Ghee

An Ayurvedic and Biochemical Treatise

Catherine Robbins, BSc, KYTA, AHE, AHP
California College of Ayurveda
AHP-Internship 2012
catherinerobbins@earthlink.net
7/14/2012
2
Introduction:
Ghee, the golden elixir of Ayurveda is an oil with a long and interesting history. A staple of Indian,
Arabic, and North African cooking, it is also found throughout Indonesian societies. Ghee is the
rendered fat of butter. Butter is made in several different ways, which result in butters with slightly
different fat, water and milk solids content. Desi ghee is the traditional Indian ghee made from
cows milk that is first collected and saved for a few days to culture. The cultured milk is then
churned to produce butter. Churning separates the emulsified fats in the milk from the liquid or
aqueous portion of the milk. The left over liquid is called buttermilk and is used for drinking and
other cooking. In American creameries, the milk is usually not cultured and it therefore produces
butter that has a slightly different fatty acid and water content [1].

The rendered oil known as ghee is called ghrita in Sanskrit, the traditional language of the ancient
texts of Ayurveda. The Brihat Treya, the three most important Ayurvedic texts are the Caraka
Samhita [2, 3], the Shushruta Samhita [4] and the Ashtanga Hrdayam [5], and date back as far as
500BC in written form. It is in these ancient writings where we learn the multiple uses and the
powerful medicinal effects of ghrita. Caraka clearly states the indications for ghee: promotes
memory, intelligence, agni, semen, ojas, Kapha and medas. It alleviates Vata, Pitta, poison,
insanity, phthisis, inauspiciousness and fever. It is the best of all fats, is cold, madhura rasa,
madhura vipaka, has 1000 potentialities and so, if used properly according to prescribed methods,
exerts 1000 types of action. Su27#231-232 [2, 3]. Caraka then goes into a greater discourse on
each use listed for ghee throughout the text.

Sushruta makes an even stronger statement on the medicinal uses of ghee, Ghrita is sweet, mild
in action, soft, cold in potency (Virya), not increasing moisture in the tissues, lubricating, relieves
upward movement in the alimentary tract, insanity, epilepsy, colic, fever, and distension of the
abdomen, mitigates vata and pitta, kindles agni, increases memory, wisdom, intelligence,
complexion, voice, beauty, softness of the body, vitality, vigor, strength, and span of life; is
aphrodisiac, good for vision, increases kapha, wards off sins and inauspiciousness, destroys
poisons and demons. He further elaborates on the properties and applications of ghees obtained
from the various types of animal milks including human, elephant and camel milk, Chap XLV
#5v1-9 [4] stating ghee from cows milk is superior for all ailments.

In the Ashtanga Samgraha, Vagbhata tells us the use of ghee for snehavidhi adyaya or oleation
therapy is best for those desirous of intelligence, memory, wisdom, good digestive capacity, for
those suffering tumors, sinus ulcers, worms, diseases of kapha, medas and vata origin Chap 25
10-11 [6]. The quotes of these authors are very strong statements and in todays medical world
where the search is on for THE one pharmaceutical magic bullet, ghee appears to be just that.

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Table 1

From the above table, it is clear that ghee can be tridoshic in small doses. It has a sweet rasa,
with a cold virya and a sweet vipaka with gunas or qualities being light, penetrating and unctuous
[2, 4, 8, 9]. Ghees unctuousness makes it an excellent internal and external lubricant for treating
Vatas dryness, roughness and emaciation and Kaphas hardness. Its cooling virya makes it
excellent for placating excessive Pitta and yet, it can stimulate agni without exacerbating Pitta
aggravations. Ghee also has a prabhav that allows it to take on the properties of herbs it is
processed with without losing its own gunas [2]. This means if it is cooked with a heating herb,
the ghee will pass on this property without giving up its own oily, cooling properties. This makes
ghee an excellent anupana and its spreading nature can take the intention of herbs in to the deep
tissues. Dr. Vasant Lad of the Ayurvedic Institute in Albuquerque, NM calls ghee a catalytic agent
or yogivahi that carries the medicinal properties of herbs it is processed or taken with in to the
tissues [10].

Again, when pondering all the possible uses for ghee from an Ayurvedic standpoint, it would seem
that ghee is like the magic bullet so sought after in Western medicine [11], however, when the
subject of dietary fat arises in the American public discourse, the first questions raised invariably
have to do with is ghee safe? Isnt ghee just rendered animal fat and shouldnt we all be avoiding
animal fat in general? Isnt ghee, being a by-product of butter, high in cholesterol?

