CCA Logo an internationally recognized Ayurveda school
Call us at 530-478-9100

Ghee: An Ayurvedic and Biochemical Treatise By: Catherine Robbins

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 cow’s 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 cow’s 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 today’s medical world where the search is on for THE one pharmaceutical “magic bullet”, ghee appears to be just that.

Table 1

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

   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]. Ghee’s unctuousness makes it an excellent internal and external lubricant for treating Vata’s dryness, roughness and emaciation and Kapha’s 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?  Isn’t ghee just rendered animal fat and shouldn’t we all be avoiding animal fat in general? Isn’t ghee, being a by-product of butter, high in cholesterol?

   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: what’s 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: triacylglycerolsa
  • 2. Membrane Lipids (phospholipids, sphingoglycolipids and cholesterolb)
  • 3. Emulsification lipids (bile acids)
  • 4. Messenger lipids (steroid hormones, cholesterolb 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 chainc 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 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 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].
 
   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 Crohn’s 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 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 6th 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 ω-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 American’s energy intake from PUFAs [24, 33].
 
   Alpha-linolenic acid (ALA) is an ω-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 ω-3 PUFAs that came to light during epidemiological studies of Eskimo/Inuit tribes who consume large amounts of ω-3 PUFAs from the fat from fish yet have low rates of CVD [24, 33, 35, 36]. Other positive effects attributed to ω-3 PUFAs, especially EPA and DHA are anti-thrombotic, anti- Alzheimer’s 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 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].
 
   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 cholesterol’s 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 Anitschkow’s 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 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.
 
   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 one’s 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 US’s 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 ----------------
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/cm3, which makes it denser than water (1 g/cm3). The density of most of the long chain FAs is ~ 0.89 g/ cm3. 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.
 
   The chemist’s 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 Ssurr, Enthalpy   H and Gibbs Free Energy G illustrate this from a thermodynamic standpoint. Entropy Ssurr 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, Ssurr >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 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 Crohn’s 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]. Alzheimer’s 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 Alzheimer’s. 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.
 
   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 ghee’s 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 NHILBI’s recommendations for a low fat/low cholesterol diet.  Further, attention is 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 Ayurveda’s 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.

Bibiliography

1. Wikipedia. Butter.  [cited; Available from: http://en.wikipedia.org/wiki/Butter.

2. Caraka, B. Dash, and K. Gupta, The Caraka samhita : anvaya (natural work order), transliteration, annotation along with, English equivalents, translation & commentary in English based on Cakrapani's Ayurveda Dipika. 1st ed. Indian medical science series. 1999, Delhi: Sri Satguru Publications. v.

3. Agnivesa, et al., Agnivesa's Caraka samhita : text with English translation & critical exposition based on Cakrapani Datta's Ayurveda dipika. 1st ed. Chowkhamba Sanskrit studies. 1976, Varanasi: Chowkhamba Sanskrit Series Office.

4. Sushruta, Sushruta Samhita. Vol. 1, Bangalore: Chaukhambra Orientalia.

5. Vagbhata, G., Atrideva, Upadhyaya, Yadunandana, Astangahrdayam : Vidyotini bhasatika- vaktavya-parisistasahitam. Samskarana 14. ed. 2003, Varanasi, Bharata: Caukhambha Samskrta Samsthana.

6. Vagbhata, Ashtanga Samgraha of Vagbhata, a Translation. 9th ed. 2005, Varanasi, India: Chaukhambhia Orientalia.

7. Valiathan, M.S., The legacy of Caraka. 2003, Chennai: Orient Longman. lxxxvi, 634 p.

8. Dash, B., Materia Medica of Ayurveda. 4th printing 2008 ed. 1991, New Delhi: B. Jain Publishers Ltd.

9. Vagbhata, A. Gupta, and Y. Upadhyaya, Astangahrdayam : Vidyotini bhasatika-vaktavya- parisistasahitam. Sa*mskara*na 14. ed. 2003, Varanasi, Bharata: Caukhambha Samskrta Samsthana. 48, 616 p.

