Diabetes type 2 can be cured

ype 2 diabetes is characterized by peripheral insulin resistance with an insulin-secretory defect that varies in severity. For type 2 diabetes mellitus to develop, both defects must exist: all overweight individuals have insulin resistance, but only those with an inability to increase beta-cell production of insulin, proportionate to insulin resistance develop diabetes type 2.

For eg if the required insulin is 100% and if there is no insulin resistance, no need of additional insulin secretion by pancreas, on the other hand if there is 30% insulin resistance then beta cells has to secrete additional 30%, so total insulin will be 70% normal insulin, 30% resistance insulin and other 30% additional insulin, so totally 130%. Usually beta cells can produce up to 60-80% additional insulin, when the insulin resistance crosses this level diabetes type 2 results in.

This process is influenced by genetic factor, life style, occupational hazards, stress, and many other multi factors.

How the modern medicine works in Diabetes type 2:

Most of the modern medicines by enzymatic actions influence the excess synthesis of insulin. The main drawback is normally insulin is released once in 5 minutes, immediately after taking food etc. But when hypoglycemic drugs were taken this will be released at once, that is why even today controlling diabetes just by taking hypoglycemic drug is always not so easy.

What should be the treatment?

Improving the insulin resistance is the treatment.

How this can be achieved?

By starvation and exercise.

Whether this will harm?

If this starvation is done systematically, this can be achieved without harming our body.

What exactly starvation means?

Here starvation means reducing carbohydrate to less than 40% in our diet. Only complex carbohydrates should be taken those with low glycemic index and high fibre content. Proprotionat mono unsaturated fat and protein should be added to the diet.

Here fat should be in higher side to protect brain. Those who are lean must take excess of fat to protect brain. Other than glucose, ketone body is the only source of energy for brain. When scarcity for carbohydrate occurs, at first insulin stimulates fat breakdown, which releases fatty acids, triglycerides and ketone bodies. Hence in obese patients no need to take excess fat.

Diet must include atleast 350 to 550 ml of milk in vegetarians and fish or meat in non vegetarians. Red meat is better but taking fish with little red meat is better.

Abundant green vegetables and low calorie vegetables should be taken.

Direct glucose, sucrose etc should be reduced to zero. Daily exercise brisk walking for more than 20 minutes.

The above diet should be continued for 1.5 years, positive result can be seen within three weeks, reversal can be seen after 6th or 8th month. But we don’t know exactly in whom reversal is possible and in whom it is not possible.

Is there any patients who already did this diet?

Yes we have totally four patients who got cured of the condition.

One is myself. I found diabetic at the age of 32. I became panic and started aggressive diet. My RBS was 240. Immediately after starting diet it came to 160-180, fasting ot 128-135 mg/dl. I continued the diet and I was observing my FBS almost on alternate days and PPBS once in 15 days. Gradually my FBS started falling down like 124 for 15-30 days then to 110-115 level, then to 100-110 level and after 8th month FBS was always between 70 and 80mg/dl. I continued the same diet for 1.5 years. During this period my weight fell down to 58 kg form 72kg. Then I stopped the diet and started taking all sweets and normal foods and in the same diet since then. Now my weight is 66-66.5 kg. Now FBS usually between 90-102, and PPBS always between 110-128mg/dl. Along with diet I also took Diabenil tablet our own preparation with more than 18 herbs and Jasada bhasma.

We conducted free diabetes cure camp about 1.5 years back. 70 patients were attended and only 16 patients could start the diet and only 3 patients could continue the diet beyond 3 weeks. All the three got cured, aged 51, 53 and 65 yr old - female, female and male patient.

But this can not be applied for Type 1 diabetes where only external insulin is the hope for the patient.

Jayagovinda Ukkinadka

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KAMALA/ Jaundice can not be a disease but a symptom

In Ayurvreda Kamala is considered as a disease, where there will be yellowish discoloration of skin, urine and mucosa. In Ayurveda Pandu and Kamala is explained in a same chapter. It is explained as, Pandu in due course if not treated will result in Kamala. This is excellent explanation available in Ayurveda. In Ayurveda mainly two types of Jaundice is explained, but in the modern science three types of Jaundice is explained.

