Article: Milk Homogenization and Heart Disease

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http://www.realmilk.com/homogenization.html

 

 

 

 

Milk Homogenization and Heart Disease

 

 

<http://www.realmilk.com/homogenization.html#author> By Mary G. Enig,

PhD

 

One widely held popular theory singles out homogenization as a cause of

the current epidemic of heart disease. The hypothesis was developed by

Kurt A. Oster, MD and studied from the early 1960s until the mid 1980s.

In studying and comparing the structure and biochemistry of healthy and

diseased arterial tissue, Oster investigated plasmalogen, an essential

fatty component of many cell membranes in widely scattered tissues

throughout the human body. Plasmalogen makes up a substantial part of

the membranes surrounding heart muscle cells and the cells that make up

the walls of arteries. It is also present in the myelin sheath

surrounding nerve fibers and in a few other tissues. But it is not found

in other parts of the human anatomy.

 

Oster discovered that heart and artery tissue that should contain

plasmalogen often contained none. It is well known that atherosclerosis

begins with a small wound or lesion in the wall of the artery. Oster

reasoned that the initial lesion was caused by the loss of plasmalogen

from the cells lining the artery, leading to the development of plaque.

 

The big question was what caused the lack of plasmalogen in the heart

muscle and the tissue lining the arteries. Oster believed that the

enzyme xanthine oxidase (XO) has the capacity to oxidize, or change,

plasmalogen into a different substance, making it appear that the

plasmalogen had disappeared. The body makes XO, but XO and plasmalogen

are not normally found in the same tissue; the heart, therefore,

normally contains plasmalogen but not XO. In a paper published in 1974,

Oster argued that the presence of XO in the liver and in the mucous

membrane of the small intestine was directly responsible for the natural

absence of plasmalogen from the cell membranes at these sites.1 If XO

somehow made its way to the heart and its arteries, that might explain

the absence of plasmalogen in the surgical specimens and autopsy tissues

from pathological hearts.

 

What was the source of the XO found in the autopsy tissues? Normal human

serum (the fluid part of the blood) does not contain XO. Oster and his

partner Ross considered two possible sources. One was liver cells;

patients with acute liver disease showed increased serum levels of

xanthine oxidase, and those with chronic liver disease occasionally

showed moderate elevations. Another potential source was cow's milk,

" .presently under investigation in this laboratory since it has been

shown that milk antibodies are significantly elevated in the blood of

male patients with heart disease. " 2

 

Cow's milk is the most widely consumed food containing high levels of

XO. Thorough cooking destroys XO, but pasteurization destroys only about

half of the XO in milk. Knowing this, Oster now looked for a link

between XO in milk and the loss of plasmalogen in arteries and heart

muscle tissue.

 

He knew that people have drunk milk for upwards of 10,000 years, and

that milk and milk products were central in the dietaries of many

cultures. But the epidemic of atherosclerosis was recent. These facts

argue against traditional milk and milk products being the culprit. But

the homogenization of milk became widespread in America in the 1930s and

nearly universal in the 1940s-the same decades during which the

incidence of atherosclerotic heart disease began to climb. Oster

theorized that the homogenization of milk somehow increased the

biological availability of xanthine oxidase.

 

According to Oster, XO that remains in pasteurized, unhomogenized milk

is found on the exterior of the membrane of the milk fat globules, where

it is broken down during digestion. XO in raw milk is similarly

digested. Oster postulated that because homogenization reduces the fat

globules to a fraction of their original size, the XO is encapsulated by

the new outer membranes of the smaller fat globules which form during

the homogenization process. He believed that this new membrane protected

the XO from digestive enzymes, allowing some XO to pass intact within

the fat globules from the gut into the circulatory system when

homogenized milk is consumed.3 He referred to these fat globules as

liposomes and argued that the liposomes carrying XO were absorbed

intact. After entering the circulation, they travel to the capillaries,

where the lipoprotein membranes appear to be digested by the enzyme

lipoprotein lipase, thus freeing the XO for absorption into the body,

including the heart and artery tissues, where it may interact with and

destroy plasmalogen.

