With increasing estrogens and its mimetics now everywhere in our society, one is not told about how to protect against it and its imitators. The most important factors to protect against estrogen in its various forms also turn out to protect:

Against shock,

Stress,

Ionizing radiation,

Free radicals,

Lipid peroxidation,

Arthritis,

Osteoporosis,

Atrophy of the Thymus,

Cells killing themselves (apoptosis) and,

Scleroderma.

All these, along with estrogen are involved in Degeneration of Tissue and Aging!

The following items, gentlemen, must be included in what you store for the very bad times just around the corner, and you should be on them now, regardless of what your tests show in terms of Thyroid Hormone, which, as you now know, are highly inaccurate!

Be on these NOW!

• Niacinamide (capsules or tablets above and beyond a multivitamin tablet),
• Progesterone (as a rub-on cream),
• Carbon dioxide, get the Bicarb tablets we have recommended,
• Thyroid Hormone (T₃), and...
• Red Light

What these things do are to protect against Prostaglandins—recall what we said about this recently, and Free Fatty Acids—Prostaglandins are made from PUFAs, polyunsaturated fatty acids.

More on Unsaturated Fats!

You learned why these oils, in the last lecture or two, are considered 'Toxic.' However, what is making them even more toxic is not the quantity of PUFAs one ingests; it is the ratio between them and Saturated Fat, which most in various countries have been taught to demonize and avoid. When we consider free radical production, age pigment formation, obesity, inflammation, blood clotting, energy production and immunity—which incidently, unsaturated fats, such as the Omegas, PEOs, etc., slow down and dam up the immune system, are given to AIDs patients to stop the immune system from overcoming them.

Can you imagine what is going to happen in a few short months or years as God's Smallest Creatures are and have been on the rise, with new diseases and no new drugs have been forthcoming (antibiotics) to destroy them, as our immune systems are stymied (or under attack) by eating all the PUFAs...the polyunsaturated fats?

All these situations man is heir to, and will increase, as just given (inflammation, obesity, free radical production, etc.,) respond to the ratio of PUFAs to Saturated Fats, and as the ratio goes higher, the probability of harm rises in the body. Hence, an important reason to eat real butter and Coconut Oil.

The relationship between these Toxic Oils and Estrogen. One example is that young girls are having periods earlier and earlier if estrogen is high in their diets from mimetics when the unsaturated oils are present in abundance in their diets, with Saturated Fat down in the child's diet!

Gentlemen! Are you beginning to get the idea how "The Killing Mechanism" is now in place for the biggest kill off the world has ever seen? Here, involved with the Kill–Off for all the 'Bio–Identical' hormones more and more women are opting for, look what is happening to the children of the world. And, this not only includes the feminine gender; it incorporates male children too.

See it this way for all humans: A 'system' in molecular biology is that which is under consideration at the moment of discussion. Hence, it is the body we are considering and thus, all body systems under the influence of the toxic oils are being damaged from three main attacks:

• Immune System Damage!

• Hormone Inequities!

• Oxidative Stress, which generates Reactive Oxygen Species!
   

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  Reactive Oxygen Species 

   

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  Superoxide Anion O2-	Produced by the electron transport chain and at other sites. Generates other reactive oxygen species but cannot diffuse far from the site of origin.
  Hydrogen Peroxide H2O2	Not a free radical, but can generate free radicals by reaction with a transition metal (e.g., iron: Fe2+). Can diffuse into and through cell membranes.
  Hydroxyl Radical OH.	The most reactive species in attacking biological molecules. Produced by water in the presence of iron (Fe2+).
  Organic Radicals R.	An organic free radical produced from RH (Polyunsaturated Lipid) by OH. attack. RH can be the carbon of a double bond in a fatty acid (resulting in -C.=C-) or RSH (organic thiol) (resulting in R-S.)
  Organic Peroxide          Radical RCOO.	An organic peroxide radical, such as occurs during lipid degradation.
  Hypochlorous Acid HOCl	Produced in bacteria during the respiratory burst to destroy invading organisms.
  Singlet Oxygen O↑↓	Oxygen with antiparallel spins. Produced at high oxygen tensions from the absorption of energy. Decays with the release of light.