Indication for ghee Dosha/Subdosha involved Reference
Promotes memory Vata (prana, samana vyana) Caraka, Sushruta,Vagbhata
Promotes intelligence/wisdom Vata (prana, samana vyana) Caraka, Sushruta,Vagbhata
Enkindles agni/digestive
capacity Pitta (pachaka) Caraka, Sushruta,Vagbhata
Promotes semen/vigor Shukra agni, apana vayu Caraka, Sushruta
Promotes ojas/vitality Kapha kshaya Caraka, Sushruta
Promotes kapha/medas Kapha kshaya Caraka, Sushruta
Cures diseases of
kapha/medas Kapha kshaya Vagbhata
Alleviates Vata Vata vruddhi Caraka, Sushruta,Vagbhata
Alleviates Pitta Pitta vruddhi Caraka, Sushruta
Poison Vata, Pitta, Kapha[7] Caraka, Sushruta
Insanity Vata Caraka, Sushruta
Epilepsy Vata Sushruta
Phthisis (tuberculosis) Vata, Pitta, Kapha[7] Caraka
Upward moving Vata in
alimentary tract Vata Sushruta
Colic, constipation/gas Vata Sushruta
Tumors Kapha Vagbhata
Sinus Ulcers Pitta Vagbhata
Fever Pitta Caraka, Sushruta
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Whenever the discussion turns to fat in the American diet, there is so much contradictory
information in the public domain, a formalized understanding of fat bio-metabolism can be truly
useful in understanding how ghee could be good. To that end, let us take a closer look at what fat
is and how, when and why humans require fat in their diet, not only to survive, but to also lead
healthy productive lives.

The skinny on fats: whats a fatty acid and why is it essential?
Lipids are one of the four major classes of bio-organic compounds required by living organisms,
the other three being carbohydrates, proteins and nucleic acids. Unlike the other three classes of
important biochemical compounds, lipids are not characterized by structure but rather, by
selective solubility in various solvents. Technically speaking, a lipid is an organic (carbon
containing) compound found in living organisms that is insoluble or sparingly soluble in water but
is very soluble in non-polar solvents [12, 13] such as oil. There is great structural diversity among
lipids leading to the following five classifications:

1. Energy Storing lipids: triacylglycerols
a

2. Membrane Lipids (phospholipids, sphingoglycolipids and cholesterol
b
)
3. Emulsification lipids (bile acids)
4. Messenger lipids (steroid hormones, cholesterol
b
and eicosanoids)
5. Protective coating lipids (plant waxes)

Fatty Acids (FAs) are naturally occurring monocarboxylic acids which generally contain an even
number of carbons in their carbon chain
c
where Long Chain FAs = 12-26 carbons, Medium Chain
FAs = 6-10 carbons and Short Chain FAs = 4-6 carbons in length. FAs are rarely found free in
nature as they are usually part of more complex lipid molecules [13, 14].
a* b*
Triacylglycerol , aka Triglyceride Cholesterol

c*
Butyric acid, a short chain saturated fatty acid found in ghee and butter
*structures constructed using MarvinSketch Freeware[15]

A further delineation of FAs is the degree of saturation. Saturated FAs (SFAs) have no carbon-
carbon double bonds in the carbon chain. Monounsaturated FAs (MUFAs) have one carbon-
carbon double bond in the carbon chain and Polyunsaturated FAs (PUFAs) have two or more
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carbon-carbon double bonds in the carbon chain. Up to 6 double bonds are found in biologically
important PUFAs. Double bonds are significant to the biochemistry of FAs because it is at these
high-energy bonds that important biochemical reactions take place.

In plants, FAs are found mostly esterified to glycerol as triglycerides and they make up ~7% of the
dry weight of a plant [14]. Plant FAs are generally unsaturated (UFAs) as demonstrated by the
fact that they are liquids at room and body temperature. Seed and nut oils have much higher FA
content, but again are mainly unsaturated and in the form of triglycerides. Coconut oil is heavily
saturated at 86.5% while olive and safflower oil have 13.8% and 7.5% saturation, respectively
[16].

In general, SFAs come from animal sources and UFAs come from plant sources although there is
great variability in the FA makeup of various types of plants and animals. Ruminant animals such
as cows, goats and sheep have much higher SFAs than fish or fowl. Ruminant animals rely on
gut bacteria to breakdown plant based foods such as grass, forage or corn into usable energy via
the anaerobic process of fermentation.

