reduced Bone Mineral Density makes the bones fragile

Osteoporosis is a silent disease that causes thinning and weakening of bones

There is decrease in Bone Mineral Density making the bones weak and brittle

Risk Factors of Osteoporosis

  • AGE  and SEX – as age advances chances of osteoporosis increases, Bone Mineral density reached its peak at around 30 yrs of age. Then after certain years it gradually starts depleting due to depleting levels of Growth hormone and later more pronounced after 48 in women and after 60 in men, its attributed to depletion of oestrogen in females and depletion of testosterone in males. its more common and severe in females as oestrogen depletion in females affects more compared to effect of testosterone depletion in males.
  • Genetics and Familial Predesposition
  • Habitat  – in region or lifestyle with lesser exposure to sunlight.
  • Vitamin D deficiency
  • Parathyroid Dysfunctions
  • Thyroid Dysfunctions
  • Kidney diseases
  • Diabetes Mellitus
  • Acromegaly
  • Certain rheumatological conditions
  • Parkinson’s Disease
  • Sedentary lifestyle lack of exercise and physical activity
  • Excessive tobacco smoking
  • High Protein diet
  • High intake of phosphoric acid, usually its through areated soft drinks
  • Prolonged increased exposure to Cadmium.
  • Malabsorption and Malnutrition

Pathophysiology of Osteoporosis

(this part is under construction)

Bone constitutes major portion of Human Skeleton

There Are Over 206 bones in skeleton primarily it consists 270 bones at birth later they fuse together during development

Bones Differs in various size shapes and structures

Bones not only performs the functions of protection protection and support to the body but also helps in storage of minerals lipids and nutritients

Tissue that constitute bone are of two types that gives strength and rigidity to bones viz:

  1. Cortical bone – Cortical Bone forms the outer layer of most of the bones. It is stiffest and hardest. It helps in supporting and protecting the soft tissues of body and gives shape to the body. It Consists of Osteons that in turn consists of Haversion Canal that allows the blood vessels and nerves to travel through them.
  2. Cancellous Bone – It occur at the end of the Long Bones. It is less stiff and weaker compered to the Cortical Bone. They Consists of Red Bone Marrow that produce Blood Cells

The Bone tissue exibits following type of cells:

  • Osteoblast
  • Osteoclast
  • Osteocyte

They help in Synthesization, Bone Resorption as well as Maintainence and repair of bones

Osteoporosis most commonly occurs due to the imbalance in bone resorption and bone formation and insufficient mass

Low Bone Density occurs when osteoclast degrads bone matrix faster than osteoblasts.

Role of Parathyroid Gland in Calcium Metabolism and Osteoporosis

•Hyperparathyroidism-Hyperparathyroidism can be defined as a condition when one or more of the parathyroid glands become hyperactivie and increases in size.
This leads to increased PTH levels in blood
Parathyroid Hormone Vitamin D and Calcium Metabolism –
•Parathyroid hormone is secreted by parathyroid glands.
•PTH along with vit D helps in regulation of calcium level in human body.
•PTH is secreted through negative feedback mechanism of the body when the serum calcium levels are decreased.
•Vit D regulates intestinal absorption of calcium.
•Calcitrol the active form of vit D regulates calcium metabolism.
•Vit D3 is produced from 7-dehydrocholestrol when the skin is exposed to Ultraviolet rays
•Vit D3(Cholecalciferol) is then carried to liver via blood where it undergoes two hydroxylation process.
•First it goes under hydroxylation in liver forming Calcidol 25(OH) and then in kidneys forming Calcidol(1,25 dihyrdroxy vit D).
•The decreased serum calcium level stimulates PTH secretion.
•As Bones are the major store house of calcium,the secreted PTH corrects calcium level by mobilizing calcium from bone through destruction of bones by osteoclasts.
•This leads to osteoporosis where there is weakening of bone decreasing it’s density.