10. V, L., Textbook of Ayurveda General Principles of Management and Treatment. 1st ed. Vol.

3. 2012, Albuquerque: The Ayurvedic Press. 646.

11. Magic Bullets. Amer J Pub H, 1953. 43(7): p. 917-918.

12. Nelson, D.L., A.L. Lehninger, and M.M. Cox, Lehninger principles of biochemistry. 5th ed. 2008, New York: W.H. Freeman. 1 v. (various pagings).

13. Stoker, S., General, Organic, and Biological Chemistry. 3rd ed. 2004: Houghton Mifflin Co. 797.

14. Hoffmann, D., Medical herbalism : the science and practice of herbal medicine. 2003, Rochester, Vt.: Healing Arts Press. 666 p.

15. ChemAxon. Marvin Sketch Freeware.  [cited; Available from: https://www.chemaxon.com/products/marvin/.

16. Lawrence, V., et al., Garlic effects on cardiovascular risks and disease, protective effects against cancer, and clinical adverse effects, in Evidence report/technology assessment, no.

20. 2000, Agency for Healthcare Research and Quality: Rockville, MD.

17. R, B. Rumen Physiology and Rumination. 2009 [cited; Available from:  http://arbl.cvmbs.colostate.edu/hbooks/pathphys/digestion/herbivores/rumination.html.

18. Solomons TWG, F.C., Organic Chemistry. 9th ed. 2007, Hoboken, NJ: Wiley & Sons.

19. Wikipedia. File:Rasyslami.jpg. Wikipedia  [cited; Available from:  http://en.wikipedia.org/wiki/File:Rasyslami.jpg.

20. Burr GO, B.M., Miller ES, On The Essential Fatty Acids in Nutrition. J Biol Chem, 1932.

97(1): p. 1-8.

21. Burr GO, B.M., A NEW DEFICIENCY DISEASE PRODUCED BY THE RIGID EXCLUSION OF FAT FROM THE DIET. J Biol Chem, 1929. 82(2): p. 345-367.

22. H, P., The Genesisi of Atherosclerosis. Bull. N.Y. Acad. Med, Feb 19, 1963.

23. Kinsell LW, e.a., Amer J Clin Nutr, 1958. 6(6).

24. Clancy, K., Greener Pastures: How grass-fed beef and milk contribute to healthy eating. 2006, Union of Concerned Scientists.

25. Steinberg, D., Thematic review series: the pathogenesis of atherosclerosis. An interpretive history of the cholesterol controversy: part I. J Lipid Res, 2004. 45(9): p. 1583-93.

26. Steinberg, D., Thematic review series: the pathogenesis of atherosclerosis. An interpretive history of the cholesterol controversy: part II: the early evidence linking hypercholesterolemia to coronary disease in humans. J Lipid Res, 2005. 46(2): p. 179-90.

27. German JB, D.J., Saturated Fats: What Dietary Intake? Amer J Clin Nutr, 2004. 80.

28. Di Sabatino A, e.a., Oral Butyrate for Mildly to Moderately Active Crohn's Disease. AIlment Pharmacol Ther, 2005. 22.

29. Gao Z, e.a., Butyrate Improves Insulin Sensitivity and Increases Energy Expendeture in Mice. Diabetes, 2009. 58.

30. Sossi, P., Butyric Acid: what is the future for this old substance? Swiss Medical Weekly, 2012. 142: p. W13596.

31. Kris-Etherton, P.M., et al., High-monounsaturated fatty acid diets lower both plasma cholesterol and triacylglycerol concentrations. Am J Clin Nutr, 1999. 70(6): p. 1009-15.

32. Wikipedia. Linoleic acid.  [cited; Available from: http://en.wikipedia.org/wiki/Linoleic_acid.

33. Kris-Etherton, P.M., W.S. Harris, and L.J. Appel, Omega-3 fatty acids and cardiovascular disease: new recommendations from the American Heart Association. Arterioscler Thromb Vasc Biol, 2003. 23(2): p. 151-2.

34. Wikipedia, Alpha Linolenic Acid.

35. Simopoulos, A.P., Omega-3 fatty acids and cardiovascular disease: The epidemiological evidence. Environ Health Prev Med, 2002. 6(4): p. 203-9.

