Optimum Health

I received this comment on my blog;

“Everyone has they’re opinion on what is right or wrong to eat? "God" speaks in the bible about what is clean and unclean to eat of that of which was provided to us. And also, the grains,fruits,etc.. Anything beyond that would be bad for you. So, it’s not what we eat or don’t eat that is detrimental or not to our health, but the man-made additives that are put into making the foods we eat so it will taste better. I do not condone the slaughter industry and the way they produce meat, however, I am not a vegetarian, but I do try to stay more vegan than meat. I’m still learning how to balance what is better, in a long run,for my health, for our bodies are not our own”.

I replied;

While I do appreciate your opinion and input, but it just so happens that humans get very sick on just eating grains and vegetables. That’s science, not religion. I have my own "belief" system when it comes to God, but I study science and nutrition. If God had not provided meat for us to eat, and the knowledge to prepare it, the human race would not have evolved this far. Since we need meat and fats to be healthy, and God has instructed us to eat well and treat out body as a temple…so we can go forth and do his work, it cannot be wrong morally for us to eat meat.

I speak from the perspective of a recovering vegetarian. I followed that way of eating for almost 25 years…because we had no clean meat to eat!  I had problems with it, it didn’t give me the right fats, I developed an allergy to EVERY SINGLE PROTEIN SOURCE associated with a vegetarian diet; SOY (after eating it for 15 years it made me start going into anaphylactic shock), DAIRY (I became seriously allergic to all dairy),  NUTS (same reaction as to soy, after eating them all my life). I also became highly sensitized to grains. I got well when I stopped eating these very common allergens. Meats, fats and meats broths have enabled me to repair my immune system. I now eat a diet that man has been evolving on for thousands of years; meat, meat stocks, vegetables and fruits.  Remember we have only been eating more grains after we stopped living as hunter-gatherers and began living in cities, somewhere around 1000 to 1100 AD>

Even though Kosher meat is killed kindly, it is not organic. Grass-fed gives me meat and fats that are clean; organic, full of life preserving, immune system building Vitamins A,D and E, and the right composition of fats.

I totally agree with the part of your statement about the additives and chemicals doing us harm. It is PART of the picture…but the most crucial nutrients that Americans are deficient in (calcium, Vitamin A and D, saturated fats) are only available in meat and fats from animals that have been raised in the sun!

So hang on to the limited diets that you are eating in the name of “a belief system”, but know that you will develop health problems and deficiencies as you age… Living on mostly carbs (grains and vegetables) will lead to obesity, a breakdown in your immune system, delicate skin that is prone to dryness and skin cancer, depression for lack of the right saturated fats and lack of energy and endurance.

Please read- The Ethics of Eating Meat by Charles Eisenstein

 

The Response-to-Injury Rabbit Never Developed Atherosclerosis — Why Not?

by Chris Masterjohn

From Cholesterol and Health.com

The pop science version of cholesterol goes something like this: when you eat fatty foods, especially foods rich in animal fat, the saturated fat and cholesterol in these foods wind up in your blood and stick to your arteries. Since saturated fats are solid outside your body, they will be solid inside your body too — depsite the 30-degree increase in average temperature. Arteries are much like pipes. When they get caked up with grease, blood flow is impaired, and a heart attack ensues.

None of the prominent scientists who promoted the idea that cholesterol is a critical factor in the development of heart disease ever believed anything remotely resembling this nonsense. From the beginning, they recognized that atherosclerotic plaque accumulates behind the layer of the artery in contact with the blood, called the endothelium, and that the cholesterol and fat within it is engulfed in white blood cells.

The theory these scientists promoted looked something like this: when the cholesterol level in the blood increases, it penetrates the arterial wall and gets stuck; white blood cells circulating in the blood then enter the arterial wall and gobble up the cholesterol; the accumulation of lipid-loaded white blood cells causes local injury, leading to cell death, calcification, and the development of a collagen-laden "fibrous cap" over the atherosclerotic lesion. When the cap ruptures, the blood clots, blocking the artery and causing a heart attack. This is called the lipid hypothesis.

But is this true? Books and web sites devoted to debunking this theory have come out of the woodwork over the last decade; books defending it have followed suit. Consider the following titles to see just how controversial the idea really is:

• The Cholesterol Myths: Exposing the Fallacy That Saturated Fat and Cholesterol Cause Heart Disease by Uffe Ravnskov, MD, PhD (2000).
• The Great Cholesterol Con: Why everything you’ve been told about cholesterol, diet, and heart disease is wrong! by Anthony Colpo (2006).
• The Cholesterol Wars: The Skeptics vs. the Preponderance of the Evidence by Daniel Steinberg, MD, PhD (2007).
• The Great Cholesterol Con: The Truth About What Really Causes Heart Disease and How to Avoid It by Malcolm Kendrick, MD (2007).

So is the theory that cholesterol causes heart disease just a myth? Or are the skeptics truly waging a war against the preponderance of the evidence?

The Cholesterol Debate — What Causes Atherosclerosis?

The truth is that each of these authors makes important points. Were there never any good evidence that cholesterol was involved in heart disease, there would be no National Cholesterol Education Program, no statin empire, and Daniel Steinberg could never have written a book plus over 200 scientific papers on the subject. On the other hand, were there never anything seriously wrong with the mainstream dogma on the issue, Ravnskov, Colpo, Kendrick, and many other authors could never have built their careers around pointing out the gaping holes in the theory.

There is no one cause of "heart disease." "Heart disease" is a heterogeneous compliation of diseases of the heart and blood vessels with many different causes. Some of these include disturbances of the rhythm of the heart, calcification of the middle portion of the blood vessels and calcification of the heart valves, and congestive heart failure. The question I address in this article is whether and in what sense cholesterol is involved in atherosclerosis, the development of fatty and calcified plaques in isolated, raised lesions, which can cause heart attacks by rupturing, clotting, and blocking arteries.

In 1933, the famous proponent of the cholesterol-fed rabbit model Nikolai Anitschkov declared that atherosclerosis had been shown to be of an "infiltrative" character rather than a "degenerative" character and was driven by lipids (fatty substances) rather than by inflammation. He did not deny inflammation was involved, but believed that it was secondary to lipid infiltration. Many opponents continue to claim that the root cause driving heart disease has nothing to do with lipids and everything to do with inflammation and that it is degenerative rather than infiltrative in character.

As we will see below, these are all correct! Atherosclerosis is largely driven by the degeneration of lipids which infiltrate the blood vessel and thereby cause inflammation. Inflammation from other sources may accelerate the process or further the degeneration of the atherosclerotic plaques once they are formed, but the initiating factor for fatty plaques appears to be the degeneration of lipids — especially the degeneration of polyunsaturated fatty acids (PUFA).

In order to begin looking at the evidence, we must go back a century in time to the cholesterol-fed rabbit. The cholesterol-fed rabbit model came on the heels of extensive investigations into what would later be termed the "response-to-injury hypothesis."

The Response-to-Injury Rabbit Model

Around the turn of the twentieth century, research into the cause or causes of heart disease was in full throttle. A 1933 compilation edited by E.V. Cowdry entitled Arteriosclerosis: A Survey of the Problem (New York: Macmillan) contained twenty reviews of investigations into the matter, including statistical relationships, the distribution of the disease in wild animals, the distribution in humans according to race and climate, nutritional influences, the physical and chemical nature of the changes that occur in atherosclerotic tissues, and experimental models of the disease.

Nikolai Anitschkov, who developed the cholesterol-fed rabbit model, wrote the 50-page review of experimental animal models.¹ Much of this research was published in German, so Anitschkov’s review is an invaluable resource.

According to Anitschkov, early ideas about the origin of arteriosclerosis — a general term for hardening and damage to the arteries, of which atherosclerosis is a specific type — saw the diseases as a response to injury. The injury was primarily seen as either a mechanical or a toxic factor, and was sometimes believed to be injury to the nerves rather than injury to the blood vessels. Researchers carried out a multitude of experiments on rabbits and other animals, including the following:

• Mechanical damage to the blood vessels including ligating, pulling, pinching, and wounding them, and cauterizing them with galvanic wire or silver nitrate.
• Increasing blood pressure by constricting the blood supply through the aorta, damaging the kidneys, or hanging rabbits up by their feet.
• Severing or irritating certain nerves.
• Injecting rabbits with adrenalin.
• Injecting rabbits with a multitude of toxic factors, including digitalin, strophanthin, adonidin, ergotin, theocin, barium chloride, hydrastin, nicotine, caffeine, formalin, ergosterol, and various salts of acids and heavy metals.
• Injection of diphtheria toxin and many other bacteria cultures or bacterial byproducts.

Most of these methods caused substantial damage to the arteries and resulted in a "regenerative thickening" of one or another type. So the response-to-injury concept is quite real.

Atherosclerosis is Just One Type of Arteriosclerosis

None of these methods, however, produced anything resembling human atherosclerosis. While arteriosclerosis refers to hardening and degeneration of the arteries in general, atherosclerosis is a specific type of arteriosclerosis in which a plaque rich in lipid-loaded white blood cells, cholesterol, fatty acids, calcium, various debris — called an atheroma — invades the innermost layer of the blood vessel wall called the intima, just behind the one-cell-thick layer called the endothelium. If you are not familiar with the anatomy of a blood vessel, you can see a diagram of it here.

The research in Anitschkov’s day suggested that, while various types of arteriosclerosis occurred in humans, atherosclerosis was a much more important cause of death. Anitschkov thus concerned his research with what caused atherosclerosis.

The mechanical injuries to blood vessels or nerves produced a local repair process that involved the proliferation of cells, their congregation around the damaged area, and a resultant thickening of the vessel wall. The results were local rather than systemic, however, and never produced a lesion resembling an atheroma.

Injections of adrenalin produced much more interesting changes that were much more relevant to humans. They produced necrosis (death) of cells in the media followed by extensive calcification. A similar process was observed in some of the blood pressure experiments and in many of the experiments involving injections of metallic, bacterial, or other toxins. These changes, however, were fundamentally different from atherosclerosis, which occurs in the intima.

Medial Calcification and the Vitamin K₂ Connection

That does not mean this research is irrelevant. Humans experience this type of medial calcification in diabetes, kidney disease, and aging. It appears to assault the media of arteries and the valves of the heart together. It increases arterial stiffness and decreases the artery’s ability to accomodate moderately high levels of blood pressure. One of the most important factors in this type of calcification appears to be vitamin K₂.

Vitamin K-dependent proteins protect against cell death, help clear away the debris that cells leave behind when they do die, and protect against the calcification of soft tissues. In the absence of sufficient vitamin K, these proteins are deformed and fail to work properly. It appears that vitamin K₂, found in animal fats and fermented foods, is far more important in this respect than vitamin K₁, found in green plant foods. I have written extensively on this subject and argued that vitamin K₂ is the "activator X" of Weston Price in my article, On the Trail of the Elusive X Factor: Vitamin K₂ Revealed.

Despite the research in Anitschkov’s day suggesting that only atherosclerosis had major clinical importance, research in our own day shows that calcification of the media and valves is critically important to, at a minimum, the 324 million people worldwide who will be diabetic come 2025. For the US population born in 2000, the estimated lifetime risk of type 2 diabetes is one in three.² In type 2 diabetics, medial calcification increases the risk of mortality from heart disease, stroke, and all causes. It also predicts the incidence of heart disease and stroke, including events that do not produce fatalities, and predicts the likelihood that peripheral artery disease will require limb amputation.³

So the response-to-injury hypothesis has a solid basis of evidence for arteriosclerosis of the media, and this is clinically important — but what causes atheroma, that is, the fatty plaque that causes raised lesions in the intima of the blood vessels?

To answer this question, we must look to the cholesterol-fed rabbit.

The Cholesterol-Fed Rabbit Controversy

In 1909, a researcher at the Military Medical Academy in St. Petersburg named Ignatowski produced atherosclerosis in rabbits by feeding them a diet of meat, eggs, and milk. He was pursuing a hypothesis put forward by Nobel Prize-winning microbiologist I. Metchnikov that dietary protein accelerated aging.⁴

In 1913, Anitschkov and his partner Chalatov were studying at the same academy and were assigned to follow up Ignatowski’s work. They progressively narrowed down the causative factor to cholesterol by feeding different foods and fractions of foods, finally producing the diease by feeding pure cholesterol dissolved in sunflower oil.⁴

Rabbits fed sunflower oil alone did not develop atherosclerosis. In the cholesterol-fed rabbits, however, lesions developed that exhibited a remarkable similarity to the human disease. They began as fatty streaks in the intima; circulating white blood cells then invaded the intima and engulfed the cholesterol and fat deposited there, eventually growing into large phagocytic cells that Anitschkov called xanthoma cells and we now call foam cells; eventually the developing plaque protruded into the intima in the form of a raised lesion. The lesion possessed a fatty core rich in crystalized and calcified cholesterol deposits and was covered with a fibrous cap.¹

The lesions did not appear everywhere equally, but occurred in specific areas. They were most prominent in the aorta and other large arteries, especially in the areas of the artery wall that experience disturbed blood flow such as the points where the arteries branch. While they did not occur in exactly the same places as human atherosclerotic lesions, the pattern was largely similar and the underlying physiological principle dictating the location of the lesions — mainly the type of blood flow experienced by the artery wall — was the same.¹

The rabbits developed cholesterol deposits all throughout their bodies, in their eyes and internal organs. Anitschkov produced a more mild form of the disease, however, by feeding the rabbits milk. In these experiments, the rabbits received a much more moderate amount of cholesterol over a much longer period of time and the resulting disease was much more focused in the arteries.¹

One curious difference between rabbits and humans is that when rabbits develop atherosclerosis, their plaques never rupture and they never get heart attacks. The main determinant of plaque rupture according to the current scientific literature is the balance between collagen degradation and collagen synthesis.⁵ Collagen synthesis requires vitamin C. Most animals, including rabbits, make their own vitamin C, but humans do not.

Atherosclerosis itself probably diminishes the quality of life in many different ways by impeding blood flow and blood vessel function, but it clearly does not inexorably lead to heart attacks. The reason why atherosclerosis produces heart attacks in humans and not rabbits or many other animals might be that humans cannot produce their own vitamin C.

Cholesterol in the Blood, Not the Food

Anitschkov argued against calling cholesterol "the cause" of atherosclerosis, but he considered cholesterol the primary causal factor and the necessary causal factor. Mechanical injuries, adrenalin injections, and other methods used to induce various types of arteriosclerosis would accelerate the development of atheroma when they were combined with cholesterol-feeding, but they would never result in human-like atherosclerosis by themselves.

Anitschkov never concluded from his experiments that cholesterol in the diet caused atherosclerosis in humans, however. To the contrary, he wrote the following:

[I]n human atherosclerosis the conditions are different. It is quite certain that such large quantities of cholesterin are not ingested with the ordinary food. In human patients we have probably to deal with a primary disturbance of the cholesterin metabolism, which may lead to atherosclerosis even if the hypercholesterinemia is less pronounced, provided only that it is of long duration and associated with other injurious factors.

Cholesterol skeptics often argue that the rabbit is irrelevant to the human because it is an herbivore. Cholesterol-feeding has failed to produce atherosclerosis in many other species. This is true, but it misses the point. In the species where cholesterol-feeding alone does not produce atherosclerosis, the blood level of cholesterol does not rise as much as in rabbits. But in all of these species when the level of cholesterol in the blood rises high enough, atherosclerosis ensues. For example, feeding dogs cholesterol alone does not produce atherosclerosis because they turn the cholesterol into bile acids; but inhibiting thyroid hormone stops them from making this conversion, and when combined with cholesterol-feeding, it induces atherosclerosis.

As Steinberg points out, raising blood levels of cholesterol has produced atherosclerosis in baboons, cats, chickens, chimpanzees, dogs, goats, guinea pigs, hamsters, monkeys, mice, parrots, pigs, pigeons, rabbits and rats.

The role of blood cholesterol in human heart disease was supported by research showing that people with a disorder that would eventually be called familial hypercholesterolemia had dramatically increased blood levels of cholesterol and, in youth and middle age, dramatically increased relative risks of heart disease and atherosclerosis. But what caused their high cholesterol levels, and did those levels cause the atherosclerosis, and if so, did this phenomenon have any relevance to the rest of us?

And, if cholesterol was somehow the culprit in all of this, was it merely its concentration in the blood that was at play, or was something very different going on?