In Ayurveda Kamala is a disease but as science advanced now Kamala is considered as just a symptom, where this condition is seen in different diseases like Malaria, Dengue fever, Leptosopirosis, Haemolytic anaemia, Amoebic liver abscess, Viral and bacterial hepatitis, Hydatid cyst, Cirrhosis of the liver, Hepatoma, Metastasis in Liver, Malignancy of head of pancreas obstructing the common bile duct, gall stone impacted in common bile duct and so on.

Bilirubin:

It is very important to understand the mode of production and function of bilirubin.

Haemoglobin when breaks down will form Haem+globin. Where haem is iron, which is partially reutilised for the production of haemoglobin, and rest is excreted. Globin is a protein, after breakdown one of the end products is biliverdin and after four levels of enzymatic action will be converted in to unconjugated bilirubin. This unconjugated bilirubin is not soluble in water and commonly known as indirect bilirubin.

The unconjugated bilirubin, in blood stream when enters liver will be converted in to conjugated bilirubin commonly known as direct bilirubin, which is water soluble and some portion of Bilirubin is destroyed in the liver. This conjugated bilirubin will be secreted into intestine through common bile duct and is called as stercobilinogen. Here this will color the stool and 95% of the same will be reabsorbed to blood stream. This in turn in circulation will enter the kidney and is called as urobilinogen and here also this will colour the urine and other 95% will be reabsorbed to blood stream and later most of it will be destroyed in the liver.

So the main function of Bilirubin is colouring the stool and urine. But this is a very good marker to identify Liver diseases, to asses over destruction of RBCs and any obstruction in common bile duct. Further to understand this it is very important to understand three types of Jaundice.

Three types of Jaundice:

Prehepatic Jaundice- Here due to over destruction of RBCs there will be excess production of unconjugated biiirubin and liver fails to convert this excess uncojugated to conjugated one, so there will be high indirect bilirubin in the blood stream. But direct bilirubin will be normal or slightly elevated. In this variety usually color of urine will be normal because unconjugated bilirubin is not water soluble.

Hepatic Jaundice- Here liver fails to completely conjugate the unconjugated bilirubin and fails to destroy the conjuagated bilirubin due to liver disorder, so both direct and indirect bilirubin will be elevated

.

Post hepatic jaundice- Here unconjuagated bilirubin will be normal but destruction of conjugated bilirubin will be delayed because of obstruction in common bile duct, so only direct bilirubin will be elevated. Colour of stool will be whitish, thick and sticky.

By understanding the above differences it is very easy to understand the site of pathology. After identifying the type of jaundice we have to search for the root cause of jaundice.

In diseases like Malaria, Dengue fever, the cause for jaundice is excess destruction of RBCs, but in Leptospirosis cause is hepatitis, so it is very important to identify the type of jaundice along with other criteria in patients with suspected dengue or leptospirosis. In amoebic liver abscess there will be high fever along with tenderness over liver area, fever will be usually along with rigors. In all viral hepatitis the typical onset will be with fever and vomiting followed by jaundice, fever and vomiting usually persists for 3-5 days, afterwards which subsides spontaneously and in Hepatitis A jaundice will subiside within 15-20 days, in Hep B, 50% will be subsided and cured in the same way and other 48% will continue as carriers, and 2% will die due to hepatic failure, in Hep C immediate fatal rate is low but carrier possibility is same as in Hep B, in Hep D it is same as A, and in Hep E Jaundice will usually last for 3 months and then subsides.

In our area we come across with many jaundice patients because almost all people both educated and illiterate people of this place believe that Ayurveda is the only remedy for Jaundice and I had to refer many cases of Malaria, some of dengue, one case of Leptospirosis and amoebic liver abscess to higher instituition and many other condition we could manage with Ayurveda medicines.

