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P
ISSN No. : 2584-2757
Volume : 03
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DOI
: 10.5281/zenodo.21369257
Reg. No. : MAHA-703/16(NAG)
Year of Establishment – 2016
INTERNATIONAL JOURNAL OF DIAGNOSTICS AND RESEARCH
Corresponding Author: Prof. Dr. Subhash Waghe
ORCID ID: 0009-0006-2776-5549
ISI Impact Factor (2025-26): 1.345
IIFS Impact Factor (2026-27): 6.0
Article Info: Article Received on : 09/05/2026 Article Reviewed on: 25/06/2026 Article Published on : 15/07/2026
Cite this article as: - Waghe, S. (2026). Clinical Study of Aetiology of Cirrhosis of Liver with special reference to Ayurvedic
Dietary and Lifestyle factors and Systemic Involvement. International Journal of Diagnostics And Research, 3(4), 1–18.
https://doi.org/10.5281/zenodo.21369257
Abstract
Background – Recent observations suggest that the true rate of chronic infection after clinically apparent acute
hepatitis B is as low as 1 per cent in normal individuals. Also, only 10 to 15 per cent of alcoholics develop Cirrhosis
of the liver, suggesting that other factors might be influencing the impact of the above factors on the liver. In view of
the above facts and the obscure concepts of Prakriti, Agni, Dincharya, Ritucharya, Ahar vidhi-visheshyatan, and
healthy lifestyle in modern medicine, it is essential to study cirrhosis of the liver with respect to the factors
mentioned above and to examine their role in its development.
Aims and Objectives - The aims and objectives of the present work is to study the aetiopathogenesis of
Kumbhakamala (Cirrhosis of liver) in terms of Ayurvedic dietary, lifestyle factors and systemic involvement.
Material and Method – 40 Patients having clinical features of cirrhosis of the liver were selected without any
prejudice from the O.P.D. & I.P.D. sections of Pakwasa Samanvaya Rugnalaya and All India Ayurveda Research
Institute, Hanuman Nagar, Nagpur.
Observations – Proper observations are recorded in tabular format, along with their analyses.
Discussion –Pittavardhak dietary and lifestyle regimen in conjunction with faulty dietary habits like samshan,
adhyshan, vishmashan, virruddhashan is commonly observed in patients of cirrhosis of the liver. Pitta dominance is
observed in the genetic body constitution of cirrhotic patients.
Conclusion - After assessing the clinical features, aetiological factors, and pathology explained in both Ayurvedic
and modern science, we can fairly correlate Kumbhakamala with cirrhosis of the liver. Ayurvedic pitta-enhancing
dietary and lifestyle factors may contribute to the severity of pathology.
Keywords: Cirrhosis of the liver, Pittvardhak ahar, pitta prakriti
Clinical Study of Aetiology of Cirrhosis of Liver with special reference to Ayurvedic Dietary and
Lifestyle factors and Systemic Involvement
Prof. Dr. Subhash Waghe
1
1
Dept. of Rog Nidan, SAM College of Ayurvedic Sciences, Raisen (MP) – 464 551
G
A
R
V
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Introduction :
Ayurveda, the science of life, studies life with
respect to health and disease, as well as the various
factors that promote and deteriorate health. Ahara
(diet) and Vihara (lifestyle) are the two most
important factors. A healthy diet and lifestyle
promote health, and vice versa. Along with
Brahamacharya (celibacy and good conduct) and
Nidra (sleep), Ahar forms the three sub-pillars
(Trayopstambha) of life. In Ayurveda, the
unwholesome conjugation of sense organs and
objects (Asatmya Indriyartha Samyog), purposeful
intellectual errors (Pradnyapradh) and the
consequences of time (Parinam) with respect to
Ahar and Vihar have been told as the three basic
causes responsible for the development of the
disease. Ayurveda is of the view that "microbes, no
matter how virulent they are, will not create any
disease in the body, unless the equilibrium stage of
Doshas gets disturbed". This equilibrium is
governed by many intrinsic and extrinsic factors,
such as Ahara, Vihara, Agni, and Prakriti, related
to vyadhikshamatva (immunity), etc. According to
Acharya Vagbhata, all diseases are due to Mand-
Agni (decreased appetite), which in turn depends on
a number of factors, such as Ahara, Vihara,
Prakriti, Vikriti, Season, Time, etc. This Mand-
Agni is unable to digest the diet as a result of which
the accumulation (Sanchaya) of toxic material
(Ama) takes place, which is the first stage of
pathogenesis of any disease. This stage leads to
further stages of pathogenesis and causes the
disease at the site of affection. There are a number
of diseases that are caused by the vitiation of
specific doshas (basic humours), which in turn are
aggravated by specific dosha-aggravating diet and
lifestyle. Kamala is one of them. In Ayurveda,
Kamala is defined as a disease characterised by
deep yellow discolouration of the eyes, nails, skin,
and face, along with fatigue, malaise, indigestion,
anorexia, etc.