Lessons From Familial Hypercholesterolemia

Familial hypercholesterolemia (FH) bears a striking resemblance to the cholesterol-fed rabbit model. In mild cases, it produces earlier and more rapidly developing atherosclerosis compared to the general population. In its severe cases, it results in cholesterol deposits all throughout the body, especially in the liver, kidneys, and eyelids.⁴

In the mid-1970s, Brown and Goldstein discovered that FH resulted from a single genetic defect in the LDL receptor that made the cells unable to absorb LDL from the bloodstream. Steinberg argues that, since cells jealously guard their cholesterol concentrations by adjusting their synthesis of cholesterol as needed, this showed that FH patients differed from the general population in only one single way: the concentration of cholesterol in their blood.⁴

The finding drew several more parallels between FH and Anitschkov’s cholesterol-fed rabbits. Anitschkov argued that it was not the mere feeding of cholesterol to the rabbits that produced atherosclerosis, but the overwhelming of their capacity to use and dispose of that cholesterol. FH cells could absorb free cholesterol, but not cholesterol from LDL. Anitschkov’s rabbits developed atherosclerosis when they ate cholesterol, but not when they were injected with it — in which case it would not be packaged into lipoproteins such as LDL, which contain many other substances besides cholesterol. Looking backward, it appears that the common thread running through each model was that the level of LDL in the blood exceeded the capacity of the LDL receptors to move that LDL from the blood to the cells.

The LDL receptor highway was blocked, and the LDL traffic was jammed.

Is Steinberg correct, however, that this changes nothing but the concentration of LDL in the blood? Consider what happens in a traffic jam:

• The concentration of cars in the road increases.
• It takes you longer to get home.

When LDL can’t get from the blood into the cells, its concentration in the blood rises, but it also spends a longer amount of time in the blood. Why would that matter? This would become clear just several years later. At the end of the 1970s, the role of oxidative stress in heart disease would finally become clear.

The Role of Oxidized LDL in Heart Disease

Anitschkov believed that his research showed that atherosclerosis was of an infiltrative character rather than a degenerative character. He believed that cholesterol and other substances naturally permeated the endothelium in order to nourish the other layers of the blood vessels, and proceeded from there into the lymph fluid. When the blood level of cholesterol rose sufficiently, he argued, it entered the intima at a faster rate than it could exit and began to accumulate.

Anitschkov was correct that the disease was driven by an infiltration of lipid, and he was correct that the degeneration of the blood vessel wall was secondary to this infiltration. What he failed to realize, and could not have realized at the time, was that the entire process depended on the degeneration of the lipid.

The Discovery of Oxidized LDL

Beginning in 1979, investigators made a series of revolutionary discoveries revealing this degenerative process. When they incubated cells with LDL in the absence of other serum components, the cells underwent severe damage and began to die within 24 hours. Adding serum or HDL prevented the toxicity.⁴

In 1981, these researchers discovered that culturing endothelial cells with LDL caused dramatic changes to the LDL, making it denser, more electronegative, and giving it a dramatic ability to accumulate in white blood cells called macrophages. Macrophages are phagocytic, meaning they like to gobble up other things, and they are the precursors to the "foam cells" that populate atherosclerotic plaques. The researchers called this LDL "endothelial cell-modified LDL." Soon after, they discovered that the LDL was being "oxidatively modified" and that not only HDL but vitamin E (which HDL is rich in) prevented the effect.⁴

Oxidized LDL Causes Injury and Inflammation

Since those early findings, thousands of papers have now been published on the role of oxidized LDL in the development of atherosclerosis. Oxidized LDL causes endothelial cells to secrete "adhesion molecules" and "chemoattractants" that allow white blood cells called monocytes to penetrate in between the endothelial cells and stick to them in the subendothelial space where fatty streaks and atherosclerotic plaques develop.⁶

Oxidized LDL turns on the expression of genes in monocytes which cause them to convert into macrophages and eventually into foam cells, which makes them gobble up more and more oxidized LDL endlessly — but these macrophages use "scavenger receptors" rather than LDL receptors, so they never take up meaningful amounts of non-oxidized LDL; they only take up oxidized LDL, and it is oxidized LDL itself that initates this endless cycle.⁷

Oxidized LDL initiates the inflammatory process by causing foam cells to secrete molecules that attract T cells and other inflammatory cells.⁶ Oxidized LDL enhances the process whereby T cells, foam cells, smooth muscle cells and endothelial cells decrease collagen production and increase collagen degradation, which leads to the rupture of the fibrous plaque.⁵

Endothelial cells produce nitric oxide, a gas that protects LDL from oxidation, increases blood flow, decreases the adhesion of monocytes to the endothelium, and decreases blood clotting. Oxidized LDL impairs the endothelial cell’s ability to produce nitric oxide.⁸

In short, oxidized LDL contributes to the entire atherosclerotic process from start to finish. Writers who argue that atherosclerosis has nothing to do with lipids but is all about inflammation and response to injury must contend with the fact that oxidized LDL injures endothelial cells and causes inflammation!

Small, Dense (Pattern B) LDL and Oxidation — Which Comes First?

If it is oxidized LDL rather than LDL per se that contributes to atherosclerosis, the question arises of what causes LDL to oxidize. Since polyunsaturated fatty acids (PUFA) in the LDL membrane are the components that are most vulnerable to oxidation, excess PUFA and insufficient antioxidants would seem to be the most obvious culprits. Endothelial cells, however, secrete a number of oxidative enzymes such as myeloperoxidase and lipoxygenase. LDL is always exposed to endothelial cells in the blood, but if it makes its way into the subendothleial space where it can get stuck in a network of sugary proteins called proteoglycans, it would be exposed to them even more directly. Some researchers have therefore put forward the "response-to-retention hypothesis," wherein the LDL oxidizes in response to getting stuck in the subendothelial space.

In 1988, a case-control study showed that people with a preponderance of small, dense LDL were three times more likely to suffer from a heart attack.⁹ Researchers subsequently showed that the smaller and denser LDL gets, the more quickly it oxidizes when they subject it to oxidants in a test tube.¹⁰ Then the "response-to-retention" crowd jumped in on the game a few years later and showed that small, dense LDL were much more likely get stuck in test tube versions of the proteoglycan network of the subendothelial space.¹¹

If the response-to-retention hypothesis is true, we are back to the infiltration hypothesis where the accumulation of LDL in the subendothelial space is driving the whole process because the accumulation causes the oxidation. This would be a convenient way of circumventing the enormously embarassing fact that the medical establishment has been pushing highly oxidation-prone PUFA oils for fifty years.

The question is, how are these LDL getting small and dense?

Within the response-to-retention paper, the authors stated that "with decreasing size and increasing density the LDL particles have less of the non-polar core covered with a surface monolayer made of phospholipids and cholesterol."

Where did the phospholipid membrane go?

A group working on lipoprotein (a), or Lp(a), published a paper in July of this year showing that virtually all oxidized LDL in the blood circulates attached to Lp(a). Lp(a) is essentially LDL stuck to a protein called apolipoprotein (a) or apo(a). This group showed that when oxidized LDL and apo(a) are incubated together, many of the oxidized phospholipids transfer directly to the apo(a).¹² In other words, when the membrane of LDL begins to oxidize, parts of it hop right off the LDL particle. Could that explain why "less of the non-polar core" would be "covered with a surface monolayer" on some LDL particles?

When Steinberg and his coworkers first described the characteristics of "endothelial cell-modified LDL," one of the most conspicuous changes that occurred to the LDL particles was a marked increase in density.¹³

A 1997 study confirmed that the LDL taken from people with a preponderance of the small, dense type does indeed oxidize quicker in a test tube, but the oxidation status of the LDL was different before they subjected it to oxidation. The predominantly small, dense LDL had a higher ratio of oxidized-to-reduced coenzyme Q₁₀ and a lower CoQ₁₀-to-vitamin E ratio.¹⁴ Since CoQ₁₀ is the first line of defense against LDL oxidation, this study strongly suggested that oxidation of the small, dense LDL had already started.

So here we have a chicken-and-egg question. Does small, dense LDL oxidize more rapidly in a test tube because it is small and dense, or because it is already partially oxidized, and its antioxidant defenses are already partially depleted? Is small, dense LDL more vulnerable to oxidation, or does LDL become small and dense when it becomes oxidized?

If LDL becomes small and dense through oxidation, then even if the test tube studies on its "stickiness" are correct and small, dense LDL is more likely to get stuck in the sugary protein network behind the endothelium, it is the oxidation driving the stickiness and not the stickiness driving the oxidation.

So we are back to square one wondering why the medical establishment never announed an emergency measure to put all the research dollars into discovering just how much damage it had done to everyone who followed its recommendations to use high-PUFA vegetable oils in place of saturated animal fats over the last fifty years.

Oxidized LDL and the PUFA Connection

Let us return to the traffic analogy for a moment. Why would an "LDL traffic jam," wherein the "LDL receptor highway" is blocked contribute to atherosclerosis?

The membrane of LDL contains polyunsaturated fatty acids (PUFA), which are highly vulnerable to oxidation. Cells continuously make antioxidant enzymes and other antioxidant compounds to protect their membrane PUFA. If PUFA start to oxidize, the cell ramps up its antioxidant production. When the liver packs cholesterol into a VLDL particle and secretes it into the blood (where it eventually becomes an LDL particle after delivering some of its nutrients to other tissues), it puts some antioxidants into the package. The PUFA have now left the comparative safety of the liver cell and have only a limited supply of antioxidants. When those antioxidants are used up, the PUFA begin to oxidize, and their oxidation products proceed to damage other components of the lipoprotein. When the oxidation becomes severe, the oxidized LDL winds up in a foam cell in an atherosclerotic plaque.

Let’s draw another analogy, this time to a jar of oil. If you use a jar of oil, you open it, exposing the PUFA within it to the oxygen in the air, but quickly put the cap back on and put it back in the fridge. What would happen if you opened the jar and let it sit on the table at room temperature? Over time, the limited amount of antioxidants in the oil would run out and the PUFA would begin to oxidize. The oil would go rancid.

Pumping LDL into the blood but letting it sit there circulating round and round exposed to oxidants rather than taking it into the shelter of the cell is like opening a jar of oil and leaving it on the table.

LDL taken from people who consume more PUFA, whether from vegetable oil or fish oil, oxidizes more easily in a test tube. Alpha-tocopherol, the major form of vitamin E, does not help.¹⁵

The specific components of the oxidized LDL particle that interact with the DNA of monocytes to transform them into macrophages and then into foam cells are oxidized derivatives of linoleic acid, a PUFA found in vegetable oils.¹⁶

A 2004 study from Brigham and Women’s Hospital and Harvard School of Public Health showed that in postmenopausal women, the more PUFA they ate, and to a much lesser extent the more carbohydrate they ate, the worse their atherosclerosis became over time. The more saturated fat they ate, the less their atherosclerosis progressed; in the highest intake of saturated fat, the atherosclerosis reversed over time.¹⁷

I will cover the topic of saturated fat, PUFA, and heart disease in greater detail in another article on the diet-heart hypothesis. Additionally, I have written a Special Report entitled How Essential Are the Essential Fatty Acids? that provides accurate and thoroughly researched information on the true requirement for PUFA, which is negligible for healthy adults. As part of my Special Reports series, I will be publishing a second PUFA Report later this year that will cover the benefits and dangers of consuming PUFA in amounts larger than the minimum requirements.

Shear Stress Explains the Locations of Plaques and the Benefits of Exercise

As in the cholesterol-fed rabbit, human atherosclerosis occurs in discrete plaques at specific locations. In both species, these plaques occur in locations that experience disturbed blood flow, such as the points where the arteries branch.

Anitschkov showed that the endothelium was more permeable to molecules labeled with dye at these points. Experimental vessel injuries that caused inflammatory responses made the endothelium even more permeable, but even in the absence of any treatment, the endothelium was naturally permeable in these areas.¹

Sections of the arterial wall in these areas experience a lower level of shear stress than sections in other areas. Shear stress is the type of pressure that is caused by laminar blood flow, or the flow of blood parallel to the blood vessel wall. Shear stress decreases the permeability of the endothelium by stimulating the production of the proteins that form the junctions between the endothelial cells. Under levels of shear stress approximating those that exist at locations where atherosclerosis develops, easily visualizable gold particles the size of LDL particles slip right in between the endothelial cells, whereas the permeability to these particles is very low under levels of shear stress approximating those that exist where plaques do not develop.¹⁸

Shear stress also increases nitric oxide production. Nitric oxide increases blood vessel dilation and blood flow, decreases the adhesion of monocytes to the endothelium, decreases blood clotting, and prevents the oxidation of LDL.⁶

By increasing blood flow, exercise increases shear stress. Since the average shear stress over time seems to be the critical factor, exercise might help prevent atherosclerosis by decreasing the permeability of the endothelium and increasing nitric oxide production in those areas of the blood vessels where the resting level of shear stress is insufficient for protection.

What About Correlations with High Cholesterol?

Much of the cholesterol debate focuses on correlations with cholesterol. How strong are they? How consistent are they? Why do they show up in young people but not in old, in men more than women?

The debate really misses the point, because since the early 1980s the molecular evidence has made very clear that it is oxidized LDL that contributes to atherosclerosis.

Correlations with cholesterol are likely to be confounded by a variety of factors that simultaneously increase cholesterol levels and contribute to heart disease, like stress and inflammation. In fact, inflammation seems to increase cholesterol synthesis essentially as an accidental byproduct of activating the stress response through an enzyme called Rho. Rho slashes nitric oxide production and thus almost certainly makes a contribution to atherosclerosis. For more information on Rho activation, click here.

Researchers have only recently developed methods for testing levels of oxidized LDL. One group has developed an antibody that recognizes oxidized but not non-oxidized phospholipids. They have shown that the proportion of LDL-associated phospholipids that are oxidized is a much more impressive risk factor for heart disease than LDL, and when it is multiplied by the level of LDL, thus indicating the total concentration of oxidized phospholipids, it is even better. Its predictive value is lower in older people, but still strong.¹⁹

Why would the association decline with age? If we look at the totality of the evidence about the mechanisms of atherosclerosis, it appears that oxidized LDL is the necessary initiating factor, but that we should expect its prominence as a contributing factor to decrease over time. Atherosclerosis probably does not develop in the absence of oxidized LDL. Once it does develop, however, and once the oxidized LDL stimulates the formation of foam cells, those foam cells recruit T cells that make their own contribution to the inflammatory process. Animal experiments show that independent sources of inflammation cannot initiate atherosclerosis, but they can aggravate it or accelerate it. Vitamin C deficiency, systemic infection, stress, and many other factors likely make contributions alongside oxidized LDL to the weakening and rupture of the fibrous cap that ultimately leads to a heart attack.

Virtually everyone develops substantial atherosclerosis by the time they are old. In people with more oxidized LDL, it occurs faster, and consequently reaches an advanced stage at a younger age. Inflammation will not help rupture a plaque that does not exist, so it will be much less likely to cause a heart attack in a younger person unless that person has high levels of oxidized LDL and consequently advanced atherosclerosis. In an older population wherein most people have advanced plaques, the factors that weaken the plaque will become much more important than the factors that create the plaque.

Studying the issue is complicated by the fact that we are looking at oxidized LDL in the blood. Once LDL gets oxidized enough, presumably it will wind up in arterial plaque. If there are factors that protect circulating LDL from contact with the tissues it could harm, they could confound the association.

Finally, studies looking at cardiovascular incidence or mortality are confounded by the fact that atherosclerosis is only one type of arteriosclerosis, and arteriosclerosis is only one cause of cardiovascular disease. Medial calcification, arrhythmia, congestive heart failure, or other causes of emboli (particles that can cause vessels) may all contribute to cardiovascular events. Oxidized LDL should only, or at least primarily, correlate with those events caused by atherosclerosis.

So is the Lipid Hypothesis Correct?

So is the lipid hypothesis correct? Not in its original form. The weight of the evidence clearly supports a role for the oxidation of LDL and not the concentration of LDL in the blood in the development of atherosclerosis.