Signs and Symptoms of Osteoporosis

  • Osteoporosis itself may stay silent and show no symptom untill bone becomes weak and break down.
  • Acute and chronic pain in bones and muscles.
  • May precipitate or trigger osteoarthritis
  • Deformities and anomalies to carry out normal daily activities.
  • Stooped posture, loss of height, collapse (loss of consciousness).
  • Fractures are most dangerous aspect of osteoporosis. Fractures most commonly occurs in spine, hip, rib, shoulder, wrist.

Diagnosis of Osteoporosis

The normal Bone Density is within +/-1 SD(+1 or-1)(Standard Deviation) in young adults.

The Score Between -1 and -2.5 is indication of low bone mass.

The score of -2.5 or lower indicates osteoporosis.

  • X rays to an extent helps in detecting reduced Bone Mass also in detecting the complications of osteoporosis like fractures.
  • CT Scan and MRI helps in detecting complications of reduced bone mass, preosteoporosis or follow up examination.
  • Dual Energy X ray Absorptiometry(DEXA) is mostly used for evaluating Bone Mineral Density and its grading for diagnosis of Osteoporosis.
  • Quantitave Ultrasound is a non-invasive method of estimating bone density and risk of bone fracture.
  • Certain Biomarkers are also useful in detecting bone degradation.

Homoeopathic Medicines for Osteoporosis

  • CALCAREA PHOSPHORICA 

    It affects the nutrition of bones and glands indicated in it Homoeopathic form when bones becomes soft brittle and thin, promotes ossification of bones in non union of fractures, pain and burning along the sutures, shifting pain, malassimilation.

  • CALCAREA CARBONICA

    Improper assimilation of calcium gives rise to defective nutrition of bones glands and skin. Swelling of the joints especially knee weakness and trembling of limbs.

  • SYMPHYTUM OFFICINALE 

    injuries to cartilage, periosteum, comminuted fractures, non union of fractures, deficient callus, arthralgia of knees, carries of vertebrae.

  • RUTA GRAVEOLENS 

    Sore tendons, injured or bruised bones, formation of deposit or nodes in periosteum and tendons, ill effects of bruise, fractured bones, brittle paralytic rigidity of injured or affected part.

  • FLOURICUM ACIDUM

    This remedy should be thought of when osteoporosis secondary to some chronic metabolic digestive or autommune condition or post chronic debilitating deep seated  infections  produces slow deeply destructive effects carries of long bones ulceration varicose veins bedsores calcareous degeneration tissues are puffy indurated and fistulus.

  • Ammonium Muriaticum 

    A good remedy to combat secondary effects and complications of osteoporosis especially those due to nerve compression due to degenerative changes of spine as a complication of osteoporosis. Patient has tension and tightness as if muscles or tendons are too short neuralgic pain in stumpsof amputed limbs sciatica pain in heels.

 

VITAMIN D DEFICIENCY HYPOVITAMINOSIS D

HOMEOPATHIC PATENT MEDICINES – Your Life Is At Stake – Are They Actually Homoeopathic!

Homoeopathic Patent Medicines – Homoeopathy for NAME-SAKE!

Homoeopathic Patent Medicines – Over the Counter – So Called Homoeopathic Medicines.

Are they actually Homoeopathic?

Are you being cheated in name of Homoeopathy?

There are lots of controversies related to So Called “Homoeopathic Patent Medicines” available over the counter in pharmacies.

And no one wants to dare to raise their voice against it as most of these are owned by major manufacturers having good contacts with central councils and no one wants to mess with them!

There are many flaws in the homoeopathic patent medicines that are available in market and about the rules and regulations governing them and without any doubt this need to be corrected in system as soon as possible, as its affecting the credibility of Homoeopathy  as  whole and its our resposibility to act and regularise certain things.

There are 5 Gross Irregularities that I have noticed in OTC Homoeopathic patent Medicines are:

1)Many of these medicines mention the effect/indications of each of the used drug seperately on the labels, where as its being administered in combination, and when more than substances are combined the new combination may not retain individual properties of original components. So only effects of newly prepared combination as a whole should be allowed to be mentioned on label.