But in Viral hepatitis really we treat the self limiting condition with Ayurveda medicines and people believe that Jaundice is cured because of our medicine, even many Ayurvedists claim in that way. But any how even in hepatitis A 0.07% of patients die due to hepatic failure, so complete bed rest low fat, low protein and carbohydrate rich diet should be advised to the patient for fast recovery and even we many times feel that patient recovers fast when treated with Ayurveda medicines. I have treated three cases of Hepatitis E during last 12.5 years, in all the three jaundice recovered after 1.5 to 3 months period, which is really the normal course of the illness. I have treated many cases of chronic carriers of Hepatitis B, but I have not seen even single patient with negative HBsAg after Ayurveda treatment. (here we can consider only chronic carriers, not the recent below one year, because in many carriers HBsAg becomes negative after one year spontaneously)

But we have seen very good result in many cases of Cirhosis of the liver. I can give two very good eg of Cirhosis, one patient with cirrhosis of liver with portal hypertension took treatment for one year and had very good symptomatic recovery and the condition recovered after 7 years and that time his condition became worse and died after 3 months. In this case, doctors in KMC Mangalore had given 6 months deadline for his survival, but with Ayurvedic medicines he recovered miraculously and survived for the next seven years without any problem. But he was not in the state of hepatic failure during the first visit. I have also advised him to take vaso dilators for long time to prevent easophageal varices, and advised for endscopy twice during the seven years, but he has had not developed oesophageal varices even after seven years, but he died due to hepatic failure. Another important thing is he was not alcoholic nor he was obese, his lipid profile tests were normal, so the cause could be genetic.

In another case, he was alcoholic very young of about 34years of age, when he visited my clinic he was in stage of hepatic failure and was using antibiotics continuously to prevent intestinal infection and his haemoglobin level used to fall down below six once in twenty days, was regularly going for blood transfusion. After 5.5 months treatment he required no blood transfusion, he started doing his work of catering, recovered well and he could manage his work for next 6 months, but in between he started taking alcohol and once again the condition aggravated came back for treatment but this time condition became worst and died in modern hospital.

As per our record these two are the best observed result in cirrhosis of the liver. We have treated number of cases of cirrhosis, but most of the cases in end stage, but in above two cases we got very good result in end stage. In the second case he could stop blood transfusion after 5.5 months of treatment; even I could not believe that.

So we have very good scope in treating cirrhosis like organ failure illness and can improve the condition. But mere two or 3 case is not sufficient to prove the efficacy of drug, we need lot of research activities to prove the action of drug in liver diseases. There are more than 50 herbs identified as liver tonics, and we have to show the real efficacy of these herbs through evidence based analysis, which will help not only the patients but also the Ayurvedic doctors.

I remember a word of one scholar he was of the opinion that, if we conduct such research activities and prove the efficacy of such herbs then modern physicians can easily prescribe Ayurveda medicines in many diseases, but what I say is, if this really happens then we have to consider this as our victory, because our treatment should be acceptable by all and should be result oriented. Otherwise prescribing Ayurveda medicines will be difficult, not only to allopathic physicians but also for Ayurvedic doctors.

Jayagovinda Ukkinadka
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A tough disease to treat: FIBROMYALGIA

"Fibromyalgia is a name in search of a meaning."

-Anonymous Canadian rheumatologist

Fibromyalgia syndrome (FMS) is a specific, chronic non-degenerative, non-progressive, noninflammatory, truly systemic pain condition. Diseases have known causes and well-understood mechanisms for producing symptoms. FMS is a syndrome, which means it is a specific set of signs and symptoms that occur together. This in no way means that fibromyalgia is any less serious or potentially disabling than a disease. Rheumatoid arthritis, lupus, and other serious afflictions are also classified as syndromes.

Sleep disorders. Inflammatory cell abnormalities. A small fiber neuropathy. There is evidence suggesting that these conditions, along with many others, are associated with what is often diagnosed as fibromyalgia. In particular, sleep apnea and chronic hypoxia to the brain's pain centers were frequently proposed by readers as potential inciters of fibromyalgia symptoms, and a number of commenters recommended ordering a sleep study in patients in whom the condition is suspected.

A family practice doctor of osteopathy wrote: "After finishing residency I was bombarded with patients who had tender points and the diagnosis of fibromyalgia. I started to screen [them] for sleep apnea and was flabbergasted at the number of patients who had hypoxic/apneic episodes at night. Now, after several years of screening patients, about 75% of my patients diagnosed with fibromyalgia have nocturnal oxygen or a CPAP [continuous positive airway pressure] machine."