 

The unsaturated fats generate many changes in hormones! The most easily understood effect is what it does to the thyroid gland operation.

• The unsaturated fats inhibit the secretion of the thyroid gland.

• It blocks the thyroid hormone movement in the entire body's circulatory system. Even worse than this, if some were to get through,

• The unsaturated fats inhibit tissue response to the hormone;

Hence, this is why I see so many clients 'beat down'; yet, their TSH is normal. The biofeedback mechanism is hindered.

So, one's physician, not knowing this, simply says, "Your TSH is normal; it's in your head"; or, "You have something else. Get out and exercise more."

Then, comes the 'Big Rub'! Keeping in mind all that we have been discussing, since the Thyroid Hormone is deficient, one's body is more often than not exposed to increasing/increased levels of the so–called, female hormone, estrogen. And, with thyroid hormone down and barely being used, and the patient feeling tired, no energy, lethargy, having memory problems, high cholesterol, then he is not using his cholesterol efficiently; nor is the patient making the hormones, progesterone and the mother of all hormones, pregnenolone, when thyroid hormone is low!

One is then set–up for 'The Killing Mechanism' coming! When thyroid hormone is present in sufficient amount, it, as just given, causes the body to use cholesterol and eliminate cholesterol. Therefore, anything that inhibits Thyroid Hormone probably causes cholesterol to be raised, as when something blocks this hormone from being secreted by the thyroid gland and from being used in the tissues!

Beware of This!

I am seeing the following research quoted quite often in some new books and Life Extension Companies for proof as to why one should increase their PEOs, Omegas, unsaturated oils such as Flax, Borage, etc.

The reference is to Dr. George Burr and Mildred Burr. From what I am reading, the publications are usings the references from quoted references from other quoted references referring to the Burr's! Here's the problem: Evidently they have not gone and looked at the the time surrounding this work the Burr's did in 1929. I will give it here.

Again, something is happening in our ability to read, grasp, understand, and reason. The norm is, 'If its in a research journal; or some other publication, the reference must be without fault.'

What The Burr's Research Showed!

George and Mildred Burr published a paper, in 1929, on their research in which they claimed that unsaturated fats, primarily linoleic acid, an Omega–6, are necessary to stop a disease from occurring that caused dermatitis, slowed growth, kidney degeneration that was fatal, dandruff, and sterility. They claimed that these oils are 'Essential' to life!

At that time, during the 1920s, especially 1929, most of the essential trace minersals and most of the B vitamins were not known to nutritionists. What the Burrs claimed that was caused by lack of unsaturated oils in the diet, is easily caused by vitamin and mineral deficiencies, of which they had no knowledge what–so–ever!

What they observed in the animals of their lab, that were given no unsaturated fats in their diet was:

• Increased nutritional needs.

• An extremely high metabolic rate. But, at that time, the Burrs or anyone else, did not know that animals on such a died need more, an increased need, for minerals and vitamins; especially B6. What the PUFAs actually did was create a very slow metabolism in the animals! This effect is good for agriculture; the animals get fat, grow fast; gain fat weight; but, not muscle weight. And, they drink more water, adding to their weight! However, this effect is not good for you!

• Animals on this type of diet resist disease and sickness more easily. And, with added vitamins and minerals, fare much better.

• Animals on a low to no unsaturated fat diet, have less dementia, aging, autoimmune problems, and resists various type of inflammation. However, they have a high, as we are illustrating, metabolic rate, since the thyroid is running higher; adding proper vitamins and minerals, including B6, tames the problems the Burrs described from their observation of the lab animals.

When the Burrs listed other research, which there was not that much during this era regarding fats, they had to have seen, as they quoted several abstracts, from Biological Abstracts, from Germany, a German study done in 1927, showing that a diet free in fat just about eliminated cancers developing spontaneously in rats (Bernstein and Elias). The Burrs did, on later dates, cite a number of German journals, of several studies, but dismissed those that said opposite to their study!

Why they did this is anyone's guess! Scientific dishonesty, I can only assume! Since 1927, the so–called 'essential' fatty acids, have been shown to be essential for the development of cancer!