2) Indications/effects should be strictly scrutinised before letting them mentioning it on their Label. Though generalising of medicine as per disease is against certain laws of organon but still “Genus Epidemicus” section does provide liberty on this aspect to some extent.

But the claimed effects should be confirmed by not only as per Homoeopathic Drug Proving Principles under high vigilance but also double blind placebo controlled trials with most modern techniques as they are not giving classical or constitutional approach in their combination disease specific medicines and is based only on theraputic model, which can easily be checked by modern techiniques.

3) The dosing which they mention on their labels should be strictly banned as  almost all of these medicines mention a fixed dose pattern without time-frame in a generalised manner for all . Organon strictly mentions that one cannot generalise the dosages as its too dangerous and should only be administered as per the susceptibility of an each individual also its a well known fact that organon strictly warns unnecessary repetition of doses in same potency one the effect has started.

4)Label of “Homoeopathic Medicine” should not be allowed if the indications are not based on same cures same principle, as its not the substance thats being used makes it homoeopathic in nature its the way its administered on a diseases condition determines wether  its Homoeopathic or Unhomoeopathic in its mode of action. There are many substances that are being used in common in Ayurveda  Homoeopathy and other systems of medicines but application and indication is different as in Homoeopathy we administer as per “LIKE CURES LIKE” or “Same Cures Same” principle where as most of other system use “Opposite Cures”.

Let me give you an example that if homoeopathy used X substance for cure of  diarrhoea then the other system will use  that substance X for cure of cobstipation.

Organon clearly mentions that when a substance is administered first it shows a primary action which is due to material dosw of that substance that act directly on the body and then come secondary response that is the body’s reaction towards that direct primary medicinal action, which we all know as response to stimulus, So in homoeopathy we rely on response to stimulus and not the primary action of the drug substance that is the stimulus, so in homoeopathy we just stimulate the organism as a whole and wait for its reaction towards that stimulus unlike other systems where they simply keep stimulating and stimulatimg by repeating ever increasing material doses whereas we just administer initial few doses untill we find satisfactorily that the organism is being stimulated sufficiently then we stop dosing it further as it will only create medicinal aggravation or even dangerous – the killers aggravation which under certain condition is fatal.

So its important wether the mentioned indication is homoeopathic in nature or unhomoeopathic and wether the indicated dosing are corresponding to laws of organon or not, otherwise they can simply mention to consult physician for dosing of those medicines.

5)Most of these medicines mention “No Side Effects” on their label,  Now this fact is not commonly known that if Homoeopathy if not taken as per principles of homoeopathic it can produces severe aggravations which might deteriorate patient’s condition and in some cases patient may even die, this type of aggravations are well known in Homoeopathic community as “Killers aggravation”. And by mention such dosing and with other irregularities most of these medicines are not homoeopathic medicines at all!

Considering all above facts most of the so called Patent Homoeopathic Medicines alvailable in market are not at all homoeopathic!

Setbacks:

  • The consumers are being cheated
  • Their life is at stake
  • Goodwill of homoeopathy is perishing

All these are gross irregularities not only on the part of Manufacturers but also the Governing body and the lax rules and ruglations governing them.

Its causing lots of critisicism about homoeopathy globally and homoeopathy has started losing its credibility because of all such issue this wonderful system of gentle medicine needs to be preserved properly and its in our hands.

Its time for all of us to come forward not only the physicians and consumers but also governing body and manufacturers to find a proper solution to this mess and lay down stringent laws not only as per Homoeopathic pharmacopia but also keeping into effect the bare homoeopathic laws as mentioned in homoeopathic organon of medicine. Though many of those need to be ammended but still the basic essence and priciple can never be Violated or Amennded  to proudly call our self HOMOEOPATHS And That Law Is “LIKE CURES LIKE”.

