Errors in Nutrition: Essential Fatty Acids

Also see:
Charts: Mean SFA, MUFA, & PUFA Content of Various Dietary Fats
Unsaturated fatty acids: Nutritionally essential, or toxic? by Ray Peat, PhD
“Curing” a High Metabolic Rate with Unsaturated Fats
Fat Deficient Animals – Activity of Cytochrome Oxidase
Anti-Inflammatory Omega -9 Mead Acid (Eicosapentaenoic acid)
Protective “Essential Fatty Acid Deficiency”
Cholesterol and Thyroid Connection
Thyroid Status and Cardiovascular Disease
Hypothyroidism and Gallbladder Disease
Thyroid Status and Oxidized LDL
Unsaturated fatty acids: Nutritionally essential, or toxic?
Suitable Fats, Unsuitable Fats: Issues in Nutrition
Fats, functions & malfunctions
Fats and degeneration.

Cliff’s Notes:
1. In 1929 and 1930, the Burrs’ discovered that polyunsaturates slow the metabolic rate and lower nutrition requirements. They did not discover “essential fatty acids” (EFA).
2. “EFA” deficiency can be cured by nutrients other than “EFA,” like vitamin B6 and B5.
3. Animals with an “EFA” deficiency have a much higher respiratory quotient relative to animals that are not “EFA” deficient.
4. A human study involving a prolonged fat-free diet (i.e. “EFA” deficient) reversed many of the health ailments suffered by the subject (William Brown).
5. Since the so-called “EFA” are in all natural foods, it’s unlikely to develop a deficiency.
6. The refining of liquid “EFA” rich oils was originally intended to go towards the production of paints and varnishes. The loss of this market to petroleum interests fueled the marketing of “EFA” as a health promotive, essential nutrient. The Burr’s faulty research served as the basis for this promotion.
7. “EFA” and other polyunsaturated fatty acid (PUFA) are environmentally-derived & toxic. Dietary choices and the intensity of a person’s metabolic rate determine to pace at which these fats accumulate. As consumption of these fats accumulates, the metabolic rate is progressively decreased.
8. An essential nutrient is a nutrient the body doesn’t make in the needed amounts that allow the organism to function normally, therefore, the diet must provide the nutrient.
9. Our body doesn’t synthesize “EFA” from carbohydrate because they’re toxic.

“The fact that no relief is obtained from the symptoms of the fat-deficiency disease by the fat thus formed from carbohydrate indicates that the curative linolic and linolenic acids are not formed by the rat from the carbohydrate or from the fat.” -Wesson & Burr, 1931 (WESSON, L. G., AND G. O. BURR. The metabolic rate and respiratory quotients of rats on a fat-deficient diet. J. Biol. Chem., vol. 91, pp. 525-539. 1931)

10. The false belief in “EFA” is harming millions as it converges with the lipid hypothesis and anti-sugar propaganda to make a perfect storm of metabolic suppression, stress, hormone imbalance, inflammation, and immunodeficiency. Salt avoidance and supplemental use of estrogen, “the woman’s hormone,” add further fuel to the inflammatory fire. This explosive cocktail is a recipe for age-related degeneration, obesity, and diseases of all kinds.

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“Claiming that certain fatty acids are essential, a scientific approach would require showing what was wrong with the experiments that showed that they were not essential, and especially, those that showed that they were positively harmful.” – “Unsaturated fatty acids: Nutritionally essential, or toxic?” by Ray Peat

Errors about a nutritional concept affects many particularly when the concept is engrained deeply into the nutritional psyche and is accepted as truth without question. The idea of essential fatty acids is a faulty theory promoted by industry interests and holding on to it as truth is harming our ability to live well and progress further into the nutritional learning landscape. However, it does help sell liquid oils.

Burr’s Disease
Anyone supportive of the idea of essential fatty acids (EFA) will mention the study done by George and Mildred Burr in 1929.(1,2) The work of the Burrs apparently showed that certain fats were essential to the diet meaning that these fats must be present in the diet for normal body function because the body cannot manufacture these nutrients in the needed amounts.

Based on the experiment done by the Burrs, some polyunsaturated dietary fats (linoleic and linolenic acids) became known as essential fatty acids. EFA appeared to cure a scaly skin condition (“rat dermatitis”) observed in rates. The introduction of EFA into the rats’ fat-deficient diet cured the dermatitis and what was coined an essential fatty acid deficiency.

