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<h1>Unsaturated fatty acids: Nutritionally essential, or toxic?</h1>
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<div style="text-align: center;">
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<a href="/"><img class="epic" src="/icons/chads/chad.png"></a>
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<p class="nav"><span class="nav-left">Listed under <a href="/ray-peat.html">Ray Peat</a>.</span><span class="nav-right"><a href="/theme.html">Theme</a></span></p>
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<p>From the <a href="https://raypeat.com/articles/articles/unsaturatedfats.shtml" target="_blank">original article</a> in 2007. Author: <a href="https://raypeat.com/" target="_blank">Ray Peat</a>.</p>
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<p>In
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1929 George and Mildred Burr published a paper claiming that unsaturated
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fats, and specifically linoleic acid, were essential to prevent a particular
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disease involving dandruff, dermatitis, slowed growth, sterility, and
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fatal kidney degeneration.</p>
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<p>In
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1929, most of the B vitamins and essential trace minerals were unknown
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to nutritionists. The symptoms the Burrs saw are easily produced by
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deficiencies of the vitamins and minerals that they didn't know about.</p>
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<p>What
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really happens to animals when the "essential fatty acids"
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are lacking, in an otherwise adequate diet?</p>
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<p>Their
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metabolic rate is very high.</p>
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<p>Their
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nutritional needs are increased.</p>
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<p>They
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are very resistant to many of the common causes of sickness and death.</p>
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<p>They
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are resistant to the biochemical and cellular changes seen in aging,
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dementia, autoimmunity, and the main types of inflammation.</p>
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<p>The
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amount of polyunsaturated fatty acids often said to be essential (Holman,
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1981) is approximately the amount required to significantly increase
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the incidence of cancer, and very careful food selection is needed
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for a diet that provides a lower amount. </p>
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<p>When
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I was studying the age pigment, lipofuscin, and its formation from polyunsaturated
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fatty acids, I saw the 1927 study in which a fat free diet practically
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eliminated the development of spontaneous cancers in rats (Bernstein
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and Elias). I have always wondered whether George and Mildred Burr were
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aware of that study in 1929, when they published their claim that polyunsaturated
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fats are nutritionally essential. The German study was abstracted in
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Biological Abstracts, and the Burrs later cited several studies from
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German journals, and dismissively mentioned two U.S. studies* that claimed
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animals could live on fat-free diets, so their neglect of such an important
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claim is hard to understand. (*Their bibliography cited, without further
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comment, Osborne and Mendel, 1920, and Drummond and Coward, 1921.)</p>
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<p>Since
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1927, others have demonstrated that the polyunsaturated fats are essential
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for the development of cancer (and some other degenerative diseases),
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but the Burrs' failed to even mention the issue at any time during their
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careers. How could they, studying fat-free diets, have missed an important
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contemporary publication, if I, 40 years later, saw it? There were very
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few publications on dietary fats in those years, so it was hardly possible
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to miss it.</p>
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<p>When
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researchers at the Clayton Foundation Biochemical Institute at the University
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of Texas demonstrated that "Burr's disease" was actually a
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vitamin B6 deficiency, rather than a fatty acid deficiency, the issue
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was settled. Later studies failed to confirm the existence of the Burr
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disease caused by a deficiency of fatty acids, though many similar conditions
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were produced by a variety of other dietary defects. In 1938, a group
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in Burr's own laboratory (Brown, et al.) failed to produce dermatitis
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in a man during a six month experiment. Neither of the other major features
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of the Burr disease, male sterility and kidney degeneration, has been
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subsequently confirmed. The claim that polyunsaturated fatty acid deficiency
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caused sterility of male animals ("A new and uniform cause of sterility
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is shown") was quickly dropped, probably because an <strong><em>excess</em></strong>
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of polyunsaturated fats was discovered to be an important cause of testicular
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degeneration and sterility.</p>
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<p>One
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of the features of the Burrs' rats on the fat-free diet was that they
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ate more calories and drank much more water than the rats that received
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polyunsaturated fatty acids in their diet. They believed that the animals
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were unable to synthesize fat without linoleic acid, although in another
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context they cited a study in which the fat of rats on a fat-free diet
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was similar in composition to lard<strong>:</strong> "McAmis, Anderson, and
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Mendel <em>[37]</em> fed rats a high sucrose, fat-free diet and rendered
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the fat of the entire animal. This fat had an iodine number of 64 to
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71, a fairly normal value for lard." </p>
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<p>The
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"wasteful" food consumption, and the leanness of animals that
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weren't fed polyunsaturated fats became fairly common knowledge by the
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late 1940s, but no one repeated the Burrs' claim that the absence of
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those fatty acids led quickly to the animals' death. Meanwhile, "crazy
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chick disease" caused by feeding an excess of polyunsaturated fats,
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and a little later, "yellow fat disease," caused by too much
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fish fat, were being recognized by farmers. In the 1950s, the seed oil
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industry created the anti-cholesterol diet culture, and a few decades
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later, without any new "Burr-like" publications, the omega
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minus 3 oils, especially fish oils, were coming to be represented as
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the overlooked essential fatty acids, which were capable of preventing
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the toxic effects of the original "essential" linoleic acid.</p>
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<p>Although
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the 1929 Burr paper is still often cited as proof of the essentiality
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of PUFA, Burr's younger colleague (at the University of Minnesota Hormel
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Institute), Ralph Holman, has cited an infant (1970), and a 78 year
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old woman (in 1969), who developed dermatitis while receiving fat-free
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intravenous feedings. Dermatitis, with dandruff, similar to Burr's disease,
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has been produced by various nutritional deficiencies besides vitamin
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B6, including a trace mineral deficiency and a biotin deficiency, so
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there is no valid reason to associate dermatitis with a fat deficiency.