The fermentation carried out by the gut bacteria and the rumen stomach together are considered
more or less a hydrogenation chamber where plant based UFAs are hydrogenated with the main
waste product being gaseous methane. Usable byproducts of ruminant fermentation are volatile
short chain SFAs such as acetic acid, proprionic acid and butyric acid and they are a main source
of energy for the animal. They also occur in the food we get from the animals such as meat, milk,
cheese and butter. Other animal meats such as chicken and fish are generally lower in SFAs
because those animals do not ruminate or, ferment their food before digesting it as do cows [17].

The chemical properties of FAs and the lipids that contain them are a function of the length of the
carbon chain they contain and the degree of saturation. SFAs that have fewer than 8 carbons are
liquid at body temperature and those containing 10 or more carbons are solid at body
temperature. The presence of double bonds lowers the melting point, hence SFAs have a higher
melting point than UFAs with the same number of carbons in the chain. The greater the degree of
unsaturation, the lower the melting point and this is due to decreased molecular attraction
between carbon chains [12, 13, 18]. The carbon-carbon double bonds in UFAs are usually (but
not always) in a cis configuration, which introduces a bend in the carbon chain. Such bends
prevent UFAs from packing as tightly together as SFAs. The greater the number of double bonds,
the less efficient this packing is and the lower the melting point of the lipid [12].

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[19]

In humans, most FAs come from the diet although the body can make many fatty acid containing
molecules with two key exceptions: the highly unsaturated linoleic acid and alpha-linolenic acid.
These two FAs have unsaturation beyond carbons nine and ten which the human body cannot
synthesize. Because these two FAs cannot be synthesized from lipid precursors in the body, they
are considered essential and must be obtained from the diet. These are PUFAs and their
exclusion from the diet leads to severe gastrointestinal and skin lesions similar to Pellegra (vitamin
B3 deficiency). Since FAs are abundantly available in both plant and animal based foods, it is a
rare situation where an individual is suffering from essential FA depletion. On the other hand, it is
generally accepted that diets very low in fat need to be supplemented with linoleic and alpha-
linolenic acid [20, 21].

Saturated FAs have been long associated with cardiovascular disease, cerebro-vascular disease
and atherosclerosis [22, 23]. Although the data have not always been strong, they appear to be
consistent across years of published research indicating that a diet high in saturated fats
increases the risk of coronary artery disease (CAD) [24]. Mechanistically, this increase for CAD
risk appears to involve increased Low Density Lipoprotein (LDL), which has been linked to
atherosclerosis, a precursor to cardiovascular disease CVD [25, 26]. On the other hand, some
SFAs such as caproic acid (5 carbons), caprylic acid (8 carbons), decanoic acid (10 carbons) and
stearic acid (18 carbons) have been shown to have no effect on LDL cholesterol [27].
Interestingly, butyric acid, the 4 carbon volatile SFA which is found at 2-5% by weight in butter and
ghee has been shown to be anti-inflammatory in Crohns disease, to improve insulin sensitivity,
increase energy expenditure in a diabetic mouse model, and to be a modulator of the immune
response and inflammation as well as an anti-tumor agent [27-30].

Unsaturated FAs come in 2 types: Monounsaturated (MUFAs) and polyunsaturated (PUFAs). The
one carbon-carbon double bond in MUFAs is generally in the cis configuration and the dietary
effect seen in many studies is to reduce cardiovascular risk [31]. Examples of MUFAs are
palmitoleic acid and oleic acid. Examples of PUFAs are linolenic acid and alpha-linoleic acid.
PUFAs have more than one carbon-carbon double bond and another important differentiating
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factor is where along the carbon chain the double bonds occur. !-3 PUFAs have their first double
bond at the third carbon from the methyl end of the carbon chain and the !-6 PUFAs have their
first double bond at the 6
th
carbon from the methyl end of the carbon chain. These two families of
PUFAs have received a lot of attention in Western science ever since it was discovered that
linoleic acid and alpha-linolenic acid are essential [20, 21].