“SIMILIA SIMILIBUS CURENTUR”

THE KILLER’s AGGRAVATION -Homoeopathic Medicines Can Kill You!

OBESITY

Obesity has reached at pandemic levels and has become a subject of concern as it is directly related to many diseases.

As obesity is directly associated with many diseases, so it needs to be studied properly in all its dimensions so as to prevent it, treat it and also to understand all the underlying factors related.

Diagnostic Measurements and Evaluation Methods for Level of Obesity

To measure fat ratio in our body there are many highly technical ways but clinically feasible and practical are the following 3 ways which are widely used.

  1. BMI – Body Mass Index, where the body weight is related with height BMI=Body Mass/ (Body Height)². It is measured as kg/m². BMI of 18.5 to 25kg/m² is considered to be normal, below 18.5kg/m² underweight, 27-30kg/m² overweight, above 30kg/m² Obese. In general a subject having BMI above  27kg/m² and below 18.5 kg/m² is considered to be at health risk.
  2. Various Circumferences of body and their relation and ratio with each other, especially waist to hip circumference ratio. Distribution of fat also determines the risk factor as it is observed that central or visceral obesity where fat accumulates in belly around abdominal organs and on trunk is observed to have more health risk compared to diffused subcutaneous fat accumulation.
  3. Skin Fold Measurement is also one of the ways to measure fat proportion. This method which gives us better idea about subcutaneous fats. Skinfold measurement when taken along with the other two above mentioned methods gives us a better comparative ratios and evaluation of body fat measurements.

Risk Factors of Obesity

Not only genetics but also environment plays a major role e.g. Its observed that Asian shifting to USA (the obesity capital of world), ratio wise more tend to become obese compared to their counterparts in their country.

Few of the risk factors are mentioned below

  • Genetics and familial predesposition
  • Enviroment and staple food of the region
  • Sedentary lifestyle
  • Irregular sleep pattern
  • lrregular meal pattern
  • Low protein intake
  • High carbohydrate and sugar intake
  • Certain Metabolic Disorders
  • Hypothyroidism
  • Diabetes Mellitus
  • PCOS polycystic ovarian disease
  • Certain Medications
  • Certain Psychiatric Eating Disorders
  • Bigorexia/muscle dysmorphia
  • Body Dismorphic Disorder
  • Anorexia Nervosa
  • Orthoxia nervosa
  • Depression
  • Anxiety
  • Night Eating Syndrome
  • Certain injuries deformities and disabilities that makes patient immobile which causes weight gain.

Pathophysiology of Obesity

To simplyfy the understanding of causation of obesity; which otherwise is too complicated to comprehend with a single article; I have explained it in a broader sense and summarised its essense as follows:

“Obesity is the disease of low energy utilisation compared to intake!”

“When the intake of energy exceeds its utilisation, it then get converted into triglycerides and is stored in adipose tissues causing obesity”

There are many factors that are responsible for obesity but the recent research has come up with an interesting mind boggling study of one of such factor that is the molecule Leptin.

Leptin and Ghrelin with other endocrinal molecules controls Appetite and Satiety centers through hypothalamus. Is a complex Hypothalamo-pitutary-endocrinal axis that is inovolved in the mechanism.

Of all the other various factors, Leptin needs a special reference and attention when it comes to obesity. As Leptin not only controls Apetite but also controls Thermogenesis and other Catabolic processes.

Role of Leptin in Apetite Control

Adipocytes communicate with satiety centers present in hypothalamus by secreting a polypeptide called Leptin. The levels of Leptin are determined by the amount of fat stores in the body. Leptin interacts with the hypothalamus by attaching to Leptin receptors.

When Lateral Hypothalamus(LH) is stimulated it increases appetite and vice a versa.

When Venteromedial Hypothalamus(VMH) is stimulated it creates satiety and vice a versa.