In modern science, a similar condition is called
jaundice, which can be caused by various factors.
Hepatitis Viruses like A, B, C, D, E, G and
alcoholic hepatotoxicity are the commonest causes
responsible for it.
[1]
The human knowledge of Kamala is as old as the
Vedas. The first reference to Kamala, along with its
treatment, is observed in the Atharvaveda, where it
is called 'Hariman'. (Hymen 1-22/1, 2 & 4). The
period of the Atharvaveda is approximately 2500-
3000 BC. For a long time, the disease kamala
(jaundice) has been affecting the masses and is one
of the major health problems throughout the world,
responsible for considerable morbidity and
mortality from its acute or chronic sequelae.
According to one study, there are more than 200
million (20 crore) HBsAg carriers in the world. In
India, approximately 4.5 crore people are infected
with HBV, and 1 crore with HCV, and with a lack
of satisfactory treatment and awareness, it remains
the 5th single most important factor responsible for
mortality in the age group between 14 and 45 years,
averaging nearly 2.5 lakh deaths per year.
[2]
Kumbhakamala (Cirrhosis of liver) is a chronic
stage of the disease Kamala which can be fairly
correlated with modern syndrome of cirrhosis of
liver in which pathologically there is necrosis of
hepatocytes, followed by fibrosis and nodule
formation and the liver architecture is diffusely
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abnormal interfering with the liver blood flow,
producing the features of portal hypertension like
hematemesis, malena, encephalopathy, ascites with
or without edema feet, etc.
[3]
which are also seen in
kumbhakamala.
Recent observations suggest that the true rate of
chronic infection after clinically apparent acute
hepatitis B is as low as 1 per cent in normal
individuals. Also, only 10 to 15 per cent of
alcoholics develop Cirrhosis of the liver, suggesting
that other factors might be influencing the impact
of the above factors on the liver.
[4,5]
In view of the
above facts and the obscure concepts of Prakriti,
Agni, Dincharya, Ritucharya, Ahar vidhi-
visheshyatan, and healthy lifestyle in modern
medicine, it is essential to study cirrhosis of the
liver with respect to the factors mentioned above
and to examine their role in its development. The
present literary and clinical study will also help in
understanding Kumbhakamala (cirrhosis of the
liver) and various other types of Kamala in the light
of modern science.
Review Of Literature:
Charaka in Chikitsasthan 16/34-37 described the
pathogenesis of Koshthashakhashrit Kamala,
Kumbhakamala. Haleemaka in 16/132-134 and
Shakhashrit Kamala in 16/124-126.
[8]
According to
him, if a patient of Pandu consumes Pitta
aggravating factors, then that vitiated Pitta burns
(dagdhwa) the blood and flesh, resulting in Bahu-
Pitta Koshthashakhashrit Kamala, which, after
chronicity, leads to Kumbhakamala.