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The cases of "EFA deficiency" produced by intravenous feedings
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that have been widely cited were probably the result of a deficiency
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of zinc or other trace mineral, since so-called "Total Parenteral
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Nutrition" was in use for many years before the trace minerals
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were added to the "total" formula. In 1975, I learned that
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our local hospital was putting all premature babies on what they called
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total intravenous feeding, without trace minerals, for weeks, or months.
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There is still more emphasis on polyunsaturated fat in intravenous feeding
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than on the essential trace nutrients. </p>
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<p>Holman
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and the Hormel Institute have been extremely influential in promoting
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the doctrine of the essentiality of PUFA, including fish oils and the
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omega -3 oils, but their best evidence, the Burr experiment, doesn't
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make their case. Far worse than that is the effect it has had in distracting
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attention from the profoundly toxic effects of the so-called essential
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fatty acids. Long after he should have known better, Holman was arguing
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that butter was a nutritionally inferior fat.</p>
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<p>When
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the Burrs were doing their study, Raymond Pearl was one of the most
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famous biologists in the country, and his "rate of living"
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theory of aging was very widely known. According to that theory, an
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organism has an intrinsic potential to produce a certain total amount
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of energy during its lifetime, and if it metabolizes at a higher than
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normal rate, its life span will be proportionately shorter than normal.</p>
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<p>There
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is general agreement that animals on a fat free diet have a very high
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metabolic rate, but the people who believe the "rate of living"
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theory will be inclined to see the increased rate of metabolism as something
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harmful in itself. It is clear that this is what the Burrs thought.
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They didn't attempt to provide a diet that provided increased amounts
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of all vitamins and minerals, in proportion to the increased metabolic
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rate. </p>
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<p>Pearl
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did an experiment, sprouting cantaloupe seeds in a dish with water.
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The sprouts that grew rapidly died sooner than those that grew more
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slowly. They died as soon as the nutrients stored in the endosperm had
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been consumed. Naturally, when nutrients are depleted, growth and metabolism
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must stop. If food and air and water are rationed, then slow metabolizers
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are going to live longer. But when nutritional needs are met, the organisms
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with the highest metabolic rate generally are healthier and live longer.
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In a study of nurses, those who habitually consumed the most calories
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lived longer than those who consumed the least. Even while Pearl was
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promoting his theory, other famous biologists, for example John Northrup
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in Jacques Loeb's lab at the Rockefeller Institute, were making observations
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that contradicted the rate of living theory. For example, around 1916,
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Northrup observed that fruit flies that metabolized at the highest rate
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lived the longest. Northrup was doing biology, Pearl was doing propaganda,
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following Weismannism.</p>
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<p>The
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idea of extending life span by slowing metabolism and growth was a logical
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implication of the "rate of living" theory of aging, and it's
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an idea that is still popular. Many people have supposed that eating
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less would slow metabolism. Caloric restriction does extend the life
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span of many species, but it generally preserves the high metabolic
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rate of youth, so that at a given age the calorie-restricted animal
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has a higher rate of oxygen consumption per gram of body weight than
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the unrestricted eaters.</p>
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<p>Roy
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Walford, a gerontologist who wrote about extending the human life span
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to 120 years by caloric restriction, spent 30 years limiting his diet
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to about 1600 calories, with little animal protein, almost no saturated
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fat--fish once or twice per week, poultry or beef about once, and a
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fat free milkshake for breakfast--and after about 15 years, began developing
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a degenerative brain disease, ALS, one of the nerve diseases involving
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lipid peroxidation and excitotoxicity. When he died from the disease,
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he had lived a year longer than the normal life expectancy.</p>
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<p>V.
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Stefannson, one of the early polar explorers, spent a winter living
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entirely on caribou meat, and felt that it had prevented the scurvy
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that had killed so many of the other explorers, who had counted on fruit
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and vegetables to prevent it. But he believed that meat was a metabolic
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stimulant that made people age prematurely, as Pearl's rate of living
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theory predicted. Stefannson said that Eskimo women were getting old
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in their twenties, and that at the age of 60 they looked as old as Europeans
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did at 80. He was a well informed anthropologist, and his observations
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were probably accurate. The Eskimos he observed ate large amounts of
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fish, and other unsaturated fats, and sometimes ate highly decayed fish.
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An accelerated rate of aging would be expected from such a diet, because
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of the toxic lipid peroxides.</p>
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<p>Calorie-restricted
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animals (on a diet of normal composition) have a lower degree of fat
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unsaturation in their mitochondria as they age, preserving the relatively
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more saturated fats of youth. </p>
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<p>Birds'
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mitochondrial fats are much less polyunsaturated than those of mammals,
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and birds' metabolic rates are much higher, and they live much longer
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than mammals of a similar size.</p>
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<p>With
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aging, the highly peroxidizable fatty acids, arachidonic and docosahexaenoic
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acid, increase greatly in a variety of tissues, and lipid peroxidation
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increases with aging. Peroxidation slows mitochondrial respiration,
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lowering the metabolic rate. Caloric restriction slows the accumulation
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of the highly unsaturated fatty acids in mitochondria, and reduces peroxidation.</p>
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<p>Over
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the years, it has become evident that the polyunsaturated fats are not
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very compatible with a high rate of metabolism, though they are necessary
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for organisms that live at low temperatures and metabolize slowly, such
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as fish and vegetables. The saturated fats solidify at low temperature<strong>; </strong>
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beef fat is very stiff at refrigerator temperature, and in a fat fish,
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such stiffness would be lethal. </p>
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<p>Even
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some hibernating rodents can stay alive with their body tissues close
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to the freezing point, and their stored fats have to be unsaturated.