Level of Leptin and its relation with certain appetite controling molecules through Stimulation or inhibition of LH and VMH is as follows:

  • Inversely proportional to a powerful appetite stimulators like Neuropeptide Y(NPY) and Agouti Related Peptide(AgRP). Resultant Stimulating LH and Inhibiting VMH
  • Directly proportional to powerful appetite inhibitors like Glucagon Like Peptide-1(GLP-1), Pro-opiomelanocortin(POMT) and Cocaine and Amphetamine Regulated Transcript(CART). Resultant Stimulating VMH and inhibiting LH

Role of Leptin in Catabolic Processes.

Leptin receptor stimulation increases

  • Energy expenditure
  • Physical activity
  • Thermogenesis(heat production)

Role of leptin in Energy Expenditure, Physical Activity and Thermogenesis

  • Stimulation of leptin receptors in hypothalamus stimulates secretion of Norepinephrine from sympathetic nerve endings in adipose tissue.
  • This stimulates β3-adrenergic receptors expressed by fat cells which results into hydrolysis of fatty acids.
  • This results into release of energy which is dissipated in the form of heat.

Also there are other catabolic effects of leptin which are mediated through Hypothalamo-Pitutary axis which goes through the channel of endocrinal system by stimulating endocrinal glands.

Deletion or SNP of Leptin producing gene causes leptin deficiency resulting into extreme obesity.

Complications and Diseases Associated with Obesity

Obesity complicates almost all the diseases and precipitates many life threatening chronic diseases.

Few of them which needs special reference are

  • Hypertension
  • Diabetes Mellitus
  • Osteoarthritis
  • Gout
  • Lumbar spondylodis
  • Sciatica
  • Meralgia Paraesthetica
  • Artherosclerosis
  • Hypertriglyceridemia
  • Hypercholestrolemia
  • Low HDL
  • Cardiomegaly
  • Congestive Cardiac Failure
  • Ischemic Heart Diseases
  • Deep Vein Thrombosis
  • Pulmonary Embolism
  • Fatty Liver
  • Cholelithiasis
  • Hypoventilation syndrome
  • PCOS
  • Infertility
  • Erectile Dysfunction
  • Hypogonadism
  • Burried male genitals
  • Depression
  • Certain Cancers

HOMEOPATHIC MEDICNES AND MANAGEMENT FOR OBESITY

To Lose Weight in obese patient who wants to reduce weight it is necessary to rule out all the pathological factors which may be responsible for obesity and if any found then first the underlying abnormalities needs to be treated first.

Each case preferably needs to be individualised properly as per homoeopathic principles for medicine selection, to yield best results of homoeopathic medicines.

Though , there are some generally used common homoeopathic medicines to lose weight which I have simplified to select by providing basic guidelines which are hard to fail in most of the cases,

  1. Phytolacca Berry well proven homoeopathic medicine for weightloss in general.
  2. Fucus Vesiculosus compliments well to phytolacca berry and when both given intermittently during weightloss treatment works wonders.
  3. Calcarea Carbonica Generalised obesity, for fair, fat and flabby women especially in their forties, mentally and physically sluggish , well suited to women with thyroid disorders.
  4. Thuja Occidentalis obesity due to excessive hunger and abnormally high appetite.
  5. Ignetia Amara obesity in females due to depressing emotion and PCOS.
  6. Thyroidinum obesity due to thyroid disorder
  7. Sepia obesity in female do to Polycystic Ovarian Syndrome (PCOS)
  8. Iodium obesity due to disorder in thyroid glands
  9. Bromium obesity due to disorder in thyroid gland
  10.  Nux Vomica for weight gain due to sedentary lifestyle, irregular dietary habbits, irregular routine, lack of sleep, typical central obesity.

Weight Management

  • To lose weight a person needs to keep strict control on his diet and need to do exercise on regular basis along with medicines for faster and better results.
  • One needs to keep check that he doesnt lose muscle mass in the process
  • I recomend to completely stop sugar and jaggery
  • Oil and Ghee not more than 1-2 tsp throughout the day
  • Increase protien intake as per intensity of workout
  • Increase fiber intake in form of salads and fruits that are not too sweet
  • 4-5 small meals throughout the day
  • Ample of water throughout the day
  • 1 hour yoga or brisk walk
  • Intense workout under professional guidance for those wants to achieve subnormal so called ripoed and defined body.
  • Atleast 7 hours of continious sleep at a stretch is recomended.