Kaphasamurchhit Vayu, vitiated due to excess
intake of dry, cold, sweet, heavy diet, suppression
of natural urges, intense exercise, etc., forces out
Pitta from its obstructed site (Pittasya Patham
Kaphen Rudhham) and throws it into circulation,
causing Shakhashrit Kamala. In a patient of Pandu,
specific vitiation of Vata & Pitta results in a
greenish, yellowish, greenish-blackish complexion;
that stage is called Haleemaka.
Vagbhata followed Charaka's view, but he held that
Koshthashakhashrit Kamala can occur without the
preexistence of anemia in a person of Pitta Prakriti.
(A.S. Ni. 13/17-21, A.S. Chi. 18/40-43)
[10] [11]
Sushruta in Uttaratana 44/11-14 mentioned that if a
person, after Pandu roga or any other disease,
consumes alcohol, sour/rotten food, or
harmful/toxic/antagonistic food in excess, then
vitiated Pitta causes Kamala. If this patient of
Kamala develops generalised edema and arthralgia,
then that stage is called as Kumbhasahv
(Kumbhakamala - Dalhan)
[8]
If this patient of
Kumbhasahav develops fever, fatigue, listlessness,
giddiness, drowsiness, greenish, greenish-blackish
or bluish tint due to specific vitiation of Vata and
Pitta, then that stage is called as Haleemaka. After
analysing the views of Charaka, Sushruta,
Vagbhata, commentators like Chakrapani, Dalhan,
the pathogenesis of Koshthashakhashrit Kamala,
Shakhashrit Kamala, Kumbhakamala, and
Haleemaka can be given as:
In the first type of pathogenesis, the said patient of
Pandu is the patient of Pittaj Pandu (Hemolytic
anemia) where there is already jaundice is present
but to a lesser extent (indicated by the word 'peeta
chakshu') as we usually notice in patients of
hemolytic anemia (low serum bilirubin) But as
these patients consumes Pitta aggravating aetiology
like alcohol, smoking, hot, chilly, pungent food etc.
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Pitta aggravates further, and weak, friable RBCs
begin to break down, resulting in a more
pronounced jaundice
[6, 7]
, indicated by the word
Haridra (deep yellow like turmeric), reflected in
yellow eyes, yellowish urine, etc. Here, the prime
pathology is of Asruk dagdhwa (Hemolysis). Prime
strotodushti is Atipravritti (excessive production).
This is Koshthashakhashrit Kamala Panduroga-
purvika. After cessation of the acute episode, when
the chronic sequelae of this pathology produce
extensive edema and bony pain, that stage is called
Kumbhakamala. And if repeated episodes produce
greenish, yellowish or greenish-blackish hue, then
that stage is called Haleemaka.
[9]
In the second type of pathogenesis, if a patient with
any Pitta-dominated disease or a person of Pitta
constitution consumes Pitta-aggravating factors like
alcohol, excess sexual intercourse, hot, chilly,
pungent diet, etc., then there occurs intense
vitiation of Pitta resulting in acute hepatic necrosis.
Here, the primary pathology is of the Mansa
dagdhwa type (Hepatolysis), as there is an
ashrayashrayi relationship between the liver and
Pitta. The term 'Mansa dagdhwa' here refers to
hepatic necrosis (hepatolysis). The predominant
strotodushti here is of Atipravritti and sang type.
(Excessive production and defective excretion)
This type of hepatocellular jaundice in Ayurveda is
called Koshthashakhashrit Kamala
Pandurogavina.
[12]
If this condition is left untreated,
then it becomes chronic, and although there is no
apparent jaundice, the internal pathology involving
the liver continues, leading to hepatic fibrosis,
indicated by the word 'Kharibhuta', giving rise to a
condition called Kumbhakamala. The meaning of
Kharibhuta given by Chakrapani is hardness
(kathortamup-gata) and intense dryness (Ati
rukshitaha). In Ayurveda, there are three types of
paka described viz. mridu, madhyam and khara. Of
these, mridu paka is one which formed by mild
heating, madhyam by moderate heating and khara
by excessive heating. The relevance of paka theory
here is very important because the term used in the
pathology of K.S.Kamala is dagdhwa (meaning 'to
Heat/burn'). Notably, one of Pitta's functions is
heating.From the above, one can understand the
nature of the pathology. The only difference
between ancient and modern science is the way it is
described and the terminology used. They have
used the terminology prevailing at the time, or
sometimes examples, to describe various aspects.