!-3 and !-6 Fatty Acids:
Linoleic acid (LA) is an !-6 PUFA, an 18 carbon mono-carboxylic acid with two cis conjugated
(separated by one carbon with a single bonds) carbon-carbon double bonds, one that is six
carbons from the methyl end and one nine carbons from the methyl end [12, 13] and it has a
melting point of -5 C. This means LA is a liquid at body temperature 37 C [18]. The word
linoleic comes from the Greek linon for flax and oleic meaning of or relating to oleic acid
(found at high concentrations in olive oil) and it is the most common PUFA found in both plant and
animal tissue [12, 13]. LA is further metabolized to arachidonic acid (AA), which is metabolized
into the pro-inflammatory type eicosanoid prostaglandins, thromboxanes and leukotrienes [12, 18,
24, 32]. When it became clear that a diet high in PUFAs had positive effects on heart health,
people were encouraged to increase the intake oils high in PUFAs such as corn, peanut and
safflower. Currently, LA provides approximately eighty-five percent of Americans energy intake
from PUFAs [24, 33].

Alpha-linolenic acid (ALA) is an !-3 PUFA, an 18 carbon mono-carboxylic acid with three cis
conjugated carbon-carbon double bonds the first of which is at the third carbon from the methyl
end of the molecule and has a melting point of -11 C [12, 13, 18, 34]. Like LA, ALA is a liquid at
room and body temperature. In the human body, ALA is a precursor to eicosapentaenoic acid
(EPA) (20 carbons) and docosahexaenoic acid (DHA) (22 carbons), two long chain !-3 PUFAs
that came to light during epidemiological studies of Eskimo/Inuit tribes who consume large
amounts of !-3 PUFAs from the fat from fish yet have low rates of CVD [24, 33, 35, 36]. Other
positive effects attributed to !-3 PUFAs, especially EPA and DHA are anti-thrombotic, anti-
Alzheimers and pro-immune response [35, 37-40].

cis and trans FAs:
Most, but not all high energy carbon-carbon double bonds that occur in nature and the human
body are in the cis configuration where the substituent groups on either carbon involved in the
double bond are on the same side of the molecule in three dimensional space. The trans
configuration is when the substituent groups are on the opposite sides of the molecule around the
carbon-carbon double bond. Carbon-carbon double bonds introduce rigidity to chains of carbon
molecules and energetically speaking the trans configuration is the most chemically stable. This is
why hydrogenated FAs as in shortening are in the trans configuration; industrial hydrogenation is
an uncontrolled reduction reaction where hydrogen is added to the double and triple bonds of
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vegetable oils in a random, energetically favored way [18]. Biochemical hydrogenation as takes
place in ruminant animals gives rise to mostly the cis configuration and the products are
recognized by other biological systems such as in humans. Also, during industrial hydrogenation,
some of the cis FAs are also converted to trans FAs through a process call cis-trans isomerization
and this dramatically alters the shape of the fatty acid chain. Not surprisingly, trans FAs produced
by uncontrolled hydrogenation are not recognized structurally by the enzymes that normally
process FAs in the body and tend to collect in the liver and at sites of atheroma growth, hence
they are now associated with higher CVD risk [18, 41].

Cholesterol: What is it and is it really bad?
Cholesterol is a steroid. A steroid is a lipid structure based on a fused-ring system that involves
three 6-membered carbon rings and one 5-membered carbon ring. Cholesterol in an integral
component of cell membranes and a precursor for other steroid based lipids [12, 13, 18].

[42]

Cholesterol is the most abundant steroid in the human body. It is found in cell membranes, nerve
tissue and brain tissue and is also found in nearly all bodily fluids in some form or another. Some
cholesterol is taken up from the diet in the small intestine, but the majority of cholesterol is
synthesized in the liver and to some degree in other organs [12, 13, 18, 22]. Ingested cholesterol
decreases the amount of cholesterol produced by the body via a negative feed back system.
Since cholesterol is not water soluble, it is packaged with FAs and protein by the body for
circulation to where it is needed. These proteins are called lipoproteins [12, 13]. Low density
lipoproteins (LDL) generally carry cholesterol from the liver to the tissues and high density
lipoproteins (HDL) carry excess cholesterol back to the liver.