BPH BENIGN PROSTATIC HYPERPLASIA

BPH or Benign Prostatic Hyperplasia is a disease of males. It is a non-malignant(non-cancerous) enlargement of prostate glands.

Anatomical and Physiological basics of Prostate Gland

Prostate is an exocrine gland about the size of walnut and weight about 7-14gms with median of 11gms it lies below urinary bladder surrounding the urethra with its glandular duct opening in prostatic part of urethra.

It is partly Glandular and partly Muscular. The Glanduloalveolar part produces alkaline prostatic fluid and the Muscular part helps to ejaculate this fluid into prostatic part of Urethra to mix it with sprems produced by testes and form the semen.

Externally it seems to be divided into 4 lobes

  • Anterior lobe or isthemus,
  • Posterior lobe
  • Right and left Lateral lobes
  • Median lobe or middle lobe

The cut section of prostate doesnt show distribution as that of lobe pattern as seen externaly also the morphological distribution is different at different age so in pathology its divided into zones rather than studying in lobes.

  • Peripheral Zone
  • Central Zone
  • Transition Zone
  • Anterior Fibromuscular zone

Pathophysiology of Benign Prostatic Hyperplasia BPH

As the men age the production of Aromatase and 5 alpha reductase increases.

Both Aromatase and 5 alpha reductase converts Androgens(male hormones) into Oestrogen and Dihydroxytesterone. Which results into reduced levels of testosterone and increased levels of Dihydroxytesterone and Oestrogen. Oestrogen stimulates growth of prostatic cells and Dihydroxytesterone a powerful anabolic hormone synergestically aids in to the action of oestrogen in growth of prostatic cells.

In which not only the stromal cells but also glandular cells undergo hyperpalsia. Although stromal hyperplasia is more predominant than the glandular, contadicting this the lateral and median lobe that have more glandular tissue and they are seen to enlarge more compared to anterior which has comparatively lesser glandular tissue.

BPH is closely associated with malignancy and its usually found in transition zone.

Risk Factors for Benign prostatic Hypertrophy BPH

  • Aging
  • Genetic and Familial predesposition
  • Smoking and alcohol
  • Sedentary and Stressful lifestyle
  • Obesity and Metabolic syndrome
  • Diabetes and hypertention
  • Abuse or frequent use of Anabolic hormones and aphrodisiac drugs.

Symptoms of Benign Prostatic Hypertrophy BPH

  • Patient typically presents with symptoms of lower urinary tract symptoms like
  • Stangury.
  • Slow and feeble stream of urine.
  • Frequent Urge to urinate.
  • Retention of urine.
  • Urge to urinate soon after passing it once
  • Post void terminal dribbling of urine
  • Intermittent stream of urine
  • Sensation as if some urine is left back, which he ineffectually tries to clear it up.
  • Involuntary passing of urine.
  • Nocturnal Enuresis.
  • Lack of confidence to hold urine on urge to pass
  • May show complications like urinary bladder stones, freqient urinary tract infections which may potentially damage bladder spincter or kidney, retention of urine.
  • Bleeding in urination or per rectum is a sign of severity and needs urgent intervention to rule out the cause and need proper eveluation for presence of malignancy

Diagnosis of Benign Prostatic Hypertrophy BPH

  • Per rectal examination to check any enlargement in size by palpating prostate per rectum.
  • Sonography shows enlarged glands and size shape and echotexture are to some extent helpful indicator of malignancy
  • PSA test -Prostate Specific Antigen if elevated it indicates probablilty of malignancy though not specific but many its most of the times elevated in patient with malignancy but it is not specific to it as patients without malignancy also many times shows elevated levels but in maligmamt cases its much more frequent.
  • PSA should not be done few days after sonography as its observed that PSA levels tend to alter after sonography.
  • Biopsy to rule out malignancy in cases where the USG report shows unusually enlarged prostate or abnormal shape or echotexture or changes in surrounding tissues or elevated PSA levels or in patients with unusual symptoms.
  • CT scan may be required in severe cases with complications and or doubt of malignancy.