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When their diet doesn't allow them to store enough polyunsaturated fat,
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they fail to go into hibernation. This is probably a clue to some of
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the general biological effects of the PUFA.</p>
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<p>A
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series of studies about 20 years ago showed that the functions of the
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thyroid hormone are all inhibited by unsaturated fats, with the inhibition
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increasing in proportion to the number of unsaturations (double bonds)
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in the fat molecule.</p>
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<p>When
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the tissues are saturated with those antithyroid fats, metabolism slows,
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especially when any stress, such as cold or hunger, increases the concentration
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of free fatty acids in the blood stream. Stress and hypothyroidism increase
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the formation of serotonin, which is an important factor in producing
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the torpor of hibernation, and lowering the body temperature. The polyunsaturated
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fatty acids themselves directly contribute to the formation of serotonin,
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for example by increasing the ability of tryptophan to enter the brain.
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In a certain cold climate, the PUFA are essential for hibernation, but
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under other conditions, the rodent would be able to continue gathering
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food and eating, instead of hibernating.</p>
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<p>The
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direct effects of the PUFA on the endocrine and nervous systems, as
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illustrated by the hibernating squirrel, interact with their effects
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on intercellular communication (including the formation of prostaglandins
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and related substances), and the effects of their oxidative breakdown
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products, such as acrolein. But the people who claim that they are absolutely,
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rather than conditionally, essential, base their argument on the idea
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that they are needed for the formation of prostaglandins and cell membranes.
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The fact that cells can replicate in fat free conditions shows that
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the argument from membranes is unfounded. The argument from prostaglandins
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is more complex, but has no firmer foundation. </p>
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<p>When
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a dose of PUFA is administered to a lizard, which isn't a hibernator,
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the lizard's body temperature is lowered by several degrees. There are
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probably many ways in which the PUFA produce that effect, besides increasing
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serotonin and decreasing thyroid. The PUFA are increased by estrogen,
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and they increase estrogen, and have some directly estrogen-like effects.
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Estrogen itself tends to lower body temperature and shift metabolism
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away from oxidative energy production. Aging, like estrogen, increases
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the body's content of the PUFA<strong>:</strong> Linoleic, linolenic, dihomo-gamma-linolenic,
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docosahexaenoic and docosapentaenoic acids are increased by age, and
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the longer chain acids increase more rapidly in women than in men (Bolton-Smith,
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et al., 1997). (Women are apparently relatively protected by progesterone,
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which inhibits lipolysis and prostaglandin formation, and protects the
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brain, thymus, and other tissues from lipid peroxidation and other effects
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of the PUFA.)</p>
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<p>Aging
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involves a decreasing metabolic rate, an increased tendency toward inflammation,
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and a decreased ability to synthesize proteins. Inflammation contributes
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to the decreasing ability to use oxygen, and the slowed renewal of proteins
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combined with lower ability to produce energy impair the organism's
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ability to control peroxidative damage and inflammation. </p>
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<p>The
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fragments of deteriorating PUFA combine with proteins and other cell
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materials, producing immunogenic substances. The so-called "advanced
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glycation end products," that have been blamed on glucose excess,
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are mostly derived from the peroxidation of the "essential fatty
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acids." The name, “glycation,” indicates the addition of sugar
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groups to proteins, such as occurs in diabetes and old age, but when
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tested in a controlled experiment, <strong>lipid peroxidation of polyunsaturated
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fatty acids produces the protein damage about 23 times faster than the
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simple sugars do</strong> (Fu, et al., 1996). </p>
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<p>Several
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autoimmune disease models in animals (involving the eye, kidney, and
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pancreas) have been prevented by a deficiency of the EFA (Schreiner,
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et al., 1989, Bazan, et al., 1990, Benhamou, et al., 1995).</p>
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<p>Besides
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causing a general slowing of metabolism, aging and toxic PUFA have specific
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actions on the detoxifying system. The enzymes that help to detoxify
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PUFA and estrogen and serotonin are inhibited by both PUFA and estrogen.
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All systems, including blood vessels and the intestine, are made leaky
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by estrogen and the PUFA and their products.<strong> </strong>A reduced ability to regulate the excitatory
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amino acids, resulting from PUFA toxins, tends to produce excitotoxicity,
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damaging nerves (Ou, et al., 2002).</p>
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<p>Although
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the interplay of the various types of nerve is very complex, a variety
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of experiments suggest that the PUFA are acting directly on serotonergic
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nerves, rather than just increasing the conversion of tryptophan to
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serotonin.</p>
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<p>For
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example, a deficiency of the so-called essential fatty acids, EFA, makes
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animals more sensitive to some anesthetics, and more resistant to others.
