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) .