As of today, we know that liver fibrosis occurs in
cirrhosis, which in Ayurveda is known as Kumbha-
kamala. Extensive edema (Mahan Shofa), including
ascites at this stage, suggests hypoalbuminaemia
reflecting severe liver pathology. Hematemesis
(Sraktachhardi), Malena (Krishna Shakrita), and
encephalopathy indicate portal hypertension. In this
condition, an additional superinfection or acute
hepatic necrosis may produce features such as low-
grade fever, anorexia, malaise, and icterus. Or long-
standing jaundice (on oxidation of bilirubin to the
greenish-yellowish or greenish-blackish biliverdin)
produces a greenish-yellowish or greenish-blackish
hue; that stage is called Haleemaka.
[13]
Whenever in
patients of Kamala, Kumbhakamala or Haleemaka,
intense vitiation of Apan Vayu results in diarrhoea
and other G.I. disturbances, then that stage is called
Apanaki.
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Material And Methods:
Place of the study
Patients having clinical features of cirrhosis of the
liver were selected without any prejudice from
O.P.D. & I.P.D. sections of Pakwasa Samanvaya
Rugnalaya and All India Ayurveda Research
Institute, Hanuman Nagar, Nagpur.
Sample Size
40 diagnosed patients of cirrhosis of the liver is
taken for the present study
Selection Of the Patient:
A detailed case history and clinical-pathological
findings were recorded on the clinical proforma
specifically designed for the present research study.
Diagnostic criteria
Diagnostic criteria were established to cover both
modern and Ayurvedic aspects of the disease. The
patients having a history of prolonged or excessive
alcohol intake or patients chronically infected with
the hepatitis B or C virus, having the following
clinical features and supported by radiological
findings as well as deranged liver function tests,
were termed patients of cirrhosis of the liver.
Clinical Features Of Cirrhosis of the Liver:
Symptoms:
Specific
 Abdominal distention due to ascites
 Ankle swelling due to fluid retention
 Haematemesis and melena due to
gastrointestinal haemorrhage.
 Pruritus
 Gynecomastia in males
 Loss of libido in males
 Amenorrhoea in females
 Confusion and drowsiness
Non-Specific
 Anorexia
 Fatigue
 Emaciation/weight loss
 Weakness
 Listlessness
 Indigestion
 Constipation
 Malaise
Signs :
General
compensated
Decompen-sated
Fever
Hepatomegaly
(initially)
Disorientation
Jaundice
Spleenomegaly
Drowsiness
Loss of
hairs
Gynaecomastia
Coma
Scratch marks
over
Flapping tremors
Spider naevi
Fetor hepaticus
Perpura
Ascites
Testicular
atrophy
Dilated veins over
the abdomen
Palmer erythema
Edema feet
Dupuytren's
contractures
History And Clinical Examination:
After confirming the diagnosis, the detailed history
with respect to age, sex, habitat, socio-economic
status, mode of onset of the disease, family history,
drug history, previous or associated disease history
with duration, dietary habits, addiction with
duration, and state of mind were recorded on the
specially prepared clinical proforma.
Examination Of Patients By Ayurvedic Method:
All patients were thoroughly examined for vitiated
Doshas, Dooshyas, Strotas, and Nidanpanchak.
Dash-Vidh and Ashta-Vidh pariksha were also
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conducted as described in ancient Ayurvedic
classics.
Study Of Nidan:
Each case was carefully interviewed to assess the
presence of various risk factors in patients, as
explained by modern as well as Ayurvedic science.