And then there was inflammation. As one reader pointed out, a 2010 article from Clinical Rheumatology suggests that mast cells (MCs) may play a key role in the condition. The study reported significantly increased MC counts in the papillary dermis of patients with fibromyalgia. The authors wrote: "MCs are present in skin and mucosal surfaces throughout the human body, and are easily stimulated by a number of physical, psychological, and chemical triggers to degranulate, releasing several proinflammatory products which are able to generate nervous peripheral stimuli causing CNS [central nervous system] hypersensitivity, local, and systemic symptoms."

A recent abstract presented at the International Association for the Study of Pain's 2010 conference in Montreal, Quebec, Canada, reported that patients with fibromyalgia have more symptoms of depression and alterations in peripheral and central nervous pain pathways compared with healthy individuals. A neurologist commented, "[Fibromyalgia] symptoms are the same as in small fiber neuropathy, and amenable to the same treatments. [This] study reports that patients with fibromyalgia have decreased epidermal nerve fiber density, as in small fiber neuropathy." Another neurologist suggested "testing patients for small fiber neuropathy before telling them anything."

Fibromyalgia is considered as pain due to over stimulation, over sensitivity to pain.

(copied from emedicine artilcles (medscape.com), small portion of article)

Even though there is no definite criteria for diagnosis, eleven tender points out of 18 points, sleepless ness, extreme bodyache, anxiety, triggering of pain by infection, stress etc, spontaneous remission and exacerbation makes the diagnosis.

In Ukkinadkas Ayurveda:

We have treated number of fibromyalgia cases some with good results, some with temporary results, some with satisfactory results and some with no results. We have treated many patients in OP and in IP levels.

Shastikashali pindasweda gives imminent result but later usually pain reccurs after heavy work.

We have also tried with Pindasweda and Dhara, and shodhana treatments in many, the immediate response from patient was excellent in most of the patients, some patients had good recovery, there was no recurrence of pain and they could manage their routine without much pain, but some patients with all these medicines and follow up medicines, their pain aggravated when they started their routine works.

But recently surprisingly we got very good result with our new product developed for skin allergies, tablet Ukkinadkas Alaril. Accidentally we came to know that this works in fibromyalgia, we have treated more than six cases of FMS with this tablet with satisfactory result. None of the patients had undergone any of pre panchakarma or panchakarma procedures. But to conclude this result we need another 50 to 60 patients of Fibromyalgia. We have administered tablet Ukkinadkas Alaril aong with other vathahara combinations(usually we prescribe Maharasnadi, Rasnadi, Sahacharadi, Prasaranyadi, Erandadi gana kwatha, Vamshatwagadi kwatha, …….. depending up on the severity and symptoms, many times we also add herbal antipsychotic and tranquilisers with good result, guggulu preparations, sometimes rasa preparations, in case if we note mild inflammatory signs which is not a common sign in FMS)

Also it is very difficult to find a similar disease mentioned in Ayurveda. But we can well correlate with the Samanya lakshana of AMAVATHA for Fibromyalgia. I request all the doctors to share your experience and your view regarding Fibromyalgia.

Jayagovinda Ukkinadka
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Rheumatoid Arthritis/ Rakthavatha of Charaka

FREQUENCY

Approximately 12 to 15 million people in India are suffering from RA

70 to 90 million suffering world wide

Female to male ratio is 4:1

Age of onset is usually 25 to 50 years, peak during 4th and 5th decade

Juvenile arthritis, named when occurs below the age of 16, 3 phases- polyarticular, pauciarticular, and systemic.

CAUSES

Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown etiology involving primarily the synovial membrane and articular structures of multiple joint.

Associated factors may include

1. Genetic predisposition
2. Female sex
3. Psychological stress
4. Immune response
5. Hormone interaction
6. Viral infection

PATHOPHYSIOLOGY

In short

Patho physiology of RA is not well understood

Factors associated with RA include possibility of

1. Infectious triggers
2. Genetic predisposition
3. Autoimmune response

The disease course may be short and limited or progressive and severe

SIGHNS AND SYMPTOMS

Pain & morning stiffness in the smaller joints of the hands & feet.

Joints of wrist, elbows, shoulders, knees & ankles are also affected.

Symmetrical involvement of the joints.        

Patient feels tired & unwell.

Pain & stiffness are worse in morning & patient gets little relief with gentle activity.

Disturbed sleep.

Joints will be warm & tender with swelling.

Deformities & rheumatic nodules develop as the disease progresses.