B Vitamin Deficiency
In the late 1920s, most of the B vitamins and trace mineral had not been identified at the time. As a result, citing a study from 1929 as the study to prove the existence of an essential nutrient appears odd.

The years following the Burrs’ discovery, more knowledge had been attained regarding the B vitamins and other nutrients. Studies post-dating the Burrs’ experiment indicated that what was previously thought to be a skin abnormality induced by a lack of EFA was actually a vitamin B6 and B5 deficiency (and likely other nutrients).(3-8) The rats’ skin condition the Burrs’ witnessed were produced by deficiencies of nutrients that had yet to be discovered.(9) Over 50 years ago, the essentiality of EFA was called into question. Ray Peat expands on this topic in the article, “Fats and degeneration.”

“Several publications between 1936 and 1944 made it very clear that Burr’s basic animal diet was deficient in various nutrients, especially vitamin B6. The disease that appeared in Burr’s animals could be cured by fat free B-vitamin preparations, or by purified vitamin B6 when it became available. A zinc deficiency produces similar symptoms, and at the time Burr did his experiments, there was no information on the effects of fats on mineral absorption. If a diet is barely adequate in the essential minerals, increasing the metabolic rate, or decreasing intestinal absorption of minerals, will produce mineral deficiencies and metabolic problems.

Although “Burr’s disease” clearly turned out to be a B-vitamin deficiency, probably combined with a mineral deficiency, it continues to be cited as the basis justifying the multibillion dollar industry that has grown up around the “essential” oils.”(10)

Benefits of an EFA deficiency
Attempts to intentionally induce an EFA deficiency in humans provided interesting results.(11) To test the effects of a very low fat diet on a human, biochemist William Brown volunteered to go six months in Burr’s laboratory eating such a diet. Chris Masterjohn discusses the results of this experiment in his article “Precious Yet Perilous: Understanding the Essential Fatty Acids.”

“Inducing an essential fatty acid deficiency in an adult human proved much more difficult than curing one…Each day, he consumed three quarts of defatted milk, a quart of cottage cheese made from it, sucrose, potato starch, orange juice and some vitamin and mineral supplements. His blood lipids became more saturated and their concentrations of linoleic and arachidonic acids were cut in half. He experienced a marked absence of fatigue, his high blood pressure returned to normal, and the migraines he had suffered from since childhood completely disappeared.”(12)

Brown experienced no skin abnormalities and “in spite of a supposedly adequate caloric intake” he lost weight as a result of improved metabolic function. The attempt to create an essential fatty acid deficiency improved the measured parameters in the experiment and Brown’s previous symptoms vanished. How could avoiding something dietarily essential create such marked improvements and produce NO skin abnormalities in six months?

Animal studies where an EFA deficiency is induced by eating a no fat diet echo this same result as the animals in such experiments exhibit increased metabolic rate, low chance of cancer, and better withstood stress and trauma. Ray Peat further mentions the following in “Fats and degeneration”:

“…a few experimenters were finding that animals which were fed a diet lacking the “essential” fatty acids had some remarkable properties: They consumed oxygen and calories at a very high rate, their mitochondria were unusually tough and stable, their tissues could be transplanted into other animals without provoking immunological rejection, and they were very hard to kill by trauma and a wide variety of toxins that easily provoke lethal shock in animals on the usual diet. As the Germans had seen in 1927, they had a low susceptibility to cancer, and new studies were showing that they weren’t susceptible to various fibrotic conditions, including alcoholic liver cirrhosis.”(10)

Some of the effects seen in the animal model were seen in the experiment done on Brown. Applying this same ideology (i.e. avoiding EFA) to human models would appear beneficial.

Unessential EFA
So what was the potential mechanism that allowed the Burrs to falsely conclude that the fats that cured the rats’ skin conditions were essential?

The use of EFA to remedy an “EFA deficiency” was actually an indication of polyunsaturated fats’ metabolism suppressing tendencies. An organism with a lower metabolic rate has a decreased need for nutrients so one can “cure” a vitamin deficiency by taking something (“EFA”) that slows metabolism. Those organisms with an “EFA deficiency” experience a higher metabolic rate and thus an increased need for B vitamins and other nutrients. So you can either use B vitamins and other nutrients or “EFA” to cure the deficiency.

One strategy actually addresses the deficiency while the other suppresses metabolism and cellular respiration giving the appearance of a cure. The Burrs’ study, it turns out, didn’t prove essentiality but was actually evidence of just one of the toxic effects of polyunsaturated fats – suppression of metabolism. A change in perspective produces a change in the experiment’s interpretation.