Because of cholesterols abundance in the body in both healthy and pathological conditions, it has
been closely studied for its role in atherosclerosis for over a century [43]. Originally, it was found
as a crystalline component of atherosclerotic plaques and gallstones. It is also known that there is
a direct correlation to age and the lipid and cholesterol content of the aorta of humans [44]. This
led to Anitschkows landmark study where he showed that feeding rabbits pure cholesterol
dissolved in oil led to the development of atherosclerotic lesions [45]. Normally rabbits do not
ingest measurable amounts of cholesterol as the cholesterol content of plants is considered
negligible [43] and rabbits are obligate herbivores. Clearly, rabbits are not the best cholesterol
model on which to base human medicine. Regardless of the fact that rabbits and humans process
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dietary cholesterol differently, the Lipid Hypothesis [46] was born and cholesterol found in LDL
as a therapeutic target has been doggedly pursued by the Western medical and scientific
community in the search for a treatment for atherosclerotic diseases ever since. With the advent
of statins in the 1980s, the lipid hypothesis gained solid acceptance and the data show that for
people suffering from hyperlipidemia, dietary and lifestyle changes along with the use of a statin
can dramatically normalize dyslipidemia and reduce the primary and secondary risk for
cardiovascular disease [47, 48].

Although the cholesterol in LDL as a primary therapeutic target has shown great success at
reducing cardiovascular risk over the years, there is a plethora of data that suggest cholesterol
alone is not the causative agent in cardiovascular disease [22, 27, 31, 33, 49-51]. In fact,
inhibition of cholesterol biosynthesis has also been associated with impaired insulin secretion and
other cholesterol mediated membrane processes involving exocytosis [52]. Exocytosis is the main
process by which cells secrete bioactive molecules such as insulin, neurotransmitters and
hormones. These data suggest that when cholesterol levels are unnaturally low due to
medications such as statins, a whole host of serious medical syndromes are experienced by a
small subset of patients [48, 53, 54] ranging from rhabdomyolysis to death [55].

One of the most interesting findings was in the ENHANCE study of a combination of Simvastatin,
a statin and Ezetimibe, a cholesterol uptake inhibitor. This was an imaging study looking at
regression of fatty plaques in the arteries due to combination therapy. Combination therapy of
statins with other lipid lowering medications has shown additive results in normalizing
dyslipidemias [56]. On the other hand, the data on the regression of plaques due to aggressive
statin and/or combination therapy have been mixed suggesting that statins play more of a role in
plaque stabilization and that plaques rarely regress very much quantitatively [57]. Patients on the
combined therapy of Simvastatin + Ezetimibe achieved tremendous reductions in LDL cholesterol
and yet the patients experienced growth of fatty plaques in their arteries [58]. The study was
subsequently stopped early [59] because of this. There were also a slightly higher number of
patients on combination therapy who developed cancer, but the study did not continue long
enough to determine if this was a significant outcome. This result and similar results in other
studies where the LDL and total cholesterol levels have been severely reduced and yet have not
resulted in greater health benefit to the patient have left Western researchers puzzled as to what
actually contributes to atherosclerotic plaque growth [48, 57, 59, 60]. It has also caused many
researchers to re-evaluate cholesterol not as a bad or a good thing, but rather as an integral
membrane steroid responsible for many important physiologic activities that can under certain
conditions contribute to the pathology of atherosclerotic plaques. On the other hand, it is now
being established that one can lower the cholesterol too much with unhealthy outcomes in certain
patients.

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The original Lipid Hypothesis is actually a consensus on the idea that there is a direct correlation
between plasma levels of cholesterol and the development of coronary artery disease [61]. At the
time of its development, it was quite plausible. In fact, as stated before, many lives have been
saved, improved and prolonged as a result of making the treatment of elevated plasma cholesterol
in LDL a primary therapeutic target. However, this hypothesis completely fails to explain the
results seen in the ENHANCE study and other, lesser known instances where a patient cohort
with high LDL cholesterol fail to develop cardiovascular disease [62, 63] or where statin therapy
does not reduce CVD risk [63].

Attention is now turning more to the role of fat in the diet and more specifically, the role of the !-3
and !-6 MUFAs and PUFAs. This new body of evidence points to the importance of a high !-3:
!-6 ratio not only for cardiovascular health, but overall health in general. The historical diet in this
country 100 years ago favored !-3 FAs because our food animals were fed mainly a diet high in
forage and grass. As stated before, !-3s have been associated with the anti-inflammatory
pathways in the body. !-3: !-6 ratios are estimated to have been ~ 9:1 for ruminant animals who
were grass fed [24]. With the advent of the post WWII corn-based feed for cattle and other food
animals in the United States, that ratio has turned in favor of the !-6s at a ratio of 20-30:1
depending on ones diet [24]. Recall again, that the !-6 FAs, although considered essential, are
highly correlated with the inflammatory pathways in the body. The Union of Concerned Scientists
has suggested that returning the feeding of the USs food animals to a grass and forage based
system could not only restore farmland ecosystems depleted under the strain of chemical
fertilizers and pesticides, but that doing so could go a long way in improving the baseline health of
the population at large [24]. Other data further demonstrate that even the saturated fats from
plants are associated with less CVD risk than saturated fats from animals and that by substituting
2% of energy from meat SFAs with energy from dairy SFAs was associated with a 25% reduction
in CVD risk [64]. It seems a more thorough understanding about the metabolic processes
involving fats in the body may lead to a better understanding of atheroma formation, CVD risk and
prevention.