Other extra articular symptoms may develop.

DIAGNOSTIC CRITERIAS

Morning stiffness for more than 1 hour.

Arthritis of 3 or more joints with tenderness & symmetric involvement.

Arthritis of hand joints & wrists

Above symptoms for 6 weeks or more.

Subcutaneous nodules & deformities.

Positive serum RA factor.

Radiographic evidence of RA.

Presence of four or more above criterias – confirms the diagnosis of RA.

INVESTIGATIONS

HB, TOTAL COUNT, DIFFERENTIAL COUNT, ESR.

CCP ANTIBODIES

RHEUMATOID FACTOR

C REACTIVE PROTIEN

X RAY OF AFFECTED JOINTS

IMMUNOGLOBULINS

PLATELET COUNT

DIFFERENTIAL DIAGNOSIS

Systemic Lupus Erythematosus

Rheumatic fever

Gout and Pseudogout

Inflammatory Bowel Disease

Polymyositis

Psoriasis

Carpal Tunnel Syndrome

Sarcoidosis

Sjogren Syndrome

Amyloidosis

Osteoarthritis (erosive)

Tendonitis

Tenosynovitis

Polyarteritis nodosa

Viral arthritis (eg, rubella, hepatitis B, parvovirus)

Scleroderma

Paraneoplastic syndromes

Multicentric reticulohistiocytosis

Cauda Equina Syndrome

Costochondritis

Polymyalgia Rheumatica

These are the main there are still more

TREATMENT IN MODERN MEDICINE

NSAID’S

Ibuprofen

Indomethacin etc

Disadvantage: Risk of gastritis, internal bleeding, nephrotic syndrome, glmerulo nephritis by short term or long term use.

Cox-2 inhibitors

Celecoxib: action similer to NSAID’s but with less adverse affects.

GOLD COMPOUNDS

Auranofin.

Disadvantage: Dermatitis, stomatitis, protenuria, cytopenia. Exacerbation after due course.

ANTI MALARIAL AGENTS

Comparitively safe but action seen is not the same in all, very slow, majority of the patients not benefited.

DISEASE MODIFYING AGENTS

Methotrexate: A well known, said to be the most effective immune modifying agent , widely used in present practice.

Disadvantage: MTX has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems. So should be used with caution. May become fatal if co administered with NSAID’s

Sulfasalazine: Another immune modifying agent usually co administered with methotrexate.

Disadvantage: weak action, but toxic.

IMMUNOSUPPRESSANT AGENTS

TNF alfa inhibitors:

Eg: Infliximab, Etanercept

T-cell inhibitor

Abatacept

Disadvantage: Although these medicines improves the clinical symptoms, and stops the progression, the major disadvantage is serious infection and malignancies.

CORTICO STEROIDS

Prednisolone

Disadvantage: Reduces the symptoms, but not the damage and progression.Risk of serious side affects makes it very difficult to administer for long term and also this will not check the progression.

OVERALL DISADVANTAGE WITH MODERN MEDICINES

All the medicines mentioned do not give definite improvement. Exacerbation of the symptoms during the course of treatment is very common, and the same medicine may not work further.

Adverse affects of DMRD drugs like Methotrexate which is hepatotoxic, neurotoxic and nephrotoxic many times forced to stop medication du to adverse reactioins.

Immuno modulators like TNF alfa inhibitors, T cell inhibitors etc almost always ends with severe infection, and sometimes malignancy.

IgM, IgG, IgA, IgE RF ISOTYPES

n      Role of genetic factors in the regulation of RF isotype level production

n      HLA-DR3 & DR4 antigen was associated with low IgA RF

n      HLA-DR1 & DR2 antigen was associated with high IgA RF, IgM RF, AND IgE RF

n      IgM RF was positive in almost all sero positive patients and most of seronegative.

n      IgA RF was negative in sero negative patients but was mostly positive in other groups .

n      Patients with negative IgM and IgA RF had incactive or recent RA.

n      Anti nucleic antibodies with the highest values were significantly associated with high levels of IgM and IgA RF.

n      Almost all patents with extra articular features had higher level positive IgA, IgM, IgE RF when compared with RA without extra articular symptoms

n      Most of the researchers believe that IgA RF is associated with RA with poor prognosis and systemic symptoms.

n      IgE RF is associated with poor prognosis but without extra articular involvement.