Reread this last part again until it is imprinted on your brain! Think of what is about to happen to the mankind with all the proffering and telling one to eat the PUFAs, when we go through the Radiations Coming, The Galactic Plane; The Prophesied Comet; The Roiling Sun; The Pole Shift!

 

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Dr. Roger Williams, who is a discoverer of one of the B vitamins and author of, 'Biochemical Individuality,' sometime in the 1940s, at his laboratory at the Clayton Foundation Biochemical Institute, at the University of Texas, produced the same results as the Burrs on laboratory animals, and discovered that the "Fat Deficiency Disease" of the Burrs animals was in actuality, a Vitamin B6 deficiency!

How–About–That!

And to this day, you are still paying for that failed oversight to investigate those animals' high rate of metabolic activity!

You Are Paying For It In Terms Of:

• Obesity!

• Immune Dysfunction When Disease Hits Hard!

• Tiredness and Sluggisness!

• Increased Susceptibility To Cancers. . . And More!

 The Williams animals also had a high rate of metabolism that were on a fat free diet in their cages. Yet, the Burrs made an inductive leap into the dark, and did not investigate their observation for its important ramifications . . . which should have been, an increased need for vitamins and minerals in relation to their extreme rate of metabolism.

  I wonder if the hyperactive child would fare better in learning and discipline and behavioral changes if given a good B–Complex, along with an excellent mineral tablet?

Two Very Sobering Thoughts:

From

The Two-Fold Chastisement:

Visions of the Coming Earth Changes

Pages 83-84

Many holy people, seers, and other instruments of God have referred in their prophecies to the vast numbers of dead that will cover the earth when the Chastisement is over. And…there will be no one to bury the bodies. Rose Colomba spoke of "large multitudes" of corpses.

Saint Gaspar du Bufalo, founder of the Precious Blood Fathers, and who died in 1837, said "The earth will be covered with cadavers. All survivors will therefore think they are alone."

Some References From Dr. "B" Compiled By Dr. Ray Peat, Endocrine Physiologist, Ph.D

REFERENCES (Fats and Degeneration)

Alcohol Clin Exp Res 1998 Feb;22(1):192-6. Increased circulating products of lipid peroxidation in patients with alcoholic liver disease. Aleynik SI, Leo MA, Aleynik MK, Lieber CS

Ann N Y Acad Sci. 1976;275:28-46. Metabolic influences in experimental thrombosis. Antoniades HN, Westmoreland N.

Nutr Cancer. 2001;41(1-2):91-7. Vaccenic acid feeding increases tissue levels of conjugated linoleic acid and suppresses development of premalignant lesions in rat mammary gland. Banni S, Angioni E, Murru E, Carta G, Melis MP, Bauman D, Dong Y, Ip C.

Obstet Gynecol. 1987 Sep;70(3 Pt 2):502-4. The treatment of retroperitoneal fibromatosis with medroxyprogesterone acetate. Barnhill D, Hoskins W, Burke T, Weiser E, Heller P, Park R. Wide excision is the recommended primary therapy for retroperitoneal fibromatosis. Radiation therapy and a variety of medications have been used to treat patients with recurrent tumors, but the response to these agents has not been uniform. The patient presented was successfully treated with medroxyprogesterone acetate for recurrent retroperitoneal fibromatosis that was refractory to multiple operative resections and radiation therapy.

Medicina (B Aires). 1978 Mar-Apr;38(2):215-6. [Fibromatosis, relaxin and progesterone] [in Spanish] Barousse AP. [Letter]

Medicina (B Aires). 1985;45(2):159-63. Progesterone as therapy for retroperitoneal fibrosis. Bilder CR, Barousse AP, Mazure PA.

Adv Exp Med Biol. 1976;75:497-503. Effect of ionizing radiation on liver microcirculation and oxygenation. Bicher HI, Dalrymple GV, Ashbrook D, Smith R, Harris D.

Lipids. 1981 May;16(5):323-7. Iodination of docosahexaenoic acid by lactoperoxidase and thyroid gland in vitro: formation of an lodolactone. Boeynaems JM, Watson JT, Oates JA, Hubbard WC. "In the presence of iodide, hydrogen peroxide and lactoperoxidase, docosahexaenoic acid (22:6 omega 3) was converted into iodinated compounds."