What is the Fat and Cholesterol Content of Ghee?
Ghee is the rendered fat of butter, therefore it is considered to be 100% fat. As discussed earlier,
not all fats are created equal, so what is the chemical fatty composition of ghee?
Table 2
FA Composition of 100 g ghee[65]
Component
Home made ghee
[65]
Commercial ghee
[65] Melting Point [66]
Triglycerides 97.8% 98.6% ----------------
Cholesterol 178.2 mg/100g 161.7 mg/100g
148-150 C
Phospholipids 28.6 mg/100g 10.4 mg/100g ----------------
Vitamin E 305 ug/100g 491 ug/100g -----------------
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Vitamin A 447 ug/100g 584 ug/100g -----------------
Butyric acid C4
SFA 4.5-6% by wt[67] --------------
-7.9 C
Decanoic C10
SFA 1.8% by wt 1.3% by wt
31.6 C
Lauric C12 SFA 2.1 % by wt 2.6% by wt
43.2 C
Myristic C14 SFA 13.8% by wt 14.3% by wt
54.2 C
Palmitic C16 SFA 33.0% by wt 32.8% by wt
62.9 C
Stearic C18 SFA
11.8% by wt
12.0% by wt
69.6 C
Oleic C18 MUFA 30.2% by wt 30.0% by wt
13-14 C
Linoleic C18
PUFA 2.1% by wt 2.6% by wt
-5 C

These fatty acids exist in ghee in the form of triglycerides, which make up the bulk(~98%) of ghee.
In order to identify them, they are hydrolyzed to liberate them from the triglyceride molecule [65].
Butyric acid is one of the volatile fatty acids found in butter and ghee and when it is hydrolyzed to
the free form, it gives off the well known rancid smell associated with spoiled dairy products. It is
included here because it is found in a relatively high concentration in ghee compared to other
volatile FAs [67] and has been associated with decreased inflammation in and normalization of
several pathological processes, especially gastrointestinal inflammation [27-30].

What is surprising is actually how low the cholesterol concentration reported here is, yet it is
consistent with other reports [67] of the cholesterol content of ghee. People who have been
advised by their doctors to follow a low fat/low cholesterol diet are counseled to take in less than
300 mg of cholesterol a day from a 1000 kcal/day diet where 30% of the calories come from fat,
as outlined in the Step I diet by the NIH Heart, Lung and Blood Institute [68]. 100 g of ghee is
reported here to contain 178.2 mg cholesterol and reported elsewhere to contain ~900 kcal [67] of
total energy. If one tablespoon of ghee weighs ~ 14 g (data empirically determined), then it
contains ~ 126 kcal of total energy and ~25 mg of cholesterol. Vagbhata suggests using the least
quantity of ghee that is effective for treating the patient, Chap 25 sutra19-20 [6], depending on the
agni and the disease being treated. It is reasonable then, to assume one tablespoon of ghee a
day can be part of a low fat/ low cholesterol Step I diet without putting the patient at risk for
complications of too much cholesterol.

The melting point data are very telling about the nature of cholesterol. A melting temperature of
150 C is very high and it tells the chemist that cholesterol is a compound with strong
intermolecular attractions. The density of cholesterol is 1.067 g/cm
3
, which makes it denser than
water (1 g/cm
3
). The density of most of the long chain FAs is ~ 0.89 g/ cm
3
. In an effort to make
cholesterol less dense for transport through the blood, the body esterifies it to a FA carbon tail and
packs it into LDL.
12