POSSIBLE VARIETIES OF RA WHICH MAY HELP IN AYURVEDIC TREATMENT

n      IgG RF

n      IgM RF

n      IgA RF

n      IgE RF

n      COMBINED ISOTOPES (IgA & IgG etc.)

n      SERO POSITIVE

n      SERO NEGATIVE

n      RA WITH HIGH ESR WITH SEVERE SYMTPOMS

n      RA WITH CONSTANT LOW ESR WITH SEVERE SYMPTOMS

n      RA WITH EXTRA ARTICULAR SYMPTOMS

n      RA WITHOUT EXTRA ARTICULAR SYMPTOMS

n      RA WITH ORGAN INVOLVEMENT (ENDOCARDITIS,NEPHRITIS,VASCULITIS etc)

n      IgG, M, A, OR E DOMINANT IMMUNOGLOBULINS

n      OR RELATION BETWEEN ANY OF THE ABOVE GROUPS.

n      ANA POSITIVE(LOW TITRE) RA GROUP

n      HLA DR 1

n      HLA DR 2

n      HLA DR 3

n      HLA DR 4

We have filtered these to 16 varieties to consider the treatment. Right now, no facility to do Ig RF tests in near by place.

RA IN AYURVEDA- RAKTHAVATHA AND AMAVATHA

n      VATHARAKTHA & AMAVATHA are the two diseases where we see many similarities with the symptomatology.

n      Amavatha is a disease mentioned only in laghu thrayees that is after the 7th century, not mentioned in the previous texts.

n      Vatha raktha is the only disease mentioned in Brihath thrayees that can be co related with RA.

VATHARAKTHA- DIFFERENCE OF OPENION AMONG SCHOLARS

n      It seems that explanation regarding vatharaktha in Charaka and Sushrutha school of thought is different.

n      Lot of difference is there in the symptomatology.

n      Charaka mentions a joint condition whereas Sushrutha explains Vatharaktha briefly, but he has not given importance to the involvement of multiple joints nowhere mentioned the involvement of joint, but explains symptoms related with skin lesion, which is painful, reddish, with swelling and burning sensation or whitish with itching. But the main site of lesion is mainly feet, but sometimes hands, and symptom may spread to whole body as poisonous rat bite.

n      While explaining the symptoms he says that there may be severe tenderness at the site of lesion or sometimes numbness.

n      Sushrutha while explaining incurable vathashonitha, says that, if the lesion spreads up to knee (from foot), and ulcerates with secretion of serum, blood and pus & in case of muscle wasting & in a debilitated person,it is incurable. So here he clearly mentions ulceration in the leg, from foot up to knee as a complication and also incurable.

  

GAMBHIRA and UTHANA Vatharaktha are not two types according to Sushrutha

n      Sushrutha says that gambhira and Uthana are not two types of vatharaktha, but two stages of disease. This may be because Sushrutha was explaining skin condition with regards to ulcer and its stage as superficial and deep. Charakas two types depending upon the severity of illness as seen in RA.

n      So Sushruthas explanation may not be related with RA, or he may not have given much importance to vathashonitha as his main subject was surgery.

n      Hence explanation of Sushrutha holds good for Gout, Pseudogout, Peripheral vascular obstruction,ischemic ulcers,  venous ulcers etc.

n      Hence here we consider Vatharaktha of charaka as a co relative study to RA and also AMAVATHA.

WHY VATHARAKTHA IS RA?

THASYA STHANAM KARAU PADAVANGULYAHA SARVASANDHAYAHA.

HASTHAPADE THU MOOLAM- DEHE VIDHAVATHI. Charaka samhitha chi. Sthana.

n      Leading symptoms seen in sandhis, mainly phalangeal joints and toes, and then multiple joints.