Am Rev Respir Dis 1989 Oct;140(4):1104-7. Leaky vessels, fibrin deposition, and fibrosis: a sequence of events common to solid tumors and to many other types of disease. Brown LF, Dvorak AM, Dvorak HF Medicina (B Aires). 1979 Sep-Oct;39(5):652-4. [Effect of progesterone in the treatment of a patient with idiopathic retroperitoneal fibrosis] [in Spanish] Casadei DH, Najun Zarazaga C, Leanza HJ, Schiappapietra JH.

Biochem Mol Biol Int 1993 Jan;29(1):175-83. Influence of antioxidant vitamins on fatty acid inhibition of lymphocyte proliferation. Calder PC, Newsholme EA. "Vitamin E (10 microM) increased human lymphocyte proliferation by 35%. However, vitamin E did not prevent the inhibitory effects of fatty acids upon lymphocyte proliferation. It is concluded that inhibition of lymphocyte proliferation by fatty acids is not caused by their conversion to peroxidised products."

Clin Sci (Lond). 1992 Jun;82(6):695-700. Polyunsaturated fatty acids suppress human peripheral blood lymphocyte proliferation and interleukin-2 production. Calder PC, Newsholme EA.

J Neurochem 1980 Oct;35(4):1004-7. Transient formation of superoxide radicals in polyunsaturated fatty acid-induced brain swelling. Chan PH, Fishman RA

Int J Cancer 2001 Mar 15;91(6):894-9. Tumor invasiveness and liver metastasis of colon cancer cells correlated with cyclooxygenase-2 (COX-2) expression and inhibited by a COX-2-selective inhibitor, etodolac. Chen WS, Wei SJ, Liu JM, Hsiao M, Kou-Lin J, Yang WK.

Free Radic Biol Med. 1999 Jul;27(1-2):51-9. Arachidonic acid interaction with the mitochondrial electron transport chain promotes reactive oxygen species generation. Cocco T, Di Paola M, Papa S, Lorusso M.

Clin Exp Metastasis 1997 Jul;15(4):410-7. Influence of lipid diets on the number of metastases and ganglioside content of H59 variant tumors. Coulombe J, Pelletier G, Tremblay P, Mercier G, Oth D.

BJU Int. 2003 Jun;91(9):830-8. Fibrin as an inducer of fibrosis in the tunica albuginea of the rat: a new animal model of Peyronie's disease. Davila HH, Ferrini MG, Rajfer J, Gonzalez-Cadavid NF.

Carcinogenesis 1994 Jul;15(7):1399-404. Peroxidation of linoleic, arachidonic and oleic acid in relation to the induction of oxidative DNA damage and cytogenetic effects. de Kok TM, ten Vaarwerk F, Zwingman I, van Maanen JM, Kleinjans JC.

Biochem Biophys Res Commun. 2000 Oct 14;277(1):128-33. Arachidonic acid causes cytochrome c release from heart mitochondria. Di Paola M, Cocco T, Lorusso M.

J Physiol. 1998 Mar 1;507 ( Pt 2):541-7. Arachidonic acid increases cerebral microvascular permeability by free radicals in single pial microvessels of the anaesthetized rat. Easton AS, Fraser PA.

Am J Physiol. 1992 May;262(5 Pt 1):E637-43. ATP depletion stimulates calcium-dependent protein breakdown in chick skeletal Muscle. Fagan JM, Wajnberg EF, Culbert L, Waxman L.

Cancer Res 1998 Aug 1;58(15):3312-9. Dietary omega-3 polyunsaturated fatty acids promote colon carcinoma metastasis in rat liver. Griffini P, Fehres O, Klieverik L, Vogels IM, Tigchelaar W, Smorenburg SM, Van Noorden CJ.

J Indian Med Assoc 1997 Mar;95(3):67-9, 83. Association of dietary ghee intake with coronary heart disease and risk factor prevalence in rural males. Gupta R, Prakash H

Transplantation 1995 Sep 27;60(6):570-7. The effect of dietary polyunsaturated fatty acids (PUFA) on acute rejection and cardiac allograft blood flow in rats. Haw MP, Linnebjerg H, Chavali SR, Forse RA. "The immunosuppressive effect of dietary PUFA warrants further investigation, and their use as a possible adjunctive treatment in organ transplantation should be considered."

