Skrevet av Emne: ...en liten pust i bakken.  (Lest 166831 ganger)

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Sv: Dangermouse... need any more?? :)
« #1200 : 29. april 2008, 14:18 »
Dagens lille sommerøkt:
---------------------------------------------
Chins:
15x60kg
12x70kg
10x80kg
8x90kg
8x90kg
10x75kg

BP:
15x70kg
12x90kg
8x110kg
7x130kg
6x140kg (+1 som neeesten gikk)
4x140kg (+1 som ikke ville gått)
9x120kg (+1 som ikke ville gått)

Stående roing:
15x40kg
10x60kg
7x70kg
7x70kg
12x50kg
-----------------------------------------------------

Ryggen fremdeles på bedringens vei, men strekk tar tid folkens. Det tar tid.

Godt fornøyd med BP. Ny rekord, men irritert over siste repp. Den skulle ha gått med litt tenning, og ikke bare vanlig løfting... tror jeg Wink

halla! rå benkpress, god styrke der! 1rm på 165? stå på videre dette går jo veien Cheesy
gutt 1988

bildeprofil; http://www.treningsforum.no/forum/index.php?topic=48442.0

treningslogg; http://www.treningsforum.no/forum/index.php?topic=58782.0

Not with the lights on honey, im bulking!

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  • The secret of steel - Its heavy!!!
Sv: Dangermouse... need any more?? :)
« #1201 : 29. april 2008, 14:53 »
halla! rå benkpress, god styrke der! 1rm på 165? stå på videre dette går jo veien Cheesy

Takker Smiley

Burde selvsagt ha klemt til i dag på 170-175kg siden formen var fin, men jeg tenkte på ryggen først og fremst.
Litt surt, men jeg får stå for mitt valg Smiley
Min treningslogg - sterke saker
BILDER - Ta en titt Smiley
Maks per 5.7.2006    Mål til jul 2006
---------------------------------------------
KB:  170 kg (180kg)      200 kg
BP:  150 kg (165kg)      170 kg
ML:  170 kg  MÅL NÅDD 200 kg

Er dette mulig? Klart det er Grin

Utlogget DangerMouse

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  • The secret of steel - Its heavy!!!
Sv: Dangermouse... need any more?? :)
« #1202 : 02. mai 2008, 14:22 »
Grunnet mitt fravær av treningsrapportering (og trening sådan) poster jeg 2 artikler som jeg mener er et must for oss alle. Enig eller uenig.

De har sikkert blitt lagt ut før, men det vet jeg ei noe om.

Link: http://www.westonaprice.org/knowyourfats/skinny.html

So here goes:

The Skinny on Fats
By Mary Enig, PhD, and Sally Fallon

From: Nourishing Traditions: The Cookbook that Challenges Politically Correct Nutrition and the Diet Dictocrats, Second Edition by Sally Fallon with Mary G. Enig, PhD. © 1999 New Trends Publishing, Inc. All Rights Reserved. To order contact www.newtrendspublishing.com

Table of Contents

Introduction
The Lipid Hypothesis
The "Evidence" Supporting the Lipid Hypothesis
Studies that Challenge the Lipid Hypothesis
Understanding the Chemistry of Fats
Classification of Fatty Acids by Saturation
Classification of Fatty Acids by Length
The Dangers of Polyunsaturates
Too Much Omega-6
Too Little Omega-3
The Benefits of Saturated Fats
What About Cholesterol?
The Cause and Treatment of Heart Disease
Modern Methods of Processing Fat
Nutrients in Butter
Composition of Different Fats
Summary
About the Authors
References
 
Introduction
Fats from animal and vegetable sources provide a concentrated source of energy in the diet; they also provide the building blocks for cell membranes and a variety of hormones and hormonelike substances. Fats as part of a meal slow down absorption so that we can go longer without feeling hungry. In addition, they act as carriers for important fat-soluble vitamins A, D, E and K. Dietary fats are needed for the conversion of carotene to vitamin A, for mineral absorption and for a host of other processes.

Politically Correct Nutrition is based on the assumption that we should reduce our intake of fats, particularly saturated fats from animal sources. Fats from animal sources also contain cholesterol, presented as the twin villain of the civilized diet.

The Lipid Hypothesis
The theory—called the lipid hypothesis—that there is a direct relationship between the amount of saturated fat and cholesterol in the diet and the incidence of coronary heart disease was proposed by a researcher named Ancel Keys in the late 1950's. Numerous subsequent studies have questioned his data and conclusions. Nevertheless, Keys' articles received far more publicity than those presenting alternate views. The vegetable oil and food processing industries, the main beneficiaries of any research that found fault with competing traditional foods, began promoting and funding further research designed to support the lipid hypothesis.

The most well-known advocate of the lowfat diet was Nathan Pritikin. Actually, Pritikin advocated elimination of sugar, white flour and all processed foods from the diet and recommended the use of fresh raw foods, whole grains and a strenuous exercise program; but it was the lowfat aspects of his regime that received the most attention in the media. Adherents found that they lost weight and that their blood cholesterol levels and blood pressure declined. The success of the Pritikin diet was probably due to a number of factors having nothing to do with reduction in dietary fat—weight loss alone, for example, will precipitate a reduction in blood cholesterol levels—but Pritikin soon found that the fat-free diet presented many problems, not the least of which was the fact that people just could not stay on it. Those who possessed enough will power to remain fat-free for any length of time developed a variety of health problems including low energy, difficulty in concentration, depression, weight gain and mineral deficiencies.1 Pritikin may have saved himself from heart disease but his lowfat diet did not spare him from cancer. He died, in the prime of life, of suicide when he realized that his Spartan regime was not curing his leukemia. We shouldn't have to die of either heart disease or cancer—or consume a diet that makes us depressed.

When problems with the no-fat regime became apparent, Pritikin introduced a small amount of fat from vegetable sources into his diet—something like 10% of the total caloric intake. Today the Diet Dictocrats advise us to limit fats to 25-30% of the caloric intake, which is about 2 1/2 ounces or 5 tablespoons per day for a diet of 2400 calories. A careful reckoning of fat intake and avoidance of animal fats, they say, is the key to perfect health.

The "Evidence" Supporting the Lipid Hypothesis
These "experts" assure us that the lipid hypothesis is backed by incontrovertible scientific proof. Most people would be surprised to learn that there is, in fact, very little evidence to support the contention that a diet low in cholesterol and saturated fat actually reduces death from heart disease or in any way increases one's life span. Consider the following:

Before 1920 coronary heart disease was rare in America; so rare that when a young internist named Paul Dudley White introduced the German electrocardiograph to his colleagues at Harvard University, they advised him to concentrate on a more profitable branch of medicine. The new machine revealed the presence of arterial blockages, thus permitting early diagnosis of coronary heart disease. But in those days clogged arteries were a medical rarity, and White had to search for patients who could benefit from his new technology. During the next forty years, however, the incidence of coronary heart disease rose dramatically, so much so that by the mid fifties heart disease was the leading cause of death among Americans. Today heart disease causes at least 40% of all US deaths. If, as we have been told, heart disease results from the consumption of saturated fats, one would expect to find a corresponding increase in animal fat in the American diet. Actually, the reverse is true. During the sixty-year period from 1910 to 1970, the proportion of traditional animal fat in the American diet declined from 83% to 62%, and butter consumption plummeted from eighteen pounds per person per year to four. During the past eighty years, dietary cholesterol intake has increased only 1%. During the same period the percentage of dietary vegetable oils in the form of margarine, shortening and refined oils increased about 400% while the consumption of sugar and processed foods increased about 60%.2

The Framingham Heart Study is often cited as proof of the lipid hypothesis. This study began in 1948 and involved some 6,000 people from the town of Framingham, Massachusetts. Two groups were compared at five-year intervals—those who consumed little cholesterol and saturated fat and those who consumed large amounts. After 40 years, the director of this study had to admit: "In Framingham, Mass, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person's serum cholesterol. . . we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active."3 The study did show that those who weighed more and had abnormally high blood cholesterol levels were slightly more at risk for future heart disease; but weight gain and cholesterol levels had an inverse correlation with fat and cholesterol intake in the diet.4

In a multi-year British study involving several thousand men, half were asked to reduce saturated fat and cholesterol in their diets, to stop smoking and to increase the amounts of unsaturated oils such as margarine and vegetable oils. After one year, those on the "good" diet had 100% more deaths than those on the "bad" diet, in spite of the fact that those men on the "bad" diet continued to smoke! But in describing the study, the author ignored these results in favor of the politically correct conclusion: "The implication for public health policy in the U.K. is that a preventive programme such as we evaluated in this trial is probably effective. . . ."5

The U.S. Multiple Risk Factor Intervention Trial, (MRFIT) sponsored by the National Heart, Lung and Blood Institute, compared mortality rates and eating habits of over 12,000 men. Those with "good" dietary habits (reduced saturated fat and cholesterol, reduced smoking, etc.) showed a marginal reduction in total coronary heart disease, but their overall mortality from all causes was higher. Similar results have been obtained in several other studies. The few studies that indicate a correlation between fat reduction and a decrease in coronary heart disease mortality also document a concurrent increase in deaths from cancer, brain hemorrhage, suicide and violent death.6

The Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT), which cost 150 million dollars, is the study most often cited by the experts to justify lowfat diets. Actually, dietary cholesterol and saturated fat were not tested in this study as all subjects were given a low-cholesterol, low-saturated-fat diet. Instead, the study tested the effects of a cholesterol-lowering drug. Their statistical analysis of the results implied a 24% reduction in the rate of coronary heart disease in the group taking the drug compared with the placebo group; however, nonheart disease deaths in the drug group increased—deaths from cancer, stroke, violence and suicide.7 Even the conclusion that lowering cholesterol reduces heart disease is suspect. Independent researchers who tabulated the results of this study found no significant statistical difference in coronary heart disease death rates between the two groups.8 However, both the popular press and medical journals touted the LRC-CPPT as the long-sought proof that animal fats are the cause of heart disease, America's number one killer.

Studies that Challenge the Lipid Hypothesis
While it is true that researchers have induced heart disease in some animals by giving them extremely large dosages of oxidized or rancid cholesterol—amounts ten times that found in the ordinary human diet—several population studies squarely contradict the cholesterol-heart disease connection. A survey of 1700 patients with hardening of the arteries, conducted by the famous heart surgeon Michael DeBakey, found no relationship between the level of cholesterol in the blood and the incidence of atherosclerosis.9 A survey of South Carolina adults found no correlation of blood cholesterol levels with "bad" dietary habits, such as use of red meat, animal fats, fried foods, butter, eggs, whole milk, bacon, sausage and cheese.10 A Medical Research Council survey showed that men eating butter ran half the risk of developing heart disease as those using margarine.11

Mother's milk provides a higher proportion of cholesterol than almost any other food. It also contains over 50% of its calories as fat, much of it saturated fat. Both cholesterol and saturated fat are essential for growth in babies and children, especially the development of the brain.12 Yet, the American Heart Association is now recommending a low-cholesterol, lowfat diet for children! Commercial formulas are low in saturated fats and soy formulas are devoid of cholesterol. A recent study linked lowfat diets with failure to thrive in children.13

Numerous surveys of traditional populations have yielded information that is an embarrassment to the Diet Dictocrats. For example, a study comparing Jews when they lived in Yemen, whose diets contained fats solely of animal origin, to Yemenite Jews living in Israel, whose diets contained margarine and vegetable oils, revealed little heart disease or diabetes in the former group but high levels of both diseases in the latter.14 (The study also noted that the Yemenite Jews consumed no sugar but those in Israel consumed sugar in amounts equaling 25-30% of total carbohydrate intake.) A comparison of populations in northern and southern India revealed a similar pattern. People in northern India consume 17 times more animal fat but have an incidence of coronary heart disease seven times lower than people in southern India.15 The Masai and kindred tribes of Africa subsist largely on milk, blood and beef. They are free from coronary heart disease and have excellent blood cholesterol levels.16 Eskimos eat liberally of animal fats from fish and marine animals. On their native diet they are free of disease and exceptionally hardy.17 An extensive study of diet and disease patterns in China found that the region in which the populace consumes large amounts of whole milk had half the rate of heart disease as several districts in which only small amounts of animal products are consumed.18 Several Mediterranean societies have low rates of heart disease even though fat—including highly saturated fat from lamb, sausage and goat cheese—comprises up to 70% of their caloric intake. The inhabitants of Crete, for example, are remarkable for their good health and longevity.19 A study of Puerto Ricans revealed that, although they consume large amounts of animal fat, they have a very low incidence of colon and breast cancer.20 A study of the long-lived inhabitants of Soviet Georgia revealed that those who eat the most fatty meat live the longest.21 In Okinawa, where the average life span for women is 84 years—longer than in Japan—the inhabitants eat generous amounts of pork and seafood and do all their cooking in lard.22 None of these studies is mentioned by those urging restriction of saturated fats.

The relative good health of the Japanese, who have the longest life span of any nation in the world, is generally attributed to a lowfat diet. Although the Japanese eat few dairy fats, the notion that their diet is low in fat is a myth; rather, it contains moderate amounts of animal fats from eggs, pork, chicken, beef, seafood and organ meats. With their fondness for shellfish and fish broth, eaten on a daily basis, the Japanese probably consume more cholesterol than most Americans. What they do not consume is a lot of vegetable oil, white flour or processed food (although they do eat white rice.) The life span of the Japanese has increased since World War II with an increase in animal fat and protein in the diet.23 Those who point to Japanese statistics to promote the lowfat diet fail to mention that the Swiss live almost as long on one of the fattiest diets in the world. Tied for third in the longevity stakes are Austria and Greece—both with high-fat diets.24

As a final example, let us consider the French. Anyone who has eaten his way across France has observed that the French diet is just loaded with saturated fats in the form of butter, eggs, cheese, cream, liver, meats and rich patés. Yet the French have a lower rate of coronary heart disease than many other western countries. In the United States, 315 of every 100,000 middle-aged men die of heart attacks each year; in France the rate is 145 per 100,000. In the Gascony region, where goose and duck liver form a staple of the diet, this rate is a remarkably low 80 per 100,000.25 This phenomenon has recently gained international attention as the French Paradox. (The French do suffer from many degenerative diseases, however. They eat large amounts of sugar and white flour and in recent years have succumbed to the timesaving temptations of processed foods.)