The chemists interpretation of the phenomenon of observing crystalline cholesterol in arterial
plaques and gallstones depends on Density (D) and Melting Point (MP). The magnitude of both
properties makes cholesterol a happier molecule when it is nice and orderly next to another
cholesterol molecule until a crystal is formed. The concepts of Entropy "S
surr
, Enthalpy "H and
Gibbs Free Energy "G illustrate this from a thermodynamic standpoint. Entropy "S
surr
is a
measure of disorder in the universe and in general, is always increasing or becoming more
positive. Enthalpy "H is a measure of the energy required or released from a process. Here we
are looking at the enthalpy of fusion between molecules of cholesterol. Gibbs Free Energy "G is a
measure of the energy available in a system to do work. Here we are looking at the free energy of
cholesterol crystallization at body temperature. In general, for a process to be spontaneous,
"S
surr
>0, "H <0, and "G <0. A process is spontaneous in the direction in which Gibbs Free
Energy, "G decreases [69]. The free energy, "G required to hydrolyze the ester bond between
the FA tail and its cholesterol molecule is supplied from the tremendous free energy given up
during cholesterol crystallization ("G becomes more negative) because heat flows out of the
system when cholesterol molecules crystallize. How do we know heat must flow out when the
cholesterol crystallizes? The Melting Point: MP tells us a lot of energy must be put into the system
in order to begin to separate molecules of cholesterol from each other, the Enthalpy "H of fusion.
This is the same amount of energy or heat that will be given up by the molecules coming together
and it is exactly this kind of thermodynamic balancing act that drives all the chemical reactions in
the body[12] including the crystallization of cholesterol in fatty plaques and blockages.

Further, if one compares the relative melting points of all the lipids present in ghee to that of
cholesterol, one would expect to see cholesterol as the only crystallized lipid at body temperature.
None of the other lipids present in ghee could even begin to crystallize under the conditions
present in the body as 37 C is very close to their respective melting points. Body temperature,
37 C is 111 C below the melting point of cholesterol. What this means is that from a chemical
perspective, cholesterol molecules want to adhere to each other strongly and are making relatively
slow molecular motions. In contrast, 37 C being above or very close to the other FA melting
points means these other FAs are undergoing relatively fast molecular interactions and they
experience much poorer intermolecular attractions than cholesterol. Does observing cholesterol
crystals in plaques make cholesterol the causative agent for plaque formation?

The answer is no, as plaque formation has been demonstrated to begin with endothelial insult
followed by fatty streak formation from macrophages attempting to clear away the initial injury [25,
26, 61]. Plaques form over these areas of injured endothelium attracting more macrophages,
cytokines and other inflammatory biomolecules as the body attempts to heal the injury. Further, it
is now widely accepted that the kind of plaques most likely to rupture are not the large crystalline,
stable plaques seen in angina pectoris, but rather, plaques causing only 20-30% stenosis or
13
lumen narrowing. These smaller plaques have no cholesterol or other crystalline deposition, yet
are highly associated with inflammation and the data show it is these lesser plaques that do not
even show up by angiography which carry the highest risk for rupture and thrombosis formation
[70, 71].

Biochemistry and the Doshic Effects of Ghee
How does ghee accomplish all the medicinal effects listed in the ancient texts? Table 1 lists some
of the actions of ghee given by the ancient authors and yet, there has been very little formal
Western investigation into these claims. On the other hand there has been some research done
on biochemical components of ghee and some of these data will be reviewed here.

The ancient texts tell us that ghee has anti-pitta properties and that small amounts of it can
stimulate agni without aggravating pitta [2, 4, 6]. Ghee is relatively high in a volatile FA called
Butyric Acid (BA) and it is this acid in the free form that gives the rancid smell of spoiled dairy
products [1, 72]. BA is an important short chain (4 carbon) FA, and is one of the several short
chain FAs that is also produced by anaerobic fermentation of undigested dietary fibers in the
colon. Recent data have shown that colonic irrigation with solutions of BA not only relieve the
inflammation associated with Crohns disease, but also results in transcriptional changes in gut
mucosal cells that are associated with increased FA metabolism and decreased oxidative stress
[27, 28, 73].

Ghee is said to increase agni [2-4, 6]. Increased agni can be viewed as an increase in energy
expenditure. When one is burning calories effectively, the body will respond by increasing hunger
to take in more food to support that expenditure. In the diabetic mouse model, BA has been
shown to increase energy expenditure and reverse insulin insensitivity, which from an Ayurvedic
standpoint is viewed as compromised agni of Kapha origin [74, 75]. Further, BA has been shown
to have anti-tumor activity [29, 30] which can be attributed to pacifying Kapha dosha. These data
can be interpreted as increasing agni by pacifying Kapha but without aggravating Pitta.