It’s also worthy to note that saturated fats (stearic, palmitic, myristic, lauric acids) did not cure the skin condition in the Burrs’ experiment which would be expected from something that doesn’t lower the metabolic rate and nutritional needs.

Seed Oil Industry
“U.S. consumption of seed oils had been almost doubling every decade since the first world war, but the technological advances of the 1960s which allowed paints to be made from petroleum derivatives, rather than from linseed oil, safflower and soy oil, stimulated the redirection of large amounts of these substances from paint production into the food market. Clever marketing tricks are in some cases creating price mark-ups of 10,000%.” -Ray Peat, PhD

One of the reasons why the myth of “essential fatty acids” continues is simple economics. The supplement industry is big business. It is the goal of the supplement marketer to place the importance of their product in the forefront of the minds of consumers. Is there a better way to market the necessity of a product than by saying that a supplement or food is essential to human health?

The faulty premise of EFA became the basis by which a cleverly contrived seed oil industry marketing scheme came about despite it being based largely on a 1920s study and having no basis in scientific reality. Nevertheless, the seed oil biz has done a great job of convincing people that the cheap essential oils are heart protective and better than animal fats which contain cholesterol that clogs your arteries. Whatever the public hears the most, they come to believe as fact. The need for essential fats has been heard so often by the masses and professionals that it is now believed as fact without any question of its validity.

Before WWII, seed oils were used as varnishes, paints, and in plastics. The introduction of petroleum into the marketplace quickly left the seed oil industry without a substantial market to sell their product. A new market had to be made and unfortunately for us it was the supermarket. The same reason why seed oils make good varnishes is the same reason why you should not consume such foods — their propensity to oxidize.(8)

Degeneration and Inflammation
The so called “EFA” are at the center of age-related degenerative processes.(12-16) When we view health through that periscope, the rampant disease, chronic fatigue, and obesity that pervades western culture is easy to figure out as the food supply and supplement business is drowning people in destructive PUFA.

As mentioned earlier, eliciting an EFA deficiency on purpose in an otherwise adequate diet proved beneficial in both human and animal models. A new nutritional paradigm encourages an intentional EFA and PUFA deficiency as such a state improves our metabolic function, adaptability to stress, resistance to disease, and allows us to synthesize our own unsaturated fats (omega -9 Mead Acid) from carbohydrate which are anti-inflammatory and protective.

EFA, being polyunsaturated, are prone to oxidation and thus are responsible in many ways for degeneration on a wide scale. Ray Peat, in his article “Membranes, plasma membranes, and surfaces,” says that EFA do the following:

“If you want to use a polyunsaturated oil as a drug, it is worthwhile to remember that the “essential fatty acids” suppress metabolism and promote obesity; are immunosuppressive; cause inflammation and shock; are required for alcoholic liver cirrhosis; sensitize to radiation damage; accelerate formation of aging pigment, cataracts, retinal degeneration; promote free radical damage and excitoxicity; cause cancer and accelerate its growth; are toxic to the heart muscle and promote atherosclerosis; can cause brain edema, diabetes, excessive vascular permeability, precocious puberty, progesterone deficiency, skin wrinkling and other signs of aging.”(17)

At this point, taking the approach of doing the exact opposite of what the public is told regarding nutrition would afford you a better chance of achieving good health and avoiding disease. The current state of nutritional affairs are that bad. Supporting industry and profits are at the heart of nutritional recommendations, never health. Weeding through the piles of dogma preached by industry and special interests is near impossible. The truth is hard to find. Marketing is dominating the thought of the masses by exposing them to cleverly contrived falsehoods.

What to do?
The very foods touted as health foods or healthy fats appear anything but. Even if the essential fats were indeed essential, people would be unlikely to be deficient in them since all natural foods contain polyunsaturated fats.

When it comes to dietary fats, avoiding foods rich in polyunsaturated fats (grains, beans, fatty fish, fish oils, seed, seed oils, nuts, above ground vegetables, vegetable oils) could be a strategy you could employ to avoid the degenerative(18-19) and metabolism suppressing effects created by these foods.

The ability to fatten farm animals quickly with little feed using a diet consisting of corn, soy, and grain is due to these PUFA rich foods’ ability to slow metabolism by poisoning the thyroid gland. PUFA-rich corn, soy, and grain are now used widely in processed foods and for raising industrial poultry and pork (omnivores). This has widespread, toxic consequences on cellular energy, cellular health, and the hormones.