The oxidized lipid hypothesis has an enormous amount of evidence supporting it. The cholesterol-fed rabbit model was a model not merely of hypercholesterolemia but of hyper-oxidized-lipoproteinemia. Antioxidants cause major decreases in atherosclerosis in cholesterol-fed or Watanabe familial hypercholesterolemic rabbit models independent of cholesterol levels.^4,20

We should not expect antioxidants to be fully capable of preventing the oxidation of LDL by themselves. As I discuss in my PUFA Report, antioxidants can stop oxidized PUFA from damaging other PUFA, but they can never fully repair the oxidized PUFA. The best they can do is convert it to a hydroxy-fatty acid, and it is the hydroxy versions of linoleic acid that have been shown to convert monocytes to foam cells!

Thus, all three of the following critical factors must be addressed:

• Increasing antioxidant status, especially coenzyme Q₁₀, but also alpha- and gamma-tocopherol.
• Reducing PUFA intake.
• Increasing LDL receptor function to minimize the amount of time LDL spends in the bloodstream.

If concentrations of LDL rise in the blood because the LDL is not being utilized — for example, in familial hypercholesterolemia — then the LDL is exposing its vulnerable PUFA to conditions promoting oxidative stress for too long. The solution should not be to diminish cholesterol synthesis, imparing CoQ₁₀ synthesis along with it, but to increase LDL utilization. The appropriate nutritional strategies for increasing LDL utilization desperately need to be researched.

A recent study showed that curcumin, a component of tumeric, increases the expression of the LDL receptor. This study may provide valuable clues. Thyroid hormone is important to the function of the LDL receptor, and many people likely have suboptimal thyroid status.

The irony in all of this is that there is no evidence to suggest that cholesterol is the culprit. In the rabbit, consuming large amounts of cholesterol increases the exposure of LDL membrane-associated PUFA to oxidation because it causes their translocation from the liver to the blood where they are detached from the cellular environment and less protected. In humans, eating cholesterol in the form of several eggs per day probably decreases the vulnerability of LDL to oxidation. See here.

The higher the concentration of free cholesterol within the LDL particle, the less vulnerable it is to oxidation. By contrast, the higher the concentration of cholesterol that is linked to fatty acids, called "esterified cholesterol," the more vulnerable the LDL is to oxidation.⁹ Esterified cholesterol primarily exists in the core of the particle. Free cholesterol primarily exists in the surface membrane where the initial oxidation takes place, so cholesterol seems to protect the PUFA from oxidation.

So, does cholesterol cause atherosclerosis? No!

But do blood lipids? Yes. Atherosclerosis is a disease in which degenerating lipids infiltrate the blood vessel wall and cause inflammation and degeneration of the local tissue once they arrive there. Solid evidence has amassed in favor of this view for the last 100 years.

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References

1. Anitschkow N, Experimental Arteriosclerosis in Animals. In: Cowdry EV, Arteriosclerosis: A Survey of the Problem. 1933; New York: Macmillan. pp. 271-322.

2. Cheng D. Prevalence, predisposition and prevention of type II diabetes. Nutrition & Metabolism. 2005;2:29.

3. Lehto S, Niskanen L, Suhonen M, Ronnemaa T, Laakso M. Medial Artery Calcification. A Neglected Harbinger of Cardiovascular Complications in Non-Insulin-Dependent Diabetes Mellitus. Arteriosis, Thrombosis, and Vascular Biology. 1996;16:978.

4. Steinberg D, The Cholesterol Wars: The Skeptics vs. The Preponderance of the Evidence.2000; San Diego: Academic Press.

5. Libby P. The molecular mechanisms of the thrombotic complications of atherosclerosis. J Intern Med. 2008;263(5):517-27.

6. Libby P. Inflammation and cardiovascular disease mechanisms. Am J Clin Nutr. 2006;83(suppl):456S-60S.

7. Tontonoz P, Nagy L, Alvarez JG, Thomazy VA, Evans RM. PPARgamma promotes monocyte/macrophage differentiation and uptake of oxidized LDL. Cell. 1998;93(2):241-52.

8. Laufs U, Fata VL, Plutzky J, Liao JK. Upregulation of Endotelial Nitric Oxide Synthase by HMG CoA Reductase Inhibitors. Circulation. 1998;97:1129-1135.

9. Austin MA, Breslow JL, Hennekens CH, Buring JE, Willet WC, Krauss RM. Low-density lipoprotein sublass patterns and risk of myocardial infarction. JAMA 1988;260(13):1917-21.

10. Tribble DL, Holl LG, Wood PD, Krauss RM. Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis. 1992;93:189-99.

11. Camejo G, Hurt-Camejo E, Wiklund O, Bondjers G. Association of apo B lipoproteins with arterial proteoglycans: Pathological significance and molecular basis. Atherosclerosis 1998;139:205-222.

12. Bergmark C, Dewan A, Orsoni A, Merki E, Miller ER, Shin M-J, et al. A Novel Function of Lipoprotein (a) as a Preferential Carrier of Oxidized Phospholipids in Human Plasma. J Lipid Res. 2008 Jul 3;[Epub ahead of print]

13. Henriksen T, Mahoney EM, Steinberg D. Enhanced macrophage degradation of low density lipoprotein previously incubated with cultured endothelial cells: Recognition by receptors for acetylated low density lipoproteins. Proc Natl Acad Sci USA. 1981;78(10):6499-6503.

14. de Rijke YB, Bredie SJH, Demacker PNM, Vogelaar JM, Hak-Lemmers HLM, Stalenhoef AFH. The Redox Status of Coenzyme Q10 in Total LDL as an Indicator of In Vivo Oxidative Modification. Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:127-133.

15. Nenseter MS, Drevon CA. Dietary polyunsaturates and peroxidation of low density lipoprotein. Curr Opin Lipidol. 1996;7(1):8-13.

16. Nagy L, Tontonoz P, Alvarez JG, Chen H, Evans RM. Oxidized LDL regulates macrophage gene expression through ligand activation of PPARgamma. Cell. 1998;93(2):229-40.

17. Mozaffarian D, Rimm EB, Herrington DM. Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal.

18. Conklin BS, Vito RP, Changyi C. Effect of Low Shear Stress on Permeability and Occludin Expression in Porcine Artery Endothelial Cells. World J Surg. 2007;31:733-43.

19. Tsimikas S, Brilakis ES, Miller ER, McConnell JP, Lennon RJ, Kornman KS, Witztum JL, Berger PB. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease. N Engl J Med. 2005;353(1):46-57.

20. Wang Z, Zou J, Cao K, Hsieh TC, Huang Y, Wu JM. Dealcoholized red wine containing known amounts of resveratrol suppresses atherosclerosis in hypercholesterolemic rabbits without affecting plasma lipid levels. Int J Mol Med. 2005;16(4):533-40.

Two nutrition experts argue that you can’t take marketing campaigns at face value

By Adam Voiland

With America’s obesity problem among kids reaching crisis proportions, even junk food makers have started to claim they want to steer children toward more healthful choices. In a study released earlier this year, the Centers for Disease Control and Prevention reported that about 32 percent of children were overweight but not obese, 16 percent were obese, and 11 percent were extremely obese. Food giant PepsiCo, for example, points out on its website that "we can play an important role in helping kids lead healthier lives by offering healthy product choices in schools." The company highlights what it considers its healthier products within various food categories through a "Smart Spot" marketing campaign that features green symbols on packaging. PepsiCo’s inclusive criteria—explained here—award spots to foods of dubious nutritional value such as Diet Pepsi, Cap’n Crunch cereal, reduced-fat Doritos, and Cheetos.

But are wellness initiatives like Smart Spot just marketing ploys? Such moves by the food industry may seem to be a step in the right direction, but ultimately makers of popular junk foods have an obligation to stockholders to encourage kids to eat more—not less—of the foods that fuel their profits, says David Ludwig, a pediatrician and the co-author of a commentary published in this week’s Journal of the American Medical Association that raises questions about whether big food companies can be trusted to help combat obesity. Ludwig and article co-author Marion Nestle, a professor of nutrition at New York University, both of whom have long histories of tracking the food industry, spoke with U.S. News and highlighted some things that junk food makers don’t want you to know about their products and how they promote them.

1. Junk food makers spend billions advertising unhealthy foods to kids.
According to the Federal Trade Commission, food makers spend some $1.6 billion annually to reach children through the traditional media as well the Internet, in-store advertising, and sweepstakes. An article published in 2006 in the Journal of Public Health Policy puts the number as high as $10 billion annually. Promotions often use cartoon characters or free giveaways to entice kids into the junk food fold. PepsiCo has pledged that it will advertise only "Smart Spot" products to children under 12.

2. The studies that food producers support tend to minimize health concerns associated with their products.
In fact, according to a review led by Ludwig of hundreds of studies that looked at the health effects of milk, juice, and soda, the likelihood of conclusions favorable to the industry was several times higher among industry-sponsored research than studies that received no industry funding. "If a study is funded by the industry, it may be closer to advertising than science," he says.

3. Junk food makers donate large sums of money to professional nutrition associations.
The American Dietetic Association, for example, accepts money from companies such as Coca-Cola, which get access to decision makers in the food and nutrition marketplace via ADA events and programs, as this release explains. As Nestle notes in her blog and discusses at length in her book Food Politics, the group even distributes nutritional fact sheets that are directly sponsored by specific industry groups. This one, for example, which is sponsored by an industry group that promotes lamb, rather unsurprisingly touts the nutritional benefits of lamb. The ADA’s reasoning: "These collaborations take place with the understanding that ADA does not support any program or message that does not correspond with ADA’s science-based healthful-eating messages and positions," according to the group’s president, dietitian Martin Yadrick. "In fact, we think it’s important for us to be at the same table with food companies because of the positive influence that we can have on them."

4. More processing means more profits, but typically makes the food less healthy.
Minimally processed foods such as fresh fruits and vegetables obviously aren’t where food companies look for profits. The big bucks stem from turning government-subsidized commodity crops—mainly corn, wheat, and soybeans—into fast foods, snack foods, and beverages. High-profit products derived from these commodity crops are generally high in calories and low in nutritional value.

5. Less-processed foods are generally more satiating than their highly processed counterparts.
Fresh apples have an abundance of fiber and nutrients that are lost when they are processed into applesauce. And the added sugar or other sweeteners increase the number of calories without necessarily making the applesauce any more filling. Apple juice, which is even more processed, has had almost all of the fiber and nutrients stripped out. This same stripping out of nutrients, says Ludwig, happens with highly refined white bread compared with stone-ground whole wheat bread.

6. Many supposedly healthy replacement foods are hardly healthier than the foods they replace.
In 2006, for example, major beverage makers agreed to remove sugary sodas from school vending machines. But the industry mounted an intense lobbying effort that persuaded lawmakers to allow sports drinks and vitamin waters that—despite their slightly healthier reputations—still can be packed with sugar and calories.

7. A health claim on the label doesn’t necessarily make a food healthy.
Health claims such as "zero trans fats" or "contains whole wheat" may create the false impression that a product is healthy when it’s not. While the claims may be true, a product is not going to benefit your kid’s health if it’s also loaded with salt and sugar or saturated fat, say, and lacks fiber or other nutrients. "These claims are calorie distracters," adds Nestle. "They make people forget about the calories." Dave DeCecco, a spokesperson for PepsiCo, counters that the intent of a labeling program such as Smart Spot is simply to help consumers pick a healthier choice within a category. "We’re not trying to tell people that a bag of Doritos is healthier than asparagus. But, if you’re buying chips, and you’re busy, and you don’t have a lot of time to read every part of the label, it’s an easy way to make a smarter choice," he says.

8. The food industry funds front groups that fight antiobesity public health initiatives.
Unless you follow politics closely, you wouldn’t necessarily realize that a group with a name like the Center for Consumer Freedom (CCF) has anything to do with the food industry. In fact,Ludwig and Nestle point out, this group lobbies aggressively against obesity-related public health campaigns—such as the one directed at removing junk food from schools—and is funded, according to the Center for Media and Democracy, primarily through donations from big food companies such as Coca-Cola, Cargill, Tyson Foods, and Wendy’s.

9. The food industry works aggressively to discredit its critics.
According to the new JAMA article, the Center for Consumer Freedom boasts that "[our strategy] is to shoot the messenger. We’ve got to attack [activists'] credibility as spokespersons." Here’s the group’s entry on Marion Nestle.

The bottom line, says Nestle, is quite simple: Kids need to eat less, include more fruits and vegetables, and limit the junk food.

What I want to tell you is to NOT buy food out of packages, if it needs are label to list all the ingredients, you don’t want it!  Buy unprocessed food; meat, coconut oil, butter, eggs, vegetables…and a tiny amount of fruit.  That’s it, leave the cereals, granola bars, chips, sodas, juices on the grocery shelf.  Eat enough healthy fat and protein at each meal, the rest should be veggies.  And include traditionally made meat stocks for calcium and iron (think soup from scratch).

 

From The Weston Price Foundation

Group Cites Key Roles of Cholesterol in Body Chemistry, Hormone Balance, Longevity

WASHINGTON, DC, September 1, 2009–September is National Cholesterol Education Month, when government officials will stress cholesterol reduction as a top priority, claiming that “high levels of cholesterol significantly increase the risk of heart disease.” However, the Weston A. Price Foundation, a nonprofit nutrition education organization, urges citizens to celebrate September by learning about the vital roles of cholesterol in the body chemistry and by embracing nutrient-dense, cholesterol-rich foods.

“Cholesterol is deemed a deadly poison. Most people are afraid of eating foods containing cholesterol and of receiving a diagnosis of ‘high’ cholesterol,” says Sally Fallon Morell, president of the Weston A. Price Foundation. “Yet, having adequate cholesterol levels in the body is key to good health. The notion that cholesterol is a villain in the diet is a myth, based on flimsy evidence and opposed by many honest scientists, including prominent lipids researcher, Dr. Mary Enig. But, this theory was promoted by the food processing industry to demonize animal fats, which are competitors to vegetable oils and by the pharmaceutical industry to create a market for the sales of cholesterol-lowering drugs.”

Cholesterol is an important building block of the cell, providing structure and impermeability to the cell membrane, making it waterproof.  “Without adequate cholesterol in the cell membrane, our cells become ‘leaky’ and cannot function properly,” says Fallon. “In addition, many important substances are made out of cholesterol, including stress hormones like cortisol, sex hormones like estrogen and testosterone, the bile salts for digesting fats, and vitamin D.”

Cholesterol is vital to proper neurological function, playing a key role in the formation of memory and the uptake of hormones in the brain, including serotonin, the body’s feel-good chemical. When cholesterol levels drop too low, the serotonin receptors cannot work, leading to depression and anti-social behavior. Cholesterol is a major component of the brain, much of it in the myelin sheaths that insulate nerve cells and in the synapses that transmit nerve impulses.

Fallon notes that cholesterol-lowering is associated with numerous health problems including depression, cognitive impairment, amnesia, cancer, muscle pain, weakness and neuropathy. “The all-cause death rate is higher in those with cholesterol under 180 mg/dl, yet this is the level the medical profession urges us to meet. People with low cholesterol levels have more deaths from cancer, stroke, intestinal diseases, accidents and suicide.  And having low cholesterol does not necessarily protect against heart disease—many people with low cholesterol suffer heart attacks.”

National Cholesterol Education Month is focusing on cholesterol lowering in the elderly; however a 2001 report from the on-going Honolulu Heart Study, published in the Lancet,  found  “increased mortality in elderly people with low serum cholesterol. . . [and that] long-term persistence of low cholesterol concentration actually increases risk of death.” Corroborating studies indicate that high cholesterol levels in the elderly are associated with a longer lifespan, partly because cholesterol protects against infectious diseases like pneumonia and influenza.

However, Fallon’s biggest concern is the effect of cholesterol fear-mongering on growing children, noting that, “Cholesterol is vital for normal growth and development of the nervous system. Pregnant and nursing women and growing children need cholesterol-rich foods like whole milk, butter, egg yolks and liver to ensure optimal development. Children are being denied these foods on the spurious claim that they will cause obesity and heart disease later in life. The result is an epidemic of learning disabilities and growth problems, and later in life the specter of infertility and chronic disease.”

The Foundation urges parents to learn the other side of the story during National Cholesterol Education Month, by educating themselves on the benefits of a cholesterol-rich diet and by feeding nutrient-dense foods like cheese, eggs, bacon and meat to their children, so that they can do well in school and enjoy protection from disease.