Dtsch Med Wochenschr. 2003 Jun 20;128(25-26):1395-8. [Rare cause of chronic abdominal pain: retractile mesenteritis] [in German] Hermann F, Speich R, Schneemann M. "Retractile mesenteritis is a rare cause of chronic abdominal pain with variable symptoms. Its aetiology is unknown. In case of bowel ischemia a surgical approach is preferred, milder forms may be treated with immunosuppressive agents as well as oral progesterone. Progesterone has exhibited positive effects on fatty tissue with successful treatment in desmoid tumors and retroperitoneal fibrosis. Here in we could demonstrate its safe and efficient use in a patient with retractile mesenteritis."

Mech Ageing Dev 2001 Apr 15;122(4):427-43. Effect of the degree of fatty acid unsaturation of rat heart mitochondria on their rates of H2O2 production and lipid and protein oxidative damage. Herrero A, Portero-Otin M, Bellmunt MJ, Pamplona R, Barja G. "Previous comparative studies have shown that long-lived animals have lower fatty acid double bond content in their mitochondrial membranes than short-lived ones. In order to ascertain whether this trait protects mitochondria by decreasing lipid and protein oxidation and oxygen radical generation, the double bond content of rat heart mitochondrial membranes was manipulated by chronic feeding with semi-purified AIN-93G diets rich in highly unsaturated (UNSAT) or saturated (SAT) oils. UNSAT rat heart mitochondria had significantly higher double bond content and lipid peroxidation than SAT mitochondria. They also showed increased levels of the markers of protein oxidative damage malondialdehyde-lysine, protein carbonyls, and N(e)-(carboxymethyl)lysine adducts." "These results demonstrate that increasing the degree of fatty acid unsaturation of heart mitochondria increases oxidative damage to their lipids and proteins, and can also increase their rates of mitochondrial oxygen radical generation in situations in which the degree of reduction of Complex III is higher than normal. These observations strengthen the notion that the relatively low double bond content of the membranes of long-lived animals could have evolved to protect them from oxidative damage."

Biochem J. 1994 May 15;300 ( Pt 1):251-5. Regulation of fibrinolysis by non-esterified fatty acids. Higazi AA, Aziza R, Samara AA, Mayer M. "Examination of the fatty acid specificity showed that a minimal chain length of 16 carbon atoms and the presence of at least one double bond, preferably in a cis configuration, were required for inhibition of the fibrinolytic activity of plasmin."

Science. 1976 Feb 27;191(4229):861-2. Nicotinic acid reduction of plasma volume loss after thermal trauma. Hilton JG, Wells CH. Intravenous administration of nicotinic acid to the anesthetized dog prior to thermal trauma reduced plasma loss at 10 minutes after burn from 7 milliliters per kilogram to less than 2 millimeters per kilogram. During the next 50 minutes plasma loss was the same in treated and untreated animals. An additional dose of nicotinic acid 30 minutes after burn prevented this further loss.

Z Gesamte Inn Med. 1976 Oct 15;31(20):838-43. [Age-dependence of catecholamine effects in man. IV. Effects of specific inhibitors on the lipolytic action of alpha and beta adrenergics] [in German] Hoffmann H.

Neurochem Res. 2000 Feb;25(2):269-76. Cortical impact injury in rats promotes a rapid and sustained increase in polyunsaturated free fatty acids and diacylglycerols. Homayoun P, Parkins NE, Soblosky J, Carey ME, Rodriguez de Turco EB, Bazan NG. "At day one, free 22:6 and 22:6-DAGs showed the greatest increase (590% and 230%, respectively). These results suggest that TBI elicits the hydrolysis of phospholipids enriched in excitable membranes, targeting early on 20:4-phospholipids (by 30 min post- trauma) and followed 24 hours later by preferential hydrolysis of DHA-phospholipids. These lipid metabolic changes may contribute to the initiation and maturation of neuronal and fiber track degeneration observed following cortical impact injury."