Sannikrishta Nidan (acute) is a recent provoking
factor leading to the acute onset of the disease,
while Viprakrishta Nidan is an old (chronic) risk
factor.
General Examinations:
General clinical examinations were done for height,
weight, blood pressure, pulse rate, temperature,
pallor etc.
Systemic Examinations:
Under it following systems were examined and
special stress was given on gastrointestinal and
nervous system.
Respiratory system (RS):- It was examined for
breathing pattern, air entry, presence of any other
abnormality.
Cardiovascular system (CVS) :- Under it the
heart was examined for rate, rhythm, heart sounds
and any other abnormality.
Gastro-Intestinal system (GIS) :- It was examined
for the presence of hepatomegaly, spleenomegaly,
and ascites. The abdominal girth on, above and
below the umbilicus was noted in patients with
ascites.
Central Nervous System (CNS):- It was
examined for the presence of features of
encephalopathy, such as disorientation,
confusion, dysgraphia, drowsiness, coma, etc.
Laboratory Investigations
Hematological: - The routine hematological
examinations like Haemoglobin percentage (Hb%),
Total Leukocyte Count (TLC), Differential
Leukocyte Count (DLC), Erythrocyte
Sedimentation Rate (ESR), Peripheral Smear (PS)
to see the degree of anemia, its type and also for
evidence of infective pathology.
Biochemical:
Liver Function Tests:
1. Serum Bilirubin (Conjugated & Unconjugated):
To assess the severity of jaundice and to know its
type.
2 Serum AST & ALT: To assess the severity of
hepatocellular damage.
3. Serum Alkaline Phosphatase: To assess the
severity of cholestasis wherever thought necessary.
4. Serum Proteins (Albumin & Globulin): To assess
the severity of functional pathology of the liver.
5 Serum Prothrombin Time: To assess the severity
of dysfunction of the liver and the coagulopathy.
6. Serum Viral Marker: - To know the type of
hepatitis virus.
Serum Electrolytes:
1. Serum Sodium: To assess the severity of
hyponatremia.
2. Serum Potassium: To assess hypo or
hyperkalemia.
Kidney Function Tests:
To assess the presence of hepato-renal failure and
the severity of functional pathology of the kidneys.
1. Serum Creatinine
2. Blood urea
Peritoneal Fluid Examination:
To assess the fluid for transudation or exudation,
and also for evidence of bacterial peritonitis and
other pathologies.
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Miscellaneous:
Blood sugar and other appropriate investigations as
required and based on the presence of associated
disease.
Radiological:
Ultrasound: To assess the type of liver pathology,
as well as for evidence of portal hypertension and
the presence of ascites.
Endoscopy:
For evidence of varices.
Result & Observations:
The results and observations of the present study
are given as follows.
1. Age incidence in cirrhotic patients:
Table No. 1 (n = 40)
Sr
Age
group
(years)
No. of
patients
%
1
20-40
6
15%
2
40-60
29
72.5%
3
60-80
5
12.5%
Total
40
100%
Age incidence in cirrhotic patients
2. Sex incidence in cirrhotic patients:
Table No. 2 (n=40)
Sr
Sex
No. of
patients
Percentage
1
Male
36
90 %
2
Female
4
10 %
Total
40
100%
Sex incidence in cirrhotic patients
Habitat (Desha) in cirrhotic patients:
Table No. 3 (n = 40)
Sr
Area
No. of patients
%
1
Rural
13
32.5 %
2
Urban
27
67.5 %
Total
40
100%
Out of 40 patients registered in the present study,
the majority of patients (72.5%) were in the age
range of 40 to 60 years, 90% of the patients were
male, and the majority of them (67.5%) were from
an urban area.
Incidence Of Socio-Economic Status:
The patients with an annual income of less than Rs.
35,000/- were placed in the lower-income group.
The annual Income between Rs. 35,000 and
65,000/- were placed in the middle-class income
group. And patients having an annual income of
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more than Rs. 65,000/- were categorised under the
higher-class income group.