For further information:

• The Oiling of America (History of the anti-cholesterol movement)
• Dangers of Statin Drugs

The Weston A. Price Foundation is a 501(c)3 nutrition education foundation with the mission of disseminating accurate, science-based information on diet and health. Named after nutrition pioneer Weston A. Price, DDS, author of the book Nutrition and Physical Degeneration, the Washington, DC-based Foundation publishes a quarterly journal for its 11,000 members, supports 400 local chapters worldwide and hosts a yearly conference. The Foundation headquarters phone number is (202) 363-4394, website is westonaprice.org, and general email address is info@westonaprice.org.

From The Grist

by Tom Philpott

“The whole problem of health—in soil, plant, animal, and man—is one great subject.”
—Albert Howard, The Soil and Health

Ezra Klein and I are engaged in a little debate over the value of organic food. I’m honestly a little surprised to be arguing with the Washington Post’s food-policy columnist about the desirability of removing toxic, ecologically damaging chemicals from food production. But no matter.

I got the ball rolling here; and here’s Ezra’s riposte. Narrowly, we’re debating whether organically grown foods offer more nutritional value than ones raised with synthetic chemicals.

I say they almost certainly do; Ezra is skeptical. From reading Ezra’s post and several comments from his readers, I find that people seem downright nonplussed by the idea that soil conditions and growing methods might affect the nutritional content of the resulting food. Their puzzlement in turn puzzles me. If we are what we eat, then so are plants; and plants are mainly eating soil (and the various nutrients and substances contained therein).

It makes me wonder what—or if?—people in our post-agricultural society think about the whole question of soil. Yet methods of soil stewardship are key to this debate. So before I dig into the details with the celebrated policy wonk—which study says what, funded by whom—I want to take a broad look at soil. In the process, I hope to open people’s minds to the idea that soil stewardship could affect food quality.

In his In Defense of Food, Michael Pollan pretty much debunked the tenets of what he called “nutritionism”—the idea that human nutrition could be reduced to a set of macronutrients (vitamin A, the B vitamins, etc.), which could then be isolated and fed to be people to keep them healthy. Scientists have known for a while that a given dose of, say, isolated vitamin A in pill form (or added to bread as fortification)  does not provide anything close to the same benefit as an equal dose in the context of a carrot. You can’t live well on 2,500 calories from sugar water plus oat fiber and a One a Day vitamin. Scientists now know that, but haven’t quite figured out why. Human nutrition turns out to be more mysterious than people in white lab coats have so far been able to decipher.

For about 100 years now, a form of nutritionism has also held sway among soil scientists, too. Where human nutritionists focused on vitamin A, etc., soil scientists seized upon N, P, and K—nitrogen, phosphorous, and potassium. No one disputes that these are basic building blocks of plant life—without sufficient access to each of them, plants can’t flourish. But just as human nutritionists at one time thought that nutrition could be isolated into macronutrients and delivered to people out of the context of food, so plant scientists decided that N, P, and K were sufficient, in isolated form, for plant life.

This idea marked the rise of what become known as NPK thinking—the nutritionism of soil scientists. By learning to synthesize nitrogen and mine phosphorous and potassium, technologists sparked an agricultural revolution. Farmers could abandon the time-consuming task of recycling nutrients and building soil; instead, they could merely purchase newly available inputs (on the installment plan, of course).  Society had “solved” the whole vexing problem of soil fertility; farmers could now focus on growing food, and lots of it (meaning fewer farmers).

In the NPK-think that still rules conventional agriculture, soil is essentially an inert medium for conveying isolated blasts of synthesized and mined NPK to crops. The effect on soil quality has been dreadful. Writing in The Fatal Harvest Reader (2002), the California farmer Jason McKenney describes the effect:

We now know that massive use of synthetic fertilizers to create artificial fertility has had a cascade of adverse effects on natural soil fertility and the entire soil system. Fertilizer application begins the destruction of soil biodiversity by diminishing the role of nitrogen-fixing bacteria and amplifying the role of everything that feeds on nitrogen. These feeders then speed up the decomposition of organic matter and humus. As organic matter decreases, the physical structure of soil changes. With less pore space and less of their sponge-like qualities, soils are less efficient at storing water and air. More irrigation is needed. Water leeches through soils, draining away nutrients that no longer have an effective susbstrate on which to cling. With less available oxygen the growth of soil microbiology slows, and the intricate ecosystem of biological exchanges breaks down.

I saw it in extreme form on a trip last spring to Immokalee, Florida—source of 90 percent of the winter tomatoes grown in the United States. As I and many others have pointed out, workers are abused there as a matter of course.

But the growing conditions are also quite startling. When you look down in an Immokalee tomato field, what you see is sand—there’s no evident organic matter in the growing medium (the word “soil” doesn’t quite apply here). To prepare for tomato growing, you start by sterilizing the ground with an extremely toxic pesticide—and in the process wipe out any beneficial microbes that might be lingering there. Then you inject the doses of NPK to maximize output, and you’re ready to go. (You may need more insecticide sprayings as the season wears on.)

More than in any other place I’ve seen, plants there live on a diet equivalent to sugar water, oat fiber, and vitamin pills. Can there be any real wonder that the resulting tomatoes are so pathetically lacking in flavor? And do people still doubt that they may be less healthful as well?

Indeed, there’s strong evidence that the nutritional value of industrially grown vegetable crops has declined significantly since 1950.

In contrast to industrial agriculture’s reliance on NPK, organic ag focuses on building soil as a living ecosystem. Even large-scale industrial-organic farms nourish their soil with nitrogen-fixing cover crops and well-composted manure, which along with NPK deliver loads of organic matter and micronutrients. And the nitrogen available from legume cover crops and manure releases slowly, not jolting crops into rapid growth like straight anhydrous ammonia. And whereas the harsh chemicals and poisons of conventional farming squeeze out microbial life in the soil, organic farmers seek to nourish it.

Given all of this, I would be surprised if a tomato grown in Immokalee’s chemical-infused sands delivered as much health-giving properties as one grown in rich, living humus.

All right, so back to the details of the debate.

I pointed to a literature review conducted by the U.S.-based Organic Center, which is funded by Big Organic groups like Horizon and Whole Foods; Ezra pointed to one funded by the U.K. Food Safety Agency, the equivalent of the U.S. FDA. And like that agency, the FSA has not managed to remain free of food-industry influence. For example, its current chief executive is Tim Smith, whose bio reads like this:

Tim Smith is the former Chief Executive of Arla Foods UK plc. The company, which is responsible for a number of major food brands, is now part of Arla Foods amba, Europe’s largest dairy manufacturer. He was appointed Chief Executive of Arla Foods in early 2005.

Tim Smith graduated from Leeds University with a degree in microbiology and zoology. He has spent his entire career in the food business: from 1979 to 1994 he was at Northern Foods, finishing his career there as a Divisional Director. After five years at Sara Lee Corporation, where he was President of UK operations, he joined Express Dairies plc as Executive Director. Express Dairies merged with Arla Foods in October 2003.

Impressive. I don’t think even a U.S. president would appoint a career Big Food exec to the top food-safety post upon his first swing through the revolving door. Even Michael Taylor, the former Monsanto exec (and before that, lawyer) Obama recently handed a top position at FDA, served a few stints in government before the appointment.

At any rate, neither Ezra nor I is leaning on a pristine study untainted by special interest. And in this age of industry dominance of research agendas, there may be no pristine studies. So let’s look at details.

Ezra makes two major points to refute my position: 1) organic food may have more total antioxidants than conventional, but that’s irrelevant, because of the “wealth of studies showing that antioxidants do not appear to reduce the risk of cancer or heart disease or anything else”; and 2) that my contention that the lower nitrogen content of organic foods makes them healthier is based on a “circumstantial argument” about the danger of nitrates “that is plausible, but hasn’t been studied.”

Ezra links to two studies to back up his claim about the irrelevance of antioxidants. The first one is itself irrelevant, because it is measuring the value of antioxidant supplements—ie, isolated antioxidants—and we’re talking about antioxidants in whole foods. I agree that taking, say, beta-caratene pills is probably worthless; I doubt that beta-caratene in, say, the context of a carrot is worthless.

The second study is more interesting. This investigates whether “natural antioxidants, i.e. Vitamin C, Vitamin E and carotenoids” fight certain kinds of heart damage. It concludes:

Animal studies indicate that dietary antioxidants may reduce atherosclerosis progression, and observational data in humans suggest that antioxidant vitamin ingestion is associated with reduced cardiovascular disease, but the results of randomised controlled trials are mainly disappointing.

I assume that by “dietary antioxidants,” the researchers mean nutrients from whole foods and not isolated supplements. So the finding would seem to support Ezra’s claim. But then we get this:

The favorable effects shown by some studies relating antioxidant dietary intake and cardiovascular disease, may have been exerted by other chemicals present in foods. Flavonoids are the ideal candidates, since they are plentiful in foods containing antioxidant vitamins (i.e. fruits and vegetables) and are potent antioxidants. Tea and wine, rich in flavonoids, seem to have beneficial effects on multiple mechanisms involved in atherosclerosis.

So flavonoids may actually help, according to this study. Now, both the FSA and Organic Center studies measured something called “total phenolics,” a category than encompasses flavonoids. The FSA study found no difference; and the Organic Center study showed a more than 20 percent advantage for organic food. Both studies are essentially gathering results from past studies and consolidating their results. As such, they’re looking at much the same data. So why the difference? According to the Organic Center’s critique of the FSA study:

Unlike the London study, The Organic Center review focused on nutrient differences in “matched pairs” of crops grown on nearby farms, on the same type of soil, with the same irrigation systems and harvest timing, and grown from the same plant variety. It also rigorously screened studies for the quality of the analytical methods used to measure nutrient levels, and eliminated from further consideration a much greater percentage of the published literature than the FSA team.

While the FSA team found 80 comparisons of phenolic compounds, the TOC [Organic Center] team focused on the more precise measure of total phenolic acids, or total polyphenols, and found just 25 scientifically valid “matched pairs.” By mixing together in their statistical analysis the results of several specific phenolic acids, the FSA team likely lost statistical precision.

The “matched pairs” thing seems legit. Crops draw nutrients from soils; different soils have different levels and types of nutrients. Different vegetable varieties, too, have different properties—including levels of nutrient uptake.

At the University of California-Davis, scholars at the Long Term Research on Agricultural Systems project have been examining “matched pairs” of organic and conventional crops since 1993. In a 2007 paper, the group compared the nutritional content of organic and conventional tomatoes grown between 1994 and 2004. The result: organic tomatoes showed significantly levels of two flavonoids called quercetin and kaempferol that were on average, respectively, 79 percent and 97 percent higher than conventional. Moreover:

The levels of flavonoids increased over time in samples from organic treatments, whereas the levels of flavonoids did not vary significantly in conventional treatments. This increase corresponds not only with increasing amounts of soil organic matter accumulating in organic plots but also with reduced manure application rates once soils in the organic systems had reached equilibrium levels of organic matter.

Okay, on to the question of nitrogen. As I wrote in the earlier post, both the FSA and Organic Center studies acknowledge that organic foods show lower levels of nitrogen in organic food. I cited that fact as a serious nutritional advantage for organic food, and pointed to a recent study by a Brown researcher linking type-2 diabetes and Alzheimer’s disease to increased exposure to nitrogen-related compounds.

Ezra dismissed the argument as “circumstantial.”

I should have been more precise. As the Organic Center put it in its rebuttal to the FSA, “Elevated levels of nitrogen in food are regarded by most scientists as a public health hazard because of the potential for cancer-causing nitrosamine compounds to form in the human GI tract.”

And it’s nitrosamine compounds that the Brown study linked to diabetes and Alzheimer’s. The researcher makes a circumstantial link between the explosion in nitrogen fertilizer applications after 1960 and the abrupt rise in Alzeimer’s and diabetes over the same period. But they also demonstrate the ability of nitrosamines to cause significant cellular damage. According to the study’s press release:

Nitrosamines basically become highly reactive at the cellular level, which then alters gene expression and causes DNA damage. The researchers note that the role of nitrosamines has been well-studied, and their role as a carcinogen has been fully documented. The investigators propose that the cellular alterations that occur as a result of nitrosamine exposure are fundamentally similar to those that occur with aging, as well as Alzheimer’s, Parkinson’s and Type 2 diabetes mellitus.

Given that information, it seems wise to minimize the level of nitrogen—which can turn to nitrosamines in the digestive process—in food. Moreover, the researchers evidently aren’t finished with the topic. The press release adds, chillingly: “Two subsequent papers have been accepted for publication in the near future that demonstrate experimentally that low levels of nitrosamine exposure cause neurodegeneration, NASH [non-alcoholic steatohepatitis], and diabetes.”

Nor are these the only ways that organics are “better for you.” Here’s an important one: they carry drastically lower pesticide residues. The Chicago Tribune recently obtained USDA data showing that “more than 50 pesticide compounds showed up on domestic and imported peaches headed for U.S. stores.” Moreover:

Five of the compounds exceeded the limits set by the Environmental Protection Agency, and six of the pesticide compounds present are not approved for use on peaches in the United States.

Ezra ended his response like this: “[W]hat we do know is that organic produce is more expensive and harder to find.”

I agree completely; but it seems clear to me that the answer is not to marginalize organics, but rather to stop using government cash and lax antitrust/environmental/labor regulation to prop up a destructive food system. We get the food system that we as a society pay for.

by Sally Fallon and Mary G. Enig, PhD

With the exception of butter, no other food has been subjected to such intense demonization in recent years as red meat, particularly beef. The juicy hamburger, that delicious marbled steak and the Sunday roast have been accused of terrible crimes. Beef causes heart disease, say the Diet Dictocrats. Beef causes cancer, particularly colon cancer, beef causes osteoporosis, beef causes autoimmune diseases like asthma, beef harbors E. coli leading to food-borne illness, beef causes Creutzfeldt Jakob disease.

Recently a vegetarian group called People for the Ethical Treatment of Animals placed billboard ads warning men not to eat beef because it causes impotence! Red meat is an acid-forming food, say the vegetarians, which putrefies in the gut because humans can’t digest meat. Beef production destroys the environment, according to the zealots, and takes away land that could be dedicated to grain for starving millions. Let’s examine these accusations one at a time.

Does beef cause heart disease?

First is the notion that beef causes heart disease. This actually dates back to the 1950’s when the lipid hypothesis was &taking hold on the American consciousness. At that time, scientists were grappling with a new threat to public health-a steep rise in heart disease, especially myocardial infarction (MI)-a massive blood clot leading to obstruction of a coronary artery and consequent death to the heart muscle. MI was almost nonexistent in 1910 and caused no more than three thousand deaths per year in 1930. By 1960, there were at least 500,000 MI deaths per year in the US.

Many scientists believed that the culprit was cholesterol and saturated fats found in animal foods like butter, eggs and beef. They reasoned that saturated fat and cholesterol raised the level of cholesterol in the blood which in turned caused the deposition of cholesterol as plaques in the arteries, leading to obstructions and heart disease. This, in a nutshell, is the lipid hypothesis.

This theory was tested in 1957 when Dr. Norman Jolliffe, Director of the Nutrition Bureau of the New York Health Department, initiated the Anti-Coronary Club. With great media fanfare, a group of businessmen, ranging in age from 40 to 59 years, were placed on the so-called Prudent Diet. Prudent Dieters used corn oil and margarine instead of butter, cold breakfast cereals instead of eggs and chicken and fish instead of beef. Anti-Coronary Club members were to be compared with a "matched" group of the same age who ate eggs for breakfast and had meat three times a day. Jolliffe, an overweight diabetic confined to a wheel chair, was confident that the Prudent Diet would save lives, including his own.

The results of Dr. Jolliffe’s Anti-Coronary Club experiment were published in 1966 in the Journal of the American Medical Association. Those on the Prudent Diet of corn oil, margarine, fish, chicken and cold cereal had an average serum cholesterol of 220, compared to 250 in the meat-and-potatoes control group. However, the study authors were obliged to note that there were eight deaths from heart disease among Dr. Jolliffe’s Prudent Diet group, and none among those who ate meat three times a day. Dr. Jolliffe was dead by this time. He succumbed in 1961 from a vascular thrombosis, although the obituaries listed the cause of death as complications from diabetes.

The truth is that in spite of all the propaganda you have heard, the lipid hypothesis has never been proved. In fact, inadequate protein intake leads to loss of myocardial muscle and may, therefore, contribute to coronary heart disease.