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It makes them resistant to the anesthetics that act by promoting the
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actions of serotonin, but it prolongs the effects of those that don't
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act through serotonin, and these are the anesthetics such as xenon and
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nitrous oxide, that apparently act by stabilizing the structure of water,
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as described by Linus Pauling. Progesterone and the saturated fats seem
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to act partly through the stabilizing of cell water, and estrogen and
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the PUFA have opposing effects, creating cellular excitation while interfering
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with the stable cellular water structure.</p>
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<p>Serotonin
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interferes with slow wave sleep, and promotes cortisol, both of which
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can be harmful to brain cells. (Hypothyroidism is one of the causes
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of a decrease in slow wave sleep.) Babies whose mothers' serum contained
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more DHA were more wakeful on their second day of life, than the babies
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of low-DHA mothers. The amide of oleic acid is a sleep promoter, with
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apparent antiserotonin activity (Yang, et al., 2003), and since oleic
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acid tends to be displaced by diets high in PUFA, this suggests another
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way in which the highly unsaturated fatty acids could promote serotonin's
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effects.</p>
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<p>People
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who don't have a normal amount of slow wave sleep are likely to have
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slow reaction times when they are awake, and quickness of reactions
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is a good indicator of general intelligence.</p>
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<p>Manufacturers
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of baby formulas are claiming that the highly unsaturated fatty acids
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accelerate brain development, but they neglect to mention studies that
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show either no effect, or retardation of development. In some of the
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tests that are used to measure infant development, a generalized state
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of arousal or anxiety could be interpreted as "more mature." </p>
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<p>In
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one experiment, animals that received less than 0.32% of their calories
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as EFA grew slightly less than rats on a standard diet, but their brains
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were as large as those of normal rats (Bruckner, et al., 1984). That
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is, their brain to body ratio was a little larger than normal, which
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is a typical feature of individuals with a higher metabolic rate. That
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result is very different from the claims of the baby food industry,
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that the brain is the organ most easily damaged by a PUFA deficiency.</p>
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<p>One
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of the standard signs of toxicity is the enlargement of the spleen and
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liver, and that effect is produced by larger amounts of the EFA. The
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weight of the thymus is reduced by PUFA in the diet (Guimarães, et
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al., 1990). Thymus cells tend to be easily killed by a combination of
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stress and EFA, and bone marrow cells, though less sensitive than thymic
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cells, are damaged by lipid peroxidation of the PUFA. The effects of
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PUFA on the thymus were compared to those of radiation by Soviet researchers.
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Immunodeficiency, produced largely by damage to thymic cells, increases
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when larger amounts of PUFA are eaten for a prolonged time.</p>
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<p>The
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growth and metastasis of a variety of tumors are inhibited by saturated
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fatty acids, and increased by fish oil--as much as 10 times in number
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of metastases, 1000 times in size (Griffini, et al., 1998).</p>
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<p>Mothers
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whose breast milk contains more long-chain n-3 fatty acids are more
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likely to have allergic children (Stoney, et al., 2004). (And children
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whose mothers are allergic have higher levels of DHA and EPA in their
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tissues.) These associations aren't mentioned by the manufacturers who
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speak of those fats as essential.</p>
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<p>When
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animals have been "deprived" of the EFA during gestation and
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nursing, and then given a standard diet, they develop larger bones,
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with a thicker cortex and more trabecular bone, both of which would
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suggest a lower level of stress. Many types of inflammation and stress
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are significantly reduced in "EFA deficient" animals. Inflammation
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caused by the injection of carrageenan is decreased, partly because
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of the absence of prostaglandins in these animals. The absence of the
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EFA protects against colitis and nephritis ( ). The kidneys are more
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effective in several ways in the deficient animals.</p>
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<p>Shock,
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caused by the injection of endotoxin, which is 100% lethal to normally
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fed animals, is only 24% lethal to the deficient animals.</p>
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<p>Poisons
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are much less harmful to deficient animals, for example, a cobra venom
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factor causes less tissue damage to their lungs.</p>
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<p>Concussive
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trauma and burns cause much less damage to deficient animals.</p>
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<p>The
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endothelial lining of blood vessels is protected by saturated fats and
|
|
oleic acid, damaged by polyunsaturated, and their barrier function is
|
|
improved by the absence of PUFA.</p>
|
|
<p>Alzheimer's
|
|
disease, retinal degeneration, cataracts, and liver cirrhosis all involve
|
|
reactions of oxidized PUFA with proteins. Saturated fats help to heal
|
|
alcoholic liver cirrhosis. </p>
|
|
<p>The
|
|
lesions of atherosclerosis and cataracts contain some of the same oxidized
|
|
lipids as the age pigment itself. When large deposits of age pigment
|
|
become visible, it's probably because the general reduction of metabolism
|
|
and protein synthesis has interfered with the normal processes for removing
|
|
debris. The age pigment contributes to degeneration by wasting energy
|
|
and oxygen, weakening the antioxidation, antiglycation, and other defensive
|
|
systems.</p>
|
|
<p>The
|
|
EFA amplify nearly all kinds of injury and stress, and the results of
|
|
many recent publications make it look as though serotonin interacts
|
|
harmfully with the EFA in most of these situations. The specific balance
|
|
of polyunsaturated fatty acids, and their various breakdown products,
|
|
from carbon monoxide, glyoxal, and acrolein, to the larger aldehydes
|
|
and radicals, and the stress-induced substances such as serotonin, histamine,
|
|
estrogens, can produce an immense variety of biological problems.</p>
|
|
<p>When
|
|
the various claims of an EFA "deficiency disease" or syndrome
|
|
or symptom are examined, their inconsistency over the years makes skepticism
|
|
seem increasingly justified. The Burrs' publications were typical of
|
|
others, in failing to describe and account for the evidence that contradicted
|
|
their claims. 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.</p>
|
|
<p>In
|
|
this culture that repeatedly makes such claims of essentiality, the
|
|
growing number of reports of biological superiority of "deficient"
|
|
animals suggests that nutritional research may be near the point at
|
|
which it can resume the line of study begun by Northrup, Osborne, Mendel,
|
|
Drummond, Bernstein, Elias, and others, that was interrupted for 60
|
|
years by industrial interests that promoted antiscientific opinions.</p>
|
|
<p>For
|
|
example, in 1914 F.P. Rous showed that limiting food intake reduced
|
|
the incidence of cancer, and then in 1915 and 1917, Osborne and Mendel
|
|
showed that food restriction extended the fertility and longevity of
|
|
female rats. The association between estrogen and cancer had become
|
|
known during this time, and vitamin E, which was originally known as
|
|
the fertility vitamin, was soon recognized to have antiestrogenic properties,
|
|
as well as to prevent the deadly effects of excessive polyunsaturated
|
|
fats in the diet. My endocrinology professor, A.S. Soderwall, who had
|
|
found that excess estrogen prevented (or interrupted) pregnancy, demonstrated
|
|
that increased vitamin E extended fertility in aging female rodents.</p>
|
|
<p>By
|
|
the time I began my research, it seemed clear that it had been the reduction
|
|
of PUFA in the diet which, like the addition of vitamin E, had prevented
|
|
sterility in the calorie restriction experiments, and that those treatments
|
|
had limited the effects of estrogen in the aging organisms.</p>
|
|
<p>Estrogen,
|
|
by activating phospholipase A2, acts to amplify the toxic effects of
|
|
PUFA in the tissues, and these effects increase with age, and with decreased
|
|
amounts of thyroid and progesterone. </p>
|
|
<p>Antioxidants
|
|
can slightly retard the cumulative degenerative effects of the fats
|
|
interacting with estrogen, serotonin, and other mediators of inflammation,
|
|
but real elimination of the degenerative diseases will require an exploration
|
|
of the effects of the entire series of lipid signalling substances derived
|
|
from the saturated and omega minus 9 fatty acids.