Saturated fats (butter, ghee, refined coconut oil, cheese, milk, chocolate, pastured animal foods from ruminate herbivores) support metabolism and are protective as they are not prone to lipid peroxidation and can reverse the multitude of damaging effects of a diet rich in EFA and other polyunsaturated fats (like fish oils). Forming fatty acids from sugar, since they are not of the toxic variety, is also protective. Healthy newborns are “EFA deficient”(20) since they are protected from PUFA by the mother’s placenta, and they form fats from sugar during gestation.

Resources:
(1) George O. Burr and Mildred M. Burr A NEW DEFICIENCY DISEASE PRODUCED BY THE RIGID EXCLUSION OF FAT FROM THE DIET J. Biol. Chem. 1929 82: 345-367

(2) Burr, G. O. & Burr, M. M. The nature and role of the fatty acids essential in nutrition. J. Biol Chem. 86: 587–621 (1930).

(3) WILLIAMS MA, HINCENBERGS I. Methyl arachidonate supplementation of vitamin B6-deficient rats. Arch Biochem Biophys. 1959 Aug;83:564-5.

(4) Gyôrgy, P., Poling, C. E., and Subbarow, Y.: Experiments on the anti-dermatitis component of the filtrate factor in rats. Proc. Soc. Exper. Biol.&Med., 42: 738(Dec.)1939.

(5) U.S. Department of Agriculture. Agricultural Research Administration. Office of Experiment Stations.. Experiment Station Record, Volume 87, July-December, 1942. Washington. UNT Digital Library. http://digital.library.unt.edu/ark:/67531/metadc5069/.

(6) F. W. QUACKENBUSH, H. STEENBOCK, F. A. KUMMEROW AND B. E. PLATZ. Linoleic acid, Pyroxidine, and Panthothenic Acid in Rat Dermatitis. J. Nutr. September 1, 1942 vol. 24 no. 3.

(7) H. Schneider, H. Steenbock, and Blanche R. Platz ESSENTIAL FATTY ACIDS, VITAMIN B6, AND OTHER FACTORS IN THE CURE OF RAT ACRODYNIA. J. Biol. Chem. 1940 132: 539-551

(8) “Suitable Fats, Unsuitable Fats: Issues in Nutrition” by Ray Peat, PhD

(9) “Unsaturated fatty acids: Nutritionally essential, or toxic?” by Ray Peat, PhD

(10) “Fats and degeneration” by Ray Peat, PhD

(11) Brown WR, Hansen AE, Burr GO, McQuarrie I. EFFECTS OF PROLONGED USE OF EXTREMELY LOW-FAT DIET ON AN ADULT
HUMAN SUBJECT. J. Nutr. December 1, 1938 vol. 16 no. 6 511-524

(12) “Precious Yet Perilous: Understanding the Essential Fatty Acids” by Chris Masterjohn, PhD

(13) Ip C, Carter CA, Ip MM. Requirement of essential fatty acid for mammary tumorigenesis in the rat. Cancer Res. 1985 May;45(5):1997-2001.
“Mammary tumorigenesis was very sensitive to linoleate intake and increased proportionately in the range of 0.5 to 4.4% of dietary linoleate.”

(14) Oda E, Hatada K, Kimura J, Aizawa Y, Thanikachalam PV, Watanabe K. Relationships between serum unsaturated fatty acids and coronary risk factors: negative relations between nervonic acid and obesity-related risk factors. Int Heart J. 2005 Nov;46(6):975-85.
“Oleic acid (OA), linoleic acid (LA), and eicosapentaenoic acid (EPA) were positively related to coronary risk factors (total CRFS = 2, 3, and 4, respectively), while nervonic acid (NA) exerted negative effects on these risk factors (total CRFS = -6 ). It is concluded NA may have preventive effects on obesity-related metabolic disorders.”

(15) Kouba M, Mourot J. Effect of a high linoleic acid diet on delta 9-desaturase activity, lipogenesis and lipid composition of pig subcutaneous adipose tissue. Reprod Nutr Dev. 1998 Jan-Feb;38(1):31-7.
“Diet M increased lipogenesis (estimated from the activities of acetyl-CoA-carboxylase, malic enzyme and glucose-6-phosphate dehydrogenase), and decreased delta 9-desaturase activity, in comparison to the other diets. Linoleic acid content was higher in the pigs fed diet M than in the other pigs (amounting to 26% of total tissue fatty acids versus 15%, respectively).”