There are many societies where the populace consumes high levels of animal food and saturated fat but remains free of heart disease. Dr. George Mann, who studied the Masai cattle herding peoples in Africa, found no heart disease, even though their diet consisted of meat, blood and rich milk. Butterfat consumption among Masai warriors, who consider vegetable foods as fodder for cattle, can reach one and one half pounds per day. Yet these people do not suffer from heart disease. Mann called the lipid hypothesis "the greatest scam in the history of medicine." It is a scam that has been used to convince millions of healthy people that they are sick and must take expensive drugs with serious side effects, a falsehood that has persuaded Americans to adopt a bland, tasteless diet simply because their cholesterol has been defined as being too high.

It is true that beef consumption in the United States has gone up during the last eighty years, the period of huge increases in heart disease. Today we consume 79 pounds of beef per person per year versus 54 in 1909, a 46% increase-but poultry consumption has increased a whopping 280%, from 18 pounds per person per year to 70. Consumption of vegetable oils, including those that have been hydrogenated, has increased 437%, from 11 pounds per person per year to 59; while consumption of butter, lard and tallow has plummeted from 30 pounds per person per year to just under 10. Whole milk consumption has declined by almost 50%, while lowfat milk consumption has doubled. Consumption of eggs, fresh fruits (excluding citrus), fresh vegetables, fresh potatoes and whole grain products has declined; but consumption of sugar and other sweeteners has almost doubled. Why, then, do today’s politically correct dietary gurus continue to blame beef consumption for our ills? Is it because it is the one wholesome food that has shown an increase over the past ninety years?

What’s the likely cause of heart disease?

The most likely causes of increased heart disease in America are the other changes in our diets-huge increases in consumption of refined carbohydrates and vegetable oils, particularly hydrogenated vegetable oils; and the decline in nutrient levels in our food, particularly minerals and fat soluble vitamins-vitamins found only in animal fats.

The only claim that can be made against beef as a cause of heart disease is that some studies have shown beef consumption to temporarily raise cholesterol levels in short term feeding experiments. Other studies have shown that beef consumption, including beef fat consumption, lowers cholesterol levels. But even if all studies show that beef consumption raises cholesterol levels, the only conclusion you can draw is-so what? There is no greater risk of heart disease at cholesterol levels of 300 than at 180, and people with cholesterol levels below 180 are at greater risk of death from other causes, such as cancer, intestinal diseases, accidents, violence and suicide.

In other words, it’s much more dangerous to have cholesterol levels that are too low than cholesterol levels that are too high.

Cholesterol is your best friend

The truth is that cholesterol is your best friend. It is vital for the function of the nervous system and the integrity of the digestive tract. Steroid hormones that help the body deal with stress are made from cholesterol. Sex hormones like estrogen and testosterone are made from cholesterol. Bile salts that the body uses to digest fats are made from cholesterol. Vitamin D, needed for thousands of biochemical processes, is made from cholesterol.

Cholesterol is a powerful antioxidant that protects us against cancer. It is vital to the cells because it provides waterproofing and structural integrity. And, finally, cholesterol is the body’s repair substance. When our arteries are weak and develop fissures or tears, cholesterol is sequestered and used for repair. When cholesterol levels in the blood are high, it’s because the body needs cholesterol. Blaming heart disease on cholesterol is like blaming a fire on the firemen who arrive to put out the flames.

Does beef cause cancer?

What about the accusation that beef causes cancer, in particular cancer of the colon? The genesis of this myth involves more than just muddied thinking, but actual skulduggery. In 1965 an influential physician, Ernst Wynder, took the data for the mostly processed vegetable oils, called them animal fat (which they were not) and compared them with worldwide colon cancer mortality. The table he produced showed high rates of colon cancer in European countries and low rates of colon cancer in Japan, and concluded that there was a positive effect, in other words, that saturated fat, the kind found in beef, caused colon cancer. What the data actually showed was that consumption of polyunsaturated vegetable oils, not saturated animal fats, was associated with the incidence of colon cancer. And Wynder forgot to mention that Asians have much higher rates than Americans of other types of cancers, particularly cancers of the liver, pancreas, stomach, esophagus and lungs.

Then in 1973, William Haenszel and his colleagues from the National Cancer Institute reported the findings from a study that relied on dietary recall and lacked matched controls-in other words, a very poorly designed study. The researchers stated that they found a relationship between beef and colon cancer that fit the earlier work of Wynder. Actually, what they really found was that among westernized Japanese Americans, those who said they consumed lots of macaroni, green beans and peas, as well as beef, had the highest rates of colon cancer; while among traditional Japanese Americans, those who said they consumed lots of dried cuttlefish, Chinese peas, bamboo shoots, rice and fermented soy products had the highest rates of colon cancer. Thus, the researchers singled out beef as the culprit from a choice of several foods associated with cancer in Westerners and ignored politically correct foods like soy products, fish and vegetables as a potential cause of cancer in Japanese Americans. Instead, this second-rate and inconclusive study has become firmly fixed in the consciousness of the scientific community as providing evidence for the assertion that beef causes colon cancer.

Two American studies conducted in the 1990’s have found a higher risk of colon cancer among those who eat red meat. However, no study done in Europe has ever shown an association between meat consumption and cancer. This suggests that European sausage and luncheon meat, included in the rubric of "meat consumption," are prepared by traditional methods that require few additives, while the similar products in the United States contain many carcinogenic preservatives and flavorings. Unfortunately, the American Cancer Society’s 1996 recommendation that Americans cut down on their consumption of meat-particularly fatty meat-in order to avoid cancer makes no distinction between fresh meats and those that have been embalmed with modern chemicals.

While two US studies have implicated meat consumption as a cause of colon cancer, there are several that contradict these findings. In 1975, Rowland Philips compared Seventh-Day Adventists physicians, who do not eat meat, with non-Seventh Day Adventist physicians, and found that the vegetarian doctors had higher rates of gastrointestinal and colon-rectal cancer deaths. National Cancer Institute data show that Argentina, with very high levels of beef consumption, has significantly lower rates of colon cancer than other western countries where beef consumption is considerably lower. A 1997 study published in the International Journal of Cancer found that increased risk of colon and rectal cancer was positively associated with consumption of bread, cereal dishes, potatoes, cakes, desserts and refined sugars, but not with eggs or meat. And a 1978 study published in the Journal of the National Cancer Institute found no greater risk of colon cancer, regardless of the amounts of beef or other meats ingested. The study also found that those who ate plenty of cruciferous vegetables, such as cabbage, Brussels sprouts and broccoli, had lower rates of colon cancer. So just because it’s all right to eat beef doesn’t mean you shouldn’t eat your broccoli.

Actually, we know one of the mechanisms whereby colon cancer is initiated, and it does not involve meat per se. Colon cancer occurs when high levels of dietary vegetable oils and hydrogenated fats, along with certain carcinogens, are acted on by certain enzymes in the cells lining the colon, leading to tumor formation. This explains the fact that in industrialized countries, where there are many carcinogens in the diet and where consumption of vegetable oils and carcinogens is high, some studies have correlated meat-eating with colon cancer; but in traditional societies, where vegetable oils are absent and the food is free of additives, meat-eating is not associated with cancer.

Riding piggy back on the alleged association of beef with colon cancer are supposed links with other cancers, such as breast cancer. Here the evidence shows a similarly inconsistent pattern. Cancer is a disease of rich countries where numerous factors can be fingered-altered fats, fabricated foods, low levels of protective nutrients, high levels of carcinogens-and rich countries consume lots of beef. But association is not the same as cause. Countries where there are more telephones have more cancer, but that does not mean that telephones cause cancer. Fat consumption in general also gets the blame for high rates of breast cancer. But a recent survey showed that women on lowfat diets have just as much breast cancer as those on high fat diets.

High protein diets are said to cause osteoporosis and Americans are now being advised to avoid beef in order to protect their bones. Once again, it’s important to look at the studies carefully. Research that showed a link with bone loss and protein consumption was done with purified protein powders. With meat, a natural protein food, there was no negative calcium balance. New evidence indicates that women who eat lots of meat had fewer hip fractures compared to those who avoided it.

High protein diets are said to contribute to kidney problems but, again, the evidence is contradictory. Although protein restriction can be helpful for those who are suffering kidney failure, there is no evidence that eating meat causes kidney disease. The fat-soluble vitamins found exclusively in animal fats are very important for healthy kidney function.

Does beef cause autoimmune diseases or asthma?

What about the accusation that meat contributes to autoimmune diseases and asthma? This hypothesis is predicated on the fact that meat contains arachidonic acid, a fatty acid from which the supposedly pro-inflammatory Series Two prostaglandins-local tissue hormones-are formed. This is one of the nuttiest notions to take hold in the scientific community for a long time. It was promulgated by Barry Sears, author of The Zone, and taken up with a vengeance by the anti-meat forces. These people know nothing about prostaglandins. Some of the prostaglandins that the body makes from arachidonic acid do indeed promote inflammation-which is a very important protective response when you have injured yourself. But the same arachidonic acid also forms the basis of anti-inflammatory prostaglandins that the body uses, when appropriate, to reduce inflammation. And besides, the amount of arachidonic acid in beef is very low-less than half a percent of total fat content. It is much lower than the amount of omega-3 fatty acids, the current darlings of the nutritional community, yet none of the voices promoting omega-3 fatty acids ever tell us that we can get them from beef.

What about "Mad Cow Disease"?

Beef consumption in England plummeted recently with the ‘Mad Cow Disease" scare. Mad cow disease, or bovine spongiform encephalopathy (BSE), is a wasting disease of cattle characterized by nervous disorders and weakness, said to be related to Creutzfeldt-Jakob disease (CJD) in humans. Scientists have not been able to link a virus to this disease, so they theorize that an abnormal protein particle called a prion, found in the brains of cattle with BSE and humans with CJD, is the cause. The theory is that these prions are infectious agents, passed along to cows though the practice of animal part feeding and then to humans who eat infected meat, particularly meat from the nervous system, like brain.

There’s a lot wrong with this theory. For one thing, BSE is nonexistent in the USA, where animal part feeding has been going on for almost one hundred years. Another is recorded cases of CJD among vegetarians; yet another is the absence of CJD in the Shetlands where scrapie, a disease similar to BSE, is common in sheep and where potted sheeps brain is a national dish.

The research of Mark Purdey, a diary farmer in England, indicates that the mad cow disease epidemic in England occurred in areas where farmers were forced to treat their cattle with organophosphate pesticides in a warble fly eradication program.²⁰ The warble fly makes holes in the cows’ backs-not dangerous in itself, but it reduces the value of pelts sold to leather manufacturers. These holes are open doors to the spinal cord and organophosphate pesticides are very toxic to the nervous system. By a complex process, these compounds seem to cause certain proteins to fold in pathological ways-these are the prions that are found in the brains of animals with BSE and humans with CJD. Mineral deficiencies are also involved, particularly magnesium, which is a mineral that protects the nervous system. Finally, a similar disease occurs among wild animals living in areas of volcanic soils, whose diets are high in aluminum and manganese, minerals known to be toxic to the nervous system. Clusters of human CJD cases are also found in areas where the soil has mineral imbalances, where there are cement factories and where high levels of organophosphate insecticides have been used.

So the answer to CJD and BSE is good soil management and the elimination of neurotoxic compounds in farming-but it’s easier to just blame it on beef. By the way, now that animal part feeding has been outlawed, feedlot operators are turning to soy feeds as a protein substitute. Soy is very toxic to cows’ livers. Does the use of soy in cattle feeding explain why beef-lean beef-has become politically correct again? After all, the other politically correct meats-chicken and salmon-use up vast quantities of soybean meal in battery feeding and fish farms.

What about E.Coli?

A final slur against beef is that beef is a vector for pathogenic E. coli and therefore a major cause of foodborne illness. Never mind that E. coli shows up in plant foods like apple juice and salad dressings; and never mind that E. coli is relatively benign and never caused foodborne illness in small amounts until recently. Once again, it’s easier to just blame it on beef.

Charles Walters of Acres USA points out that old fashioned all-meat hamburgers, when handled with reasonable care, did not formerly pose a foodborne illness problem. Why, then, are we getting outbreaks of foodborne illness from fast food outlets, where food handling techniques are rigidly controlled-from frozen patty to the grill? He believes that the problem lies in the fact that hamburgers are now bulked out with hydrolyzed soybeans, also called textured vegetable protein, much of it made from genetically modified soybeans. With modern processing, 100 pounds of ground meat can be bulked out to 124 pounds.

E. coli DNA is used as a vector in genetically modified soybeans. The E. coli causing problems in fast food hamburgers is called facultative bacteria, which means that it operates with or without air. Does this bacteria come from the genetically modified soy and is it more dangerous than E. coli that occurs in the guts of cattle? It’s a question that needs answering. Says Walters: "This E. coli the news releases keep talking about is not a consequence of slaughterhouse personnel not washing their hands enough, Involved is the negative spin, which is what it lives on. It is in the tissue. It is not errant E. coli leaving the intestinal tract and infecting the product. The scientists know this and this is why they’re trying to fall back on irradiation and heavy cooking."

There are studies that support Walter’s theory. One found that spoilage was greater and most rapid in "extended" than in "nonextended" (meaning pure) ground beef. Another study showed that coliform counts were significantly higher in beef mixed with textured soy protein after one day of storage in comparison to the 100% ground beef.

Does beef cause impotence?

The accusation that beef causes impotence is a tactic that can definitely be described as "below the belt." Beef causes impotence by "clogging arteries, limiting blood flow to the extremities." So goes the argument proffered by People for the Ethical Treatment of Animals. Nothing could be more unethical than the implied suggestion that vegetarianism is good for your sex life. We know that vegetarianism-the practice of not eating animal foods-can lead to many deficiencies that directly contribute to impotence, infertility and reproductive difficulties-deficiencies in protein, zinc, vitamins B₆ and B₁₂, and fat-soluble vitamins A and D.

The notion that beef is an "acid-forming" food is another favorite vegetarian argument. Beef contains lots of sulphur and phosphorus, which technically form an acid when dissolved in water, but that does not mean that eating meat causes the body to be too acid. Actually, meat provides both high-quality protein and vitamin D (if you eat the fat and organ meats, that is), both of which are needed to maintain proper acid-alkaline balance in the body.

Meat does not putrefy in the gut. Humans are admirably equipped to digest meat. That is the main job of the human stomach, which-unlike the stomach of the cow or rabbit-contains millions of cells that secrete hydrochloric acid. Our intestinal tract is much shorter than that of the vegetarian animals, but somewhat longer than that of purely carnivorous animals. Man is an omnivore-with teeth, stomach, intestines and bowel all designed to handle both animal and plant foods.

Do cattle use land that should be planted with grain?

Vegetarians argue that cows and sheep require pasturage that could be better used to raise grains for starving millions in third-world countries. This argument ignores the fact that a large portion of our earth’s land is unsuited to cultivation. The open range, desert and mountainous areas yield their fruits in grazing animals. Grasslands perfectly suited to grazing cover an area in China’s interior equal to three times the entire amount of land under cultivation in the rest of the country. Citing the arguments of vegetarians, the Chinese government has opted for more intense cultivation of existing agricultural lands rather than development of these untapped regions in order to supply much-needed animal products to the Chinese diet.

A far more serious threat to humanity is the monoculture of grains and legumes, which tends to deplete the soil and requires the use of artificial fertilizers and pesticides. The educated consumer and the enlightened farmer together can bring about the return of the mixed farm, where cultivation of fruits and vegetables is combined with the raising of livestock and fowl in a manner that is efficient, economical and environmentally friendly. Cattle providing rich manure are the absolute basis for healthy, sustainable farming. On marginal land, wise grass feeding practices can actually improve soil quality and restore pasture land. It is not animal cultivation that leads to hunger and famine but unwise agricultural practices and monopolistic distribution systems.

Do vegetarians live longer than meat eaters?

Since we’re talking about vegetarianism, let’s examine the claim that vegetarians live longer than meat eaters. The late Dr. Russell Smith, who was a statistician, took a close look at the studies purporting to show that vegetarianism was a healthier life-style. In a review of some 3,000 articles in the scientific literature, he found only two that compared mortality data for vegetarians and nonvegetarians. One was a 1978 study of Seventh Day Adventists (SDA’s). Although published analyses of this study claim that it showed that the vegetarians lived longer, Smith’s analysis of total mortality rates as a function of the frequencies of consuming cheese, meat, milk, eggs and fat attached to meat found that the total death rate decreased as the frequencies of consuming cheese, eggs, meat and milk increased.