Homoeopathic Medicines for Benign Prostatic Hypertrophy BPH

  • Sabal Serrulata
  • Chimaphilla
  • Conium Maculatum
  • Phytolacca Decandra
  • Kalium Muriaticum
  • Ustillago
  • Baryta Carbonica
  • Baryta Muriaticum
  • Calcarea Fluorica

VITAMIN D DEFICIENCY HYPOVITAMINOSIS D

Vitamin D Deficiency is also called as Hypovitaminosis D and is very common form of nutritional deficiency and it is closely associated with calcium level in blood as it plays a major role in calcium regulation in body.

Vitamin D also called Cholecalciferol is a Fat Soluble Vitamin produced naturally in skin where a precursor 7-Dehydrocholestrol is converted into Pre- Cholecalciferol through conrotatory pathway when exposed to Ultra Violet B (UV-B) rays present in sunrays having wavelenght between 290nm-315nm causing electrocyclic reaction with optimal synthesis between 295nm-300nm when exposed for several minutes to form an equilibrium.

This Pre-cholecalciferol finally undergoes (1,7) antarafacial sigmatropic rearrangement to finally isomerize into cholecalciferol, which an inactive form of Vitamin D.

Cholecalciferol further undergoes Hydroxylation in Liver whith help of 25-Hydroxylase in Hepatocytes and is converted to 25-Hydroxycholecalciferol(Calcifediol) which is an inactive form.

Calcifediol further undergoes Hydroxylation in kidney with help of 1-α-Hydroxylase to form (1,25)dihydroxycholecalciferol(Calcitriol) which is an active form of Vitamin D. Parathyroid hormone tightly regulates amount of active Vitamin D circulating in blood by controlled activation of 1-α-hydroxylase.

Vitamin D Deficiency is usually caused due to

  • Insufficient exposure to Ultra Violet B radiation from Sun. Person with  dark skin colour are more prone to its deficiency as melanin pigment absorbs UVB and doesnt let it penetrate in skin sufficient enough to activation Vitamin D synthesis. also use of sunscreen peeparations doesnt let sufficient penetration of UVB. Also time and period of exposure, altitude, longitude presence of clouds type of clothing worn by person etc determines its amount of absorption and penetration in skin.
  • Insufficient dietary in take of Vitamin D.
  • Cholecalciferol(Vitamin D) is converted into 25-Hydroxycholecalciferol in liver. In certain liver diseases this step of metabolism is disturbed and vitamin D is not converted into 25-Hydroxycholecalciferol(Calcifediol).
  • 25-Hydroxycholecalciferol(Calcifediol) is further converted into active form that is 1,25-Dihydroxycholecalciferol(Calcitriol) in kidney, certain kidney disease hampers this conversion.

Vitamin D deficiency Symptoms

Vitamin D Deficiency shows not only shows symptoms of its deficiency but also symptoms of calcium deficiency in most cases.

  • Osteomalacia
  • Osteoporosis
  • Triggers Osteoarthritis
  • Rickets
  • Periodontitis
  • Paraesthesia
  • Myalgia
  • Tetany
  • Pre-eclampsia
  • Light-Headedness
  • Depression

Vitamin D Deficiency Diagnosis 

Vitamin D Deficiency is diagnosed by measuring level of 25-hydroxycholecalciferol in blood.

Normal level of Vitamin D in blood should range between 30-100ng/ml below this upto 20ng is considered as insufficiency and level below 20 ng is considered as Vitamin D Deficiency.