Thromb Res. 1989 Jan 1;53(1):45-53. Normalization by dietary cod-liver oil of reduced thrombogenesis in essential fatty acid deficient rats. Hornstra G, Haddeman E, Don JA.

Radiographics. 2003 Nov-Dec;23(6):1561-7. CT Findings in Sclerosing Mesenteritis (Panniculitis): Spectrum of Disease. Horton KM, Lawler LP, Fishman EK.

Nutr Cancer. 1985;7(4):199-209. Isomeric fatty acids and tumorigenesis: a commentary on recent work. Hunter JE, Ip C, Hollenbach EJ. "Neither epidemiological nor experimental studies published to date have demonstrated any valid association between trans fatty acid ingestion and tumorigenesis. A recent study showed that under controlled conditions, a fat with a high content of trans fatty acids did not promote the development of mammary tumors induced in rats by 7,12-dimethylbenz[a]anthracene to any greater extent than did a comparable fat with a high content of cis fatty acids. In addition, in this study a high trans fat was less tumor promoting than was a blend of fats that simulated the dietary fat composition of the United States and had a lower level of trans fatty acids."

Medicina (B Aires). 1978 Mar-Apr;38(2):215. [Progesterone and retroperitoneal fibrosis] [in Spanish] Introzzi A.[Letter]

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

Biochim Biophys Acta. 1984 Nov 6;802(1):17-23. Activation of bovine platelets induced by long-chain unsaturated fatty acids at just below their lytic concentrations, and its mechanism. Kitagawa S, Endo J, Kametani F.

Clin Exp Metastasis 2000;18(5):371-7. Promotion of colon cancer metastases in rat liver by fish oil diet is not due to reduced stroma formation. Klieveri L, Fehres O, Griffini P, Van Noorden CJ, Frederiks WM. "Recently, it was demonstrated that dietary omega-3 polyunsaturated fatty acids (PUFAs) induce 10-fold more metastases in number and 1000-fold in volume in an animal model of colon cancer metastasis in rat liver."

Folia Haematol Int Mag Klin Morphol Blutforsch. 1977;104(1):1-10. [Review: hemorrhagic diathesis resulting from acute exposure to ionizing Radiation] [Article in German] Krantz S, Lober M. The symptoms of the acute radiopathy are chiefly characterized by a severe blood coagulation disorder. The main results and problems of research work on this haemorrhagic diathesis are shortly reviewed.

Prostaglandins. 1978 Apr;15(4):557-64. Prostaglandin I2 as a potentiator of acute inflammation in rats. Komoriya K, Ohmori H, Azuma A, Kurozumi S, Hashimoto Y, Nicolaou KC, Barnette WE, Magolda RL.

Gerontology 1993;39(1):7-18. Modulation of membrane phospholipid fatty acid composition by age and food restriction. 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." "The data revealed characteristic patterns of age-related changes in ad libitum (AL) fed rats: 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." "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."

Medicina (B Aires). 1978 Mar-Apr;38(2):123-32. [Effective treatment of several types of fibromatosis with progesterone. Fibrous mediastinitis, desmoid tumors, paraneoplastic fibrosis] [in Spanish] Lanari A, Molinas FC, Castro Rios M, Paz RA.

Medicina (B Aires). 1979 Nov-Dec;39(6):826-35. [Progesterone in fibromatosis and atherosclerosis] [in Spanish] Lanari A.

Free Radic Biol Med 1999 Feb;26(3-4):260-5. Modulation of cardiac mitochondrial membrane fluidity by age and calorie intake. Lee J, Yu BP, Herlihy JT. "The fatty acid composition of the mitochondrial membranes of the two 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." "Considered together, these results suggest that DR maintains the integrity of the cardiac mitochondrial membrane fluidity by minimizing membrane damage through modulation of membrane fatty acid profile."

Lipids 2001 Jun;36(6):589-93. Effect of dietary restriction on age-related increase of liver susceptibility to peroxidation in rats. Leon TI, Lim BO, Yu BP, Lim Y, Jeon EJ, Park DK.