36. Sinclair, H.M., Prevention of coronary heart disease: the role of essential fatty acids.

Postgrad Med J, 1980. 56(658): p. 579-84.

37. Beydoun M, e.a., Plasma n-3 fatty acids and the risk of cognitive decline in older adults: Atheroclerosis Risk in Communities Study. Am J Clin Nutr, 2007. 85(4).

38. Harris, W.S., Omega-3 fatty acids and cardiovascular disease: a case for omega-3 index as a new risk factor. Pharmacol Res, 2007. 55(3): p. 217-23.

39. Hashimoto M, H.S., Neuroprotective and Ameliorative Actions of Polyunsaturated Fatty Acids Against Neuronal Diseases: Beneficial Effect of Docosahexaenoic Acid on Cognitive Decline in Alzheimer’s Disease. J Pharmacol Sci, 2010. 116: p. 150-162.

40. Santora, R. and R.A. Kozar, Molecular mechanisms of pharmaconutrients. J Surg Res, 2010. 161(2): p. 288-94.

41. Iwata, N.G., et al., Trans fatty acids induce vascular inflammation and reduce vascular nitric oxide production in endothelial cells. PLoS One, 2011. 6(12): p. e29600.

42. Pharmacy, V.S.o.  [cited; Available from: http://www.people.vcu.edu/~urdesai/intro.htm#Numbering.

43. Frantz, I.D., Jr., Lipids and atherosclerosis. Cancer Res, 1981. 41(9 Pt 2): p. 3718-21.

44. R, S., Physiol Chem, 1926. 160.

45. N, A., Verhanderlung den Deutschen Pathologischen Gesellschaft, 1925. 20.

46. Duff, G.L. and M.G. Mc, Pathology of atherosclerosis. Am J Med, 1951. 11(1): p. 92-108.

47. Vagelos PR, G.L., Medicine, Science and Merck. 2004, Cambridge, UK: Cambridge University Press.

48. Ridker, P.M., The JUPITER trial: results, controversies, and implications for prevention.

Circ Cardiovasc Qual Outcomes, 2009. 2(3): p. 279-85.

49. Roizen M, O.M., YOU on a Diet: The Owner's Manual for Waist Management. 1 ed. 2006, New York, NY: Free Press, a division of Simon & Shuster. 369.

50. Wang, C., et al., Effects of omega-3 fatty acids on cardiovascular disease. Evid Rep Technol Assess (Summ), 2004(94): p. 1-8.

51. JS, G., Atherosclerosis: Viewing the Problem from a Different Perspective Including Possible Treatment Options. Lipid Insights, 2011. 4.

52. Xia F, e.a., Inhibition of Cholesterol Biosynthesis Impairs Insulin Secretion and Voltage- Gated Calcium Channel Function in Pancreatic Bets-cells. Endocrinology, 2008. 149.

53. Klopfleisch, S., et al., Negative impact of statins on oligodendrocytes and myelin formation in vitro and in vivo. J Neurosci, 2008. 28(50): p. 13609-14.

54. Xia, F., et al., Inhibition of cholesterol biosynthesis impairs insulin secretion and voltage- gated calcium channel function in pancreatic beta-cells. Endocrinology, 2008. 149(10): p. 5136-45.

55. Evans M, r.A., Effects of HMG-CoA reductase inhibitors on skeletal muscle: are all statins the same? Drug Safety, 2002. 25(9).

56. Brown, A.S., Use of combination therapy for dyslipidemia: a lipid clinic approach. Am J Cardiol, 2002. 90(10B): p. 44K-49K.

57. K, N., Qualitative Plaque Stabilization But Not Quantitative Plaque Regression. Circulation Journal, 2012. 76.

58. Kastelein, J.J., et al., Simvastatin with or without ezetimibe in familial hypercholesterolemia.

N Engl J Med, 2008. 358(14): p. 1431-43.

59. Berensen, A., Drug Has No Benefit in Trial, Makers Say

, in New York Times. 2008: NY, NY.