4. Table No. 4 (n=40)
Socio-Economic Status
Sr
Sex
No. of patients
%
1
Lower
15
37.5%
2
Middle
12
30 %
3
Higher
13
32.5%
Total
40
100%
Although the percentage of cirrhosis in the lower
income group is slightly on the higher side, no
significant variation is seen in the occurrence of
cirrhosis as far as socio-economic status is
concerned.
5. Incidence Of Dietary Habits (Ahar)
Table No. 5 (n = 40)
Sr
Dietary habit
No. of patients
%
1
Vegetarian
5
12.5%
2
Non-Vegetarian
0
0 %
3
Mixed
35
87.5%
Total
40
100%
In the present study, out of 40 patients suffering
from cirrhosis, 35 (87.5%) were having a mixed
diet
6. Incidence Of Addiction:
Table No. 6 (n=40)
Sr
Addiction
No. of
patients
%
1
Only alcohol
6
15%
2
Alcohol with
smoking
21
52.5%
3
Alcohol with
tobacco
4
10%
4
Only smoking
1
2.5%
5
No addiction
7
17.5%
6
Other
1
2.5%
Total
40
100%
Alcohol addiction is found in 77.5% patients. Out
of which 52.5% were also addicted to smoking and
10% with tobacco chewing. No addiction was
found in 17.5% patients. The other addiction 2.5%
found was of Fortwin. The duration of alcoholism
was in the range of 10 to 25 years. The mean
duration of alcoholism was 17.5 years.
7. Incidence of State of Mind (Mansic hetu)
Table No. 7 (n = 40)
Sr
Mental status
No. of patients
%
1
Anxious
8
20 %
2
Tense
11
27.5%
3
Irritable
9
22.5%
4
Relaxed
12
30%
Total
40
100%
A stressful state of mind was observed in 70%
patients with cirrhosis of the liver.
Incidence Of Aetiological Factors (Nidan):
Table No. 8 (n = 40)
Sr
Aetiological factors
No. of patients
%
1
Alcohol
26
65%
2
HBV
10
25%
3
HCV
4
10%
Total
40
100%
Incidence Of Aetiological Factors
(Nidan):
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In 65% of the patients, alcohol was directly
responsible for the development of cirrhosis, while
in 25% patient main aetiological factor was
hepatitis B virus, and in the remaining 10%, it was
hepatitis C virus.
9. Ahar Hetu (Dietary factors):
The criteria for specific dosha aggravation were as
follows:
Vatvardhak ahara :
Katu, Tikta, Kashay rasatmak and Laghu, Ruksha,
Vishtambhi gunatmaka etc.
Pittavardhak ahara:
Katu, Lavan rasatmak and Ushna, Tikshna, Vdahi,
gunatmak etc.
Kaphavardhak ahara:
Madhur, Amla rasatmak and Shit, Guru, Vishyandi
gunatmaka etc.
Table No. 9 showing Ahar hetu (Dietary factors)
in cirrhotic patients. (n = 40)
Sr
Ahara
No. of patients
%
1
Vatavardhak
0
0%
2
Pittavardhak
4
10%
3
Kaphavardhak
4
Vata-Pittavardhak
20
50%
5
Kapha-Vatavardhak
2
5%
6
Pitta-Kaphavardhak
10
25%
7
Tridosh Prakopak
4
10%
Total
40
100%
Incidence Of Ahar Hetu
The diet of 50% patients with cirrhosis of the liver
was Vat-Pittavardhak. In 25% of patients, it was
Pitta-Kaphavardhak, and only 10% followed a
plain Pittavardhak diet.
10. Ahar Paddhati (Dietary Habit) :
The dietary habit was divided into four parts as
follows:
1. Samshan:- Eating a healthy and an unhealthy
diet together.
2 Vishmashan - Irregularity of diet with respect to
time and quantity.
3. Adhyshan:- Taking a diet before the digestion of
the earlier one.
4. Viruddhashan :- Consuming an antagonistic
diet.