Sources of Vitamin D

  • Exposure of Skin to Sunlight
  • Fish
  • Eggs
  • Mushrooms
  • Fortified Milk and other food products like oats bread Fortified with Vitamin D.
  • Suppliments are available in both oral and injectible forms.

Excess intake of Vitamin D causes Nausea, Vomitting, Constipation , Confussion, Weakness, Kidney stones(urolithiasis).

Also read following related articles

CALCIUM DEFICIENCY

OSTEOPOROSIS

RICKETS

CALCIUM DEFICIENCY

Calcium Deficiency as commonly used  is an ambiguous and misleading term as it may refer to two conditions Dietary Insufficiency without evident Hyopcalcaemia or Hypocalcaemia without Dietary Insufficiency of Calcium both have different Causes and Implications.

Hypocalceamia means reduced calcium level in blood serum below average range of 8.8-10.7 mg/dl.

Calcium is very essential element in human body and is required for maintaining proper anatomical structure and physiological functions in human body, at cellular level of almost all tissue/ organ.

Serum Calcium levels are not indicative of general chornic calcium deficiency/insufficiency, as per body’s requirements,  as  Blood Serum Calcium levels are very tightly maintained in human body within a narrow range. If there is dietary insufficiency then it may not reflect in Blood Serum Levels as the body comprimises Bone Mineral Density to maintain normal Blood Serum Calcium levels as it is more important so as to maintain proper function of other organs and cells especially heart and nerves and other cellular processes as any disturbance in this due to low blood serum calcium level may cause severe acute life threatenig conditions.

Regular intake of calcium is necessary for proper functioning of the body, If there is dietary insufficiency of calcium then the body starts consuming it from bones to maintain normal Blood Serum Calcium level, this depletes the Bone Mineral Density which if prolonged may result into conditions like

  • Osteomalacia
  • Osteoporosis
  • May trigger or contribute to Osteoarthritis.
  • Rickets with pigeon chest open sutures and fontanalles and other anomalies in growing children.

Hypocalcaemia is a severe acute condition usually caused due to deficient calcium metabolism which is regulated by Parathyroid hormone , vitaminD and also healthy functioning of organs like liver and kidney are required for proper calcium metabolism.

Symptoms of Hyopcalceamia

Positive Bathmotropic Effect

As calcium blocks sodium channel which maintains the threshold level of depolarisation of nerve and muscle So, decreased level of calcium will decrease the threshold level for depolarisation which will result in to Positive Bathmotive Effect

Petechea

Recurrent Petechial Heamorrhages which if persists, it tends to overlace and merge with each other appearing like purpura , it appears espescially on weight bearing and dependent parts.

Paraesthesia

Tingling and numb sensation on face especially in perioral region and in limbs on extremities like fingers spreading to hands and toes spreading to feet

Myalgia

Muscular pain especially in lower limbs, its may also accompany paraesthesia.

Tetany

Painful and violent muscular cramps and contractions generalised or may be redtricted to carpopedal region.Positive Trousseau’s  and or Chvostek’s sign for Latent Tetany

Cardiac Symptoms

  • Decreased Chronotropic and Inotropic effect that is reduced heart rate and Myocardial Cantractibility.
  • Which causes decreased cardiac output.
  • ECG shows associated changes like intermittent QT prolongation, typical Ventricular Tachycardia.

Causes

  • Hypoparathyroidism
  • Low Vit D
  • Low dietary intake of calcium
  • Other pathological conditions like kidney or pancrease disease etc.

Homoeopathic Medicines for Calcium Deficiency or Hypocalcaemia

  • Calcarea Carbonica
  • Calcarea Phosphorica
  • Calcarea Fluorica
  • Silicea
  • Magnesia Carbonica
  • Magnesia Muriaticum
  • Magnesia Phosphorica
  • Zincum Metallicum
  • Natrum Mur
  • Natrum Phos
  • Kalium phos

RICKETS

VITAMIN D DEFICIENCY HYPOVITAMINOSIS D

 

OSTEOPOROSIS