Milk Homogenization & Heart Disease

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Milk Homogenization & Heart Disease

_http://www.westonaprice.org/knowyourfats/homogenization.html_

(http://www.westonaprice.org/knowyourfats/homogenization.html)

_By Mary G. Enig, PhD _

(http://www.westonaprice.org/knowyourfats/index.html#author)

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:

1. Homogenization causes a supposedly " noxious " enzyme called xanthine

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

2. 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_

(http://www.bethesdapress.com/) .

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_

(http://www.foodsci.uoguelph.ca/dairyedu/homogenization.html) .