A chorus of establishment voices, including the American Cancer Society, the National Cancer Institute and the Senate Committee on Nutrition and Human Needs, claims that animal fat is linked not only with heart disease but also with cancers of various types. Yet when researchers from the University of Maryland analyzed the data they used to make such claims, they found that vegetable fat consumption was correlated with cancer and animal fat was not.26

Understanding the Chemistry of Fats
Clearly something is wrong with the theories we read in the popular press—and used to bolster sales of lowfat concoctions and cholesterol-free foods. The notion that saturated fats per se cause heart disease as well as cancer is not only facile, it is just plain wrong. But it is true that some fats are bad for us. In order to understand which ones, we must know something about the chemistry of fats.

Fats—or lipids—are a class of organic substances that are not soluble in water. In simple terms, fatty acids are chains of carbon atoms with hydrogen atoms filling the available bonds. Most fat in our bodies and in the food we eat is in the form of triglycerides, that is, three fatty-acid chains attached to a glycerol molecule. Elevated triglycerides in the blood have been positively linked to proneness to heart disease, but these triglycerides do not come directly from dietary fats; they are made in the liver from any excess sugars that have not been used for energy. The source of these excess sugars is any food containing carbohydrates, particularly refined sugar and white flour.

Classification of Fatty Acids by Saturation
Fatty acids are classified in the following way:

Saturated: A fatty acid is saturated when all available carbon bonds are occupied by a hydrogen atom. They are highly stable, because all the carbon-atom linkages are filled—or saturated—with hydrogen. This means that they do not normally go rancid, even when heated for cooking purposes. They are straight in form and hence pack together easily, so that they form a solid or semisolid fat at room temperature. Your body makes saturated fatty acids from carbohydrates and they are found in animal fats and tropical oils.

Monounsaturated: Monounsaturated fatty acids have one double bond in the form of two carbon atoms double-bonded to each other and, therefore, lack two hydrogen atoms. Your body makes monounsaturated fatty acids from saturated fatty acids and uses them in a number of ways. Monounsaturated fats have a kink or bend at the position of the double bond so that they do not pack together as easily as saturated fats and, therefore, tend to be liquid at room temperature. Like saturated fats, they are relatively stable. They do not go rancid easily and hence can be used in cooking. The monounsaturated fatty acid most commonly found in our food is oleic acid, the main component of olive oil as well as the oils from almonds, pecans, cashews, peanuts and avocados.

Polyunsaturated: Polyunsaturated fatty acids have two or more pairs of double bonds and, therefore, lack four or more hydrogen atoms. The two polyunsaturated fatty acids found most frequently in our foods are double unsaturated linoleic acid, with two double bonds—also called omega-6; and triple unsaturated linolenic acid, with three double bonds—also called omega-3. (The omega number indicates the position of the first double bond.) Your body cannot make these fatty acids and hence they are called "essential." We must obtain our essential fatty acids or EFA's from the foods we eat. The polyunsaturated fatty acids have kinks or turns at the position of the double bond and hence do not pack together easily. They are liquid, even when refrigerated. The unpaired electrons at the double bonds makes these oils highly reactive. They go rancid easily, particularly omega-3 linolenic acid, and must be treated with care. Polyunsaturated oils should never be heated or used in cooking. In nature, the polyunsaturated fatty acids are usually found in the cis form, which means that both hydrogen atoms at the double bond are on the same side.

All fats and oils, whether of vegetable or animal origin, are some combination of saturated fatty acids, monounsaturated fatty acids and polyunsaturated linoleic acid and linolenic acid. In general, animal fats such as butter, lard and tallow contain about 40-60% saturated fat and are solid at room temperature. Vegetable oils from northern climates contain a preponderance of polyunsaturated fatty acids and are liquid at room temperature. But vegetable oils from the tropics are highly saturated. Coconut oil, for example, is 92% saturated. These fats are liquid in the tropics but hard as butter in northern climes. Vegetable oils are more saturated in hot climates because the increased saturation helps maintain stiffness in plant leaves. Olive oil with its preponderance of oleic acid is the product of a temperate climate. It is liquid at warm temperatures but hardens when refrigerated.

Classification of Fatty Acids by Length
Researchers classify fatty acids not only according to their degree of saturation but also by their length.

Short-chain fatty acids have four to six carbon atoms. These fats are always saturated. Four-carbon butyric acid is found mostly in butterfat from cows, and six-carbon capric acid is found mostly in butterfat from goats. These fatty acids have antimicrobial properties—that is, they protect us from viruses, yeasts and pathogenic bacteria in the gut. They do not need to be acted on by the bile salts but are directly absorbed for quick energy. For this reason, they are less likely to cause weight gain than olive oil or commercial vegetable oils.27 Short-chain fatty acids also contribute to the health of the immune system.28

Medium-chain fatty acids have eight to twelve carbon atoms and are found mostly in butterfat and the tropical oils. Like the short-chain fatty acids, these fats have antimicrobial properties; are absorbed directly for quick energy; and contribute to the health of the immune system.

Long-chain fatty acids have from 14 to 18 carbon atoms and can be either saturated, monounsaturated or polyunsaturated. Stearic acid is an 18-carbon saturated fatty acid found chiefly in beef and mutton tallows. Oleic acid is an 18-carbon monounsaturated fat which is the chief component of olive oil. Another monounsaturated fatty acid is the 16-carbon palmitoleic acid which has strong antimicrobial properties. It is found almost exclusively in animal fats. The two essential fatty acids are also long chain, each 18 carbons in length. Another important long-chain fatty acid is gamma-linolenic acid (GLA) which has 18 carbons and three double bonds. It is found in evening primrose, borage and black currant oils. Your body makes GLA out of omega-6 linoleic acid and uses it in the production of substances called prostaglandins, localized tissue hormones that regulate many processes at the cellular level.

Very-long-chain fatty acids have 20 to 24 carbon atoms. They tend to be highly unsaturated, with four, five or six double bonds. Some people can make these fatty acids from EFA's, but others, particularly those whose ancestors ate a lot of fish, lack enzymes to produce them. These "obligate carnivores" must obtain them from animal foods such as organ meats, egg yolks, butter and fish oils. The most important very-long-chain fatty acids are dihomo-gamma-linolenic acid (DGLA) with 20 carbons and three double bonds; arachidonic acid (AA) with 20 carbons and four double bonds; eicosapentaenoic acid (EPA) with 20 carbons and five double bonds; and docosahexaenoic acid (DHA) with 22 carbons and six double bonds. All of these except DHA are used in the production of prostaglandins, localized tissue hormones that direct many processes in the cells. In addition, AA and DHA play important roles in the function of the nervous system.29

The Dangers of Polyunsaturates
The public has been fed a great deal of misinformation about the relative virtues of saturated fats versus polyunsaturated oils. Politically correct dietary gurus tell us that the polyunsaturated oils are good for us and that the saturated fats cause cancer and heart disease. The result is that fundamental changes have occurred in the Western diet. At the turn of the century, most of the fatty acids in the diet were either saturated or monounsaturated, primarily from butter, lard, tallows, coconut oil and small amounts of olive oil. Today most of the fats in the diet are polyunsaturated from vegetable oils derived mostly from soy, as well as from corn, safflower and canola.

Modern diets can contain as much as 30% of calories as polyunsaturated oils, but scientific research indicates that this amount is far too high. The best evidence indicates that our intake of polyunsaturates should not be much greater than 4% of the caloric total, in approximate proportions of 1 1/2 % omega-3 linolenic acid and 2 1/2 % omega-6 linoleic acid.30 EFA consumption in this range is found in native populations in temperate and tropical regions whose intake of polyunsaturated oils comes from the small amounts found in legumes, grains, nuts, green vegetables, fish, olive oil and animal fats but not from commercial vegetable oils.

Excess consumption of polyunsaturated oils has been shown to contribute to a large number of disease conditions including increased cancer and heart disease; immune system dysfunction; damage to the liver, reproductive organs and lungs; digestive disorders; depressed learning ability; impaired growth; and weight gain.31

One reason the polyunsaturates cause so many health problems is that they tend to become oxidized or rancid when subjected to heat, oxygen and moisture as in cooking and processing. Rancid oils are characterized by free radicals—that is, single atoms or clusters with an unpaired electron in an outer orbit. These compounds are extremely reactive chemically. They have been characterized as "marauders" in the body for they attack cell membranes and red blood cells and cause damage in DNA/RNA strands, thus triggering mutations in tissue, blood vessels and skin. Free radical damage to the skin causes wrinkles and premature aging; free radical damage to the tissues and organs sets the stage for tumors; free radical damage in the blood vessels initiates the buildup of plaque. Is it any wonder that tests and studies have repeatedly shown a high correlation between cancer and heart disease with the consumption of polyunsaturates?32 New evidence links exposure to free radicals with premature aging, with autoimmune diseases such as arthritis and with Parkinson's disease, Lou Gehrig's disease, Alzheimer's and cataracts.33

Too Much Omega-6
Problems associated with an excess of polyunsaturates are exacerbated by the fact that most polyunsaturates in commercial vegetable oils are in the form of double unsaturated omega-6 linoleic acid, with very little of vital triple unsaturated omega-3 linolenic acid. Recent research has revealed that too much omega-6 in the diet creates an imbalance that can interfere with production of important prostaglandins.34 This disruption can result in increased tendency to form blood clots, inflammation, high blood pressure, irritation of the digestive tract, depressed immune function, sterility, cell proliferation, cancer and weight gain.35

Too Little Omega-3
A number of researchers have argued that along with a surfeit of omega-6 fatty acids the American diet is deficient in the more unsaturated omega-3 linolenic acid. This fatty acid is necessary for cell oxidation, for metabolizing important sulphur-containing amino acids and for maintaining proper balance in prostaglandin production. Deficiencies have been associated with asthma, heart disease and learning deficiencies.36 Most commercial vegetable oils contain very little omega-3 linolenic acid and large amounts of the omega-6 linoleic acid. In addition, modern agricultural and industrial practices have reduced the amount of omega-3 fatty acids in commercially available vegetables, eggs, fish and meat. For example, organic eggs from hens allowed to feed on insects and green plants can contain omega-6 and omega-3 fatty acids in the beneficial ratio of approximately one-to-one; but commercial supermarket eggs can contain as much as nineteen times more omega-6 than omega-3!37

The Benefits of Saturated Fats
The much-maligned saturated fats—which Americans are trying to avoid—are not the cause of our modern diseases. In fact, they play many important roles in the body chemistry:

Saturated fatty acids constitute at least 50% of the cell membranes. They are what gives our cells necessary stiffness and integrity.


They play a vital role in the health of our bones. For calcium to be effectively incorporated into the skeletal structure, at least 50% of the dietary fats should be saturated.38


They lower Lp(a), a substance in the blood that indicates proneness to heart disease.39 They protect the liver from alcohol and other toxins, such as Tylenol.40


They enhance the immune system.41


They are needed for the proper utilization of essential fatty acids.
Elongated omega-3 fatty acids are better retained in the tissues when the diet is rich in saturated fats. 42


Saturated 18-carbon stearic acid and 16-carbon palmitic acid are the preferred foods for the heart, which is why the fat around the heart muscle is highly saturated.43 The heart draws on this reserve of fat in times of stress.


Short- and medium-chain saturated fatty acids have important antimicrobial properties. They protect us against harmful microorganisms in the digestive tract.
The scientific evidence, honestly evaluated, does not support the assertion that "artery-clogging" saturated fats cause heart disease.44 Actually, evaluation of the fat in artery clogs reveals that only about 26% is saturated. The rest is unsaturated, of which more than half is polyunsaturated.45

What about Cholesterol?
And what about cholesterol? Here, too, the public has been misinformed. Our blood vessels can become damaged in a number of ways—through irritations caused by free radicals or viruses, or because they are structurally weak—and when this happens, the body's natural healing substance steps in to repair the damage. That substance is cholesterol. Cholesterol is a high-molecular-weight alcohol that is manufactured in the liver and in most human cells. Like saturated fats, the cholesterol we make and consume plays many vital roles:

Along with saturated fats, cholesterol in the cell membrane gives our cells necessary stiffness and stability. When the diet contains an excess of polyunsaturated fatty acids, these replace saturated fatty acids in the cell membrane, so that the cell walls actually become flabby. When this happens, cholesterol from the blood is "driven" into the tissues to give them structural integrity. This is why serum cholesterol levels may go down temporarily when we replace saturated fats with polyunsaturated oils in the diet.46


Cholesterol acts as a precursor to vital corticosteroids, hormones that help us deal with stress and protect the body against heart disease and cancer; and to the sex hormones like androgen, testosterone, estrogen and progesterone.


Cholesterol is a precursor to vitamin D, a very important fat-soluble vitamin needed for healthy bones and nervous system, proper growth, mineral metabolism, muscle tone, insulin production, reproduction and immune system function.


The bile salts are made from cholesterol. Bile is vital for digestion and assimilation of fats in the diet.


Recent research shows that cholesterol acts as an antioxidant.47 This is the likely explanation for the fact that cholesterol levels go up with age. As an antioxidant, cholesterol protects us against free radical damage that leads to heart disease and cancer.


Cholesterol is needed for proper function of serotonin receptors in the brain.48 Serotonin is the body's natural "feel-good" chemical. Low cholesterol levels have been linked to aggressive and violent behavior, depression and suicidal tendencies.


Mother's milk is especially rich in cholesterol and contains a special enzyme that helps the baby utilize this nutrient. Babies and children need cholesterol-rich foods throughout their growing years to ensure proper development of the brain and nervous system.


Dietary cholesterol plays an important role in maintaining the health of the intestinal wall.49 This is why low-cholesterol vegetarian diets can lead to leaky gut syndrome and other intestinal disorders.
Cholesterol is not the cause of heart disease but rather a potent antioxidant weapon against free radicals in the blood, and a repair substance that helps heal arterial damage (although the arterial plaques themselves contain very little cholesterol.) However, like fats, cholesterol may be damaged by exposure to heat and oxygen. This damaged or oxidized cholesterol seems to promote both injury to the arterial cells as well as a pathological buildup of plaque in the arteries.50 Damaged cholesterol is found in powdered eggs, in powdered milk (added to reduced-fat milks to give them body) and in meats and fats that have been heated to high temperatures in frying and other high-temperature processes.

High serum cholesterol levels often indicate that the body needs cholesterol to protect itself from high levels of altered, free-radical-containing fats. Just as a large police force is needed in a locality where crime occurs frequently, so cholesterol is needed in a poorly nourished body to protect the individual from a tendency to heart disease and cancer. Blaming coronary heart disease on cholesterol is like blaming the police for murder and theft in a high crime area.