The ancient texts tell us that ghee is also good for persons who desire intelligence, good memory
and wisdom [6]. Alzheimers disease is a neurodegenerative disease characterized by
progressive cognitive and memory decline leading to dementia [76]. From an Ayurvedic standpoint
it is viewed as a result of Vata dosha having relocated in the majja and mano vaha srotas. Vata is
cold, rough and dry and the unctuousness of ghee comes from the fat content. Docosahexaenoic
acid (DHA) deficiency in particular has been shown to correlate with impaired brain function [77]
as seen in Alzheimers. Not only is ghee unctuous and penetrating, it is also high in the FA
precursors for DHA lending to the Ayurvedic notion that ghee improves brain functioning. This
view can be expanded further to understand how ghee can ameliorate other brain diseases of
Vata origin such as epilepsy and insanity even in the absence of Western style data.
14

Research more specific to ghee has been done in the area of cholesterol research. Historical
data have been confusing, presenting contradictory effects of ghee on serum cholesterol levels.
This may be due to the use of vanaspati ghee or ghee made with hydrogenated vegetable oil [78]
in older studies. More recent work shows that ghee can slightly raise total cholesterol levels, but
does so by raising the HDL, the so called good cholesterol from the Western standpoint [79]. The
National Cholesterol Education Program (NCEP) recommendations for cholesterol management
state that when HDL is raised above 60 mg/dL, it is considered a negative risk factor for CVD [80].
The increase in HDL cholesterol seen with ghee can be interpreted as reducing CVD risk from the
standpoint of the NCEP guidelines.

There has also been a question about the formation of cholesterol oxidation products (COPS)
which are reported to be atherogenic and angiotoxic [81]. Kumar, et al., specifically studied the
effect of ghee and COPS found in ghee from prolonged heating on serum and liver lipids in male
Wistar rats [65]. First they demonstrated that heating did indeed decrease cholesterol levels and
increase the COPS levels in ghee. However, animals fed ghee or ghee with significant levels of
COPS both showed an overall decrease in serum lipids over a dietary range of 2.5%-10%. Later
work suggests this decrease in serum levels of cholesterol may be due to increased secretion of
biliary lipids [82], one of the main ways the body removes excess fat from ingested foods before it
can enter the systemic circulation.

Studies that take into account ghees prabhav for carrying herbs to the deep tissues have been
done using the Western scientific model. For example, Oza, et al. studied Bhringarajadi Ghrita
Rasayana in premature aging. Here they were able to demonstrate the reversal of several
Ayurvedic parameters of aging such as muscle weakness and mental acuity. They concluded that
Bhringarajadi Ghrita probably acts at the level of the dhatuagni which leads to improvement in the
overall health of the dhatus and hence, the person [83].

Conclusions:
Ghee is an important medicine in Ayurveda having tridoshic and doshic specific rasayana
properties. In the West, the use of ghee as medicine has been circumspect because of its
association with dairy products and saturated fatty acids. Ghee is a liquid at body temperature
and is only ~ 68% saturated which means it cannot go in to an organism and suddenly become
solid. Cholesterol, which is found in ghee esterified to FAs has been implicated in CVD, but
research through the years has demonstrated that cholesterol is not the causative agent for
atheroma formation. Although, cholesterol does not appear to be the causative agent, controlling
the biosynthesis of cholesterol has reduced the primary and secondary risks associated with
elevated serum cholesterol. That said, the amount of cholesterol in 1-3 tablespoons of ghee is in
line with the NHILBIs recommendations for a low fat/low cholesterol diet. Further, attention is
15
turning from cholesterol specifically to the role of !-3 and !-6 PUFAs in CVD. Our current corn
based food chain system has shifted the ratio of PUFAs favoring !-6 over !-3. Animals fed grass
based diets produce products that are higher in !-3 than !-6. !-6 PUFA involvement in pro-
inflammatory processes versus !-3 involvement in anti-inflammatory processes may explain the
high degree of CVD risk seen in the West. The body of evidence on ghee in specific, controlled
Western style clinical trials is small, yet promising for explaining the Ayurvedic actions of ghee to
the Western medical community. Regardless, the ancient texts of Ayurveda clearly state the
many medicinal applications of ghee and it is considered one of Ayurvedas most potent
medicines. Perhaps going forward, more Western style research will be done to support the many
Ayurvedic medicinal claims for ghee, but that remains to be seen. On the other hand, the
predictive value of the science that is Ayurveda should be enough for most practitioners to have
confidence using ghee in the treatment of appropriate patients.


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