|
|
</p>
|
|
<h2>References</h2>
|
|
<small>
|
|
<p>J
|
|
Nutr. 2000 Nov;130(11):2855-65. <strong>Low arachidonic acid rather than
|
|
alpha-tocopherol is responsible for the delayed postnatal development
|
|
in offspring of rats fed fish oil instead of olive oil during pregnancy
|
|
and lactation.</strong> Amusquivar E, Ruperez FJ, Barbas C, Herrera E.</p>
|
|
<p>Dev.
|
|
Psychobiol. 8(1), 59-66, 1985. <strong>"Effects of a commercial soy
|
|
lecithin preparation on development of sensorimotor behavior and brain
|
|
biochemicals in the rat,"</strong> Bell, J. M. and P. K. Lundberg.</p>
|
|
<p>Zeitschr.
|
|
Krebsforsh. 28(1), 1-14, 1927<strong> "Lipoids and carcinoma growth,".</strong>
|
|
Bernstein, S. and Elias, H.</p>
|
|
<p>J.
|
|
Biol. Chem. 82:345-367.(1929) <strong>A new deficiency disease produced by
|
|
the rigid exclusion of fat from the diet.</strong> Burr, G. & Burr, M.</p>
|
|
<p>J.
|
|
Biol. Chem. 86:587-621. (1930)<strong> On the nature and role of the fatty
|
|
acids essential in nutrition. </strong>Burr, G. & Burr, M.</p>
|
|
<p>J
|
|
Natl Cancer Inst. 1984 Jul;73(1):185-91. <strong>Dietary lipid effects on
|
|
the growth, membrane composition, and prolactin-binding capacity of
|
|
rat mammary tumors.</strong> Cave WT Jr, Jurkowski JJ. "Our results
|
|
indicated that 1) when the polyunsaturated lipid component (corn oil)
|
|
of the diet exceeded 3%, it was the quantitative level of total lipid,
|
|
rather than the level of polyunsaturated lipid alone, that best correlated
|
|
with the observed reduction in tumor latent period; 2) when the polyunsaturated
|
|
lipid content of the diet fell below 3%, there was a decrease in tumor
|
|
incidence and an increase in the mean latent period...."</p>
|
|
<p>Lipids.
|
|
1997 Sep;32(9):979-88. <strong>Modulation of adjuvant-induced arthritis by
|
|
dietary arachidonic acid in essential fatty acid-deficient rats.</strong>
|
|
Chinn KS, Welsch DJ, Salsgiver WJ, Mehta A, Raz A, Obukowicz MG. "<strong>Controlled
|
|
feeding of linoleic acid (LA) or arachidonic acid (AA) to essential
|
|
fatty acid-deficient (EFAD) rats was used to define the relationship
|
|
between dietary AA and the inflammatory response evoked during adjuvant-induced
|
|
arthritis."</strong> <strong>"Compared to rats fed the standard laboratory
|
|
chow diet (Control), edema in the primary hind footpads was decreased
|
|
by 87% in EFAD, 71% in EFAD + 1x AA, 45% in EFAD + 10x AA, and 30% in
|
|
EFAD + 0.5x LA. The decrease in edema in the footpads of EFAD rats was
|
|
nearly identical to the decrease in edema in the footpads of Control
|
|
rats dosed with indomethacin.</strong>
|
|
Hind footpad edema correlated with the final AA plasma level and eicosanoid
|
|
levels extracted from hind footpad tissue, but not with neutrophil infiltration." </p>
|
|
<p>J
|
|
Nutr. 1996 Jun;126(6):1534-40. <strong>Dietary (n-9) eicosatrienoic acid
|
|
from a cultured fungus inhibits leukotriene B4 synthesis in rats and
|
|
the effect is modified by dietary linoleic acid.</strong> Cleland LG, Gibson
|
|
RA, Neumann MA, Hamazaki T, Akimoto K, James MJ.</p>
|
|
<p>J
|
|
Nutr. 1981 Nov;111(11):2039-43. <strong>Effects of dietary fatty acids on
|
|
delayed-type hypersensitivity in mice.</strong> Dewille JW, Fraker PJ, Romsos
|
|
DR. Effects of an essential fatty acid deficient (EFAD) [0% corn oil
|
|
(CO)] diet and a diet high in polyunsaturated fatty acids [PUFA (50%
|
|
CO)] on one aspect of in vivo T cell function [delayed-type hypersensitivity
|
|
(DTH)] were assessed. After a 70-day feeding trial, <strong>DTH was reduced
|
|
by 30% in mice fed the EFAD diet,</strong> but the response of mice fed the
|
|
high PUFA diet equaled that of control mice fed a diet containing 13%
|
|
CO<strong>. The time required for the EFAD diet to reduce DTH was 42 days.
