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by Alakananda Ma
Life span, complexion, strength, health, enthusiasm, corpulence, luster, immunity, energy, heat processes and vital breath--all these depend on bodily fire. One dies if this fire is extinguished, lives long free from disorders if it is functioning properly, gets ill if it is deranged, hence agni is the root cause of all. (1)
Celiac disease (CD) is an auto-immune gluten sensitive enteropathy and is an important cause of grahani roga or sprue in all parts of the world and among people of all ages. Continuing our discussion of anna vaha srotas, in part one of this article we will consider the epidemiology, pathology and diagnosis of celiac sprue and in part two, next month, we will look at case histories and treatment.
Grahani roga is considered in detailed fashion in the fifteenth chapter of the chikitsasthan of Charak and also in chapter four of Madhav Nidhan. Given the epidemiology of the time, tropical sprue was likely to have been responsible for most cases of grahani roga or malabsorption syndromes when these texts were written. However, in wheat or barley consuming areas of Northern India, Celiac Sprue would have affected a typical three people per thousand (2,3). Today, changing patterns in the epidemiology of CD have resulted in a current estimated prevalence of 1% for this gravely under-diagnosed condition (3,4). Ayurvedic practitioners beware--far more than one percent of your patents will suffer from this condition, firstly because you are getting a cross section of chronically sick individuals rather than of the general population and secondly because you are typically seeing those who have not yet received a satisfactory diagnosis.
What has given rise to the vast increase in CD? Although improved methods of Western diagnosis may account for a fraction of the rise, our changing diet and environment are also culpable (3, 5). These include changes in infant feeding practices (6), high-gluten commercial baby foods, rotavirus infections (gastroenteritis) and higher socio-economic status with its attendant more sterile environment and richer diet. CD is an atmaja or genetic condition occurring mainly among the genetically at-risk population (7) and involves a complex interplay of genetic and environmental factors, inevitably including gluten consumption. CD, like other auto-immune disorders, is 2-3 times more common in women than in men (8). As many as 20-30% of the Western European population carries a genetic risk factor for CD. Although only a small percentage of these individuals may have clinically diagnosed CD, in this author's clinical experience, many more may respond positively to a gluten free (GF) diet. Note the following valuable abstract:
Until recently, celiac disease (CD) was felt to be a rare disease in the United States. The aim of this study was to conduct a systematic review of the prevalence of CD in general Western populations and in populations at high risk for CD. Standard systematic review methodology was used. A literature search was conducted in MEDLINE (1966 to October 2003) and EMBASE (1974 to December 2003) databases. Qualitative and quantitative prevalence estimates were produced after assessing study heterogeneity. The prevalence of CD in general Western populations is close to 1% and is somewhat higher in certain Western European populations. The prevalence of CD in populations at risk for CD is as follows: 3%-6% in type 1 diabetic patients, up to 20% in first-degree relatives, 10%-15% in symptomatic iron-deficiency anemia (IDA), 3%-6% in asymptomatic IDA, and 1%-3% in osteoporosis. The prevalence of CD in patients suspected of having CD varied depending on the reasons for suspecting CD and on whether the study was conducted in a referral center. In general, the prevalence ranged from 5% to 15%, but was up to 50% in symptomatic patients evaluated in a tertiary referral center. CD is a common medical condition. The prevalence is higher still in high-risk groups. Clinicians in a variety of specialties should have a high index of suspicion for the diagnosis of CD and in particular need to pay close attention to the identified high-risk groups ((4).
Celiac disease is diagnosed both in childhood and in adults, particularly in their forties and fifties, with current debate as to whether diagnosis in adult life is a result of late diagnosis or of true adult onset (7).
Pathology and Clinical Presentation
The lively discussion of grahani roga in Charak begins with agni and a detailed description of the digestive process, going on to consider nutrition of the dhatus. Charak then states, "When the weak digestive fire burns the food incompletely it goes either upwards or downwards. When it moves out downward...it is known as grahani roga. In such patients the foods is often half burnt and and the stool is frequent, constipated or liquid. There is presence of thirst, anorexia, abnormal taste in mouth, excessive salivation and feeling of darkness." (9).
Along with this accurate description of the gastro-intestinal rupa of malabsorption syndrome, both Charak and Madhav describe the purva rupa (premonitory symptoms) as thirst, lassitude, debility, burning sensations in the chest, delayed digestion and a feeling of heaviness (10,11).