(16) Yam D, Eliraz A, Berry EM. Diet and disease–the Israeli paradox: possible dangers of a high omega-6 polyunsaturated fatty acid diet. Isr J Med Sci. 1996 Nov;32(11):1134-43.
“Studies suggest that high omega-6 linoleic acid consumption might aggravate HI and IR, in addition to being a substrate for lipid peroxidation and free radical formation. Thus, rather than being beneficial, high omega-6 PUFA diets may have some long-term side effects, within the cluster of hyperinsulinemia, atherosclerosis and tumorigenesis.”

(17) “Membranes, plasma membranes, and surfaces” by Ray Peat, PhD

(18) Griffini P, Fehres O, Klieverik L, Vogels IM, Tigchelaar W, Smorenburg SM, Van Noorden CJ. Dietary omega-3 polyunsaturated fatty acids promote colon carcinoma metastasis in rat liver. Cancer Res. 1998 Aug 1;58(15):3312-9.
“In conclusion, omega-3 and omega-6 PUFAs promote colon cancer metastasis in the liver without down-regulating the immune system. This finding has serious implications for the treatment of cancer patients with fish oil diet to fight cachexia.”

(19) Wolfe RR, Martini WZ, Irtun O, Hawkins HK, Barrow RE. Dietary fat composition alters pulmonary function in pigs. Nutrition. 2002 Jul-Aug;18(7-8):647-53.
“We concluded that the common practice of providing calories in the form of polyunsaturated fatty acids to critically ill patients carries the risk of being detrimental to lung function.”

(20) Al MD, Hornstra G, van der Schouw YT, Bulstra-Ramakers MT, Huisjes HJ. Biochemical EFA status of mothers and their neonates after normal pregnancy. Early Hum Dev. 1990 Dec;24(3):239-48.

FPS coaches a 12 week nutrition course based solely on the methodology of Ray Peat, PhD. Please click here for more information.

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Additional Information by Ray Peat, PhD:
“I think the issue is just one of propaganda analysis, because scientifically, no one ever refuted the refutation of essentiality which occurred when the “EFA deficiency syndrome” was cured with vitamin B6. The German demonstration that spontaneous cancer was eliminated on a fat freediet preceded the really awful, incompetent study that supposedly demonstrated the essentiality of polyunsaturated fatty acids, and in the 75 years since the German study a tremendous amount of information has accumulated showing both the toxicity and the non-essentiality of the polyunsaturated fatty acids. But there has been no financial support for publicizing the protective effect of not eating vegetable oils or fish oils. To the contrary, vast amounts of money are being spent in the promotion of the various polyunsaturated fats as foods.

The animals that don’t eat them do have increased nutritional needs for vitamins and minerals, because their metabolic rate is so much greater than the PUFA-replete animals whose cardiolipin has degenerated. The recent Stanford study that shows a much greater longevity for old people who have a very high oxygen consumption capacity is consistent with the historical animal studies. PUFA-deprived animals have a very high oxygen consumption, and are resistant to practically all causes of death and disease, including trauma and poisoning.

The editorial boards of many of the journals are packed with industry flacks who are apparently willing to publish any junk that helps to sell soy oil, canola, waste fish oil, or algae oils. And researchers have to get grants to stay in business.”

“The publicity campaign against “saturated fat” as an ally of cholesterol derived its support from the commercial promotion of the polyunsaturated seed oils as food for humans. Although the early investigators of vitamin E knew that the polyunsaturated oils could cause sterility, and others later found that their use in commercial animal foods could cause brain degeneration, there were a few biologists (mostly associated with George Burr) who believed that this type of fatty acid is an essential nutrient.

George and Mildred Burr had created what they claimed to be a disease in rats caused by the absence of linoleic or linolenic acid in their food. Although well known researchers had previously published evidence that animals on a fat free diet were healthy–even healthier than on a normal diet–Burr and his wife published their contradictory claim without bothering to discuss the conflicting evidence. I haven’t seen any instance in which Burr or his followers ever mentioned the conflicting evidence. Although other biologists didn’t accept Burr’s claims, and several researchers subsequently published contrary results, he later became famous when the seed oil industry wanted scientific-seeming reasons for selling their product as an “essential” food. The fact that eating the polyunsaturated fats could cause the blood cholesterol level to decrease slightly was advertised as a health benefit. Later, when human trials showed that more people on the “heart healthy” diet died of heart disease and cancer, more conventional means of advertising were used instead of human tests.