Poor thyroid function (hypothyroidism) will often result in high cholesterol levels. When thyroid function is poor, usually due to a diet high in sugar and low in usable iodine, fat-soluble vitamins and other nutrients, the body floods the blood with cholesterol as an adaptive and protective mechanism, providing a superabundance of materials needed to heal tissues and produce protective steroids. Hypothyroid individuals are particularly susceptible to infections, heart disease and cancer.51

The Cause and Treatment of Heart Disease
The cause of heart disease is not animal fats and cholesterol but rather a number of factors inherent in modern diets, including excess consumption of vegetables oils and hydrogenated fats; excess consumption of refined carbohydrates in the form of sugar and white flour; mineral deficiencies, particularly low levels of protective magnesium and iodine; deficiencies of vitamins, particularly of vitamin C, needed for the integrity of the blood vessel walls, and of antioxidants like selenium and vitamin E, which protect us from free radicals; and, finally, the disappearance of antimicrobial fats from the food supply, namely, animal fats and tropical oils.52 These once protected us against the kinds of viruses and bacteria that have been associated with the onset of pathogenic plaque leading to heart disease.

While serum cholesterol levels provide an inaccurate indication of future heart disease, a high level of a substance called homocysteine in the blood has been positively correlated with pathological buildup of plaque in the arteries and the tendency to form clots—a deadly combination. Folic acid, vitamin B6, vitamin B12 and choline are nutrients that lower serum homocysteine levels.53 These nutrients are found mostly in animal foods.

The best way to treat heart disease, then, is not to focus on lowering cholesterol—either by drugs or diet—but to consume a diet that provides animal foods rich in vitamins B6 and B12; to bolster thyroid function by daily use of natural sea salt, a good source of usable iodine; to avoid vitamin and mineral deficiencies that make the artery walls more prone to ruptures and the buildup of plaque; to include the antimicrobial fats in the diet; and to eliminate processed foods containing refined carbohydrates, oxidized cholesterol and free-radical-containing vegetable oils that cause the body to need constant repair.

Modern Methods of Processing Fats
It is important to understand that, of all substances ingested by the body, it is polyunsaturated oils that are most easily rendered dangerous by food processing, especially unstable omega-3 linolenic acid. Consider the following processes inflicted upon naturally occurring fatty acids before they appear on our tables:

Extraction: Oils naturally occurring in fruits, nuts and seeds must first be extracted. In the old days this extraction was achieved by slow-moving stone presses. But oils processed in large factories are obtained by crushing the oil-bearing seeds and heating them to 230 degrees. The oil is then squeezed out at pressures from 10 to 20 tons per inch, thereby generating more heat. During this process the oils are exposed to damaging light and oxygen. In order to extract the last 10% or so of the oil from crushed seeds, processors treat the pulp with one of a number of solvents—usually hexane. The solvent is then boiled off, although up to 100 parts per million may remain in the oil. Such solvents, themselves toxic, also retain the toxic pesticides adhering to seeds and grains before processing begins.

High-temperature processing causes the weak carbon bonds of unsaturated fatty acids, especially triple unsaturated linolenic acid, to break apart, thereby creating dangerous free radicals. In addition, antioxidants, such as fat-soluble vitamin E, which protect the body from the ravages of free radicals, are neutralized or destroyed by high temperatures and pressures. BHT and BHA, both suspected of causing cancer and brain damage, are often added to these oils to replace vitamin E and other natural preservatives destroyed by heat.

There is a safe modern technique for extraction that drills into the seeds and extracts the oil and its precious cargo of antioxidants under low temperatures, with minimal exposure to light and oxygen. These expeller-expressed, unrefined oils will remain fresh for a long time if stored in the refrigerator in dark bottles. Extra virgin olive oil is produced by crushing olives between stone or steel rollers. This process is a gentle one that preserves the integrity of the fatty acids and the numerous natural preservatives in olive oil. If olive oil is packaged in opaque containers, it will retain its freshness and precious store of antioxidants for many years.

Hydrogenation: This is the process that turns polyunsaturates, normally liquid at room temperature, into fats that are solid at room temperature—margarine and shortening. To produce them, manufacturers begin with the cheapest oils—soy, corn, cottonseed or canola, already rancid from the extraction process—and mix them with tiny metal particles—usually nickel oxide. The oil with its nickel catalyst is then subjected to hydrogen gas in a high-pressure, high-temperature reactor. Next, soap-like emulsifiers and starch are squeezed into the mixture to give it a better consistency; the oil is yet again subjected to high temperatures when it is steam-cleaned. This removes its unpleasant odor. Margarine's natural color, an unappetizing grey, is removed by bleach. Dyes and strong flavors must then be added to make it resemble butter. Finally, the mixture is compressed and packaged in blocks or tubs and sold as a health food.

Partially hydrogenated margarines and shortenings are even worse for you than the highly refined vegetable oils from which they are made because of chemical changes that occur during the hydrogenation process. Under high temperatures, the nickel catalyst causes the hydrogen atoms to change position on the fatty acid chain. Before hydrogenation, pairs of hydrogen atoms occur together on the chain, causing the chain to bend slightly and creating a concentration of electrons at the site of the double bond. This is called the cis formation, the configuration most commonly found in nature. With hydrogenation, one hydrogen atom of the pair is moved to the other side so that the molecule straightens. This is called the trans formation, rarely found in nature. Most of these man-made trans fats are toxins to the body, but unfortunately your digestive system does not recognize them as such. Instead of being eliminated, trans fats are incorporated into cell membranes as if they were cis fats—your cells actually become partially hydrogenated! Once in place, trans fatty acids with their misplaced hydrogen atoms wreak havoc in cell metabolism because chemical reactions can only take place when electrons in the cell membranes are in certain arrangements or patterns, which the hydrogenation process has disturbed.

In the 1940's, researchers found a strong correlation between cancer and the consumption of fat—the fats used were hydrogenated fats although the results were presented as though the culprit were saturated fats.54 In fact, until recently saturated fats were usually lumped together with trans fats in the various U.S. data bases that researchers use to correlate dietary trends with disease conditions.55 Thus, natural saturated fats were tarred with the black brush of unnatural hydrogenated vegetable oils.

Altered partially hydrogenated fats made from vegetable oils actually block utilization of essential fatty acids, causing many deleterious effects including sexual dysfunction, increased blood cholesterol and paralysis of the immune system.56 Consumption of hydrogenated fats is associated with a host of other serious diseases, not only cancer but also atherosclerosis, diabetes, obesity, immune system dysfunction, low-birth-weight babies, birth defects, decreased visual acuity, sterility, difficulty in lactation and problems with bones and tendons.57 Yet hydrogenated fats continue to be promoted as health foods. The popularity of partially hydrogenated margarine over butter represents a triumph of advertising duplicity over common sense. Your best defense is to avoid it like the plague.

Homogenization: This is the process whereby the fat particles of cream are strained through tiny pores under great pressure. The resulting fat particles are so small that they stay in suspension rather than rise to the top of the milk. This makes the fat and cholesterol more susceptible to rancidity and oxidation, and some research indicates that homogenized fats may contribute to heart disease.58

The media's constant attack on saturated fats is extremely suspect. Claims that butter causes chronic high cholesterol values have not been substantiated by research—although some studies show that butter consumption causes a small, temporary rise—while other studies have shown that stearic acid, the main component of beef fat, actually lowers cholesterol.59 Margarine, on the other hand, provokes chronic high levels of cholesterol and has been linked to both heart disease and cancer.60 The new soft margarines or tub spreads, while lower in hydrogenated fats, are still produced from rancid vegetable oils and contain many additives.

Nutrients in Butter
The Diet Dictocrats have succeeded in convincing Americans that butter is dangerous, when in fact it is a valued component of many traditional diets and a source of the following nutrients:

Fat-Soluble Vitamins: These include true vitamin A or retinol, vitamin D, vitamin K and vitamin E as well as all their naturally occurring cofactors needed to obtain maximum effect. Butter is America's best source of these important nutrients. In fact, vitamin A is more easily absorbed and utilized from butter than from other sources.61 Fortunately, these fat-soluble vitamins are relatively stable and survive the pasteurization process.

When Dr. Weston Price studied isolated traditional peoples around the world, he found that butter was a staple in many native diets. (He did not find any isolated peoples who consumed polyunsaturated oils.) The groups he studied particularly valued the deep yellow butter produced by cows feeding on rapidly growing green grass. Their natural intuition told them that its life-giving qualities were especially beneficial for children and expectant mothers. When Dr. Price analyzed this deep yellow butter he found that it was exceptionally high in all fat-soluble vitamins, particularly vitamin A. He called these vitamins "catalysts" or "activators." Without them, according to Dr. Price, we are not able to utilize the minerals we ingest, no matter how abundant they may be in our diets. He also believed the fat-soluble vitamins to be necessary for absorption of the water-soluble vitamins. Vitamins A and D are essential for growth, for healthy bones, for proper development of the brain and nervous systems and for normal sexual development. Many studies have shown the importance of butterfat for reproduction; its absence results in "nutritional castration," the failure to bring out male and female sexual characteristics. As butter consumption in America has declined, sterility rates and problems with sexual development have increased. In calves, butter substitutes are unable to promote growth or sustain reproduction.62

Not all the societies Dr. Price studied ate butter; but all the groups he observed went to great lengths to obtain foods high in fat-soluble vitamins—fish, shellfish, fish eggs, organ meats, blubber of sea animals and insects. Without knowing the names of the vitamins contained in these foods, isolated traditional societies recognized their importance in the diet and liberally ate the animal products containing them. They rightly believed such foods to be necessary for fertility and the optimum development of children. Dr. Price analyzed the nutrient content of native diets and found that they consistently provided about ten times more fat soluble vitamins than the American diet of the 1930's. This ratio is probably more extreme today as Americans have deliberately reduced animal fat consumption. Dr. Price realized that these fat-soluble vitamins promoted the beautiful bone structure, wide palate, flawless uncrowded teeth and handsome, well-proportioned faces that characterized members of isolated traditional groups. American children in general do not eat fish or organ meats, at least not to any great extent, and blubber and insects are not a part of the western diet; many will not eat eggs. The only good source of fat-soluble vitamins in the American diet, one sure to be eaten, is butterfat. Butter added to vegetables and spread on bread, and cream added to soups and sauces, ensure proper assimilation of the minerals and water-soluble vitamins in vegetables, grains and meat.

The Wulzen Factor: Called the "antistiffness" factor, this compound is present in raw animal fat. Researcher Rosalind Wulzen discovered that this substance protects humans and animals from calcification of the joints—degenerative arthritis. It also protects against hardening of the arteries, cataracts and calcification of the pineal gland.63 Calves fed pasteurized milk or skim milk develop joint stiffness and do not thrive. Their symptoms are reversed when raw butterfat is added to the diet. Pasteurization destroys the Wulzen factor—it is present only in raw butter, cream and whole milk.

The Price Factor or Activator X: Discovered by Dr. Price, Activator X is a powerful catalyst which, like vitamins A and D, helps the body absorb and utilize minerals. It is found in organ meats from grazing animals and some sea food. Butter can be an especially rich source of Activator X when it comes from cows eating rapidly growing grass in the spring and fall seasons. It disappears in cows fed cottonseed meal or high protein soy-based feeds.64 Fortunately, Activator X is not destroyed by pasteurization. UPDATE: Activator X is now believed to be the fat-soluble vitamin K2; read Chris Masterjohn's article to see how this 60-year mystery was finally solved.

Arachidonic Acid: A 20-carbon polyunsaturate containing four double bonds, found in small amounts only in animal fats. Arachidonic acid (AA) plays a role in the function of the brain, is a vital component of the cell membranes and is a precursor to important prostaglandins. Some dietary gurus warn against eating foods rich in AA, claiming that it contributes to the production of "bad" prostaglandins, ones that cause inflammation. But prostaglandins that counteract inflammation are also made from AA.

Short- and Medium-Chain Fatty Acids: Butter contains about 12-15% short- and medium-chain fatty acids. This type of saturated fat does not need to be emulsified by bile salts but is absorbed directly from the small intestine to the liver, where it is converted into quick energy. These fatty acids also have antimicrobial, antitumor and immune-system-supporting properties, especially 12-carbon lauric acid, a medium-chain fatty acid not found in other animal fats. Highly protective lauric acid should be called a conditionally essential fatty acid because it is made only by the mammary gland and not in the liver like other saturated fats.65 We must obtain it from one of two dietary sources—small amounts in butterfat or large amounts in coconut oil. Four-carbon butyric acid is all but unique to butter. It has antifungal properties as well as antitumor effects.66

Omega-6 and Omega-3 Essential Fatty Acids: These occur in butter in small but nearly equal amounts. This excellent balance between linoleic and linolenic acid prevents the kind of problems associated with overconsumption of omega-6 fatty acids.

Conjugated Linoleic Acid: Butter from pasture-fed cows also contains a form of rearranged linoleic acid called CLA, which has strong anticancer properties. It also encourages the buildup of muscle and prevents weight gain. CLA disappears when cows are fed dry hay or processed feed.67

Lecithin: Lecithin is a natural component of butter that assists in the proper assimilation and metabolization of cholesterol and other fat constituents.

Cholesterol: Mother's milk is high in cholesterol because it is essential for growth and development. Cholesterol is also needed to produce a variety of steroids that protect against cancer, heart disease and mental illness.

Glycosphingolipids: This type of fat protects against gastrointestinal infections, especially in the very young and the elderly. For this reason, children who drink skimmed milk have diarrhea at rates three to five times greater than children who drink whole milk.68

Trace Minerals: Many trace minerals are incorporated into the fat globule membrane of butterfat, including manganese, zinc, chromium and iodine. In mountainous areas far from the sea, iodine in butter protects against goiter. Butter is extremely rich in selenium, a trace mineral with antioxidant properties, containing more per gram than herring or wheat germ.

One frequently voiced objection to the consumption of butter and other animal fats is that they tend to accumulate environmental poisons. Fat-soluble poisons such as DDT do accumulate in fats; but water-soluble poisons, such as antibiotics and growth hormones, accumulate in the water fraction of milk and meats. Vegetables and grains also accumulate poisons. The average plant crop receives ten applications of pesticides—from planting to storage—while cows generally graze on pasture that is unsprayed. Aflatoxin, a fungus that grows on grain, is one of the most powerful carcinogens known. It is correct to assume that all of our foods, whether of vegetable or animal origin, may be contaminated. The solution to environmental poisons is not to eliminate animal fats—so essential to growth, reproduction and overall health—but to seek out organic meats and butter from pasture-fed cows, as well as organic vegetables and grains. These are becoming increasingly available in health food stores and supermarkets and through mail order and cooperatives.