VATHARAKTHA- CLINICAL FEATURES

n      Multiple joint pain

n      Pricking pain

n      Tenderness

n      Reccurent exacerbation and remission

n      Malaise

n      Formation of nodules

n      Skin rashes, excessive or no sweating, tingling and itching sensation over joints.

n      Joint deformities, stiffness, rigidity

n      In gambhira vatharaktha, pain is severe and paka usually occurs.

n      Almost all the features of RA is explained except morning stiffness and symmetrical involvement, which is also a diagnostic criteria to consider RA.

n      Extra articular symptoms like necrotic ulcers(paka) as seen in vasculitis, mandalothpatti (butterfly rash in sle), visarpa (skin lesions with bullous ulcers, necrotic or gangrenous ulcers with systemic symptoms)

n      So considering all the criterias, RA comes under vatharaktha of Charaka and all differential diagnosis of RA should also be considered under vatharaktha.

AMAVATHA FEATURES

n      Bodyache, anorexia, malaise, heavyness, fever, lightness of the body are the common features.

n      Paka is not the symptom of amavatha (apakaha)

n      Multiple joint pain

n      Excessive urination

n      Abd distension etc are the other features.

Amavatha is mild and mild to moderate RA (and also fibromyalgia)

n      In amavatha extra articular symptoms with systemic involvemnt is not explained as in vatharaktha

n      But grahani (?enteric arthritis), abdominal pain, vomitting is said as upadrava

n      Amavatha with involvement of almost all the joints, swelling, and tridosha are considered as difficult to cure. With single dosha as sadhya, and two dosha as yapya.

n      So there is no asadhya amavatha explained in the text as in vatharaktha, vatharaktha with tridosha involvement and upadravas are asadhya.

RA AND Ukkinadkas Ayurveda

n      In our hospital we have treated more than 2800 cases of RA since last 13 years, and started keen observation since 8 years. But detailed documentation was not done. 90% of the observation is in OP level, and few of the patients might have belonged to Ankylosing spondylitis and such other collagen disorders.

For the better management we have classified RA under 3 catagories.

n      MILD (laghu) RA

n      MODERATE (madhyama) RA

n      SEVERE (theevra)RA

WHAT IS MILD RA?

n      The symptoms are similar as explained before, but the deformity of joints will not be seen even after a very lengthy course of the disease. And response to the Ayurvedic treatment is very fast, like 1 to 3 weeks. The symptoms will be reduced to ¾ th with in 1 or 3 weeks.  (? NEGATIVE IgA & IgM RF TYPE OF RA)

WHAT IS MODERATE RA?

n      In this condition also the symptoms are similar as explained earlier, but the severity of pain & other symptoms will be severe. In this case also there will not be any deformities even after a very lengthy course, but the response to the Ayurvedic treatment is slow when compared with mild RA. (? Ig E RF TYPE OF RA)

WHAT IS SEVERE RA?

n      In this condition the signs & symptoms are very severe & most of the times deformity is seen within 6 months of onset of symptoms & the sufferings (pain & systemic manifestations) are more in this variety of RA. The response to Ayurvedic treatment is poor & slow. (? IgA RF TYPE OF RA)

HOW WE TREAT THE PATIENTS?

n      In our Hospital, mild & moderate RA cases are treated as out patients.

    In mild & moderate cases we prescribe-Kashaya powder or Liquid kashayas, Herbal & Herbo-mineral tablets internally, and in moderate cases we add lehyas and herbal powder according to the need. For external application we use Lepa powders or oils  according to the need.         

IN SEVERE & CHRONIC CASES

n      In these types of patients we hospitalise the patient for three weeks in our hospital for the panchakarma treatments, which gives very good result particular group of the severe and severe to moderate cases of RA.

n      Internally we prescribe-Kashaya powder or concentrated Liquid kashayas, Herbal & Herbo-mineral tablets, lehyas and herbal powder according to the need. For external application we use Lepa powders or oils according to the need.

RESULTS OF TREATMENT

MILD RA-

n      60% of RA patients visiting our hospital comes under this group

n      Shamanoushadhis & patient education

n      Short course, multi drug combination is preferred, low dosage is usually sufficient.

n      Result is seen within 3 weeks in almost all cases (90-100%).

n      Course of the treatment usually varies from 3 months up to 1 year.

MODERATE RA           

n      25% of the patients visiting our hospital comes under this group

n      Shamanoushadhi, preferably combinations with potent medicines like rasna panchaka , in higher dose, but not multi drug combinations like maharasnadi.

n      In moderate to severe cases panchakarma is preferred.

n      Good result was seen within 1.5 to 4 months in 60-80% of the patients.

n      Course of the treatment usually varies from 6 months up to 2 years or more.