|
|
Although consumption of the EFAD diet reduced DTH,</strong> this reduction
|
|
was rapidly reversed, within 7 days, by switching the EFAD mice to the
|
|
control diet. These results indicate that :1) consumption of the EFAD
|
|
diet reduces one aspect of in vivo T cell function (DTH), but the effect
|
|
can be reversed by refeeding the control diet; and 2) a high PUFA diet
|
|
does not adversely affect DTH.</p>
|
|
<p>Biochem.
|
|
J., 1917, xi, 325. <strong>A comparative study of tumour and normal tissue
|
|
growth.</strong> Drummond, JC</p>
|
|
<p>J.
|
|
Physiol. 1920, liv, p. xxx, Proc. Physiol. Soc. <strong>Nutrition on
|
|
diets practically devoid of fats.</strong> Drummond, JC.</p>
|
|
<p>J.
|
|
Gerontol. 30(6), 647-54, 1975, <strong>"Rat brain fatty acid composition:
|
|
effect of dietary fat and age,"</strong> Eddy, D. E., and D. Harman.</p>
|
|
<p>J
|
|
Biol Chem 1996 Apr 26;271(17):9982-6. <strong>The advanced glycation
|
|
end product, Nepsilon-(carboxymethyl)lysine, is a product of both lipid
|
|
peroxidation and glycoxidation reactions.</strong> Fu MX, Requena JR, Jenkins
|
|
AJ, Lyons TJ, Baynes JW, Thorpe SR.</p>
|
|
<p>Pediatrics
|
|
31:171-192, 1963. Hansen AE, Wiese HF, Boelsche AN, Haggard ME, Adam
|
|
DJD, Davis H.</p>
|
|
<p>Am
|
|
J Clin Nutr 49:290-300, 1982. Holman RT, Johnson SB, Hatch TF.</p>
|
|
<p>Cancer
|
|
Res. 45(5), 1997-2001, 1985. <strong>"Requirement of essential fatty
|
|
acids for mammary tumor," </strong>
|
|
Ip, C., et al.</p>
|
|
<p>Food
|
|
and Nutrition Board. 1989. <strong><em>Recommended Dietary Allowances</em></strong>
|
|
10th ed. Washington, DC: National Academy of Sciences. p 48.</p>
|
|
<p>Am
|
|
J Clin Nutr. 2004 Nov;80(5):1167-74. <strong>Docosahexaenoic acid concentrations
|
|
are higher in women than in men because of estrogenic effects.</strong> Giltay
|
|
EJ, Gooren LJ, Toorians AW, Katan MB, Zock PL. "The proportion
|
|
of <strong>DHA</strong> was 15 +/- 4% (x +/- SEM; P < 0.0005) higher in the
|
|
women than in the men. <strong>Among the women, those taking oral contraceptives
|
|
had 10 +/- 4% (P = 0.08) higher DHA concentrations than did those not
|
|
taking oral contraceptives. Administration of oral ethinyl estradiol,
|
|
but not transdermal 17beta-estradiol, increased DHA by 42 +/- 8% (P
|
|
< 0.0005), whereas the</strong> antiandrogen cyproterone acetate did not
|
|
affect <strong>DHA</strong>. Parenteral testosterone decreased <strong>DHA</strong> by 22
|
|
+/- 4% (P < 0.0005) in female-to-male transsexual subjects. Anastrozole
|
|
decreased estradiol concentrations significantly and <strong>DHA</strong> concentrations
|
|
nonsignificantly (9 +/- 6%; P = 0.09). <strong>CONCLUSION: Estrogens cause
|
|
higher DHA concentrations in women than in men, probably by upregulating
|
|
synthesis of DHA from vegetable precursors.</strong>"</p>
|
|
<p>J.
|
|
American Geriatrics Soc. 24(1) 292-8, 1976<strong>, "Free radical theory
|
|
of aging: effect of dietary fat on central nervous system function,"</strong>
|
|
Harman, D., et al. </p>
|
|
<p>Adv
|
|
Exp Med Biol 266:3-15, 1989, <strong>"Lipofuscin and ceroid formation:
|
|
the cellular recycling system,"</strong> Harman, D.</p>
|
|
<p>J
|
|
Theor Biol. 2005 May 21;234(2):277-88. Epub 2005 Jan 24. <strong>On the importance
|
|
of fatty acid composition of membranes for aging.</strong> Hulbert AJ.</p>
|
|
<p>Biochim
|
|
Biophys Acta. 2005 Jan 5;1686 3:248-54. <strong>Perinatal essential fatty
|
|
acid deficiency influences body weight and bone parameters in adult
|
|
male rats.</strong> Korotkova M, Ohlsson C, Gabrielsson B, Hanson LA, Strandvik
|
|
B. Department of Pediatrics, Goteborg University, The Queen Silvia Children's
|
|
Hospital, SE 41685 Goteborg, Sweden. <a href="mailto:Marina.Korotkova@cmm.ki.se" target="_blank">Marina.Korotkova@cmm.ki.se</a> Fetal
|
|
and postnatal nutrition have long-term effects on the risk for development
|
|
of diseases late in life in humans and animals. The aim of the present
|
|
study was to investigate the effect of dietary deficiency of essential
|
|
fatty acids (EFA) in the perinatal period on later body weight and bone
|
|
mass. <strong>During late gestation
|
|
and throughout lactation, </strong>rats were fed a control or an EFA-deficient
|
|
(EFAD) diet. At 3 weeks of age the offspring were weaned onto an ordinary
|
|
chow and followed until adult age. The mean body weight of adult rats
|
|
receiving the EFAD diet during the perinatal period was significantly
|
|
increased from 12 weeks of age compared to the controls (P<0.05).