Composition of Different Fats
Before leaving this complex but vital subject of fats, it is worthwhile examining the composition of vegetable oils and other animal fats in order to determine their usefulness and appropriateness in food preparation:

Duck and Goose Fat are semisolid at room temperature, containing about 35% saturated fat, 52% monounsaturated fat (including small amounts of antimicrobial palmitoleic acid) and about 13% polyunsaturated fat. The proportion of omega-6 to omega-3 fatty acids depends on what the birds have eaten. Duck and goose fat are quite stable and are highly prized in Europe for frying potatoes.

Chicken Fat is about 31% saturated, 49% monounsaturated (including moderate amounts of antimicrobial palmitoleic acid) and 20% polyunsaturated, most of which is omega-6 linoleic acid, although the amount of omega-3 can be raised by feeding chickens flax or fish meal, or allowing them to range free and eat insects. Although widely used for frying in kosher kitchens, it is inferior to duck and goose fat, which were traditionally preferred to chicken fat in Jewish cooking.

Lard or pork fat is about 40% saturated, 48% monounsaturated (including small amounts of antimicrobial palmitoleic acid) and 12% polyunsaturated. Like the fat of birds, the amount of omega-6 and omega-3 fatty acids will vary in lard according to what has been fed to the pigs. In the tropics, lard may also be a source of lauric acid if the pigs have eaten coconuts. Like duck and goose fat, lard is stable and a preferred fat for frying. It was widely used in America at the turn of the century. It is a good source of vitamin D, especially in third-world countries where other animal foods are likely to be expensive. Some researchers believe that pork products should be avoided because they may contribute to cancer. Others suggest that only pork meat presents a problem and that pig fat in the form of lard is safe and healthy.

Beef and Mutton Tallows are 50-55% saturated, about 40% monounsaturated and contain small amounts of the polyunsaturates, usually less than 3%. Suet, which is the fat from the cavity of the animal, is 70-80% saturated. Suet and tallow are very stable fats and can be used for frying. Traditional cultures valued these fats for their health benefits. They are a good source of antimicrobial palmitoleic acid.

Olive Oil contains 75% oleic acid, the stable monounsaturated fat, along with 13% saturated fat, 10% omega-6 linoleic acid and 2% omega-3 linolenic acid. The high percentage of oleic acid makes olive oil ideal for salads and for cooking at moderate temperatures. Extra virgin olive oil is also rich in antioxidants. It should be cloudy, indicating that it has not been filtered, and have a golden yellow color, indicating that it is made from fully ripened olives. Olive oil has withstood the test of time; it is the safest vegetable oil you can use, but don't overdo. The longer chain fatty acids found in olive oil are more likely to contribute to the buildup of body fat than the short- and medium-chain fatty acids found in butter, coconut oil or palm kernel oil.

Peanut Oil contains 48% oleic acid, 18% saturated fat and 34% omega-6 linoleic acid. Like olive oil, peanut oil is relatively stable and, therefore, appropriate for stir-frys on occasion. But the high percentage of omega-6 presents a potential danger, so use of peanut oil should be strictly limited.

Sesame Oil contains 42% oleic acid, 15% saturated fat, and 43% omega-6 linoleic acid. Sesame oil is similar in composition to peanut oil. It can be used for frying because it contains unique antioxidants that are not destroyed by heat. However, the high percentage of omega-6 militates against exclusive use.

Safflower, Corn, Sunflower, Soybean and Cottonseed Oils all contain over 50% omega-6 and, except for soybean oil, only minimal amounts of omega-3. Safflower oil contains almost 80% omega-6. Researchers are just beginning to discover the dangers of excess omega-6 oils in the diet, whether rancid or not. Use of these oils should be strictly limited. They should never be consumed after they have been heated, as in cooking, frying or baking. High oleic safflower and sunflower oils, produced from hybrid plants, have a composition similar to olive oil, namely, high amounts of oleic acid and only small amounts of polyunsaturated fatty acids and, thus, are more stable than traditional varieties. However, it is difficult to find truly cold-pressed versions of these oils.

Canola Oil contains 5% saturated fat, 57% oleic acid, 23% omega-6 and 10%-15% omega-3. The newest oil on the market, canola oil was developed from the rape seed, a member of the mustard family. Rape seed is unsuited to human consumption because it contains a very-long-chain fatty acid called erucic acid, which under some circumstances is associated with fibrotic heart lesions. Canola oil was bred to contain little if any erucic acid and has drawn the attention of nutritionists because of its high oleic acid content. But there are some indications that canola oil presents dangers of its own. It has a high sulphur content and goes rancid easily. Baked goods made with canola oil develop mold very quickly. During the deodorizing process, the omega-3 fatty acids of processed canola oil are transformed into trans fatty acids, similar to those in margarine and possibly more dangerous.69 A recent study indicates that "heart healthy" canola oil actually creates a deficiency of vitamin E, a vitamin required for a healthy cardiovascular system.70 Other studies indicate that even low-erucic-acid canola oil causes heart lesions, particularly when the diet is low in saturated fat.71

Flax Seed Oil contains 9% saturated fatty acids, 18% oleic acid, 16% omega-6 and 57% omega-3. With its extremely high omega-3 content, flax seed oil provides a remedy for the omega-6/omega-3 imbalance so prevalent in America today. Not surprisingly, Scandinavian folk lore values flax seed oil as a health food. New extraction and bottling methods have minimized rancidity problems. It should always be kept refrigerated, never heated, and consumed in small amounts in salad dressings and spreads.

Tropical Oils are more saturated than other vegetable oils.

Palm oil is about 50% saturated, with 41% oleic acid and about 9% linoleic acid.
Coconut oil is 92% saturated with over two-thirds of the saturated fat in the form of medium-chain fatty acids (often called medium-chain triglycerides). Of particular interest is lauric acid, found in large quantities in both coconut oil and in mother's milk. This fatty acid has strong antifungal and antimicrobial properties. Coconut oil protects tropical populations from bacteria and fungus so prevalent in their food supply; as third-world nations in tropical areas have switched to polyunsaturated vegetable oils, the incidence of intestinal disorders and immune deficiency diseases has increased dramatically. Because coconut oil contains lauric acid, it is often used in baby formulas.
Palm kernel oil, used primarily in candy coatings, also contains high levels of lauric acid. These oils are extremely stable and can be kept at room temperature for many months without becoming rancid. Highly saturated tropical oils do not contribute to heart disease but have nourished healthy populations for millennia.72 It is a shame we do not use these oils for cooking and baking—the bad rap they have received is the result of intense lobbying by the domestic vegetable oil industry.73
Red palm oil has a strong taste that most will find disagreeable—although it is used extensively throughout Africa—but clarified palm oil, which is tasteless and white in color, was formerly used as shortening and in the production of commercial French fries, while coconut oil was used in cookies, crackers and pastries.
The saturated fat scare has forced manufacturers to abandon these safe and healthy oils in favor of hydrogenated soybean, corn, canola and cottonseed oils.

Summary
In summary, our choice of fats and oils is one of extreme importance. Most people, especially infants and growing children, benefit from more fat in the diet rather than less. But the fats we eat must be chosen with care. Avoid all processed foods containing newfangled hydrogenated fats and polyunsaturated oils. Instead, use traditional vegetable oils like extra virgin olive oil and small amounts of unrefined flax seed oil. Acquaint yourself with the merits of coconut oil for baking and with animal fats for occasional frying. Eat egg yolks and other animal fats with the proteins to which they are attached. And, finally, use as much good quality butter as you like, with the happy assurance that it is a wholesome—indeed, an essential—food for you and your whole family.

Organic butter, extra virgin olive oil, and expeller-expressed flax oil in opaque containers are available in health food stores and gourmet markets. Edible coconut oil can be found in Indian or Caribbean markets.

About the Authors:

Mary G. Enig, Ph.D. is an expert of international renown in the field of lipid biochemistry. She has headed a number of studies on the content and effects of trans fatty acids in America and Israel, and has successfully challenged government assertions that dietary animal fat causes cancer and heart disease. Recent scientific and media attention on the possible adverse health effects of trans fatty acids has brought increased attention to her work. She is a licensed nutritionist, certified by the Certification Board for Nutrition Specialists, a qualified expert witness, nutrition consultant to individuals, industry and state and federal governments, contributing editor to a number of scientific publications, Fellow of the American College of Nutrition and President of the Maryland Nutritionists Association. She is the author of over 60 technical papers and presentations, as well as a popular lecturer. Dr. Enig is currently working on the exploratory development of an adjunct therapy for AIDS using complete medium chain saturated fatty acids from whole foods. She is the mother of three healthy children brought up on whole foods including butter, cream, eggs and meat.


Sally Fallon is the author of Nourishing Traditions: The Cookbook that Challenges Politically Correct Nutrition and the Diet Dictocrats (with Mary G. Enig, PhD), a well-researched, thought-provoking guide to traditional foods with a startling message: Animal fats and cholesterol are not villains but vital factors in the diet, necessary for normal growth, proper function of the brain and nervous system, protection from disease and optimum energy levels. She joined forces with Enig again to write Eat Fat, Lose Fat, and has authored numerous articles on the subject of diet and health. The President of the Weston A. Price Foundation and founder of A Campaign for Real Milk, Sally is also a journalist, chef, nutrition researcher, homemaker, and community activist. Her four healthy children were raised on whole foods including butter, cream, eggs and meat.

References

Gittleman, Ann Louise, MS, Beyond Pritikin, 1980, Bantam Books, New York, NY
Enig, Mary G, PhD, Trans Fatty Acids in the Food Supply: A Comprehensive Report Covering 60 Years of Research, 2nd Edition, Enig Associates, Inc, Silver Spring, MD, 1995, 4-8
Castelli, William, Arch Int Med, Jul 1992, 152:7:1371-1372
Hubert H, et al, Circulation, 1983, 67:968; Smith, R and E R Pinckney, Diet, Blood Cholesterol and Coronary Heart Disease: A Critical Review of the Literature, Vol 2, 1991, Vector Enterprises, Sherman Oaks, CA
Rose G, et al, Lancet, 1983, 1:1062-1065
"Multiple Risk Factor Intervention Trial; Risk Factor Changes and Mortality Results," JAMA, September 24, 1982, 248:12:1465
"The Lipid Research Clinics Coronary Primary Prevention Trial Results. I. Reduction in Incidence of Coronary Heart Disease," JAMA, 1984, 251:359
Kronmal, R, JAMA, April 12, 1985, 253:14:2091
DeBakey, M, et al, JAMA, 1964, 189:655-59
Lackland, D T, et al, J Nutr, Nov 1990, 120:11S:1433-1436
Nutr Week, Mar 22, 1991, 21:12:2-3
Alfin-Slater, R B, and L Aftergood, "Lipids," Modern Nutrition in Health and Disease, 6th ed, R S Goodhartand M E Shils, eds, Lea and F
Min treningslogg - sterke saker
BILDER - Ta en titt Smiley
Maks per 5.7.2006    Mål til jul 2006
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BP:  150 kg (165kg)      170 kg
ML:  170 kg  MÅL NÅDD 200 kg

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« #1203 : 02. mai 2008, 14:24 »
Og her er del 2 (som er linket videre fra den første):

Link: http://www.westonaprice.org/basicnutrition/vitamin-k2.html

On the Trail of the Elusive X-Factor
A Sixty-Two-Year-Old Mystery Finally Solved

By Chris Masterjohn

Contents

Article Summary
On the Trail of the Elusive X-Factor (Main Article)
A Sixty-Year Mystery
Vitamin K: Three Discoveries Converge
Perfect Correspondence
Synergy with Vitamins A and D
Vitamin K2 and Dental Health
Vitamin K2 and Bone Health
Vitamin K2 and Heart Disease
Vitamin K2 and the Brain
Other Roles of Vitamin K2
Vitamin K2 in Foods
Figures
Figure 1: The Structure of K Vitamins and Their Chemical Behavior
Figure 2: Corresponding Characteristics of Activator X and Vitamin K2
Figure 3: Vitamin K-Dependent Carboxylation
Figure 4: Vitamin K2 Contents of Selected Foods
Sidebars
The Activator X Test
Interactions between Vitamins A, D, and K2
Is Vitamin K2 an Essential Nutrient?
The Vitamin K-Dependent Carboxylase
Vitamin K2 and the Brain: A Closer Look
Bacterial Production of Vitamin K2
Supplementing with Vitamin K2
References
About the Author
Follow Up Questions & Answers

Article Summary
In 1945, Dr. Weston Price described "a new vitamin-like activator" that played an influential role in the utilization of minerals, protection from tooth decay, growth and development, reproduction, protection against heart disease and the function of the brain.

Using a chemical test, he determined that this compound—which he called Activator X—occurred in the butterfat, organs and fat of animals consuming rapidly growing green grass, and also in certain sea foods such as fish eggs.

Dr. Price died before research by Russian scientists became known in the West. These scientists used the same chemical test to measure a compound similar to vitamin K.

Vitamin K2 is produced by animal tissues, including the mammary glands, from vitamin K1, which occurs in rapidly growing green plants.

A growing body of published research confirms Dr. Price's discoveries, namely that vitamin K2 is important for the utilization of minerals, protects against tooth decay, supports growth and development, is involved in normal reproduction, protects against calcification of the arteries leading to heart disease, and is a major component of the brain.

Vitamin K2 works synergistically with the two other "fat-soluble activators" that Price studied, vitamins A and D. Vitamins A and D signal to the cells to produce certain proteins and vitamin K then activates these proteins.

Vitamin K2 plays a crucial role in the development of the facial bones, and its presence in the diets of nonindustrialized peoples explains the wide facial structure and freedom from dental deformities that Weston Price observed.
 

Main Article (On the Trail of the Elusive X-Factor)
In 1945, Weston Price published a second edition of his pioneering work Nutrition and Physical Degeneration, to which he added a new chapter entitled, "A New Vitamin-Like Activator."1 In it, he presented evidence of a theretofore unrecognized fat-soluble substance that played a fundamental role in the utilization of minerals and whose absence from modern nutrition was responsible for the proliferation of dental caries and other degenerative diseases. Although Price quantified the relative amount of this substance in thousands of samples of dairy products sent to him from around the world, he never determined its precise chemical identity. For want of a better means of identification, he referred to it as "Activator X," also sometimes referred to as the "Price Factor."

Price found the highest concentrations of this nutrient in "the milk of several species, varying with the nutrition of the animal" and found the combination of cod liver oil and high-Activator X butter to be superior to that of cod liver oil alone. In the many butter samples he tested, Activator X was only present when the animals were eating rapidly growing green grass. In most regions, this occurred in the spring and early fall.