Burr’s experimental diet consisted of purified casein (milk protein) and purified sucrose, supplemented with a vitamin concentrate and some minerals. Several of the B vitamins weren’t known at the time, and the mineral mixture lacked zinc, copper, manganese, molybdenum, and selenium. More of the essential nutrients were unknown in his time than in Yudkin’s, so his failure to consider the possibility of other nutritional deficiencies affecting health is more understandable.

In 1933, Burr observed that his fat-deficient rats consumed oxygen at an extremely high rate, and even then, the thought didn’t occur to him that other nutritional deficiencies might have been involved in the condition he described. Ordinarily, the need for vitamins and minerals corresponds to the rate at which calories are being burned, the metabolic rate. Burr recalled that the rats on the fat free diet drank more water, and he reasoned that the absence of linoleic or linolenic acid in their skin was allowing water vapor to escape at a high rate. He didn’t explain why the saturated fats the rats were synthesizing from sugar didn’t serve at least as well as a “vapor barrier”; they are more effective at water-proofing than unsaturated fats, because of their greater hydrophobicity. The condensed and cross-linked keratin protein in skin cells is the main reason for the skin’s relatively low permeability. When an animal is burning calories at a higher rate, its sweat glands are more actively maintaining a normal body temperature, cooling by evaporation; the amount of water evaporated is an approximate measure of metabolic rate, and of thyroid function.

In 1936, a man in Burr’s lab, William Brown, agreed to eat a similar diet for six months, to see whether the “essential fatty acid deficiency” affected humans as it did rats.

The diet was very similar to the rats’, with a large part of the daily 2500 calories being provided at hourly intervals during the day by sugar syrup (flavored with citric acid and anise oil), protein from 4 quarts of special fat-free skimmed milk, a quart of which was made into cottage cheese, the juice of half an orange, and a “biscuit” made with potato starch, baking powder, mineral oil, and salt, with iron, viosterol (vitamin D), and carotene supplemented.

Brown had suffered from weekly migraine headaches since childhood, and his blood pressure was a little high when he began the diet. After six weeks on the diet, his migraines stopped, and never returned. His plasma inorganic phosphorus declined slightly during the experiment (3.43 mg./100 cc. of plasma and 2.64 on the diet, and after six months on a normal diet 4.2 mg.%), and his total serum proteins increased from 6.98 gm.% to 8.06 gm.% on the experimental diet. His leucocyte count was lower on the high sugar diet, but he didn’t experience colds or other sickness. On a normal diet, his systolic blood pressure varied from 140 to 150 mm. of mercury, the diastolic, 95 to 100. After a few months on the sugar and milk diet, his blood pressure had lowered to about 130 over 85 to 88. Several months after he returned to a normal diet, his blood pressure rose to the previous level.

On a normal diet, his weight was 152 pounds, and his metabolic rate was from 9% to 12% below normal, but after six months on the diet it had increased to 2% below normal. After three months on the sugar and milk diet, his weight leveled off at 138 pounds. After being on the diet, when he ate 2000 calories of sugar and milk within two hours, his respiratory quotient would exceed 1.0, but on his normal diet his maximum respiratory quotient following those foods was less than 1.0.

The effect of diabetes is to keep the respiratory quotient low, since a respiratory quotient of one corresponds to the oxidation of pure carbohydrate, and extreme diabetics oxidize fat in preference to carbohydrate, and may have a quotient just a little above 0.7. The results of Brown’s and Burr’s experiments could be interpreted to mean that the polyunsaturated fats not only lower the metabolic rate, but especially interfere with the metabolism of sugars. In other words, they suggest that the normal diet is diabetogenic.

During the six months of the experiment, the unsaturation of Brown’s serum lipids decreased. The authors reported that “There was no essential change in the serum cholesterol as a result of the change in diet.” However, in November and December, two months before the experiment began, it had been 252 mg.% in two measurements. At the beginning of the test, it was 298, two weeks later, 228, and four months later, 206 mg%. The total quantity of lipids in his blood didn’t seem to change much, since the triglycerides increased as the cholesterol decreased.

By the time of Brown’s experiment, other researchers had demonstrated that the cholesterol level was increased in hypothyroidism, and decreased as thyroid function, and oxygen consumption, increased. If Burr’s team had been reading the medical literature, they would have understood the relation between Brown’s increased metabolic rate and decreased cholesterol level. But they did record the facts, which is valuable.