|
|
Analysis by peripheral quantitative computerized tomography (pQCT) at
|
|
44 weeks of age showed that the trabecular volumetric bone mineral density
|
|
(BMD) of the femur was significantly decreased (P<0.05<strong>) but the
|
|
cortical bone mineral content, cortical area, and cortical thickness
|
|
were increased</strong> (P<0.05) in the EFAD group of rats. The length
|
|
of the femur was not affected. <strong>In conclusion, neonatal EFA deficiency
|
|
was in adult rats associated with increased body weight and significant
|
|
changes in both cortical and trabecular bone. The results indicate that
|
|
regulatory mechanisms related to bone mass seemed to be programmed by
|
|
EFA</strong> in the perinatal period. The nature of this modulation needs
|
|
to be identified.</p>
|
|
<p>Biochem
|
|
Biophys Res Commun. 1987 Jun 30;145(3):1185-91. <strong>Anti-lipoperoxidation
|
|
action of food restriction.</strong> Laganiere S, Yu BP. "Chronic food
|
|
restriction inhibited the age-related increase of malondialdehyde production
|
|
and lipid hydroperoxides in liver mitochondrial and microsomal membranes
|
|
of ad libitum fed Fischer 344 rats. The anti-lipoperoxidation action
|
|
of food restriction could not be attributable to the changes in membrane
|
|
lipid content nor vitamin E status. <strong>Restricting calories modified
|
|
membrane fatty acid composition by increasing linoleic acid and decreasing
|
|
docosapentaenoic acid</strong> content in both membranes." </p>
|
|
<p>Lipids
|
|
22(3), 133-6, 1987<strong>.. "Effects of parenteral nutrition with high
|
|
doses of linoleate on the developing human liver and brain,"</strong>
|
|
Martinez, M., and A. Ballabriga.</p>
|
|
<p><u>J
|
|
Nutrit</u> <strong>10</strong>:63(1935). <strong>"The effect of retarded growth
|
|
upon length of the life span and upon the ultimate body size."</strong>
|
|
McCay, CM., Crowell, MF., and Maynard, LA.</p>
|
|
<p>McCollum
|
|
EV. 1957. <strong><em>A History of Nutrition.</em></strong> Boston: Houghton Mifflin.
|
|
p 374.</p>
|
|
<p>J
|
|
Clin Invest 73:272-276,1984. Neuringer M, Connor WE, Van Petten C, Barstad
|
|
L.</p>
|
|
<p>J.
|
|
Biol. Chem., 1912, xii, 81.<strong> Feeding experiments with fat-free food
|
|
mixtures.</strong> Osborne, TB., Mendel, LB. </p>
|
|
<p>Science
|
|
45:294-295. (1917). <strong>"The effect of retardation of growth upon
|
|
the breeding period and duration of life in rats." </strong>
|
|
Osborne, TB., Mendel, LB., and Fey, EL.</p>
|
|
<p>Gerontology
|
|
1993;39(1):7-18. <strong>Modulation of membrane phospholipid fatty acid composition
|
|
by age and food restriction.</strong> Laganiere S, Yu BP. H.M. “Phospholipids
|
|
from liver mitochondrial and microsomal membrane preparations were analyzed
|
|
to further assess the effects of age and lifelong calorie restriction
|
|
on membrane lipid composition.” <strong>“The data revealed characteristic
|
|
patterns of age-related changes in ad libitum (AL) fed rats:</strong> <strong>
|
|
membrane levels of long-chain polyunsaturated fatty acids, 22:4 and
|
|
22:5, increased progressively, while membrane linoleic acid (18:2) decreased
|
|
steadily with age. Levels of 18:2 fell by approximately 40%, and 22:5
|
|
content almost doubled making the peroxidizability index increase with
|
|
age.</strong>” “<strong>We concluded that the membrane-stabilizing action
|
|
of long-term calorie restriction relates to the selective modification
|
|
of membrane long-chain polyunsaturated fatty acids during aging.</strong>”</p>
|
|
<p>Free
|
|
Radic Biol Med 1999 Feb;26(3-4):260-5. <strong>Modulation of cardiac
|
|
mitochondrial membrane fluidity by age and calorie intake.</strong> Lee J,
|
|
Yu BP, Herlihy JT. “The fatty acid composition of the mitochondrial
|
|
membranes of the two<strong> ad lib fed groups differed: the long-chain polyunsaturated
|
|
22:4 fatty acid was higher in the older group, although linoleic acid
|
|
(18:2) was lower. DR eliminated the differences.”</strong> “Considered
|
|
together, these results suggest that DR maintains the integrity of the
|
|
cardiac mitochondrial membrane fluidity by<strong> minimizing membrane damage
|
|
through modulation of membrane fatty acid profile.”</strong></p>
|
|
<p>
|
|
Lipids 2001 Jun;36(6):589-93. <strong>Effect of dietary restriction
|
|
on age-related increase of liver susceptibility to peroxidation in rats.</strong> Leon TI, Lim BO, Yu BP, Lim Y, Jeon
|
|
EJ, Park DK.</p>
|
|
<p>
|
|
Neurobiol Aging. 1982 Fall;3(3):173-8. <strong>Lipid peroxides in brain during
|
|
aging and vitamin E deficiency: possible relations to changes in neurotransmitter
|
|
indices.</strong> Noda Y, McGeer PL, McGeer EG.<strong> "Lipid peroxide levels,
|
|
were found to be significantly higher in brains of 18 month old as compared
|
|
to 4 month old rats, with particularly large increases</strong> occurring
|
|
in the olfactory bulb, globus pallidus, cerebral cortex and caudate-putamen
|
|
(CP). Eighteen month old rats fed a<strong> vitamin E deficient diet for
|
|
9 months before sacrifice had lipid peroxide levels significantly higher
|
|
than age-matched controls in the cerebral cortex,</strong> hippocampus and
|
|
hypothalamus." "Age-related decreases were seen in choline
|
|
acetyltransferase, acetylcholinesterase and 3H-QNB binding in some but
|
|
not all brain regions, while GABA transaminase and MAO showed age-related
|
|
increases." "As compared with controls, vitamin E deficient
|
|
rats showed decreases of 38% in cortical 3H-DHA binding, of 33% in 3H-QNB
|
|
binding in the CP and of 23% and 12% in choline acetyltransferase in
|
|
the CP and cerebellum, respectively." </p>
|
|
<p>J
|
|
Immunol, 1989 Nov 15, 143:10, 3192-9. <strong>The antiinflammatory effects
|
|
of essential fatty acid deficiency in experimental glomerulonephritis.