 

In essence, Oster's theory replaces cholesterol as the cause of heart

disease with another mechanism, summarized as follows:

 

Homogenization causes a supposedly " noxious " enzyme called xanthine

oxidase to be encapsulated in a liposome that can be absorbed intact.

 

XO is released by enzymatic action and ends up in heart and arterial

tissue where it causes the destruction of a specialized protective

membrane lipid called plasmalogen, causing lesions in the arteries and

resulting in the development of plaque.

 

Neither the opponents nor the proponents of the xanthine

oxidase/plasmalogen hypothesis have presented convincing evidence in all

of their writings. However, the more scientific reviews questioned the

validity of Oster's hypothesis, and pointed to some of the inconsistent

findings.

 

A fundamental flaw in Oster's theory involves the difference between a

fat globule and a liposome. Fat globules basically contain triglycerides

and cholesterol encapsulated in a lipid bilayer membrane composed of

proteins, cholesterol, phospholipids and fatty acids. They occur

naturally in milk in a wide range of sizes. The fat globules in

unhomogenized bovine milk are both very small and very large, ranging in

size from 1000 nanometers to 10,000 nanometers. After homogenization,

the average globule size is about 500 nanometers with a range from 200

nanometers to 2000 nanometers.

 

Oster considered homogenization of cow's milk to be a " procedure which

foists unnaturally small particles on our digestive tracts. " 4 Yet

sheep's milk fat globules are reported to be " very small. . . [and

consequently]. . . easier to digest " and in fact globules from this milk

are described as " naturally homogenized. " 5 The milk fat globule membrane

from sheep's milk does not separate and butter cannot be made from such

milk even though there is twice as much fat in sheep's milk as in cow's

milk. The fat globules from goat's milk are similarly small. Once again,

goat's milk is considered easier to digest than cow's milk for this

reason. So there is nothing unnatural about small milk fat globules.

 

Fat globules of all sizes are broken down during digestion, releasing

the hundreds of thousands of triglycerides as well as any enzymes they

contain. (Milk fat globules actually contain more than seven enzymes, of

which XO is one. The other major ones are NADH2, iodonitrotetrazolium,

5-nucleotidase, alkaline phosphatase, phosphodiesterase and

gamma-glutamyltranspeptidase.) These enzymes are broken down into

individual amino acids (enzymes are specialized proteins) and the

triglycerides are broken down into individual fatty acids and

monoglycerides.

 

Although Oster described these small milk fat globules in homogenized

milk as liposomes, several researchers have pointed out that liposomes

are very different in basic composition. Liposomes are typically 200

nanometers or less in size and do not contain complex protein

components. Liposomes do not occur in nature but were developed by

scientists as a way of delivering components such as drugs to the cells

in the body. They are composed of a phospholipid layer in which the

phosphorus moiety is on the outside and the lipid moiety is on the

inside. The layer encapsulates a watery liquid, not fatty acids. A

liposome is not broken down during digestion. For this reason,

scientists have looked at liposomes as a way of delivering compounds

taken orally to the cells. In fact, a 1980 study led by Oster's

colleague D. J. Ross reported that liposome-entrapped insulin effected

blood sugar-lowering in diabetic rats.6 Ross claimed that this proved

that large molecules could be absorbed.

 

A team led by A. J. Clifford looked carefully at Oster's theories. In a

study published in 1983,7 they noted that " neither liposome formation

during homogenization of milk nor absorption of intact liposomes from

the gastrointestinal tract has been demonstrated. " In reviewing the

major published findings, Clifford reported that " absorption of dietary

xanthine oxidase has not been demonstrated. " Clifford's team cites

studies showing lack of activity of serum xanthine oxidase from pigs and

humans fed diets that included milk or were without milk8,9 Further,

Clifford's team noted that " a relationship between intake of homogenized

'dairy foods' and levels of xanthine oxidase activity in the blood has

not been established. "

 

There was even one study which showed an increase in serum xanthine

oxidase when corn oil was fed, whereas milk and cream showed no such

increase.10 Oster had argued that homogenization came into widespread

use during the 1930s and 1940s, the same years during which heart

disease incidence went up dramatically. But these were the same years in

which vegetable oils came into widespread use. (And if Oster's theories

are correct, then only those who drink modern milk would get heart

disease, a conclusion that is obviously untrue.)