The discussion in Charak reminds us of the far-reaching implications of CD. Malabsorption can present with typical symptoms in Abhyantara marga (GI tract) resulting from inflammation of the small intestinal mucosa and villous atrophy. However, the cycle of nutrition of the dhatus described in Charak reminds us that CD can present with symptoms of dhatu kshay (depletion of dhatus) such as anemia (rasa/rakta kshay), osteoporosis (asthi kshay) and neurological symptoms (majja kshay). Chronic fatigue and malaise may be indication that the disease process has reached the point of creating ojo kshay (depleted ojas). The pitta inflammatory aspect of CD can manifest in Bahya marga (external pathway) as dermatitis herpetiformis, a skin inflammation and even as pitta ojo vyapad (POV). POV manifestations of CD are seen as an increased incidence of auto-immune disease including auto-immune hepatitis, auto-immune thyroiditis, Addison Disease, inflammatory arthritis, sjogren disease and psoriasis (7).
Currently CD, once seen as a pediatric sprue disorder, is understood to encompass four different rupas (7, 12). Classical CD is usually diagnosed in infancy and shows the rupa described by Charak for sprue. Endoscopy reveals villous atrophy of the intestinal mucosa. In atypical CD, there will be a history of visham agni and other minor GI symptoms, accompanied with symptoms within bahya and madhyama marga such as anemia, osteoporosis, peripheral neuropathy, cognitive disorders, infertility and recurrent miscarriages (13). On endoscopy these patients will not have classic villous atrophy although there will be abnormalities of the mucosa. More difficult still to diagnose is latent CD, which may have mild or intestinal symptoms and possibly extra-intestinal symptoms, with a gradual worsening of the symptom picture later in life. Silent celiac disease may not present any of the typical symptoms associated with CD but patients will complain of apparently unrelated conditions such as malaise, mandagni, fatigue and disorders of mood, behavior or attention, poor performance in school, as well anemia and low bone density (12,13). In Western medicine, these patients may be diagnosed by serological screening tests. For the Ayurvedic practitioner without access to such tests, a three month upashaya or therapeutic trial of gluten free diet (GFD) can be an excellent diagnostic tool. Significant improvement in general health on GFD points to atypical, latent or silent CD as a major cause of the pateints' chronic ill health. This can be confirmed by genetic testing which is available online on a patient ordered basis without need of a physician referral.
Celeac disease should be considered in the diagnosis of gastro-intestinal issues, dhatu kshay, ojo-kshay and pitta ojo vyapd as well as in non-specific malaise and poor health, depression and attention and learing disorders. In the next article we will look at some case summaries and treatment strategies for CD related illnesses.
1. Charak Samhita,Tr. .PV. Sharma Chaukhambha Orientalia Delhi 1994 Chi, XV 3-4
2. Losowsky, M. S. A history of coeliac disease. Dig. Dis. 26, 112-120 (2008).
3. Lohi, S. et al. Increasing prevalence of coeliac disease over time. Aliment. Pharmacol. Ther. 26, 1217-1225 (2007).
4. Dubé, C. et al. The prevalence of celiac disease in average-risk and at-risk Western European populations: a systematic review. Gastroenterology 128 (Suppl. 1), S57-S67 (2005)
5. Vilppula, A. et al. Increasing prevalence and high incidence of celiac disease in elderly people: a population-based study. BMC Gastroenterol. 9, 49 (2009).
6. Norris J et al. (2005) Risk of celiac disease autoimmunity and timing of gluten introduction in the diet of infants at increased risk of the disease. JAMA 19: 2343-2351
7. Greetje J. Tack; Wieke H. M. Verbeek; Marco W. J. Schreurs; Chris J. J. Mulder The Spectrum of Celiac Disease: Epidemiology, Clinical Aspects and Treatment, Nat Rev Gastroenterol Hepatol. 2010;7(4):204-213.
8. Jacobson, D. L., Gange, S. J., Rose, N. R. & Graham, N. M. Epidemiology and estimated population burden of selected autoimmune diseases in the United States. Clin. Immunol. Immunopathol. 84, 223-243 (1997).
9. Charak, op cit, Chi. XV 51-54.
10. ibid v 55
11. Madhav Nidhan tr. KR Srikantha Murthy, Chaukhambha Orientalia, Varanasi, 2007 Ch 4 v 4
12. Ferguson, A., Arranz, E. & O'Mahony, S. Clinical and pathological spectrum of coeliac disease--active, silent, latent, potential. Gut 34, 150-151 (1993).
13. Alessio Fasano, Carlo Catassi, Current Approaches to Diagnosis and Treatment of Celiac Disease: An Evolving Spectrum GASTROENTEROLOGY 2001;120:636-651