A Sixty-Year Mystery
For over sixty years, all attempts to identify this elusive "X" factor have failed. In the 1940s, Dr. Royal Lee, founder of the whole food supplement company Standard Process, suggested that activator X was the essential fatty acids.2 In 1980, Dr. Jeffrey Bland suggested more specifically that it was the elongated omega-3 essential fatty acid called EPA.3 Although these fatty acids exert some effects on calcium metabolism,4 neither the distribution of these unsaturated fatty acids in foods nor their chemical behavior corresponds to that of Activator X. Cod liver oil is much richer than butter in essential fatty acids including EPA, and the oils of plant seeds are even richer in these fats, but Price found little, if any, Activator X in these foods. Moreover, Price tested for Activator X by quantifying the ability of a food to oxidize iodide to iodine; essential fatty acids, however, do not possess this chemical ability.

In 1982, one author wrote to the Price-Pottenger Nutrition Foundation that after pursuing a number of false leads while attempting to identify the X factor, he had concluded that the "peculiar behavior" observed in Price's chemical test might be due to a "special kind of oxygen-containing heterocyclic ring," and suggested a compound called 6-methoxybenzoxazolinone (MBOA) as a likely candidate.5 Although researchers first identified MBOA as an antifungal agent found in corn,6 later studies showed that it was found in many other plant foods and acted as a reproductive stimulant in some animals by mimicking the hormone melatonin.7 Although it is present in young, rapidly growing grass, no research has ever established MBOA as an essential nutrient, attributed to it any of the physiological roles of Activator X, or demonstrated its presence in the foods that Price considered to be the richest sources of this nutrient. MBOA, then, was just another false lead; we will soon see, however, that the writer's observations about the chemical nature of Activator X were largely correct.

Vitamin K: Three Discoveries Converge
The test that Price used for Activator X, called iodometric determination, was traditionally regarded within the English language literature as a test for peroxides (carbon-containing molecules that have been damaged by oxygen).8,9 Since peroxides do not have any activity as vitamins, the relationship between the test and any nutritional substance remained a mystery. Although researchers publishing in other languages were using the test to detect a class of chemicals called quinones at least as far back as 1910,10 it was not until 1972 that Danish researchers published a paper in the British Journal of Nutrition showing that the test could be used to detect biological quinones such as K vitamins in animal tissues.12

K vitamins (Figure 1) possess oxygen-containing ring structures that are capable of oxidizing iodide to iodine and would therefore be detected by Price's Activator X test. The K vitamins are likely to go down in history as the most misunderstood group of vitamins of the twentieth century. In many ways, however, modern researchers are now rediscovering properties of these vitamins that Price had discovered over sixty years ago. It has now become clear that both Activator X and its precursor in rapidly growing grass are both members of this group.

There are two natural forms of vitamin K: vitamin K1 and vitamin K2. Vitamin K1, also called phylloquinone, is found in the green tissues of plants, tightly embedded within the membrane of the photosynthesizing organelle called the chloroplast. As the chlorophyll within this organelle absorbs energy from sunlight, it releases high-energy electrons; vitamin K1 forms a bridge between chlorophyll and several iron-sulfur centers across which these electrons travel, releasing their energy so that the cell can ultimately use it to synthesize glucose.13

When animals consume vitamin K1, their tissues convert part of it into vitamin K2,14 which fulfills a host of physiological functions in the animal that we are only now beginning to understand. The ability to make this conversion varies widely not only between species14 but even between strains of laboratory rats,15,16 and has not been determined in humans. The mammary glands appear to be especially efficient at making this conversion, presumably because vitamin K2 is essential for the growing infant.17 Vitamin K2 is also produced by lactic acid bacteria,18 although bacteria produce forms of the vitamin that are chemically different from those that animals produce, and researchers have not yet established the differences in biological activity between these forms.

Although both K vitamins were discovered and characterized over the course of the 1930s, two fundamental misunderstandings about these vitamins persisted for over sixty years: the medical and nutritional communities considered blood clotting to be their only role in the body, and considered vitamins K1 and K2 to simply be different forms of the same vitamin. The first vitamin K-dependent protein relating to skeletal metabolism was not discovered until 1978. It was not until 1997, nearly twenty years later, that the recognition that vitamin K was "not just for clotting anymore" broke out of the confines of the fundamental vitamin K research community.19

Since the amount of vitamin K1 in typical diets is ten times greater than that of vitamin K2,20 researchers have tended to dismiss the contribution of K2 to nutritional status as insignificant. Yet over the last few years, a growing body of research is demonstrating that these two substances are not simply different forms of the same vitamin, but are better seen as two different vitamins: whereas K1 is preferentially used by the liver to activate blood clotting proteins, K2 is preferentially used by the other tissues to place calcium where it belongs, in the bones and teeth, and keep it out of where it does not belong, in the soft tissues.21 Acknowledging this research, the United States Department of Agriculture, in conjunction with researchers from Tufts University, finally determined the vitamin K2 contents of foods in the U.S. diet for the first time in 2006.22

Perfect Correspondence
Because vitamin K1 is directly associated with both chlorophyll and beta-carotene within a single protein complex and plays a direct role in photosynthesis,13 the richness of the green color of grass, its rate of growth, and its brix rating (which measures the density of organic material produced by the plant) all directly indicate its concentration of vitamin K1. Animals grazing on grass will accumulate vitamin K2 in their tissues in direct proportion to the amount of vitamin K1 in their diet. The beta-carotene associated with vitamin K1 will also impart a yellow or orange color to butterfat; the richness of this color therefore indirectly indicates the amount of both vitamins K1 and K2 in the butter. Not only are the K vitamins detected by the Activator X test and distributed in the food supply precisely as Price suggested, but, as shown in Figure 2, the physiological actions that Price attributed to Activator X correspond perfectly to those of vitamin K2. It is therefore clear that the precursor to Activator X found in rapidly growing, green grass is none other than vitamin K1, while Activator X itself is none other than vitamin K2.

Ironically, Price discovered the roles of vitamin K2 in calcium metabolism, the nervous system and the cardiovascular system more than sixty years before the vitamin K research community began elucidating these roles itself, while vitamin K researchers discovered the chemical structure of activator X several years before Price even proposed its existence. Had Price been aware that his chemical test had been used for decades outside of the English language scientific community to detect quinones, a class to which the K vitamins belong, the two independent discoveries of this one vitamin may have converged sooner.

Instead, English-speaking researchers continued for decades to labor under the illusion that the iodometric method detected only peroxides; by the time this illusion was corrected, better methods for detecting peroxides had already been developed, Activator X had been forgotten, and the opportunity to make the connection between these three discoveries was lost. The twenty-first century, however, is already making radical revisions to our understanding of the K vitamins, which now make it clearer than ever that Activator X and vitamin K2 are one and the same.

Synergy with Vitamins A and D
Price showed Activator X to exhibit dramatic synergy with vitamins A and D. Chickens voluntarily consumed more butter and died more slowly on a deficiency diet when the butter was high in both vitamin A and Activator X than when it was high in vitamin A alone. Cod liver oil, which is high in both vitamins A and D, partially corrected growth retardation and weak legs in turkeys fed a deficiency diet, but the combination of cod liver oil and high-Activator X butter was twice as effective. Likewise, Price found that the combination of cod liver oil and a high-Activator X butter oil concentrate was more effective than cod liver oil alone in treating his patients for dental caries and other signs of physical degeneration.

Vitamin K2 is the substance that makes the vitamin A- and vitamin D-dependent proteins come to life. While vitamins A and D act as signaling molecules, telling cells to make certain proteins, vitamin K2 activates these proteins by conferring upon them the physical ability to bind calcium. In some cases these proteins directly coordinate the movement or organization of calcium themselves; in other cases the calcium acts as a glue to hold the protein in a certain shape.33 In all such cases, the proteins are only functional once they have been activated by vitamin K.

Osteocalcin, for example, is a protein responsible for organizing the deposition of calcium and phosphorus salts in bones and teeth. Cells only produce this protein in the presence of both vitamins A and D;34 it will only accumulate in the extracellular matrix and facilitate the deposition of calcium salts, however, once it has been activated by vitamin K2.35 Vitamins A and D regulate the expression of matrix Gla protein (MGP),36,37 which is responsible for mineralizing bone and protecting the arteries from calcification; like osteocalcin, however, MGP can only fulfill its function once it has been activated by vitamin K2.33 While vitamins A and D contribute to growth by stimulating growth factors and promoting the absorption of minerals, vitamin K2 makes its own essential contribution to growth by preventing the premature calcification of the cartilaginous growth zones of bones.38

Vitamin K2 may also be required for the safety of vitamin D. The anorexia, lethargy, growth retardation, bone resorption, and soft tissue calcification that animals fed toxic doses of vitamin D exhibit bear a striking resemblance to the symptoms of deficiencies in vitamin K or vitamin K-dependent proteins. Warfarin, which inhibits the recycling of vitamin K, enhances vitamin D toxicity and exerts a similar type of toxicity itself. Similarly, the same compounds that inhibit the toxicity of Warfarin also inhibit the toxicity of vitamin D. I have therefore hypothesized elsewhere that vitamin D toxicity is actually a relative deficiency of vitamin K2.39 The synergy with which vitamin K2 interacts with vitamins A and D is exactly the type of synergy that Price attributed to Activator X.

Vitamin K2 and Dental Health
Weston Price was primary interested in Activator X because of its ability to control dental caries. By studying the remains of human skeletons from past eras, he estimated that there had been more dental caries in the preceding hundred years than there had been in any previous thousand-year period and suggested that Activator X was a key substance that people of the past obtained but that modern nutrition did not adequately provide. Price used the combination of high-vitamin cod liver oil and high-Activator X butter oil as the cornerstone of his protocol for reversing dental caries. This protocol not only stopped the progression of tooth decay, but completely reversed it without the need for oral surgery by causing the dentin to grow and remineralize, sealing what were once active caries with a glassy finish. One 14-year-old girl completely healed 42 open cavities in 24 teeth by taking capsules of the high-vitamin cod liver oil and Activator X concentrate three times a day for seven months.

Activator X also influences the composition of saliva. Price found that if he collected the saliva of individuals immune to dental caries and shook it with powdered bone or tooth meal, phosphorus would move from the saliva to the powder; by contrast, if he conducted the same procedure with the saliva of individuals susceptible to dental caries, the phosphorus would move in the opposite direction from the powder to the saliva. Administration of the Activator X concentrate to his patients consistently changed the chemical behavior of their saliva from phosphorus-accepting to phosphorus-donating. The Activator X concentrate also reduced the bacterial count of their saliva. In a group of six patients, administration of the concentrate reduced the Lactobacillus acidophilus count from 323,000 to 15,000. In one individual, the combination of cod liver oil and Activator X concentrate reduced the L. acidophilus count from 680,000 to 0.

In the 1940s, researchers showed that menadione and related compounds inhibited the bacterial production of acids in isolated saliva.47 Menadione itself is a toxic synthetic analogue of vitamin K, but animal tissues are able to convert a portion of it to vitamin K2. The ability of vitamin K-related compounds to inhibit acid production in isolated saliva had no relationship to their vitamin activity, and the most effective of these compounds had practically no vitamin activity at all.48 Researchers unfortunately assumed that because vitamin K did not have a unique role in inhibiting acid formation in saliva within a test tube that it had no nutritional role in preventing tooth decay within living beings.

In 1945, American researchers conducted a double-blind, placebo-controlled trial of menadione-laced chewing gum and showed it to reduce the incidence of new cavities and cause a dramatic drop in the L. acidophilus count of saliva.49 The next year, the Army Medical Department attempted to repeat these results but failed, and research on vitamin K and dental health in the United States was subsequently abandoned.50 The authors of the original study assumed that the menadione exerted its effect simply as a topical anti-bacterial agent, even though it was highly unlikely to sustain a sufficient concentration in the saliva to exert this effect. Ten years later, German researchers showed that injecting menadione into the abdominal cavities of hamsters more effectively prevented tooth decay than feeding it orally.51 Although they could not rule out the possibility that some of this menadione was secreted into the saliva, their results argued in favor of a nutritional role for the vitamin K2 that would have been produced from it. Despite this finding, to this day no one has investigated the role of natural K vitamins in the prevention of dental caries.

Nevertheless, our continually expanding understanding of the physiology of both K vitamins and teeth now makes it clear that vitamin K2 plays an essential role in dental health. Of all organs in the body, vitamin K2 exists in the second highest concentration in the salivary glands (the highest concentration is found in the pancreas). Even when rats are fed only K1, nearly all of the vitamin K in their salivary glands exists as K2.15 Both vitamin K52 and vitamin K-dependent proteins53 are secreted into the saliva, although their function is unknown.

We now know that the growth and mineralization of the dentin that Price observed in response to the combination of cod liver oil and Activator X concentrate would primarily require three essential factors: vitamins A, D, and K2. There are three calcified tissues of the teeth: the cementum forms the roots, the enamel forms the surface, and the dentin forms the support structure beneath it. Cells called odontoblasts lining the surface of the pulp just beneath the dentin continually produce new dentin material. If a cavity invades the dentin and reaches these cells they can die. The pulp tissue, however, contains stem cells that can differentiate into new odontoblasts that could regenerate the lost dentin if the right conditions were present.54

Dentin is unique among the tissues of the teeth for its expression of osteocalcin, a vitamin K-dependent protein better known for its role in organizing the deposition of calcium and phosphorus salts in bone. In the infant rat, whose teeth grow very rapidly, dentin manufactures much more osteocalcin than bone does, suggesting that osteocalcin plays an important role in the growth of new dentin. Matrix Gla protein (MGP), which is required for the mineralization of bone, is also expressed in dentin.55 Vitamins A and D signal odontoblasts to produce osteocalcin,56,57 and probably regulate their expression of MGP as well. Only after vitamin K2 activates these proteins' ability to bind calcium, however, can they lay down the mineral-rich matrix of dentin. The remarkable synergy between these three vitamins exactly mirrors the process Price observed.

Vitamin K2 and Bone Health
Price also believed that Activator X played an important role in bone health. Butter oil concentrate cured rickets and increased serum levels of calcium and phosphorus in rats consuming a mineral-deficient diet. In a four-year-old boy who suffered from rampant tooth decay, seizures and a tendency to fracture, the combination of a large helping of this concentrate and a meal of whole wheat and whole milk rapidly resolved each of these symptoms.

Although the small amount of vitamin D in the butter oil was probably sufficient to cure rickets and the combination of vitamins A and D most likely produced the rise in serum calcium and phosphorus,58 vitamin K2 has a definite role in bone health. There are at least two vitamin K-dependent proteins that fulfill important functions in skeletal metabolism: matrix Gla protein (MGP) and osteocalcin.