Acta Chir Scand. 1976;142(1):20-5. Induction of endogenous fibrinolysis inhibition in the dog. Effect of intravascular coagulation and release of free fatty acids. Lindquist O, Bagge L, Saldeen T. "In all groups subjected to infusion of thrombin an increase in plasma free fatty acids (FFA) was observed. The role of this increase for the development of fibrinolysis inhibition was tested by infusion of norepinephrine alone and in combination with nicotinic acid. Norepinephrine caused an increase of FFA after 2 hours and in urokinase inhibitor activity after 24-48 hours. Both of these were diminished by high doses of nicotinic acid, indicating that the release of FFA rather than intravascular coagulation might be the principal mechanism underlying the occurrence of fibrinolysis inhibition following trauma."

Proc Natl Acad Sci U S A 1990 Nov;87(22):8845-9. Incorporation of marine lipids into mitochondrial membranes increases susceptibility to damage by calcium and reactive oxygen species: evidence for enhanced activation of phospholipase A2 in mitochondria enriched with n-3 fatty acids. Malis CD, Weber PC, Leaf A, Bonventre JV.

Prostaglandins Leukot Essent Fatty Acids 1994 Jul;51(1):33-40. Suppression of human T-cell growth in vitro by cis-unsaturated fatty acids: relationship to free radicals and lipid peroxidation. Madhavi N, Das UN, Prabha PS, Kumar GS, Koratkar R, Sagar PS.

Clin Exp Metastasis 1998 Jul;16(5):407-14. Diminution of the development of experimental metastases produced by murine metastatic lines in essential fatty acid-deficient host mice. Mannini A, Calorini L, Mugnai G, Ruggieri S.

Biochem Pharmacol. 1990 Mar 1;39(5):879-89. Histamine release from rat mast cells induced by metabolic activation of polyunsaturated fatty acids into free radicals. Masini E, Palmerani B, Gambassi F, Pistelli A, Giannella E, Occupati B, Ciuffi M, Sacchi TB, Mannaioni PF.

Journal of Lipid Research, Vol. 44, 271-279, February 2003. Arachidonic acid and prostacyclin signaling promote adipose tissue development : a human health concern? F. Massiera, P. Saint-Marc, J. Seydoux , T. Murata , T. Kobayashi , S. Narumiya , P. Guesnet, Ez-Zoubir Amri, R. Negrel and G. Ailhaud1.

Infection. 1994 Mar-Apr;22(2):106-12. Influence of dietary (n-3)-polyunsaturated fatty acids on leukotriene B4 and prostaglandin E2 synthesis and course of experimental tuberculosis in guinea pigs. Mayatepek E, Paul K, Leichsenring M, Pfisterer M, Wagner D, Domann M, Sonntag HG, Bremer HJ.

Biochim Biophys Acta 1994 Sep 15;1214(2):209-20. Reinvestigation of lipid peroxidation of linolenic acid. Mlakar A, Spiteller G. "Thus, a great number of previously unknown lipid peroxidation products was detected. It is assumed that these compounds also occur--at least as intermediates--in lipid peroxidation processes in mammalian tissue."

Prostaglandins Leukot Essent Fatty Acids. 2003 May;68(5):305-10. Synergistic effect of D-003 and aspirin on experimental thrombosis models. Molina V, Arruzazabala ML, Carbajal D, Mas R.

Chem Res Toxicol. 2001 Apr;14(4):431-7. Defining mechanisms of toxicity for linoleic acid monoepoxides and diols in Sf-21 cells. Moran JH, Mon T, Hendrickson TL, Mitchell LA, Grant DF.

J Biochem (Tokyo). 1977 Aug;82(2):529-33. Effects of free fatty acids on fibrinolytic activity. Muraoka T, Okuda H. A novel method for the estimation of fibrinolytic activity is proposed. In this method, a fibrin clot suspension is used as a substrate (fibrin is known to be a physiological substrate of plasmin). The fibrin clot suspension was prepared by homogenization of human fibrin clots. With this method, we found that free fatty acids inhibited the plasmin activity, and long-chain, unsaturated free fatty acids had a particularly strong inhibitory action on plasmin. As regards the mechanism of the inhibitory action, free fatty acids may not inhibit complex formation between plasmin and fibirin, but may make it impossible for plasmin to act on fibrin due to deformation of the surface of the fibrin clot.