The authors wrote that “The most interesting subjective effect of the ‘fat-free’ regimen was the definite disappearance of a feeling of fatigue at the end of the day’s work.””

“Burr didn’t understand that it was his rats’ high sugar diet, freed of the anti-oxidative unsaturated fatty acids, that caused their extremely high metabolic rate, but since that time many experiments have made it clear that it is specifically the fructose component of sucrose that is protective against the antimetabolic fats.

Although Brown, et al., weren’t focusing on the biological effects of sugar, their results are important in the history of sugar research because their work was done before the culture had been influenced by the development of the lipid theory of heart disease, and the later idea that fructose is responsible for increasing the blood lipids.”

“One of the observations in Brown, et al., was that the level of phosphate in the serum decreased during the experimental diet. Several later studies show that fructose increases the excretion of phosphate in the urine, while decreasing the level in the serum. However, a common opinion is that it’s only the phosphorylation of fructose, increasing the amount in cells, that causes the decrease in the serum; that could account for the momentary drop in serum phosphate during a fructose load, but–since there is only so much phosphate that can be bound to intracellular fructose–it can’t account for the chronic depression of the serum phosphate on a continuing diet of fructose or sucrose.

There are many reasons to think that a slight reduction of serum phosphate would be beneficial.”

“In the 1950s, the food and drug industries were promoting polyunsaturated “essential” fatty acids as protectors against heart disease, because they lowered cholesterol. Estrogen was being promoted as a cure for infertility, menopause, and numerous other problems, and the fact that it lowered cholesterol was seen as another marketing opportunity. The development of new diuretics to treat high blood pressure led to the demonizing of salt, and new drugs to treat diabetes led to indoctrinating the public with the idea that sugar was harmful.

For the television audience, these things became part of “mainstream medical science,” and they are still influential ideas, visible in medical journals, affecting the ways physiological events are interpreted. To understand any problem, such as malfunction of nerves, all of these stereotypes have to be reconsidered–the ways sugars, fats, cholesterol and hormones interact are involved in the normal and abnormal functions of any kind of cell.”

“There is general agreement that animals on a fat free diet have a very high metabolic rate, but the people who believe the “rate of living” theory will be inclined to see the increased rate of metabolism as something harmful in itself. It is clear that this is what the Burrs thought. They didn’t attempt to provide a diet that provided increased amounts of all vitamins and minerals, in proportion to the increased metabolic rate.”

“In the l930s, animals on a diet lacking the unsaturated fatty acids were found to be “hypermetabolic.” Eating a “normal” diet, these animals were malnourished, and their skin condition was said to be caused by a “deficiency of essential fatty acids.” But other researchers who were studying vitamin B6 recognized the condition as a deficiency of that vitamin. They were able to cause the condition by feeding a fat-free diet, and to cure the condition by feeding a single B vitamin. The hypermetabolic animals simply needed a better diet than the “normal,” fat-fed, cancer-prone animals did.”

“In 1929 George and Mildred Burr published a paper claiming that unsaturated fats, and specifically linoleic acid, were essential to prevent a particular disease involving dandruff, dermatitis, slowed growth, sterility, and fatal kidney degeneration.

In 1929, most of the B vitamins and essential trace minerals were unknown to nutritionists. The symptoms the Burrs saw are easily produced by deficiencies of the vitamins and minerals that they didn’t know about.

What really happens to animals when the “essential fatty acids” are lacking, in an otherwise adequate diet?

Their metabolic rate is very high.

Their nutritional needs are increased.

They are very resistant to many of the common causes of sickness and death.

They are resistant to the biochemical and cellular changes seen in aging, dementia, autoimmunity, and the main types of inflammation.

The amount of polyunsaturated fatty acids often said to be essential (Holman, 1981) is approximately the amount required to significantly increase the incidence of cancer, and very careful food selection is needed for a diet that provides a lower amount.

When I was studying the age pigment, lipofuscin, and its formation from polyunsaturated fatty acids, I saw the 1927 study in which a fat free diet practically eliminated the development of spontaneous cancers in rats (Bernstein and Elias). I have always wondered whether George and Mildred Burr were aware of that study in 1929, when they published their claim that polyunsaturated fats are nutritionally essential. The German study was abstracted in Biological Abstracts, and the Burrs later cited several studies from German journals, and dismissively mentioned two U.S. studies* that claimed animals could live on fat-free diets, so their neglect of such an important claim is hard to understand. (*Their bibliography cited, without further comment, Osborne and Mendel, 1920, and Drummond and Coward, 1921.)