In 1997, researchers from the University of Texas and the University of Montreal developed mice that lacked the gene that codes for MGP. These mice appeared normal for the first two weeks of their lives, after which they developed faster heart beats, stopped growing and died within two months with the rupture of their heavily calcified aortas. The disorganization of their cartilage cells not only produced short stature, but also produced osteopenia and spontaneous fractures.38

The bones of mice that lack the osteocalcin gene mineralize just as well as those of mice that do not lack the gene, but the mineral deposits are organized differently. This could mean that osteocalcin is important to the functional quality of bone and the ability to regulate its shape.59 Isolated human osteoblasts, the cells that lay down the calcified matrix of bone, secrete osteocalcin in response to vitamins A and D.34 The protein-rich matrix surrounding these cells will only accumulate this osteocalcin, however, if it is activated by vitamin K2. Calcification of the extracellular matrix occurs in parallel with the accumulation of osteocalcin, but it is not clear whether this protein plays a direct role in laying down the calcium salts or if its accumulation simply reflects the higher amount of vitamin K2 that is available to activate other proteins involved more directly in mineralization such as MGP.35

When there is an insufficient amount of vitamin K to keep up with the production of vitamin K-dependent proteins, many of these proteins are secreted into the blood in an inactive form. Circulating cells then take up these useless proteins and destroy them.40 By drawing a person's blood and testing the percentages of circulating osteocalcin that are active and inactive, we can determine whether that person's bone cells have enough vitamin K to meet their needs. People with the highest percentages of inactive osteocalcin are at a more than five-fold increased risk of hip fracture,60 confirming the value of the test.

By using this test, we can also show that vitamin K2 is the preferred K vitamin of the bones. It takes one milligram per day of a highly absorbable pharmacological preparation of vitamin K1 to maximally activate osteocalcin in human subjects;28 it appears, however, that humans are not capable of absorbing much more than one fifth this amount from whole foods.24 By contrast, large amounts of vitamin K2 are readily absorbed from foods.26 Even when using highly absorbable forms of these vitamins, vitamin K2 is much more effective. Researchers from the University of Maastricht in the Netherlands recently showed that over the course of 40 days, vitamin K2 was three times more effective than vitamin K1 at raising the percentage of activated osteocalcin. Moreover, the effect of vitamin K1 reached a plateau after just three days, whereas the effect of vitamin K2 increased throughout the entire study. Had it lasted longer, the study may have shown an even greater superiority of vitamin K2.32

We can therefore regard the percentage of inactive osteocalcin primarily as a marker for vitamin K2 status. In the healthy adult population, one hundred percent of the vitamin K-dependent blood coagulants produced by the liver are in their active form. By contrast, in this same population between ten and thirty percent of circulating osteocalcin is in its inactive form. Researchers rarely encounter individuals whose osteocalcin is fully activated.31 This suggests that vitamin K2 deficiency is universal, and that variation in K2 status within the population simply reflects varying degrees of deficiency.

Vitamin K1 supplements produce modest decreases in bone loss in the elderly. A number of Japanese trials, on the other hand, have shown that vitamin K2 completely reverses bone loss and in some cases even increases bone mass in populations with osteoporosis.31 The pooled results of seven Japanese trials show that vitamin K2 supplementation produces a 60 percent reduction in vertebral fractures and an 80 percent reduction in hip and other non-vertebral fractures.61 These studies used extremely high amounts of vitamin K2 and did not observe any adverse effects over the course of several years. Since they used such high doses of K2, however, and no studies have tested lower doses, they do not constitute definitive proof that the vitamin activity rather than some drug-like action unique to the high dose produced such dramatic results. The balance of the evidence, however, suggests that vitamin K2 is essential to skeletal health and that it is a key substance that modern diets do not adequately provide.

Vitamin K2 and Heart Disease
Price analyzed more than 20,000 samples of dairy products sent to him every two to four weeks from various districts of the United States, Canada, Australia, Brazil and New Zealand. Dividing the total area into many districts, each producing dairy products with different patterns of seasonal fluctuation in vitamin A and Activator X content, he found an inverse relationship in each district between the vitamin content of butterfat and the mortality from pneumonia and heart disease.

The role of vitamin A in the immune system is well established. We do not currently know, however, whether vitamin K2 plays an important role in the immune system. Nevertheless, lymph glands and bone marrow accumulate large amounts of it62 and a vitamin K-dependent protein called gas6 plays a role in phagocytosis,33 a process wherein immune cells destroy and consume foreign cells or the body's own cells when they are infected or no longer needed. It is therefore possible that K vitamins could play an important role in protecting against infectious diseases such as pneumonia.

Vitamin K2's ability to protect us from heart disease is much more clearly established. Research is in fact rapidly redefining heart disease largely as a deficiency of this vitamin. While it is most clearly established that vitamin K2 deficiency causes calcification of the cardiovascular system, vitamin K2 appears to protect against the inflammation and accumulation of lipids and white blood cells that characterize atherosclerosis as well.

Cardiovascular calcification can begin as early as the second decade of life, and is nearly ubiquitous in the population by the age of 65.33 There are primarily two types: calcification of the heart valves and tunica media constitutes one type, while calcification of the tunica intima constitutes the second. The tunica media is the middle layer of the artery; it contains elastic fibers that allow the artery to stretch and accommodate varying degrees of pressure. The elastic fibers of the tunica media and the valves of the heart calcify during diabetes, kidney disease and aging. The tunica intima is the innermost layer of the artery and is the site where atherosclerosis develops. In atherosclerosis, calcified deposits rich in lipids and white blood cells accumulate on the debris left behind by the blood vessel's smooth muscle cells once they have died.63

In healthy arteries, the vitamin K-dependent matrix Gla protein (MGP) congregates around the elastic fibers of the tunica media and guards them against the formation of crystals by the calcium that circulates in the blood. The inactive form of MGP, which cells produce when they do not have sufficient K vitamins to meet their needs, does not exist in healthy arteries. In early atherosclerosis, by contrast, most MGP exists in its inactive form and associates with calcified structures containing lipids, white blood cells, and the remnants of dead smooth muscle cells. Inactive MGP also accumulates within the calcified deposits of the medial sclerosis that occurs during diabetes, kidney disease and aging. Although blood tests for the percentage of inactive and active MGP are not available, patients with severe calcifications have high percentages of inactive osteocalcin, indicating a general deficiency of vitamin K2.63

Two other vitamin K-dependent proteins are likely to play a role in the development of atherosclerosis: gas6 and protein S. Gas6 promotes the survival of the smooth muscle cells that line the intima and the rapid clearance of those that die. The rapid clearance of these dead cells may be important for preventing the accumulation of the calcified lipids and white blood cells that gather around them. Protein S guides the immune system to clear away this debris from the intima gently rather than mounting a dangerous inflammatory attack against it.33 As these observations all predict, experimental and epidemiological evidence both show that vitamin K2 is a powerful inhibitor of cardiovascular disease.

Mice that lack the gene for MGP develop extensive calcification of the aorta, aortic valves and arteries soon after birth and bleed to death within two months when their heavily calcified aortas rupture.38 Warfarin, which inhibits the recycling of K vitamins40 and the conversion of K1 to K2,64 causes calcification of the tunica media in rats within two weeks,21 increases arterial stiffness, decreases the ability of the artery to accommodate moderately high levels of blood pressure, and causes the death of the artery's smooth muscle cells.65 Marcoumar, a similar drug, doubles the degree of aortic valve calcification in humans over the course of one to three years.42

Large amounts of vitamin K2 completely inhibit the ability of Warfarin to cause arterial calcification in rats. Vitamin K1, by contrast, has no inhibitory effect at all.21 Researchers from the University of Maastricht recently showed that both K vitamins can reverse calcification that has already occurred in Wistar Kyoto rats.65 The K vitamins also reduced the number of dead smooth muscle cells after Warfarin treatment, showing that vitamin K-dependent proteins not only promote cell survival but also facilitate the safe clearance of cells that have died. Although both K vitamins were effective, these rats convert vitamin K1 to vitamin K2 with great efficiency. In the absence of Warfarin, two-thirds of the vitamin K in the blood vessels of the rats that consumed K1 alone existed as K2. In the presence of Warfarin, however, which inhibits the conversion, none of the vitamin K in these blood vessels existed as K2. Apparently, vitamin K1 is effective after but not during Warfarin treatment because it can only protect against arterial calcification insofar as it is converted to vitamin K2.

In the Nurses' Health Study, the risk of heart disease was a modest 16 percent lower for those consuming more than 110 micrograms per day of vitamin K1, but there was no benefit from consuming any more than this.66 This small amount is equivalent to consuming only three servings of kale per month. The Health Professionals Follow-Up Study generated a similar finding in men, although it lost significance after adjustment for other dietary risk factors.67 It isn't clear whether the slight increase in risk associated with only the lowest intakes reflects the possibility that only very small amounts of vitamin K1 are absorbed, or simply reflects the association between K1 intake and a healthy lifestyle. People who consume more vitamin K1 weigh less, smoke less, eat more fruits, vegetables, fish, folate, vitamin E and fiber,68 and are more likely to use vitamin supplements.67

The inverse association between heart disease and vitamin K2 intake is more straightforward. In The Rotterdam Study, which prospectively followed just over 4,600 men aged 55 or older in the Netherlands, the highest intake of vitamin K2 was associated with a 52 percent lower risk of severe aortic calcification, a 41 percent lower risk of coronary heart disease (CHD), a 51 percent lower risk of CHD mortality, and a 26 percent lower risk of total mortality. Even though the study population consumed ten times more K1 than K2, vitamin K1 had no association with either the degree of aortic calcification or the risk of heart disease.20 The profound effects of variations in such small amounts of dietary K2 emphasize just how powerful this substance is in the prevention of degenerative disease.

Vitamin K2 and the Brain
Price supplied several anecdotes suggesting that Activator X plays an important role in the nervous system. Price administered a daily meal of nutrient-dense whole foods supplemented with high-vitamin cod liver oil and high-Activator X butter oil to the children of impoverished mill workers who suffered from rampant tooth decay. The treatment not only resolved the tooth decay without the need for oral surgery, but resolved chronic fatigue in one boy and by the report of their school teachers produced a marked increase in learning capacity in two others.

Price also administered the butter oil concentrate to a four-year-old who suffered from rampant tooth decay, a fractured leg and seizures. A dessert spoonful of the butter oil served over whole wheat gruel with whole milk once before bed and five times over the course of the following day immediately resolved his seizures. Rapid healing of his fracture and dental caries followed soon after. The fact that these three symptoms appeared together and resolved following the same treatment suggests a common cause for each of them. Sixty years later, modern research is now elucidating the essential role that vitamin K2 plays not only in the dental and skeletal systems, but in the nervous system as well. This strongly suggests it was the key unidentified factor in Price's protocol.

The brain contains one of the highest concentrations of vitamin K2 in the body; only the pancreas, salivary glands, and the cartilaginous tissue of the sternum contain more. When male Wistar rats consume vitamin K1 alone, 98 percent of the vitamin K in their brains exists as K2, demonstrating the overwhelming preference of the nervous system for this form. The K2 contents of these four tissues remain remarkably high on a vitamin K-deficient diet, suggesting either that the vitamin is so essential to their function that they have developed a highly efficient means of preserving it, or that it plays a unique role in these tissues that does not require as high a rate of turnover as is required by the roles it plays in most other tissues.15

An analysis of three autopsies showed that vitamin K2 makes up between 70 and 93 percent of the vitamin K in the human brain.69 It is not clear why humans exhibit greater variation in this percentage than rats, although it could be that we convert K1 less efficiently and are therefore more dependent on dietary K2.

Vitamin K2 supports the enzymes within the brain that produce an important class of lipids called sulfatides. The levels of vitamin K2, vitamin K-dependent proteins and sulfatides in the brain decline with age; the decline of these levels is in turn associated with age-related neurological degeneration.46 Comparisons of human autopsies associate the early stages of Alzheimer's disease with up to 93 percent lower sulfatide levels in the brain.70 Warfarin treatment or dietary vitamin K deficiency causes lack of exploratory behavior and reduced physical activity in rats that is suggestive of fatigue.71 Animals that completely lack the enzymes to make sulfatides and a related class of lipids, cerebrosides, progressively suffer from growth retardation, loss of locomotor activity, weak legs and seizures.72

These observations suggest that deficiencies in vitamin K, especially vitamin K2, could result in fatigue and learning difficulties in humans, and that rare, extreme deficiencies of vitamin K2 in the brain could result in seizures. If this is the case, it would explain why Price observed tooth decay, bone fracture, learning difficulties and seizures to share a common cause and a common solution.

Other Roles of Vitamin K2
Our understanding of the K vitamins is rapidly expanding and we are likely to discover many new roles for them as the twenty-first century progresses.

The highest concentration of vitamin K2 exists in the salivary glands and the pancreas. These organs exhibit an overwhelming preference for K2 over K1 and retain high amounts of the vitamin even when animals consume a vitamin K-deficient diet.15 The high presence of the vitamin in both of these organs suggests a role in activating digestive enzymes, although its apparent role in the regulation of blood sugar could explain its presence in the pancreas.76 The testes of male rats also exhibit a high preference for and retention of vitamin K2,16 and human sperm possess a vitamin K-dependent protein with an unknown function.77 The kidneys likewise accumulate large amounts of vitamin K269 and secrete vitamin K-dependent proteins that inhibit the formation of calcium salts. Patients with kidney stones secrete this protein in its inactive form, which is between four and twenty times less effective than its active form at inhibiting the growth of calcium oxalate crystals, suggesting that vitamin K2 deficiency is a major cause of kidney stones.77

The use of Warfarin during pregnancy produces developmental malformations of the face; as the nasal cartilage calcifies, growth of the nose comes to an early end, resulting in a stubby appearance.78 Vitamin K2 therefore most certainly played a role in the development of beautiful faces with broad features that Price observed among primitive peoples.

A number of cell experiments have shown that vitamin K2 has powerful anti-carcinogenic properties that may make it useful in preventing or treating cancer in humans.79

Researchers have recently discovered a whole new class of vitamin K-dependent proteins called transmembrane Gla (TMG) proteins. Their functions are unknown.33

The K vitamins perform all of their well understood roles in the part of the cell responsible for the modification of proteins. Only a portion of the vitamin K within a cell exists in this area, however. Even more exists in the inner membrane of the mitochondria where the cell produces its energy.45 The greatest concentration exists in the nucleus, which possesses a receptor for vitamin K that may be involved in regulating the expression of genes.44 Vitamin K2 has a greater affinity than vitamin K1 for both the mitochondrial membrane and the nuclear receptor. We presently know virtually nothing about these functions of the K vitamins and the plot will only thicken as the story unfolds.