The second study was published by Burr and Sweetnam in 1982. Once again, although the authors claim that their study showed that vegetarians lived longer, Smith found quite the opposite when he looked carefully at the hard data. He found that the all-cause death rates were slightly greater for vegetarian men compared to nonvegetarian men; and significantly greater for vegetarian women compared to nonvegetarian women.

Vegetarians never mention a study by Dr. Emmanuel Cheraskin who surveyed 1040 dentists and their wives. Those who had the fewest problems and diseases as measured by the Cornell Medical Index had the most protein in their diets. Yet almost all the treatments for chronic disease found in alternative publications these days begin with the recommendation of a vegetarian diet. Typical is an article by a Dr. Brodie that appeared in Issue #13 of Alternative Medicine Digest, published by Burton Goldberg. Dr. Brodie recommends a "balanced vegetarian diet" of raw fruits and vegetables, whole grains and beans with no "refined sugars, red meat, caffeine and chemically preserved foods." This is truly guilt by association!

But wait! In order to get well, Dr. Brodie recommends certain supplements including vitamin A, vitamin B6, thymus extracts, zinc, cysteine, and bovine cartilage, all of which are largely absent in plant foods and plentifully available in beef! At least they are available if you are eating the whole animal as our ancestors did-meat, organs, cartilage, bones and fat.

Is beef good for you?

What a shame we have demonized red meat because this is one modern food, enjoyed by almost everybody, that is rich in nutrients. Red meat provides complete protein, including sulphur-containing proteins like cysteine. Beef is a wonderful source of taurine and carnitine, needed for healthy eyes and a healthy heart. Beef also provides another key nutrient for the cardiovascular system-coenzyme Q10.

Beef is an excellent source of minerals like magnesium and zinc-you need zinc for clear thinking and a healthy sex life. The fuzzy-headedness that vegetarians mistake for heightened consciousness is really the fog of zinc deficiency. Vitamin B₆ is abundant in meat, especially rare meat. Red meat is one of the best sources of vitamin B₁₂, which is vital to a healthy nervous system and healthy blood. Vegetarians are especially prone to vitamin B₁₂ deficiency. One of the first signs of vitamin B₁₂ deficiency is a tendency to irrational anger–so much for vegetarian claims that we will have a more peaceful, harmonious world if we all just stop eating meat.

If you use the animal bones and hooves to make stock, and use the stock as our ancestors did in soups, stews and sauces, you will get plenty of calcium and the components of cartilage to give you healthy bones and cartilage. If you eat organ meats, as our ancestors did, you will get vital fat-soluble nutrients like vitamin A and D, both of which are essential for protein utilization and mineral absorption. See- Chicken Stock 101

What about saturated fat?

In fact, the one warning we could give you about meat is not to eat it lean. In spite of claims to the contrary, the diet of the cave man was not one of lean meat. Paleolithic man always ate his meat with fat.

Vilhjalmur Stefansson, who spent many years living with the Eskimos and Indians of Northern Canada, reports that wild male ruminants like elk and caribou carry a large slab of back fat, weighing as much as 40 to 50 pounds. The Indians and Eskimo hunted older male animals preferentially because they wanted this backslab fat, as well as the highly saturated fat found around the kidneys. Other groups used blubber from sea mammals like seal and walrus.

"The groups that depend on the blubber animals are the most fortunate in the hunting way of life," wrote Stefansson, "for they never suffer from fat-hunger. This trouble is worst, so far as North America is concerned, among those forest Indians who depend at times on rabbits, the leanest animal in the North, and who develop the extreme fat-hunger known as rabbit-starvation. Rabbit eaters, if they have no fat from another source-beaver, moose, fish-will develop diarrhea in about a week, with headache, lassitude, a vague discomfort. If there are enough rabbits, the people eat till their stomachs are distended; but no matter how much they eat they feel unsatisfied. Some think a man will die sooner if he eats continually of fat-free meat than if he eats nothing, but this is a belief on which sufficient evidence for a decision has not been gathered in the north. Deaths from rabbit-starvation, or from the eating of other skinny meat, are rare; for everyone understands the principle, and any possible preventive steps are naturally taken."

Normally, according to Stefansson, the diet consisted of dried or cured meat "eaten with fat," namely the highly saturated cavity and back slab fat that could be easily separated from the animal. Another Arctic explorer, Hugh Brody, reports that Eskimos ate raw liver mixed with small pieces of fat and that strips of dried or smoked meat were "spread with fat or lard." Pemmican, a highly concentrated travel food, was a mixture of lean dried buffalo meat and highly saturated buffalo fat. (Buffalo fat, by the way, is more saturated than beef fat.) Less than two pounds of pemmican per day could sustain a man doing hard physical labor. The ratio of fat to protein in pemmican was 80% to 20%. As lean meat from game animals was often given to the dogs, there is no reason to suppose that everyday fare did not have the same proportions: 80% fat (mostly highly saturated fat) to 20% protein-in a population in which heart disease and cancer were nonexistent.

The beef industry has been forced to be apologetic about its product because it’s very difficult to get the fat out of beef. You can reduce the fat content by using hormones, but you end up with a product that is tough and tastes terrible, not to mention full of hormones. Beef producers need to recognize that the fat is the most important part of the beef, rich in components that promote good health and that help you utilize the nutrients in all the other parts of the beef. In addition to vitamins A and D, fat contributes many important fatty acids, including palmitoleic acid, an antimicrobial fat that protects us against pathogens in the gut. If you want to be sure that you don’t get foodborne illness from your hamburger, use full fat ground beef.

Fat also provides a substance called conjugated linoleic acid or CLA, at least it does if the animals have been on green grass. CLA is a substance that protects us against cancer and that promotes weight loss-that’s right, fat can make you thin, if it’s the right kind of fat.

And the right kind of fat is also saturated fat which, in spite of what we’ve been told, plays many important roles in the body chemistry. The scientific literature delineates a number of vital roles for dietary saturated fats-they enhance the immune system, are necessary for healthy bones, provide energy and structural integrity to the cells, protect the liver and enhance the body’s use of essential fatty acids. Stearic acid and palmitic acid, found in beef tallow and butter, are the preferred foods for the heart. As saturated fats are stable, they do not become rancid easily, do not call upon the body’s reserves of antioxidants, do not initiate cancer, do not irritate the artery walls.

In fact saturated beef fat is one of the most useful fats in the culinary repertoire. As it is very stable and doesn’t go rancid when heated to high temperatures, it’s perfect for frying. While we don’t recommend a lot of fried foods, we know that our children and grandchildren are going to eat them. Fast food outlets used to fry their potatoes in healthy stable beef tallow. They were crisp, tasted delicious and provided many important nutrients. But the phony cholesterol issue has forced these outlets to switch to partially hydrogenated vegetable oil, which is known to cause a host of chronic diseases including cancer, heart disease, bone problems, infertility and autoimmune disease.

What about the beef industry?

The beef industry should know these things but it doesn’t. Instead the National Beef Checkoff Board, funded by mandatory payments from cattlemen, officially endorses consumption of only three and one-half ounce servings of lean beef, about the size of a pack of cards, and runs ads that say things like this: ". . . when it comes to lowering ‘bad’ cholesterol levels, lean red meat has the same effects as white chicken meat. That means eating lean beef may reduce the risk of heart disease. Since seven cuts of beef fall between a skinless chicken breast and chicken thigh in terms of total fat, consumers can feel good about eating beef." This is damning a good product by faint praise. The Checkoff Board had bought into the phony cholesterol theory and sides squarely with the Diet Dictocrats, calling for irradiation to kill "emerging pathogens" and subsidies to giant processors.

Steve and Jeanne Charter, ranchers from Shepherd, Montana, have refused to make the checkoff payments and are willing to take on the Beef Checkoff Board in court. At preliminary hearings the judge listened while Checkoff bureaucrats defended the Department of Agriculture’s food pyramid, based on seven to eleven servings of grain per day, while the Charters championed the juicy steak-to cheers from fellow ranchers.

We need to stand up and support people like the Charters because beef is not the demon food we’ve been told it is. Beef does not cause disease. In fact beef contributes to good health by providing many important nutrients. All this can be found in the scientific literature. So what’s the beef, then, about beef?

Perhaps it also has to do with the characteristics of cattle-herding peoples. Unlike agriculturists, who require an organized social structure highly susceptible to centralized control, the pastoral way of life favors the independent thinker. And the beef industry, for all its faults, is far less subject to monopolistic control than the grain industry is. And it’s easier to manipulate prices on grain, a commodity controlled by just a few families, than it is to control prices on an industry supported by thousands of cattlemen.

While it is not as true today as it was in the days before the barbed wire fence, cattle keeping families enjoy the luxury of greater independence than those who till the soil or tend vines. They inhabit the wide open spaces and are more accustomed to fending for themselves than relying on their neighbors.

This is not to say there is anything wrong with relying on one’s neighbors-in fact, to survive and revive, more cooperation in the beef industry will be needed-but democracy needs a critical mass of the kind of free thinking, independent businessman that you find in the cattle industry. This may be the real reason the Chinese decided not to develop their western grasslands-even small numbers of forward thinking Chinese cowboys would be a threat to that totalitarian society.

People who raise beef not only tend to be free thinkers, they are also good thinkers, because beef provides many factors needed for the modern equivalent of the quick draw-keen, quick minds-including zinc, B12, cholesterol, omega-3 fatty acids, trace minerals, saturated fat and complete protein. In fact, when it comes to good health-it’s the beef.

From The Weston Price Foundation

From Weston Price Foundation

By Sally Fallon and Mary G. Enig, PhD

An estimated 15 to 20 million Americans suffer from osteoporosis–thinning of the bones leading to back pain, increased fractures, and frailty, frequently with extensive suffering. One theory proposed to explain its prevalence in the US is a diet that is high in protein, from excessive consumption of meat.

The protein theory was first presented in 1968 and followed up in 1972 with a study comparing bone density of vegetarians and meat eaters. Twenty-five British lacto-ovo vegetarians were matched for age and sex with an equal number of omnivores. Bone density, determined by reading X-rays of the third finger metacarpal, was found to be significantly higher in the vegetarians. Two years later, a study on North Alaskan Eskimos reported that bone loss, determined by a technique called direct photon absorptiometry, was significantly greater in Eskimos than in whites, and began at an earlier age. Although growth patterns and bone densities in children were similar for both groups, by age 70, Eskimos were found to have bone densities 15% below comparable whites, with Eskimos females at 30% below comparable whites. The authors of the study attribute the decline in bone mass to the high protein diet of the Eskimos, especially its high meat content. Some studies with animals, as well as further studies with humans, given diets high in protein also indicate a greater loss of calcium and thinner bones than controls on low protein regimes.

But the pioneering research of Dr. Weston Price indicates that we should not accept the protein theory without further study. Dr. Price found many groups throughout the world subsisting on high meat diets. Although he did not directly study bone density in these peoples, he did study their teeth. He found that groups on high meat diets–including Alaskan Eskimos–had a high immunity to tooth decay, were sturdy and strong, and virtually free from degenerative disease. Groups subsisting mainly on plant foods were less robust and had more tooth decay. Pre-Columbian skeletons of American Indians whose diets consisted largely of meat show no osteoporosis, while those of Indians on largely vegetarian diets indicate a high incidence of osteoporosis and other types of bone degeneration. The implication of Dr. Price’s research and other anthropological studies is that high meat diets protect against osteoporosis. How do we explain this discrepancy?

The research of Dr. Herta Spencer, of the Veterans Administration Hospital in Hines Illinois, supplies us with clues. She notes that the animal and human studies that correlated calcium loss with high protein diets used isolated, fractionated amino acids from milk or eggs. Her studies show that when protein is given as meat, subjects do not show any increase in calcium excreted, or any significant change in serum calcium, even over a long period. Other investigators found that a high protein intake increased calcium absorption when dietary calcium was adequate or high, but not when calcium intake was a low 500 mg per day.

The textbooks tell us that the body needs vitamin D for calcium utilization, and vitamin A for both calcium and protein assimilation. Protein given as a powder lacks these fat-soluble co-factors that the body can use to build and maintain healthy bones.

Synthetic vitamin D, on the other hand, can cause hypercalcemia, a disturbance of calcium equilibrium leading to excessive blood calcium and calcification of soft tissues. Synthetic vitamin D added to commercial milk does not have the same beneficial effect as vitamin D from cod liver oil in preventing rickets and strengthening the bones.

Fats, especially animal fats, also supply usable vitamin K. This nutrient is associated with blood clotting–individuals who lack the ability to use vitamin K suffer from hemophilia and risk uncontrolled bleeding when injured. But Vitamin K also plays an important role in bone metabolism. Vitamin K is more available in dairy fats than in the oils found in green vegetables. Studies indicate that vitamin K is more completely absorbed from vegetables consumed with butter than with vegetables eaten plain. Vitamin K is also manufactured by intestinal flora. Use of antibiotics can inhibit vitamin K production, leading to bone loss. Consumption of lacto-fermented foods such as yoghurt and old fashioned sauerkraut promotes the growth of beneficial flora in the intestines, and hence contributes to healthy bones.

Fat soluble vitamin E also plays a role in promoting bone health, by protecting the calcium depositing mechanism from free radical disruption. In a recent study, investigators at Purdue University found that high levels of free radicals from omega-6 linoleic acid (found principally in corn, soy and safflower oils) interfered with bone formation, but that vitamin E gave needed protection in a diet high in polyunsaturates. In addition, they found that high levels of saturated fat also gave protection. That’s right, the much-maligned saturated fats, found in tropical oils, butter and other animal fats, play an important role in bone modeling. This may be a major reason that population groups in tropical areas, where coconut and palm oils form a major component of the diet, have very little osteoporosis.

Bone loss in women coincides with diminution of estrogen and progesterone at the onset of menopause. But archeological evidence indicates that menopause does not necessarily initiate osteoporosis. Human skeletons of Huguenot women ages fifteen to eighty-nine recently exhumed in London showed little difference in bone density between premenopausal and post menopausal women. Once again, the role of animal fats in the diet can explain this contradiction. Vitamin A in animal fats is absolutely essential for the health of the entire glandular system, and hence the continued production of regulating hormones throughout life. Hormone replacement often recommended for the prevention of osteoporosis is not an ideal substitute for the natural hormones produced in properly nourished bodies. Estrogen is also synthesized in the adipose (fat) tissue. Perhaps this is why women naturally gain some weight at menopause. The extra body fat supplies them with additional estrogen and protects them from bone loss. Maintaining a svelte figure in middle age, either through weight loss or liposuction, does not necessarily confer health benefits. Very thin women are much more at risk for bone loss than those who allow themselves to enjoy good, wholesome food and become pleasingly plump. Many women smoke cigarettes to keep their weight down, a habit that lowers estrogen concentration in the blood stream and inhibits its effects.

Only a rich, wholesome and varied diet can supply the many nutrients needed for the complex process that maintains the integrity of our bones. Dairy products, vegetables, nuts, meat and old fashioned bone broths supply calcium. Dr. Spencer’s research indicates that post-menopausal women need about 1200 mg of calcium per day–400 more that the recommended daily allowance of 800 mg.¹⁴ One quart of whole milk, or six ounces of whole natural cheese supply the optimum 1200 mg of calcium. Individuals with a poor tolerance to milk products must take extra care to obtain sufficient dietary calcium. Fish, chicken or beef broth, prepared with a little vinegar to pull calcium from the bones, are excellent sources, and have supplied easily assimilated calcium to pre-industrialized peoples throughout the globe. Leafy green vegetables and grains, nuts and seeds are also good sources if properly prepared. Vegetables and grains should be consumed with animal fats like butter or eggs; and nuts, legumes and grains should be soaked, sprouted or sour leavened to neutralize phytic acid, a substance that can block calcium absorption.

The "acid-ash" of meat is given as the reason high meat diets cause bone loss. But meats also supply phosphorus, which counteracts this acidity. Phosphorus is needed for the phosphate component of bone matter. Meats are also excellent sources of vitamin B12, which plays a recently discovered but little understood role in maintaining the integrity of the bones.