60. Rossebo, A.B., et al., Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis. N Engl J Med, 2008. 359(13): p. 1343-56.

61. Steinberg, D., Thematic review series: the pathogenesis of atherosclerosis. An interpretive history of the cholesterol controversy, part V: the discovery of the statins and the end of the controversy. J Lipid Res, 2006. 47(7): p. 1339-51.

62. Futterman, L.G. and L. Lemberg, Apo a-I Milano. Am J Crit Care, 2005. 14(3): p. 244-7.

63. Nabel, E.G. and E. Braunwald, A tale of coronary artery disease and myocardial infarction.

N Engl J Med, 2012. 366(1): p. 54-63.

64. de Oliveira Otto, M.C., et al., Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis. Am J Clin Nutr, 2012.

65. Kumar VJ, S.K., Lokesh B, Effect of dietary ghee-the anhydrous milk fat, on blood and liver lipids in rats. J Nutr. Biochem., 1999. 10.

66. Beare-Rogers J, e.a., Lexicon of lipid nutrition (IUPAC Technical Report). Pure and Applied Chemistry, 2001. 73(4).

67. S, C. COW’S GHEE-GO GHRIT -FA COMPOSITION OF COW'S GHEE. Dec 30, 2012 [cited; Available from: http://ayurvedaconsultants.com/caseshow.aspx?ivalue=engoogle3001.

68. NIH Heart, L.a.B.I. Low Calorie Step I Diet. 2012 [cited; Available from:  http://hp2010.nhlbihin.net/oei_ss/download/pdf/PRACTICAL1.pdf.

69. Zumdahl SS, Z.S., Chemistry, Ch7. 7th ed. 2007, Boston, MA: Houghton Mifflin Company. 1056.

70. Li, J.J., Inflammation: an important mechanism for different clinical entities of coronary artery diseases. Chin Med J (Engl), 2005. 118(21): p. 1817-26.

71. Li, J.J., Inflammation in coronary artery diseases. Chin Med J (Engl), 2011. 124(21): p. 3568-75.

72. Wikipedia, Butyric Acid. Wikipedia.

73. Vanhoutvin, S.A., et al., Butyrate-induced transcriptional changes in human colonic mucosa. PLoS One, 2009. 4(8): p. e6759.

74. V, L., Textbook of Ayurveda: A Complete Guide to Clinical Assessment. 2006, Albuquerque, NM: The Ayurvedic Press.

75. Halpern, M., Textbook of Clinical Ayurvedic Medicine, Part I. 2010.

76. Wikipedia, Alzheimer's Disease cited: http://en.wikipedia.org/wiki/Alzheimer's_disease

77. Cole, G.M., Q.L. Ma, and S.A. Frautschy, Omega-3 fatty acids and dementia.

Prostaglandins Leukot Essent Fatty Acids, 2009. 81(2-3): p. 213-21.

78. Sharma, H., X. Zhang, and C. Dwivedi, The effect of ghee (clarified butter) on serum lipid levels and microsomal lipid peroxidation. Ayu, 2010. 31(2): p. 134-40.

79. Shankar RS, e.a., Serum Lipid Response to Introducing Ghee as a Partial Replacement for Mustard Oil in the Diet of Healthy Young Indians. Indian J. Physiol. Pharmacol., 2005. 49(1).

80. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation, 2002. 106(25): p. 3143-421.

81. LL, S., Review of Progress in Sterol Oxidation 1987-1996. Lipids, 1996. 31.

82. Kumar VJ, S.K., Lokesh B, Hypocholesterolemic efect of anhydrous milk fat ghee is mediated by increasing the secretion of biliary lipids. J Nutr. Biochem., 2000. 11.

83. Oza DN, e.a., Evaluation of Bhringarajadi Ghrita Rasayana in Premature Aging. Ayu, 2009.

30(2).

 

About the Student Research Papers

The papers published on our website have been written by students of the California College of Ayurveda as a part of their required work toward graduation. After reviewing each paper, Dr. Halpern selects those papers that he feels are appropriate to publish. The information in each paper should not be construed as the final word on any subject nor should it be assumed that errors do not exist.