Vitamin K2 in Foods
Figure 4 shows the distribution of vitamin K2 in selected foods. Precise values for the organ meats that would be richest in K2 are not available. The pancreas and salivary glands would be richest; reproductive organs, brains, cartilage and possibly kidneys would also be very rich; finally, bone would be richer than muscle meat.15,16,69 Analyses of fish eggs, which Price found to be rich in Activator X, are not available.

Commercial butter is only a moderate source of vitamin K2. After analyzing over 20,000 samples of butter sent to him from around the world, however, Price found that the Activator X concentration varied 50-fold. Vitamin K-rich cereal grasses, especially wheat grass, and alfalfa in a lush green state of growth produced the highest amounts of Activator X, but the soil in which the pasture was grown also profoundly influenced the quality of the butter. The concentrations were lowest in the eastern and far western states where the soil had been tilled the longest, and were highest in Deaf Smith County, Texas, where excavations proved the roots of the wheat grass to pass down six feet or more through three feet of top soil into deposits of glacial pebbles cemented together with calcium carbonate. It was this amazingly vitamin-rich butter that had such dramatic curative properties when combined with high-vitamin cod liver oil and nutrient-dense meals of whole milk, whole grains, organ meats, bone broths, fruits and vegetables.

For over 50 years after Price described his discovery of Activator X, the medical and nutritional communities saw vitamin K merely as a requirement for blood clotting. The poor understanding of the functions of the K vitamins within the body and the apparent lack of any relationship between Price's chemical test and the structure of any known vitamin made it impossible to determine the identity of this mysterious substance. We now know, however, that vitamin K2 and Activator X are one and the same. Like Price's X factor, vitamin K2 is synthesized by animal bodies from its precursor in rapidly growing grass. Cereal grasses and alfalfa are rich in this precursor, and these plants accumulate it in direct proportion to their photosynthetic activity. It is critical to the ability of teeth and bones to lay down mineralized tissue, and to the prevention of degenerative diseases of the cardiovascular and nervous systems. It is the key factor that acts in synergy with vitamins A and D: these vitamins command cells to make proteins, but vitamin K brings these proteins to life. It is an "activator," then, in the truest sense of the word, and it is therefore fitting that we knew it for so many decades simply as "Activator X."

Thank you to Michael Eiseike, a health researcher from Hokkaido Japan, for originally bringing the Rotterdam Study to our attention and suggesting that vitamin K2 may be the X Factor of Weston Price; and also to David Wetzel of Green Pasture Products for his input and advice.

Figures

Figure 1: The Structure of K Vitamins and Their Chemical Behavior
Single lines represent single bonds between carbon atoms; double lines represent double bonds between carbon atoms. Hydrogen atoms are attached to most of the carbons but are not shown.

a.

Vitamin K1. The side chain extending to the right of the molecule is monounsaturated.

b.

Vitamin K2. The nucleus, composed of two ring structures, is the same as that of vitamin K1. The side chain, however, is polyunsaturated rather than monounsaturated.

c.

Either K vitamin would be expected to react with hydriodic acid (HI) by absorbing hydrogen atoms and liberating diatomic iodine (I2). The side chain is abbreviated by the letter "R."

d.

If the mixture of the vitamin K and hydriodic acid is combined with a starch indictor, the diatomic iodine liberated by the reaction would turn the starch blue.

Figure 2. Corresponding Characteristics of Activator X and Vitamin K2
Activator X Vitamin K2
Found in the butterfat of mammalian milk, the eggs of fishes, and the organs and fats of animals.
 Found in the butterfat of mammalian milk and the organs and fats of animals. Analyses of fish eggs are not available.
 
Synthesized by animal tissues, including the mammary glands, from a precursor in rapidly growing, green grass. Synthesized by animal tissues, including the mammary glands, from vitamin K1, which is found in association with the chlorophyll of green plants in proportion to their photosynthetic activity. 
The content of this vitamin in butterfat is proportional to the richness of its yellow or orange color. Its precursor is directly associated with beta-carotene, which imparts a yellow or orange color to butterfat.
Liberates diatomic iodine from hydriodic acid during chemical testing. Liberates diatomic iodine from hydriodic acid during chemical testing.
Acts synergistically with vitamins A and D. Activates proteins that cells are signaled to produce by vitamins A and D.
Plays an important role in reproduction.  Synthesized by the reproductive organs in large amounts from vitamin K1 and preferentially retained by these organs on a vitamin K-deficient diet. Sperm possess a K2-dependent protein of unknown function.
Plays a role in infant growth. Contributes to infant and childhood growth by preventing the premature calcification of the cartilaginous growth zones of bones.
Plays an essential role in mineral utilization and is necessary for the control of dental caries. Activates proteins responsible for the deposition of calcium and phosphorus salts in bones and teeth and the protection of soft tissues from calcification.
Increases mineral content and decreases bacterial count of saliva. Is found in the second highest concentration in the salivary glands, and is present in saliva.
Intake is inversely associated with heart disease.  Protects against the calcification and inflammation of blood vessels and the accumulation of atherosclerotic plaque.
Increases learning capacity. The brain contains one of the highest concentrations of vitamin K2, where it is involved in the synthesis of the myelin sheath of nerve cells, which contributes to learning capacity.
Resolved chronic fatigue in one boy. Deficiency induces fatigue in laboratory animals.
Resolved seizures in one boy. Involved in the synthesis of lipids called sulfatides in the brain, an absence of which induces seizures in laboratory animals. 

Figure 3. Vitamin K-Dependent Carboxylation
a. O=C=O

    O(-1)
|
b.C=O
      O(-1)
|
    C=O
|
c. —Glutamate—
(Glu)
 CO2
|
\/
Vitamin K-
-Dependent
Carboxylase      Ca(+2)
(-1)O   O(-1)
|   |
O=C  C=O
\  /
—γ-Carboxy—
Glutamate (Gla) 

a.) A carbon dioxide molecule
b.) a carboxyl group
c.) Vitamin K-dependent carboxylation

The vitamin K-dependent carboxylase rearranges the chemical bonds within carbon dioxide molecules. Carboxyl groups contain carbon and oxygen atoms and carry a charge of negative one. Calcium carries a charge of positive two. The side chains of the amino acid glutamate normally carry one carboxyl group; the vitamin K-dependent addition of a second carboxyl group gives these side chains a charge of negative two and thus allows them to bind to calcium, which has the equal and opposite charge. This process transforms glutamate into γ-carboxyglutamate, abbreviated Gla. For this reason, many vitamin K-dependent proteins, such as matrix Gla protein (MGP), contain "Gla" in their name.

Figure 4: Vitamin K2 Contents of Selected Foods22, 26
The percentage of vitamin K2 present as MK-4 represents that synthesized by animal tissues, while the remainder represents that synthesized by bacteria during fermentation.

FOOD  VITAMIN K2  (MCG/100G)
Natto 1103.4  (0% MK-4)
Goose Liver Paste  369.0  (100% MK-4)
Hard Cheeses  76.3  (6% MK-4)
Soft Cheeses  56.5  (6.5% MK-4)
Egg Yolk (Netherlands)  32.1  (98% MK-4)
Goose Leg  31.0  (100% MK-4)
Curd Cheeses  24.8  (1.6% MK-4)
Egg Yolk (United States)  15.5  (100% MK-4)
Butter  15.0  (100% MK-4)
Chicken Liver  14.1 (100% MK-4)
Salami  9.0  (100% MK-4)
Chicken Breast  8.9  (100% MK-4)
Chicken Leg  8.5  (100% MK-4)
Ground Beef (Medium Fat)  8.1  (100% MK-4)
Bacon  5.6 (100% MK-4)
Calf Liver  5.0  (100% MK-4)
Sauerkraut  4.8  (8% MK-4)
Whole Milk  1.0  (100% MK-4)
2% Milk  0.5  (100% MK-4)
Salmon  0.5  (100% MK-4)
Mackerel  0.4  (100% MK-4)
Egg White  0.4  (100% MK-4)
Skim Milk  0.0   
Fat-Free Meats  0.0   

Sidebars

The Activator X Test
The chemical test that Price eventually came to use for the quantification of Activator X in foods was originally suggested as an indirect test for vitamin D by Lester Yoder of the Agricultural Experiment Station of Iowa State College in 1926.8 The basic principle of the test, called iodometric determination, was most commonly utilized in the United States for detecting the presence of organic peroxides.9 Since peroxides are capable of oxidizing ionic iodide to diatomic iodine, researchers can detect them by combining the test substance with hydriodic acid and a starch indicator. Hydriodic acid releases iodide ions into a solution. If peroxides are present, they convert these iodide ions to diatomic iodine, which then turns the starch blue or purple.

This is somewhat similar to the amylase test that is used as a demonstration in many high school or college biology classes. In that test, however, preformed iodine is used; in the absence of amylase, the iodine turns the starch blue, while in the presence of amylase, the starch is broken down into sugar and the color change does not occur.

At the time, the only way to test a food for vitamin D was to feed it to rats on a mineral-deficient diet, kill the rats, and analyze the mineral content of their bones. The richer the food was in vitamin D, the more it would stimulate absorption of the small amounts of calcium and phosphorus in the diet and the higher the bone mineral content would be. Yoder suggested, however, that there was a general correlation between the ability of an oil to peroxidize (become rancid) and its vitamin D content, and advocated testing an oil's ability to oxidize iodide as an indirect indicator of its level of vitamin D. Having no other convenient chemical test, Price adopted this as his test for vitamin D.

The test was far from perfect. Yoder found peroxidation in substances with no vitamin D activity such as turpentine, a thirteen-year-old sample of cholesterol, and an aged sample of mineral oil. He further found that irradiating foods to the point at which their vitamin D activity was destroyed actually increased their score on the test.8

As Price used this test on over 20,000 samples of dairy foods sent to him from around the world, he realized that the physiological effects that correlated with a food's ranking were different from those attributable to isolated vitamin D, and began using the term "Activator X" to describe the nutritional substance that the test was measuring. He observed that the vitamin content of these butter samples varied fifty-fold, and that the samples richest in Activator X were the most potent for controlling dental caries. Clearly, Price's test was detecting something besides rancid oils.

While researchers who published in English language journals traditionally used this test to detect peroxides, researchers publishing in Russian and German language journals had been using it to detect the synthetic compound benzoquinone all along.10,11 Benzoquinone belongs to a class of chemicals called quinones that includes biological molecules such as coenzyme Q10 and the K vitamins. These quinones possess oxygen-containing ring structures whose oxygens will steal electrons and hydrogen ions from hydriodic acid and thereby oxidize ionic iodide to diatomic iodine, causing the starch to become a bluish purple color (see Figure 1).

In the 1970s, researchers from Britain and Denmark were debating whether or not healthy rat tissues contained lipid peroxides. The British researchers used the iodometric method to determine peroxide levels and argued that healthy rat tissues did contain peroxides, while the Danish researchers used a different method and argued that they did not. In a 1972 paper published in the British Journal of Nutrition, the Danish researchers demonstrated that the iodometric method was not showing the existence of peroxides in the rat tissues, but rather the existence of coenzyme Q10 and probably other quinones.12

Price's test, therefore, was not specific to any one particular chemical compound. When used for fresh oils, however, it would be able to detect a number of nutrients that include coenzyme Q10 and the K vitamins. As shown in this article, it is the K vitamins that we should expect to vary in direct proportion to the amount of richly green grass in the diet of the animals, while the physiological effects Price identified with Activator X are specifically attributable to vitamin K2.

Interactions between Vitamins A, D, and K2
SOFT TISSUE CALCIFICATION AND VITAMIN D TOXICITY
(Hypothesis)
Vitamin K
 Vitamin D
 Vitamin A
 
Fulfills demand for Vitamin K  Exerts Vitamin K sparing effect
May protect by other unknown mechanisms
Increased demand
for Vitamin K
 
Relative deficiency
of Vitamin K
 
Soft tissue calcification
Bone loss, growth retardation
Nervous system damage
 

 
 
 BONES & TEETH 
Vitamin A  Vitamin D  Vitamin A Vitamin D
     
Matrix Gla Protein  Osteocalcin
 Vitamin K 
Activated Matrix Gla Protein  Activated Osteocalcin
   
Deposition of Minerals  Organization of Minerals
 

GROWTH
 
Vitamin A Vitamin D Vitamin K
   
Synthesis of Growth Factors and Growth Factor Receptors  Absorption of Minerals Prevention of the Calcification of Growth Cartilage
   
 OPTIMAL GROWTH & DEVELOPMENT 
 Strong Bones
Straight Teeth
Good Proportions
Wide Facial Development
Long Straight Nose 
 

 

Is Vitamin K2 an Essential Nutrient?
Vitamins K1 and K2 are both effective cofactors for the enzyme that activates vitamin K-dependent proteins,23 but the liver preferentially uses vitamin K1 to activate clotting factors while most other tissues preferentially use vitamin K2 to activate the other vitamin K-dependent proteins.21 Although animals can convert vitamin K1 to vitamin K2,14 there are a number of lines of evidence strongly suggesting that humans require preformed K2 in the diet to obtain optimal health.

Humans appear to have a finite ability to absorb vitamin K1 from plant foods. In the United States, where the mean intake of vitamin K1 is less than 150 micrograms per day, blood levels increase with increasing dietary intake until the latter reaches two hundred micrograms per day, after which they plateau. In the Netherlands, where the mean intake of vitamin K1 is much higher (250 micrograms per day), plasma levels of vitamin K1 have no relationship to dietary intake at all.24 These results suggest that humans do not possess the ability to absorb much more than 200 micrograms of vitamin K1 per day from vegetables.

This interpretation is also supported by feeding experiments. Whereas the absorption of vitamin K2 from natto, a fermented soy food, is nearly complete, the absorption of vitamin K1 from servings of green vegetables ranging from two hundred to four hundred grams consumed without added fat is only between five and ten percent. The absorption of similarly sized servings of vegetables with added fat is still only between ten and fifteen percent.25-26 By contrast, smaller servings are absorbed more efficiently. For example, the absorption from a 150-gram serving of spinach is 17 percent and the absorption from a 50-gram serving of spinach is 28 percent.27 These results show that our absorption of the vitamin declines as the amount we consume increases and strengthens the interpretation that we might only be able to absorb about 200 micrograms per day. When study subjects consume a highly absorbable pharmacological preparation of vitamin K1, a dose of 1000 micrograms per day is required to maximize the activation of proteins important to bone metabolism.28 If we can only absorb one-fifth of this amount from vegetables, we cannot support our skeletal system with vitamin K1 regardless of how efficiently we may be able to convert it to vitamin K2.