Plant foods such as fruits, especially apples, nuts and grains supply boron, needed for the conversion of vitamin D to its active form, and for the formation of estrogen. Iodine found in natural sea salt, sea foods and butter helps maintain healthy ovaries and thyroid gland, both of which play a role in maintaining bone integrity. Magnesium, found in whole foods, also contributes to bone health as does natural fluoride, present in hard water as calcium fluoride. Chromium may also contribute to bone health by normalizing insulin activity. Type I diabetics are prone to osteoporosis. Chromium picolinate has been found to reduce the amount of calcium excreted in the urine and therefore may protect against bone loss. Refined carbohydrates such as sugar and white flour can cause chromium deficiency.

But sodium fluoride added to drinking water is one of a number of substances that is harmful to our bones. It causes an apparent increase in bone mass, but the bone structure is abnormal and weak. Recent studies indicate that hip fractures are more common in areas where water is fluoridated.

The late distinguished dentist, Dr. Melvin Page, demonstrated that sugar consumption upsets the natural homeostasis of calcium and phosphorus in the blood. Normally, these minerals exist in a precise ratio of ten to four. Sugar consumption causes serum phosphorus to decrease and calcium to rise. The excess serum calcium, which comes from the bones and teeth, cannot be fully utilized because phosphorus levels are too low. It is excreted in the urine or stored in abnormal deposits such as kidney stones and gallstones. Caffeine also upsets the natural balance of calcium and phosphorus, and causes increased calcium to be excreted in the urine. Phosphoric acid in soft drinks is a major cause of calcium deficiency in children and osteoporosis in adults.²¹ Aluminum from antacids, cans and pollution also contributes to bone loss.

Osteoporosis is often associated with excess consumption of alcohol. This is the likely explanation of bone loss in Eskimos, who are highly prone to alcoholism. The fact that the Eskimo is an obligate carnivore may also explain his susceptibility to both alcoholism and bone loss. Isolated groups like Eskimos and Irish sea coast peoples, whose traditional diet has been rich in marine oils, lack the desaturating enzymes needed to produce very long, highly unsaturated fatty acids needed for prostaglandin production. People with arctic or sea coast ancestry would be wise to supplement their diet with cod liver oil, a rich source of very long chain fatty acids needed for virtually every metabolic process.

Even small changes in the native diet of carnivorous populations render them vulnerable to degenerative disease like osteoporosis and alcoholism. A recent article on the Canadian Inuit’s indicates that commercial foods like jam, white bread and peanut butter have replaced some of the meat in their diet, even while they continue to maintain a traditional lifestyle.

The 1972 study comparing British vegetarians and omnivores calls for additional comment. Bone density determinations through absorptiometry or X-ray are highly subject to error, especially in unblinded studies where researchers may be biased towards obtaining pre-determined results. Subjects were matched merely for age, height and sex, but not for body composition and dietary habits such as smoking and sugar, coffee and alcohol consumption. A group of omnivores that smokes, drinks and indulges in a calcium-poor diet of refined carbohydrates will naturally have more of a tendency to bone loss than a group of health-conscious lacto-ovo vegetarians who consume plenty of dairy products. (British vegetarians do, in fact, tend to be very health conscious, avoiding not only meat but also alcohol, cigarettes, coffee and soft drinks. Unlike American vegetarians, they understand the importance of calcium-rich whole dairy products in the diet and eat plentifully of milk, cheese, butter and eggs.) When researchers compare the effects of high-meat diets to normal diets in the same person, no adverse effects are found, even over extended periods of time.

Individuals who find they do better on high meat diets need not, therefore, worry about osteoporosis, as long as their diet includes complementary animal fats, plenty of calcium and a variety of other properly prepared whole foods.

About the Authors

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.

Mary G. Enig, PhD 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 Vice-President of the Weston A Price Foundation and Scientific Editor of Wise Traditions as well as the author of Know Your Fats: The Complete Primer for Understanding the Nutrition of Fats, Oils, and Cholesterol, Bethesda Press, May 2000. She is the mother of three healthy children brought up on whole foods including butter, cream, eggs and meat.

Getting Over Soy

By Kaayla T. Daniel, PhD, CCN

Hidden soy exists in thousands of everyday foods and cosmetics as well as products such as cardboards, paints, cars, biodiesel fuels, fabric softeners, mattresses and even books printed with soy ink. This is a nightmare for people who are allergic to soy and a challenge for those who are sensitive to it or who just want to avoid it. When New Trends printed The Whole Soy Story: the Dark Side of America’s Favorite Health Food in 2005, we went "green" and boasted on the copyright page "Printed with soy ink, an appropriate use of soy." Soon after, we learned, to our dismay, that people who are highly allergic to soy cannot read the book!

Warning Labels

Books printed with soy ink don’t yet require warning labels but luckily foods now do. In January 2006, help for consumers came with the Food Allergen Labeling and Consumer Protection Act. The law requires food manufacturers to clearly state whether a product contains any of the top eight allergens—milk, eggs, peanuts, tree nuts, fish, shellfish, wheat and soy protein—and to put the warning in plain English. That means companies have to spell it out S-O-Y and not hide behind confusing and little-understood terms like "hydrolyzed plant protein" or "textured vegetable protein."

That’s good enough for people who simply prefer to avoid soy. For highly allergic people, the new labeling law is not enough. Soy oil, lecithin and vitamin E (often added as a preservative) do not fall under the labeling requirement. (The FDA reasons that such products are free of soy protein, which is only true when they are manufactured under perfect conditions.) Animal products too may unexpectedly contain "hidden" soy. Some will appear on labels such as "extenders" added to ground meat, "plasticizers" used to hold patties, meat balls and hot dogs together or soy oil pumped into pre-basted turkeys. But labeling won’t help the increasing numbers of people who are starting to react to the flesh of fish, poultry, lamb or cattle that were fattened on soy feed and to eggs laid by soy fed chickens.

Inaccurate labeling is yet another problem. Both the US Food and Drug Administration (FDA) and Canadian Food Inspection Agency recall hundreds of products each year, usually because of undeclared allergens. Three factors are usually to blame: omissions or errors on labels, cross contamination of manufacturing equipment and mistakes made by suppliers of ingredients. With the new labeling law, some health food store companies have voluntarily taken the precaution of stating clearly on their labels whether a food product was produced in a "facility that also processes soy." Likewise, some supplement companies may indicate that a probiotic was grown on a culture containing dairy and soy, even though soy is not officially an ingredient and is extremely unlikely to appear in the final product. Such companies, however, are the exception and not the rule.

Nothing to Eat

Since The Whole Soy Story came out, hundreds of allergic people have told me that they live lives of angry desperation. Trips to the supermarket or health food store mean hours of poring over food labels and finding little or nothing to eat. Making matters worse, many react to soy dust in the bulk bins and/or smells in the cleaning product and cosmetic aisles. Some of these people use up tremendous amounts of energy venting in letters to the FDA and to food manufacturers. Their entire lives revolve around fear of soy and the frustration of trying to completely avoid it. What they want is for the government to outlaw soy entirely, so they can be happy again.

Why Avoidance Isn’t Enough

The mistake most of these highly allergic people make is to put all their energy into avoiding soy. Vigilance is essential, of course, especially for those who might go into anaphylactic shock. But the downside is an increasingly limited diet that can precipitate additional food allergies. Think how many of the soy allergies develop in the first place. A baby, child or adult reacts to commercial dairy products only to be switched to soy infant formula or soy milk. Or, parents of an autistic child will go on a gluten-free and casein-free diet and end up using soy flours, soy protein and soy milk. The overuse of soy then leads to soy-related digestive disorders, allergies, thyroid damage and other health problems. Every week I get letters from people wanting "protein powders," "energy bars" and other convenience foods free of whey and soy protein. The food industry’s latest answer is pea protein, but people who take pea protein every day will likely develop allergies or sensitivities to it as well. In any case, 100 percent soy avoidance is well nigh impossible.

A better solution is to reduce—or even eliminate—the sensitivity and reactivity. This is not always easy, but is possible using the combination of right diet and high-quality soy-free supplements. To get started, here are four tips.

Tip # 1: If It Has A Label, Don’t Buy It!

Live by this rule and you’ll eliminate the frustration of poring over food labels at supermarkets. Basing their diet on readymade food products without any soy or other bad ingredients is the reason people with allergies think there’s nothing they can eat. With the time saved, put your energy into preparing real foods, whole foods and slow foods. Eat a variety of them. This is the best way to avoid soy and will give your body the nourishment it needs for soy recovery.

Tip #2: Bone Up

People with allergies and food sensitivities almost always suffer from impaired digestion and a "leaky gut." Heal both with homemade bone broths rich in gelatin, cartilage and collagen. (Canned, packaged, restaurant or deli soups won’t do the trick as they are almost never made properly.) Directions can be found in Nourishing Traditions and Eat Fat/Lose Fat. Both books contain broth-based recipes but feel free to use any of your old favorite soup or stew recipes after including the three key ingredients of bones, water and vinegar. Chicken, turkey, lamb, beef and fish broths are all good. In addition to making homemade soups and stews, use bone broth as the liquid when cooking rice and other grains to improve nutritional content and digestibility. Bone broth provides good levels of absorbable calcium for people who cannot tolerate dairy, even raw dairy.

Tip #3: Support Yourself with Coconut

The number one question I hear from readers is, "I can’t drink milk so what do you recommend instead of soy milk?" Most people choose rice milk, a beverage that is high in sugar and low in nutritional value. The best non-dairy, soy free alternative is a homemade coconut tonic made with coconut milk (full fat, not "lite"), water, dolomite, vanilla and a little maple syrup or stevia for a sweetener. Thanks to the dolomite, it’s rich in calcium and magnesium (see recipe below). Use coconut oil liberally as well. Coconut supports the immune system, always a weakness in people with allergies.

Coconut Milk Tonic

1 can whole coconut milk 3/4 cup filtered water
1-2 tablespoons maple syrup 1/2 teaspoon vanilla extract
1 teaspoon KAL brand dolomite powder

Mix all ingredients and heat gently. Serve in a mug. Note: Coconut Milk Tonic contains the same calories, fat and calcium as whole milk. However, this recipe should not be used as a substitute for raw milk in recipes for baby formula. The tonic is still missing many compounds and nutrients found in raw milk. However, Coconut Milk Tonic can be used as a substitute for milk in a diet containing a variety of whole foods.

Tip #4: Bring In the Wee Beasties

Improve your intestinal flora and fauna with unpasteurized cultured vegetables, kombucha and other fermented foods and beverages. The problem is that few people do it. Those who get past the taste often give up after experiencing uncomfortable detoxification reactions such as bowel upsets, headaches and flu symptoms. Such reactions can be minimized by going slowly but surely. In addition, I recommend working with a health professional who does laboratory testing and can recommend a high-quality probiotic, customized digestive and metabolic enzymes, and other gut-healing supplements. Enzymes are critical because allergy sufferers produce insufficient amounts of pancreatic enzymes needed for adequate digestion of protein, fats and carbohydrates. Enzymes are not only needed to break down the proteins that would otherwise incite allergic reactions, but also to block the allergic reactions themselves. Furthermore, enzymes boost immune system function by promoting the growth of healthy intestinal flora. While healing can sometimes be accomplished with diet alone, most people need time to implement a full-tilt Nourishing Traditions diet. The right combination of diet and supplements can greatly speed the way.

Super Soy Me!

Remember Super Size Me, the 2004 darkly hilarious, award-winning documentary? The film features 30 days in the life of Morgan Spurlock who risked life and love by eating breakfast, lunch and dinner at McDonalds. Human interest is provided by his vegan girlfriend who worries (appropriately) but implies (inappropriately) that Morgan’s fast weight gain, fatigue, liver toxicity and loss of libido are due not only to sugar but to the evil meat patty with its saturated fat. Truth is the amount of saturated fat in the burgers is far exceeded by soy oil on the griddle and in the French fries. And the buns, shakes and condiments all contain soy protein. Indeed, the movie might have been called Super Soy Me!

I saw two commercials last night for prescription medications.  Two were for osteoporosis, the other was for cholesterol.  All three pissed me off.  (excuse my language..)

The Boniva ad had Sally Fields talking about her osteoporosis and how she had stopped the bone loss. The other commercial had two women talking about how they had known each other all thier lives and even now “shared osteoporosis”.

Dr. Jarvis says on his commercial for Lipitor, “when diet and exercise are not enough, he turned to Lipitor.”

HELLO???   Diet and Exercise  ARE always enough if you eat right!  My chiropractor says my bone density is that of a 25 year old. My joints show very little wear and tear on an x-ray.

Our bodies do not recognize supplements as food, most are excreted. Medications bring side effects, kidney and liver are stressed. 

A few days ago I posted Eating Organically and Economically-How I Cook and Eat-Weekly

Let’s take a look at one days menu then I will show you the nutrition breakdown for that day.

Ideal Day

Breakfast:

2 whole organic eggs soft scrambled with 1 T. raw butter

1 slices organic bacon

2 slices tomato

½ cup fresh vegetable juice, mostly greens.

Lunch

3 chicken legs

2 cups sautéed red cabbage and onions using coconut oil

2 slices tomato

Mid-afternoon

½ cup blueberries

Dinner

1 cup sweet potato (136 calories) or (winter squashes) with 1 T. butter

7 ounces grass fed beef, bison or free range chicken, cooked with 1 T. coconut oil

2 cups kale or broccoli or other green LEAFY vegetable

½ cup mushrooms, peppers and onions cooked with butter

Notice the nutrient level for Vitamin C is 662 mg? Vitamin A is 57,275 I.U. a DAY!  Calcium intake is 165% of what you need daily, Iron 254%!

Perfect nutrition, not expensive, not hard to prepare…and meets your every need for protein, fats, carbs and all Vitamins and Minerals. 

Trying to use prescription medications to reach optimum health is like using a band-aid to deal with symptoms. Perfect nutrition gets rid of the symptoms, gets at the cause, detoxes you and returns you to perfect health. And reverses the ages process by drastically cutting back on free radical production.

 

ScienceDaily (Aug. 7, 2009) — Drinking beetroot juice boosts your stamina and could help you exercise for up to 16% longer. A University of Exeter led-study shows for the first time how the nitrate contained in beetroot juice leads to a reduction in oxygen uptake, making exercise less tiring.

The study reveals that drinking beetroot juice reduces oxygen uptake to an extent that cannot be achieved by any other known means, including training.

The research team believes that the findings could be of great interest to endurance athletes. They could also be relevant to elderly people or those with cardiovascular, respiratory or metabolic diseases.

The research team conducted their study with eight men aged between 19 and 38. They were given 500ml per day of organic beetroot juice for six consecutive days before completing a series of tests, involving cycling on an exercise bike. On another occasion, they were given a placebo of blackcurrant cordial for six consecutive days before completing the same cycling tests.

After drinking beetroot juice the group was able to cycle for an average of 11.25 minutes, which is 92 seconds longer than when they were given the placebo. This would translate into an approximate 2% reduction in the time taken to cover a set distance. The group that had consumed the beetroot juice also had lower resting blood pressure.

The researchers are not yet sure of the exact mechanism that causes the nitrate in the beetroot juice to boost stamina. However, they suspect it could be a result of the nitrate turning into nitric oxide in the body, reducing the oxygen cost of exercise.

The research was carried out by the University of Exeter and Peninsula Medical School and published in the Journal of Applied Physiology. The research team now hopes to conduct further studies to try to understand in more detail the effects of nitrate-rich foods on exercise physiology.

Corresponding author of the study, Professor Andy Jones of the University of Exeter’s School of Sport and Health Sciences, said: "Our study is the first to show that nitrate-rich food can increase exercise endurance. We were amazed by the effects of beetroot juice on oxygen uptake because these effects cannot be achieved by any other known means, including training. I am sure professional and amateur athletes will be interested in the results of this research. I am also keen to explore the relevance of the findings to those people who suffer from poor fitness and may be able to use dietary supplements to help them go about their daily lives."

This study follows research by Barts and the London School of Medicine and the Peninsula Medical School (published in February 2008 in the American Heart Association journal Hypertension), which found that beetroot juice reduces blood pressure.

By Cathy McNeil

Grass fed beef stock can be a Godsend for cancer patients undergoing chemotherapy. Two of the main problems faced by chemo patients are painful mouth sores which inhibit chewing and swallowing, as well as low hematocrit scores (blood iron levels), possibly resulting in malnourishment and anemia.

One woman I know of said that while undergoing chemo, all she could eat was applesauce. A recovering cancer patient undergoing chemotherapy needs far more nutritional support than just applesauce. He or she needs sufficient quantities of protein and iron.