Since 1927, others have demonstrated that the polyunsaturated fats are essential for the development of cancer (and some other degenerative diseases), but the Burrs’ failed to even mention the issue at any time during their careers. How could they, studying fat-free diets, have missed an important contemporary publication, if I, 40 years later, saw it? There were very few publications on dietary fats in those years, so it was hardly possible to miss it.

When researchers at the Clayton Foundation Biochemical Institute at the University of Texas demonstrated that “Burr’s disease” was actually a vitamin B6 deficiency, rather than a fatty acid deficiency, the issue was settled. Later studies failed to confirm the existence of the Burr disease caused by a deficiency of fatty acids, though many similar conditions were produced by a variety of other dietary defects. In 1938, a group in Burr’s own laboratory (Brown, et al.) failed to produce dermatitis in a man during a six month experiment. Neither of the other major features of the Burr disease, male sterility and kidney degeneration, has been subsequently confirmed. The claim that polyunsaturated fatty acid deficiency caused sterility of male animals (“A new and uniform cause of sterility is shown”) was quickly dropped, probably because an excess of polyunsaturated fats was discovered to be an important cause of testicular degeneration and sterility.

One of the features of the Burrs’ rats on the fat-free diet was that they ate more calories and drank much more water than the rats that received polyunsaturated fatty acids in their diet. They believed that the animals were unable to synthesize fat without linoleic acid, although in another context they cited a study in which the fat of rats on a fat-free diet was similar in composition to lard: “McAmis, Anderson, and Mendel [37] fed rats a high sucrose, fat-free diet and rendered the fat of the entire animal. This fat had an iodine number of 64 to 71, a fairly normal value for lard.”

The “wasteful” food consumption, and the leanness of animals that weren’t fed polyunsaturated fats became fairly common knowledge by the late 1940s, but no one repeated the Burrs’ claim that the absence of those fatty acids led quickly to the animals’ death. Meanwhile, “crazy chick disease” caused by feeding an excess of polyunsaturated fats, and a little later, “yellow fat disease,” caused by too much fish fat, were being recognized by farmers. In the 1950s, the seed oil industry created the anti-cholesterol diet culture, and a few decades later, without any new “Burr-like” publications, the omega minus 3 oils, especially fish oils, were coming to be represented as the overlooked essential fatty acids, which were capable of preventing the toxic effects of the original “essential” linoleic acid.

Although the 1929 Burr paper is still often cited as proof of the essentiality of PUFA, Burr’s younger colleague (at the University of Minnesota Hormel Institute), Ralph Holman, has cited an infant (1970), and a 78 year old woman (in 1969), who developed dermatitis while receiving fat-free intravenous feedings. Dermatitis, with dandruff, similar to Burr’s disease, has been produced by various nutritional deficiencies besides vitamin B6, including a trace mineral deficiency and a biotin deficiency, so there is no valid reason to associate dermatitis with a fat deficiency. The cases of “EFA deficiency” produced by intravenous feedings that have been widely cited were probably the result of a deficiency of zinc or other trace mineral, since so-called “Total Parenteral Nutrition” was in use for many years before the trace minerals were added to the “total” formula. In 1975, I learned that our local hospital was putting all premature babies on what they called total intravenous feeding, without trace minerals, for weeks, or months. There is still more emphasis on polyunsaturated fat in intravenous feeding than on the essential trace nutrients.”

“In 1927, German researchers reported that a fat-free diet prevented the occurrence of spontaneous cancers in rats. Since, a little later, other workers found that the elimination of unsaturated fats from the diet not only prevented cancer, but also caused a large increase in the metabolic rate, it might have been possible to conclude that it is not living which kills us, but something in the environment. Some people did draw that conclusion, but research funds go mainly to product-oriented research, and “the environment” has been hard to package as a product.”

“Essential fatty acids (EFA) are, according to the textbooks, linoleic acid and linolenic acid, and they are supposed to have the status of “vitamins,” which must be taken in the diet to make life possible. However, we are able to synthesize our own unsaturated fats when we don’t eat the “EFA,” so they are not “essential.” The term thus appears to be a misnomer. [M. E. Hanke, “Biochemistry,” Encycl. Brit. Book of the Year, 1948.]”