The ability to convert K1 to K2 varies widely between species and breeds of animals. The German researchers who first reported this conversion found that rats made it poorly compared to birds and that pigeons made it most efficiently.14 Every tissue tested in male Wistar rats is capable of making the conversion,15 whereas the liver, kidneys and heart of male Lewis rats will preferentially accumulate preformed K2, but, unlike the pancreas and testes of these same animals, will not synthesize it from K1.16 The K2 content of human breast milk increases when mothers consume pharmacological preparations of K1, but the K2 content of their blood does not;17 since the conversion takes place in the target tissues rather than the blood, however, we do not know how efficiently other human tissues make this conversion.

Vitamins K1 and K2 share a common ring-structured nucleus but possess different types of side chains. The first step in the conversion of K1 to K2 appears to be the cleavage of its side chain in either the liver or the gastrointestinal tract, yielding a toxic oxidizing agent called menadione; much of this metabolite is detoxified by the liver and excreted in the urine, while the remaining portion can be used to synthesize K2 in tissues.29 After this cleavage takes place, menadione must be transported to its target tissues where cellular enzymes can add a side chain to it, completing the transformation to K2. Because they are transported in different types of lipoproteins, vitamin K1 is primarily sent to the liver, whereas vitamin K2 is primarily sent to the other tissues;30 we know very little, however, about the transport of menadione in the blood. We also know very little about the rate at which our cells are capable of adding side chains to these molecules; presumably, if the supply of menadione exceeds the rate at which the cell can add these side chains, the menadione will exert toxic effects and cause oxidative damage within the cell. Preliminary evidence indicates that doses of 1000 micrograms per day of supplemental K1 may contribute to periodontal disease,31 suggesting that our bodies' resistance to absorbing this much K1 from vegetables may serve an important purpose.

The clearest demonstration that humans require dietary preformed vitamin K2 for optimal health is that epidemiological and intervention studies both show its superiority over K1. Intake of vitamin K2, for example, is inversely associated with heart disease in humans while intake of vitamin K1 is not,20 and vitamin K2 is at least three times more effective than vitamin K1 at activating proteins related to skeletal metabolism.32 This nutritional superiority makes it clear why the primitive groups that Weston Price studied expended so much effort procuring foods rich in vitamin K2 like the organs and fats of animals and the deeply colored orange butter from animals grazing on rich pastures.

The Vitamin K-Dependent Carboxylase
Most known functions of the K vitamins are mediated by the vitamin K-dependent carboxylase. The carboxylase is an enzyme bound to the membrane of the endoplasmic reticulum, a cellular organelle involved in the synthesis and modification of proteins. It uses vitamin K as a cofactor to add carboxyl groups to the side chains of the amino acid glutamate within certain vitamin K-dependent proteins (see Figure 3). This gives them a negative charge, allowing them to bind to calcium, which carries a positive charge.40

Vitamin K-dependent proteins must be carboxylated before they leave the cell or insert themselves into its membrane. They may contain anywhere from three to thirteen glutamate residues (amino acids are called "residues" when they are bound up within proteins) that must be carboxylated; the carboxylase binds to them only once, however, and carboxylates each of these before it releases the protein. On the other hand, vitamin K can only be used for the carboxylation of a single glutamate residue and the carboxylase must release it after each carboxylation and allow it to be recycled and returned. A different enzyme, vitamin K oxidoreductase, recycles the vitamin; this enzyme is the target of the anticoagulant drug Warfarin and its relatives.40 Since Warfarin targets the recycling of vitamin K rather than the vitamin K-dependent coagulation proteins themselves, it not only acts as an anticoagulant, but also causes arterial and aortic valve calcification in both rats21 and humans41,42 and inhibits the mineralization of bone matrix.35

The distribution of the carboxylase among species and among tissues within an organism can help us understand its significance and that of its cofactor, vitamin K. With the exception of some microorganisms that have "stolen" the enzyme by incorporating the genetic material of other species,43 the carboxylase is present only in multicellular animals, underscoring its importance to intercellular communication. In the growing embryo, it is first expressed in skeletal and nervous tissue; vitamin K is therefore almost certainly essential to the development of the skeletal and nervous systems from their very beginnings.40

Vitamin K's activity as a cofactor for the carboxylase may only be the tip of the iceberg. In osteoblasts, the cells responsible for bone growth, the greatest concentration of vitamin K2 exists in the nucleus where the genetic material is; the second greatest concentration exists in the mitochondria, the so-called "power house"
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Maks per 5.7.2006    Mål til jul 2006
---------------------------------------------
KB:  170 kg (180kg)      200 kg
BP:  150 kg (165kg)      170 kg
ML:  170 kg  MÅL NÅDD 200 kg

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« #1204 : 05. mai 2008, 12:30 »
Vil først og fremst gratulere et par herrer fra Hommersåk Atletklubb for kanonbra innsats under mesterskapet i helgen  >Cheesy

Dagens økt:
-------------------------------------
7 min medium sykling
KB:
10x60kg
6x90kg
3x110kg
3x110kg
3x110kg

ML:
5x60kg
5x110kg
3x140kg
3x140kg
3x140kg

Beinpress:
8x200kg
8x200kg
8x200kg

Legg extension:
10x70kg
10x70kg

Lår curl:
10x40kg
10x40kg

Sittende tåhev:
8x40kg
8x40kg
------------------------------------------------------------

Ryggen er sliten i bunnen. I løft vil det si at selve toppen/utretting er lite god...
Kommer til å kjøre forsiktig frem til ryggen sier go go go igjen Smiley

Ellers er det full gang med jobbing ute i hagen. Innkjørsel skal spaes opp, stein skal legges. Eiendom skal planeres og mures ut. Gjerde, grill m/benk og plen skal tilføyes. Hus skal males, samt få nytt overbygg/halvtak over inngangspartiet....

Jeg vet hva jeg skal i sommer Grin
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BILDER - Ta en titt Smiley
Maks per 5.7.2006    Mål til jul 2006
---------------------------------------------
KB:  170 kg (180kg)      200 kg
BP:  150 kg (165kg)      170 kg
ML:  170 kg  MÅL NÅDD 200 kg

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« #1205 : 06. mai 2008, 13:23 »
Dagens sommerkropp-økt:
---------------------------------------------------
Chins:
15x60kg
10x70kg
7x80kg
7x80kg
10x70kg

Nedtrekk bak:
10x80kg
6x90kg
10x80kg

BP:
15x70kg
12x90kg
10x110kg
6x130kg
4x140kg
3x150kg
4x140kg (+1 m/hjelp)

Flyes i cross cable:
10x40kg
8x40kg

Stående roing:
12x40kg
10x60kg
8x70kg
10x60kg
----------------------------------------------------

Spadde 7 tonn med grus i går kveld, så armen (høyre) likte ikke noen av øvelsene idag. Tok det med ro, og valgte å kjøre piano i noen øvelser.

Uansett, ny rekord i BP mht antall reps (og på en passe grei dag)...
 Cool
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Maks per 5.7.2006    Mål til jul 2006
---------------------------------------------
KB:  170 kg (180kg)      200 kg
BP:  150 kg (165kg)      170 kg
ML:  170 kg  MÅL NÅDD 200 kg

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« #1206 : 08. mai 2008, 14:01 »
Dagens beinøkt:
-----------------------------------------
5 min lett sykling

KB:
8x80kg
6x100kg
5x120kg
5x120kg
5x120kg

ML:
5x70kg
5x110kg
5x140kg
5x140kg
5x140kg

Legg extension:
10x70kg
10x70kg

Lår curl:
12x40kg
8x40kg

Sittende tåhev:
10x25kg
6x50kg
6x50kg
----------------------------------------------

Sommer og sol... Smiley

Begynte bra mht bein i dag. En god del trøkk, men tok det rolig som planlagt.
That's it.... Smiley
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Maks per 5.7.2006    Mål til jul 2006
---------------------------------------------
KB:  170 kg (180kg)      200 kg
BP:  150 kg (165kg)      170 kg
ML:  170 kg  MÅL NÅDD 200 kg

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« #1207 : 09. mai 2008, 02:04 »
ville økter på deg for tiden mann! Cheesy
maks:                                    
benk: 150kg x 1 RAW              
markløft: 210 x 1 RAW           
knebøy: 160kg x 1 Bind          
Treningsveileder, NIH
Kettlebells instruktør
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« #1208 : 09. mai 2008, 07:35 »
ville økter på deg for tiden mann! Cheesy

Labre økter egentlig, men kjenner at formen begynner å nærme seg nye perser av en eller annen merkelig grunn. Håper jeg for en gangs skyld ikke tar feil Grin
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Maks per 5.7.2006    Mål til jul 2006
---------------------------------------------
KB:  170 kg (180kg)      200 kg
BP:  150 kg (165kg)      170 kg
ML:  170 kg  MÅL NÅDD 200 kg

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« #1209 : 09. mai 2008, 12:39 »
det lukter maksing framover med andre ord? Wink
maks:                                    
benk: 150kg x 1 RAW              
markløft: 210 x 1 RAW           
knebøy: 160kg x 1 Bind          
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« #1210 : 09. mai 2008, 14:14 »
det lukter maksing framover med andre ord? Wink

I en eller annen form: Ja Smiley

Dagens for-madammen-sin-del økt:
-----------------------------------------------------------------
Chins omvendt grep:
10x60kg
10x75kg
8x90kg
6xmeg
6xmeg
6xmeg

BP smalt omvendt grep:
10x60kg
10x80kg
8x100kg
7x100kg

Stående roing:
15x40kg
10x60kg
7x70kg
4x80kg
4x80kg
13x60kg

Dips:
15xmeg
10xmeg+25kg
10xmeg+25kg

Manual curl:
10x22,5kg
7x20kg

Skulderpress manual:
10x15kg
10x20kg
8x20kg
7x20kg

Franskpress:
15x35kg
15x35kg

Skulder manual (5 øvelser i supersett):
12x5kg
12x5kg
----------------------------------------------------------

Tunge armer gitt ...uvant med slikt Smiley
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Maks per 5.7.2006    Mål til jul 2006
---------------------------------------------
KB:  170 kg (180kg)      200 kg
BP:  150 kg (165kg)      170 kg
ML:  170 kg  MÅL NÅDD 200 kg

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« #1211 : 13. mai 2008, 12:07 »
Dagens økt:
------------------------------------
6 min lett sykling

KB:
8x80kg
6x100kg
5x120kg
3x140kg
2x140kg
2x140kg
5x120kg

Legg extension:
8x75kg
8x75kg

Lår curl:
8x45kg
8x45kg

Sittende tåhev:
10x25kg
8x40kg
8x40kg
----------------------------------------------
Min treningslogg - sterke saker
BILDER - Ta en titt Smiley
Maks per 5.7.2006    Mål til jul 2006
---------------------------------------------
KB:  170 kg (180kg)      200 kg
BP:  150 kg (165kg)      170 kg
ML:  170 kg  MÅL NÅDD 200 kg

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« #1212 : 14. mai 2008, 09:35 »
Har endt opp med en rar tilstand. Jeg skal si noen korte ord om tilstanden i håp om at andre har opplevd det samme, men i motsetning til meg funnet svar på tiltalen...

I går etter trening merket jeg at kroppen begynte å gå i dvale. Stoffskiftet gikk ned, appetitten likeså, energien stupte hodestups ned i en sølepytt av tiltaksløshet...
Hva skjedde egentlig??

Utover ettermiddagen ble det bare værre. Jeg orket ikke tanken på mat, og vann var vanskelig å få i seg. Kunne ikke tenke, kunne ikke finne lyspunkter og visste ikke når jeg ville føle gnisten av liv igjen... (satt på spissen). Magen vridde seg i tango rundt mine innvolder. Jeg kunne også kjenne en viss kvalme som kom og gikk igjen. Heldigvis svakt.

Utover kvelden stabiliserte det seg, og jeg fikk dyttet i meg mer vann, c-vit, vitaminbjørner og litt snacks... Men mat: Ikke snakk om en liten bit engang. Lå strak ut hele ettermiddagen og kvelden.
Ære være madammen som stod på med våres 3 små, laget mat, jobbet ute og spadde sand mens lille uduglige meg bare lå inne og kunne ikke annet enn å prate...
Tok meg en ZMA før jeg sovnet, og sov som en bjørn Smiley

Våknet opp i dag, og var igjen bra utvilt. Men ikke noe overskudd, ingen appetitt og middels konsentrasjon.
Fremdeles i skrivende øyeblikk er jeg fornøyd med dagens inntak av en banan!!!

Hva er det som er galt?? Har ingen symptomer på magesår, utbrenthet eller stress....
Er det virus?? Er det blåmandag av værste sort, eller er det noe annet??
Magen virker som om den helt har sluttet og ta til seg næring, og er for det meste lett urolig og bare "tom".

Jeg aner lite, og ser ei heller noe stort poeng med en allmennpraktiserende lege... De er snille og greie, men kan litt om mye. Jeg får så sjeldent gode svar at jeg har gitt dem opp...

Forslag taes med takk.
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Maks per 5.7.2006    Mål til jul 2006
---------------------------------------------
KB:  170 kg (180kg)      200 kg
BP:  150 kg (165kg)      170 kg
ML:  170 kg  MÅL NÅDD 200 kg

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Sv: Dangermouse... need any more?? :)
« #1213 : 14. mai 2008, 10:22 »
Dumt å høre. Jeg aner i all fall ikke hva det er, men det kan jo virke som det går den rette veien dagen etter? Jeg har også en dose skepsis til legestanden, men de kan ta visse prøver som kanskje kan vise noe, men du får se om det går den rette veien først. Merkelig er det jo uansett, og det hadde vært greit for deg å bli klokere på hva det er. (Unødig å si...) Tvi, tvi, kompis, så håper jeg å se deg frisk og rask snart.

Jeg trener for øvrig som før, og driver med jobbsøking rundt forbi. Regner med å flytte på meg til høsten.

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Sv: Dangermouse... need any more?? :)
« #1214 : 14. mai 2008, 11:49 »
Jeg ville i utgangspunktet tippet matforgiftning eller en eller annen type infeksjon. Ville...hm...gått til legen.... Wink  de kan måle om du har dette. Kjedelig uansett..God bedring  Smiley

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