Grass fed beef is a perfect source of protein and iron, as almost all producers raise it without the use of added growth hormones, antibiotics, or pesticides; all things that a recovering cancer patient wants to be sure to avoid.

However, as good for a recovering cancer patient as grass fed beef is, it is of no value if the patient cannot chew or swallow it. The mouth sores that often come as a side effect of chemo can make it almost impossible to chew, much less swallow, steak, roast beef, or hamburger. That is where grass fed beef stock is the perfect solution!

Full of health supporting nutrients such as protein, iron, Omega 3, CLA, Vitamin E, Beta Carotene, B vitamins, and minerals, grass fed beef stock requires no chewing and is easy to swallow, thus making it so much easier to ingest. Not only that, grass fed beef stock is delicious and satisfying, even for chemo patients who have experienced changes in their taste buds and have found most food to be less desirable.

The other great thing about grass fed beef stock is that it is so easy and affordable to make. Soup bones are the most inexpensive cut of beef, and you can brew up a large pot of stock almost effortlessly. See the recipe below:

Quick and easy grass fed beef stock

• Roast 3 pounds of grass fed beef soup bones in 350 degree F oven for an hour
• Start large stockpot of water boiling
• Add roasted soup bones, with meat, fat, and drippings, to boiling water
• Add a whole, peeled onion to boiling water
• Add six whole celery stocks to boiling water
• Boil at hard boil for about 15 minutes
• Turn to simmer, and let simmer for an hour or two
• Strain or remove bones, meat, onion, and celery
• Add a pinch of ground celery seed, thyme, and chervil to taste
• Strip the meat off of the bones and add it to the individual soup bowls for those who are not undergoing chemo

A caution about salt
It is best not to add salt to the broth, as it can aggravate and irritate the mouth sores of chemo patients. The rest of the family can add clean and pure sea salt to their own individual bowl rather than to the stockpot. Once the sores start to heal, the chemo patient can begin to add salt as tolerated. Yes, the stock is a bit bland without salt, but the additional herbs, especially the celery seed, can make the broth quite flavorful without it.

As the patient begins to recover
As the mouth sores begin to heal, you can introduce more solid food to the stock. Start by blending the meat, along with sautéed carrots, celery, and other vegetables and adding it all to the stock. After a while you will not need to blend it up, and the patient can begin to enjoy delicious, full and hearty soups made from a base of grass fed beef stock.

Health benefits for the whole family
Not only is grass fed beef stock great for chemo patients, but is chock full of other wonderful properties that are beneficial to the whole family. Studies have shown that bone broth can help improve joint functioning and relieve digestive problems. It makes intuitive sense that the nutrients leached from bones and joints into a beef stock would be good for our own bones and joints.

Grass fed beef stock is a delicious, hearty, healthy, and nutritious solution to the dietary needs of the recovering cancer patient undergoing chemotherapy, as well as the whole family.

If you or a loved one has cancer, and are undergoing chemotherapy, our hearts go out to you! We appreciate the trials and tribulations that you are going through, and for that reason are offering a special on grass fed beef soup bones so you can get the nutritional support you need.

from The Organic Consultancy

by Simon Wright

History

Palm oil is produced from the fruit of the oil palm Elaeis Guinnesis which is found in Africa, South East Asia and Latin America. Although humans have eaten the oil palm for over 5000 years commercial planting and cultivation did not begin until the mid-1990’s in Malaysia.

Production and Uses

Palm oil is extracted and refined through pressing and crushing rather than through using chemical solvents such as hexane. Palm oil can be further refined into palm olein (liquid) and palm stearine (solid). Palm olein is used as a frying oil because it is very stable to heat, whilst palm stearine is used in biscuits and cakes and in non-hydrogenated margarine. Palm stearine is also used to stop peanut butter from separating. Palm oil resists oxidation and rancidity, which means products made using palm oil have extended shelf lives.

Organic palm oil

The fact that palm oil is solid at room temperature, has a neutral taste and can be extracted without the use of solvents has made organic palm oil a very useful ingredient in organic food processing. The only other organic fats which are solid at room temperature are butter and coconut oil, both of which are highly saturated.

But I thought palm oil was highly saturated?

Palm oil is frequently confused with palm kernel oil, which is highly saturated. In contrast palm oil contains a balance of polyunsaturated, monounsaturated and saturated fatty acids. In addition palm oil contains essential substances such as linoleic acid (an essential fatty acid which the body cannot manufacture) and tocopherols and tocotrienols, which act as natural anti-oxidants against damaging free-radicals.

What about cholesterol?

Like other vegetable fats palm oil is free from cholesterol. Because palm oil is solid at room temperature there is no need to use hydrogenation, a technique which hardens liquid oil but also produces damaging trans fatty acids and raises cholesterol levels in the process. Human feeding studies have shown that palm oil does not ordinarily raise blood cholesterol levels and in some cases has been found to lower harmful LDL-cholesterol.

Any other health benefits?

Rats fed on a palm-oil enriched diet had a reduced tendency to form blood clots. Unrefined palm olein (which is bright red in color) is a major source of carotenoids which inhibit some types of cancer. The unrefined oil is also a major source of beta-carotene, which is a precursor to Vitamin A.

It is also a rich source of phytonutrients such as beta-carotene, alpha-carotene, vitamin-E, lycopene and other carotenoids. These carotenoids are responsible for the striking red color of the oil.

Red palm oil has been used for thousands of years as a cooking oil in the East, but has only recently become available in the West. Importers in the West intend to make it more readily available. At the moment, red palm oil is available at selected health shops and supermarkets.

Why is red palm oil a super-healthy oil?
Red palm oil is particularly healthy because it contains the above-mentioned carotenoids and a special form of vitamin E. Most people are not aware of the fact that many different kinds of vitamin E occur in nature and that some forms of vitamin E are more beneficial than others. Red palm oil contains tocotrienols, a powerful form of vitamin E, which acts as a super-antioxidant.

The carotenoids in red palm oil also act as antioxidants and one of these carotenoids, namely lycopene, is associated with reducing the risks of certain types of cancer.

Our bodies need antioxidants to counteract ‘free radicals’. When we are exposed to pollutants in cigarette smoke, industrial pollution, stress, unbalanced diets, pesticide residues in food, and many other negative environmental influences, we are also exposed to free radicals.

A build-up of free radicals in the body is associated with degenerative diseases such as heart disease and cancer, as well as general ageing. It is, therefore, in our own best interests to ensure that we eat a diet rich in antioxidants that will counteract the damage to our bodies by free radicals.

What about heating?
Most people are aware of the fact that important nutrients can be broken down or destroyed when food is cooked. Research has shown that red palm oil can be heated during cooking without destroying its rich phytonutrient content.

What are tocotrienols?
Tocotrienols are super-antioxidants that belong to the vitamin E family. Red palm oil is particularly rich in these tocotrienols and is the only vegetable oil that has an abundant tocotrienol content.

Research results
Scientific studies conducted at the Universities of Louisiana and Wisconsin in the USA, the University of Reading in the UK, and the University of Western Ontario in Canada, have identified the following health benefits of red palm oil:

• a reduction in the incidence of arteriosclerosis (hardening of the arteries which can result in heart disease);

• a reduction in blood cholesterol levels;

• a reduction in blood clotting, combined with blood vessel dilation, thus preventing heart attacks and strokes;

• inhibition of the growth of breast cancer cells, which suggests that red palm oil may act as a chemopreventive agent;

• a 45% enhancement of the efficiency of breast cancer drugs such as Tamoxifen.

These research results are indeed good news and may herald a new chapter in the prevention of heart disease and various types of cancer.

Interesting comparisons
The following table illustrates the nutritional benefits of red palm oil:

Nutrient   Red Palm Oil   Sunflower Oil   Safflower Oil   Maize Oil   Olive Oil

Vitamin E (mg)  80              39                  27.4              20.7            7.6

Carotene (mg)  50               0                    0                    0               0

It is evident that the vitamin E and carotene contents of red palm oil are superior to those of the above-mentioned cooking and salad oils.

So why does palm oil have such a bad reputation?

In the 1980’s the American Soya Oil processors were worried about losing domestic sales to imports of palm oil from Malaysia. They set up organizations with names like American Heartsavers which purported to promote good health to consumers but in reality these organizations were a front for attacking “tropical” oils such as palm oil. The campaign culminated in full page newspaper advertisements carrying headlines such as “Stop The Poisoning Of America”. Some of this misinformation trickled across the Atlantic and has left residual doubts in the minds of UK consumers and industry figures even today.

Palm oil is a very common cooking ingredient in the regions where it is produced.

Its heavy use in the commercial food industry elsewhere can be explained by its comparatively low price, being one of the cheaper vegetable or cooking oils on the market, and by new markets in the USA, stimulated by a search for alternatives to trans fats after the Food and Drug Administration required food labels to list the amount of trans fat per serving.

Red palm oil is known to be healthier than refined (discolored) palm oil. This is a result of several mitigating substances found in the red palm oil. These compounds are:

• betacarotenes (present in higher amounts than in regular palm oil),
• co-enzyme Q10 (ubiquinone),
• squalene,
• vitamin A
• vitamin E.

Refining these oils makes them unhealthy for us;

Palm oil products are made using milling and refining processes: first using fractionation, with crystallization and separation processes to obtain solid (stearin), and liquid (olein) fractions. By melting and degumming, impurities can be removed and then the oil filtered and bleached. Next, physical refining removes smells and coloration, to produce refined bleached deodorized palm oil, or RBDPO, and free sheer fatty acids, used as an important raw material in the manufacture of soaps, washing powder and other hygiene and personal care products. RBDPO is the basic oil product which can be sold on the world’s commodity markets, although many companies fractionate it out further into palm olein, for cooking oil, or other products.

We were all brought up with the myth that "milk does a body good." This is why most parents believe that milk is a desirable and essential part of a child’s diet. But 70% of the world’s population doesn’t drink milk. The fact is mother nature never intended mammals to drink milk after weaning. In fact, in no mammalian species, except for a small percentage of humans, is milk consumption continued after weaning. In the words of Dr. Frank Oski, Director of Pediatrics at Johns Hopkins School of Medicine, "No one should drink milk." Mother’s milk is actually a perfect food—for infants. The chemical composition of milk is uniquely designed for the infants of each species. Consumption by adult mammals or cross-feeding to other mammals is a bad idea. Feeding elephant milk to cats, mouse milk to giraffes, or cow milk to humans will damage health. Cow milk is a major contributor to our chronic disease problems. When people stop consuming dairy—health improves. The reason for this is that the sugar, fat, protein, and minerals in cow’s milk are not appropriate for human consumption. In addition, virtually all milk is pasteurized which further changes the chemistry of the milk and makes it even more damaging.

Milk contains a sugar, called lactose, which is found only in milk. Mammals are born with the ability to make an enzyme, called lactase, which digests the lactose. All mammals, including the majority of humans, lose the ability to make this enzyme after weaning. Without this enzyme, consuming milk causes numerous medical problems ranging from mild to serious. Many people have this problem without knowing it. I have met people who wonder why they have so much gas after drinking milk. Most likely they are lactase deficient. Milk is contaminated with low-level residues of pesticides, hormones, antibiotics, sulfa drugs, dioxin, PCBs, and other chemicals. According to the USDA, "No milk available on the market today, in any part of the U.S., is free of pesticide residues." These chemical residues can bioaccumulate in our tissues and eventually reach concentrations where they cause birth defects, cancer, and other problems. About 80% of the average person’s pesticide load comes from consuming meat and dairy. One example of what happens after years of this bioaccumulation was cited by John Robbins in Diet for a New America. Robbins noted that the milk of most American mothers who are breast feeding is so contaminated with PCBs, dioxin, and various pesticides that, "…it would be subject to confiscation and destruction by the FDA were it to be sold across state lines." These chemicals store in the mother’s fat which is then used to make the mother’s milk. Robbins goes on to say, "The EPA has concluded that the average American breast-fed infant ingests nine times the permissible level of dieldrin, one of the most potent of all cancer causing agents known to modern science." It shouldn’t be a surprise that cancer has become the leading cause of death for children under the age of fourteen. All this is happening because of the mother’s bioaccumulation of toxins from her own consumption of meat and dairy.

Milk is also contaminated with viruses and bacteria. Government regulations state that after pasteurization milk should contain no more than 20,000 bacteria per milliliter. A study done by Consumer Reports found that seven out of twenty-five milk samples had in excess of 130,000 bacteria per milliliter. One sample had almost three million, and others had too many to count. Exposing yourself to this level of bacterial contamination is not a good idea. A host of infectious diseases have been traced to consumption of pasteurized milk. In addition, you may be putting an unnecessary and injurious load on your immune system.

Cow milk contains the wrong proteins for human consumption. It is rich in proteins called caseins which are difficult for humans to digest. Cows have four stomachs so they don’t have a problem, but we do. These undigested proteins enter the lower intestines where they putrefy. This creates highly toxic by-products which poison us. Undigested proteins can also enter into systemic circulation, provoking allergic reactions. This is why milk is so highly allergenic. Dr. Frank Oski says that, "At least 50% of all children are allergic to dairy." An even higher percentage of adults are allergic. Allergic reactions tax the immune system, and lower resistance to infection and other diseases. Cow milk is rich in calcium, but is a poor source of calcium. It can also cause calcium losses. Cow milk contains 1200 mg. of calcium per quart while human milk contains only 300 mg. However, an infant actually absorbs more calcium from a quart of human milk because the calcium in the cow milk is less bioavailable. While there is a lot of calcium in cow milk, there is also a lot of phosphorous. The calcium combines with the phosphorous in the digestive tract and prevents its absorption. In addition, cow milk is low in magnesium and magnesium is necessary for calcium metabolism. Calcium that is not properly metabolized ends up as kidney stones, gout, and atherosclerotic plaques.

Another problem is that cow milk is high in protein which metabolizes to strong acids. These strong acids could harm us, so the body uses calcium to neutralize them, thus robbing bones of calcium and causing calcium losses. The U.S. has only 4% of the world’s population but it consumes more dairy than the other 96% combined. If milk was good for our bones, we would have the strongest bones in the world. Instead we have one of the highest osteoporosis rates in the world. The countries with the highest dairy consumption have the most osteoporosis. Vegetables like broccoli, chard, and kale are rich sources of calcium. We need to get our calcium the same place cows get theirs—from plants.

Milk contains too much fat. Fifty percent of the calories in milk come from fat, 60% of which is saturated. Children as young as two and three already have early signs of atherosclerosis because of excessive fat intake, and heart disease is our number one cause of death.

Pasteurizing milk adds additional health risks by changing the entire physio-chemical state of the milk. For instance, pasteurization reduces the bioavailability of milk’s calcium by 50 percent. Enzymes are deactivated. The structure of protein molecules is changed. The milk chemistry is substantially altered so that when pasteurized milk is fed to calves, for which it was intended as a perfect food, all the calves die within two months. Experiments feeding pasteurized dairy to cats, mice, rats, and calves all had the same result. The animals get sick and die. If pasteurized milk kills all these animals, why do we think it’s good for us?

Milk consumption is clearly connected to a variety of diseases. One is iron-deficiency anemia in infants. According to Dr. Frank Oski in Don’t Drink Your Milk, about 20% of all children under the age of two suffer from iron-deficiency anemia. In about half of these cases, an allergy to milk causes intestinal bleeding leading to loss of iron and anemia. Ear infections are another problem. Most ear infections can be prevented by removing dairy from a child’s diet. Multiple sclerosis has a striking correlation with the amount of milk consumed. Juvenile delinquents were found to consume ten times more dairy than other adolescents of similar age and background. Diabetes, kidney disease, eczema, asthma, rheumatoid arthritis, appendicitis, streptococcal infections, leukemia, Lou Gehrig’s disease, colds, flu, enlarged tonsils and adenoids, and ovarian cancer also have strong connections to milk consumption.

According to the American Journal of Epidemiology, ovarian cancer is highest in those countries with the highest dairy consumption. Cottage cheese and yogurt appear to be the worst offenders because their dairy sugars have been pre-digested into a sugar called galactose, which is thought to be instrumental for this cancer.

In conclusion, there is little scientific evidence that cow’s milk is of much nutritional benefit to humans, while there is ample evidence that it causes disease. Infants should be breast fed for more than a year. After that, milk is unnecessary. Cow milk and its products should be avoided by children and adults alike, and especially by potential mothers.