|
|
The modulation of macrophage migration and eicosanoid metabolism.</strong>
|
|
Schreiner GF, Rovin B, Lefkowith JB.</p>
|
|
<p>Br
|
|
J Nutr. 2003 Aug;90(2):385-94. <strong>Dietary docosahexaenoic acid-induced
|
|
production of tissue lipid peroxides is not suppressed by higher intake
|
|
of ascorbic acid in genetically scorbutic Osteogenic</strong> <strong>Disorder
|
|
Shionogi/Shi-od/od rats. </strong>Sekine S, Kubo K, Tadokoro T, Maekawa A,
|
|
Saito M.</p>
|
|
<p>Cancer
|
|
Res. 2004 Sep 15;64(18):6482-8. <strong>Estrogen enhances angiogenesis through
|
|
a pathway involving platelet-activating factor-mediated nuclear factor-kappaB
|
|
activation.</strong> Seo KH, Lee HS, Jung B, Ko HM, Choi JH, Park SJ, Choi
|
|
IH, Lee HK, Im SY.</p>
|
|
<p>Clin
|
|
Exp Allergy. 2004 Feb;34(2):194-200. <strong>Maternal breast milk long-chain
|
|
n-3 fatty acids are associated with increased risk of atopy in breastfed
|
|
infants.</strong> Stoney RM, Woods RK, Hosking CS, Hill DJ, Abramson MJ,
|
|
Thien FC.</p>
|
|
<p>Proc
|
|
Natl Acad Sci U S A. 1988 Aug;85(16):6137-41. <strong>Essential fatty acid
|
|
deficiency prevents multiple low-dose streptozotocin-induced diabetes
|
|
in CD-1 mice.</strong> Wright JR Jr, Lefkowith JB, Schreiner G, Lacy PE.</p>
|
|
<p>Mech
|
|
Ageing Dev. 2005 May 10; [Epub ahead of print] <strong>Membrane alteration
|
|
as a basis of aging and the protective effects of calorie restriction.</strong>
|
|
Yu BP. </p>
|
|
<p>Acta
|
|
Paediatr 1996 Jun;85(6):679-83. <strong>Phospholipid fatty acids in cord
|
|
blood: family history and development of allergy.</strong> Yu G, Kjellman
|
|
NI, Bjorksten B.</p>
|
|
<p>Fiziol
|
|
Cheloveka. 2005 Mar-Apr;31(2):108-15. <strong>[Age-related changes in lipid
|
|
peroxidation in various regions of the central nervous system]</strong> [Article
|
|
in Russian] Volchegorskii IA, Shemiakov SE, Telesheva IB, Malinovskaia
|
|
NV, Turygin VV.</p>
|
|
<p>Surg
|
|
Today. 2003;33(8):600-5. <strong>Beneficial effects of n-9 eicosatrienoic
|
|
acid on experimental bowel lesions.</strong> Yoshida H, Soh H, Sando K, Wasa
|
|
M, Takagi Y, Okada A. PURPOSE: Dietary fortification of n-9 polyunsaturated
|
|
fatty acids (PUFA) or 5,8,11-eicosatrienoic acid (ETrA) as well as n-3
|
|
PUFA might contribute to the suppression of leukotriene B4 (LTB4) synthesis
|
|
and thereby reduce inflammatory bowel lesions. As a result, the effect
|
|
of an ETrA-enriched diet on experimental bowel lesions was examined
|
|
in this study. METHODS: In Expt. 1, rats were freely fed either an ETrA-enriched
|
|
or a standard diet. After 7 days of feeding, acute bowel lesions were
|
|
induced by the subcutaneous injection of 10 mg/kg indomethacin. In Expt.
|
|
2, chronic bowel lesions were made by performing subcutaneous injections
|
|
of 7.5 mg/kg indomethacin twice. After the first injection, the rats
|
|
were freely fed either an ETrA-enriched or a standard diet for 7 days.
|
|
RESULTS: In both experiments, the rats fed an ETrA-enriched diet showed
|
|
increased levels of ETrA in the plasma and intestinal mucosa, and a
|
|
decreased inflammation score. However, there was no significant decrease
|
|
in plasma and intestinal mucosal LTB4 in the ETrA-enriched diet-fed
|
|
rats. CONCLUSION: These results suggest that the dietary supplementation
|
|
of ETrA may have both prophylactic and therapeutic effects on experimentally
|
|
produced bowel lesions. Further investigations are necessary to clarify
|
|
the effects of ETrA on bowel lesions and its mechanisms.
|
|
</p>
|
|
</small>
|
|
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</html>
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