SEVERE RA

15% of total RA cases visiting our hospital come under this group.

n      Very difficult to treat.

n      As deformities occur very fast, risk of systemic involvement, organ damage, and delayed action makes the treatment much difficult.

n      But still with the shamanoushadhis we get very good result in about 15 to 20 % of severe RA and moderate result in other 20% of cases. But rest of the severe RA patients develop joint deformities very fast and in such patients we have tried with the combination of shamanoushadhis and panchakarma, the response was very good and many patients who had no response earlier started improving, so now a days in severe RA we start with panchakarma treatment and the overall result raised up to 40%.

n      In rest of the severe RA patients prognosis was poor with Ayurvedic medicines alone. But integrated approach was beneficial in about another 30% of the patient

n      Course of the treatment is 2 to 5 years, may extend up to life time also in this group.

SEVERE RA & INTEGRATED APPROACH WITH DMRD

n      Since last 2 years in severe RA trying with integrated approach with DMRD(under rheumatologists prescription), presently we have such many patients under treatment, symptomatic improvement is excellent, but complete withdrawal of modern medicine is not possible in most of the cases because of fear of aggravation. But we noted remarkable improvement with the symptoms, HB and ESR in all cases after starting Ayurvedic medicines.

n      In a female patient aged 28 years, we have successfully reduced the dose of DMRD drugs to 100% with very good result. She was taking TNF alfa inhibitor and suffered from TB. So switched over to other mild DMRD, her symptoms aggravated, then she approached us, treated initially with panchakarma followed by shamanaushadhis for next two years. Now she is working in London without any symptoms and medicines. Another important thing is she had deformity in left elbow, the progression could be stopped and she is devoid of any symptoms of RA now except for the damage which already happened

OTHER INTEGRATED APPROACH

n      In many cases of severe RA with unsatisfactory result, we have tried our medicines along with NSAID’s (Indomethacin 25 mg, 1 OD or BD),.

n      We have observed positive result in many cases after a very long course of treatment, in few cases we could stop the NSAID after long time.

n      Some patients had intermittent exacerbation and required NSAID’s in between.

WHY AYURVEDA IS A SUPERIOR TREATMETN IN MILD AND MODERATE RA?

As per our observation over all –by Ayurvedic management we can control 60% of RA cases very easily with simple treatments, other 25% of patients with some long duration. But another 15% of the patients are the most unfortunate patients with greater difficulties & still we can control the disease in 40% of the severe RA cases.

NEED OF A DEFINITE CURATIVE REMEDY

None of the system gives or claims cure or standardised treatment for RA.

Ayurvedic treatment many times proved to be a superior treatment. But evidence based study in terms of both Ayurveda and modern parameters in a vast group of patient are necessary to assess the effectiveness and safety of the treatment.    

CONCLUSION

n      In modern medicine there is no remedy for mild, mild to moderate and moderate types of RA. Other than NSAID’s, no other medicines are advisable in this stage, none of the medicines reverse the process of auto immunity, but just blocks the chain of auto immunity as well as normal immunity, so it’s systemic adverse affect restricts the use at this stage.(Now a days Rheumatologists suggest use of immunosuppressive from beginning!!)

n      If not treated some mild to moderate & moderate RA may turn in to moderate or moderate to severe RA in due course.

n      So Ayurveda is a treatment of choice for those with mild and mild to moderate and moderate RA.

n      In moderate to severe and severe cases, the main disadvantage of ayurveda.treatment is lack of effective pain killer, controlling  the pain is very important to improve the patients work efficiency.

n      In severe RA- controlling the fast progressive nature and early deformity as early as possible is a challenge in getting good result.

n      Getting result in 30 to 40% of severe RA is really not bad.

n      But in many patients the trial & error method of drug selection & delayed action makes it difficult to treat severe RA cases as the deformity is fast.

n       So by considering the various gene isotopes and other factors, we can try to make the 40% success rate of severe RA to even more. By administering the medicine in a vast group of RA patients, we can study the action of different groups of medicine in patients with different groups of gene isotopes and other factors.

n      Hopefully this may give us some guide to use specific group of medicine in particular type of RA to achieve fast and accurate result in large number of RA patients.

Jayagovinda Ukkinadka
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