 

As for Ross's study on insulin, Clifford argued that recent evaluation

by others showed the insulin phenomenon to be an artifact of the methods

used and not due to the delivery of insulin to the cells. Thus one of

Oster's published proofs turned out to be erroneous. (In fact,

scientists have subsequently tried to use liposomes in humans as a way

of delivering insulin taken orally to the cells but without success.

However, liposomes have been used successfully to deliver an enzyme

needed for the treatment of Gaucher disease.) When the Clifford team

examined the electron micrograph presented in Ross's 1980 paper, he

reported that it did not match the typical liposome stucture as reported

by a noted authority in liposomes.11

 

In the second part of his theory, Oster maintains that XO causes the

destruction of plasmalogen. However, Clifford's team reported that " a

direct role for xanthine oxidase in plasmalogen depletion under

physiological conditions has not been established. " They cite animal

studies where bovine xanthine oxidase was given intravenously in large

doses.12 This treatment failed to deplete plasmalogen in the arteries or

in the coronary tissue, nor did it introduce formation of plaque.

 

The fact that Oster's theory has been disproven does not mean that the

homogenization process is benign. During homogenization there is a

tremendous increase in surface area on the fat globules. The original

fat globule membrane is lost and a new one is formed that incorporates a

much greater portion of casein and whey proteins.13 This may account for

the increased allergenicity of modern processed milk.

 

About the Author

Mary G. Enig, PhD is the author of Know Your Fats: The Complete Primer

for Understanding the Nutrition of Fats, Oils, and Cholesterol, Bethesda

Press, May 2000. Order your copy here: www.enig.com/trans.html.

 

References

 

1. Oster, K., Oster, J., and Ross, D. " Immune Response to Bovine

Xanthine Oxidase in Atherosclerotic Patients. " American Laboratory,

August, 1974, 41-47

 

2. Oster, K., and Ross, D. " The Presence of Ectopic Xanthine

Oxidase in Atherosclerotic Plaques and Myocardial Tissues. " Proceedings

of the Society for Experimental Biology and Medicine, 1973.

 

3. Ibid.

 

4. Oster KA. Plasmalogen diseases: a new concept of the etiology of

the atherosclerotic process. American Journal of Clinical Research

1971:2;30-35.

 

5. Sheep's milk

 

6. Ross DJ, Sharnick SV, Oster KA. Liposomes as proposed vehicle

for the persorption of bovine xanthine oxidase. Proceedings for the

Society of Experimental Biology and Medicine. 1980:163;141-145.

 

7. Clifford AJ, Ho CY, Swenerton H. Homogenized bovine milk

xanthine oxidase: a critique of the hypothesis relating to plasmalogen

depletion and cardiovascular disease. American Journal of Clinical

Nutrition. 1983:38;327-332.

 

8. McCarthy RD, Long CA. Bovine milk intake and xanthine oxidase

activity in blood serum. Journal of Dairy Science. 1976:59;1059-1062.

 

9. Dougherty TM, Zikakis JP, Rzucidlo SJ. Serum xanthine oxidase

studies on miniature pigs. Nutrition Report International.

1977:16;241-248.

 

10. Ho CY, Crane RT, Clifford AJ. Studies on lymphatic absorption of

and the availability of riboflavin from bovine milk xanthine oxidase.

Journal of Nutrition. 1978:108;55-60.

 

11. Bangham AD. Physical structure and behavior of lipids and lipid

enzymes. Advances in Lipid Research. 1963:1;65-104.

 

12. Ho CY, Clifford AJ. Bovine milk xanthine oxidase, blood lipids

and coronary plaques in rabbits. Journal of Nutrition. 1977:107;758-766.

 

 

13. http://www.foodsci.uoguelph.ca/dairyedu/homogenization.html.

 

_____

 

This article appeared in Wise Traditions in Food, Farming and the

Healing Arts,

the quarterly magazine of the Weston A. Price Foundation, Summer 2003

 

 

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<http://www.westonaprice.org/> The Weston A. Price Foundation

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