Alcohol Clin Exp Res. 1986 Jun;10(3):271-3. Dietary factors and alcoholic cirrhosis. Nanji AA, French SW.

Gastroenterology. 1995 Aug;109(2):547-54. Dietary saturated fatty acids: a novel treatment for alcoholic liver disease. Nanji AA, Sadrzadeh SM, Yang EK, Fogt F, Meydani M, Dannenberg AJ.

J Pharmacol Exp Ther. 1996 Jun;277(3):1694-700. Medium chain triglycerides and vitamin E reduce the severity of established experimental alcoholic liver disease. Nanji AA, Yang EK, Fogt F, Sadrzadeh SM, Dannenberg AJ.

Hepatology. 1997 Dec;26(6):1538-45. Dietary saturated fatty acids down-regulate cyclooxygenase-2 and tumor necrosis factor alfa and reverse fibrosis in alcohol-induced liver disease in the rat. Nanji AA, Zakim D, Rahemtulla A, Daly T, Miao L, Zhao S, Khwaja S, Tahan SR, Dannenberg AJ.

J Pharmacol Exp Ther. 2001 Nov;299(2):638-44. Dietary saturated fatty acids reverse inflammatory and fibrotic changes in rat liver despite continued ethanol administration. Nanji AA, Jokelainen K, Tipoe GL, Rahemtulla A, Dannenberg AJ.

Gastroenterology 1995 Apr;108(4):1124-35. Accumulation and cellular localization of fibrinogen/fibrin during short-term and long-term rat liver injury. Neubauer K, Knittel T, Armbrust T, Ramadori G "Fibrinogen/fibrin deposition in damaged livers was studied by immunohistology." "Immunohistology showed striking amounts of fibrinogen and fibrin deposits in pericentral necrotic areas (short-term damage) and within fibrotic septa (long-term damage)." "The results show fibrinogen/fibrin deposition during short-term liver injury and liver fibrogenesis, which may suggest the involvement of a "clotting-like process" in short-term liver damage and liver fibrosis. The data might indicate that fibrin/fibronectin constitute a "provisional matrix," which affects the attraction and proliferation of inflammatory and matrix-producing cells."

Ophthalmic Res. 1999;31(4):273-9. Age-related accumulation of free polyunsaturated fatty acids in human retina. Nourooz-Zadeh J, Pereira P.

Chem Res Toxicol. 2002 Mar;15(3):367-72. Formation of cyclic deoxyguanosine adducts from omega-3 and omega-6 polyunsaturated fatty acids under oxidative conditions. Pan J, Chung FL.

Radiobiologiia. 1985 Nov-Dec;25(6):763-7. [Mechanism of circulatory disorders in animals irradiated at high doses] [in Russian] Pozharisskaia TD, Vasil'eva TP, Sokolova EN, Alekseeva II. Some data are reported on pathoanatomical changes, a status of the microcirculatory channel and the coagulogram of animals affected by high doses of ionizing radiation. The signs of disseminated intravascular blood coagulation have been revealed.

J Biol Chem. 1998 May 29;273(22):13605-12. Formation of isoprostane-like compounds (neuroprostanes) in vivo from docosahexaenoic acid. Roberts LJ 2nd, Montine TJ, Markesbery WR, Tapper AR, Hardy P, Chemtob S, Dettbarn WD, Morrow JD.

Nutr Cancer 1995;24(1):33-45. Effects of linoleic acid and gamma-linolenic acid on the growth and metastasis of a human breast cancer cell line in nude mice and on its growth and invasive capacity in vitro. Rose DP, Connolly JM, Liu XH

Arch Toxicol. 1997;71(9):563-74. Impaired cellular immune response in rats exposed perinatally to Baltic Sea herring oil or 2,3,7,8-TCDD. Ross PS, de Swart RL, van der Vliet H, Willemsen L, de Klerk A, van Amerongen G, Groen J, Brouwer A, Schipholt I, Morse DC, van Loveren H, Osterhaus AD, Vos JG.

Nutr Cancer 1998;30(2):137-43. Effects of dietary n-3-to-n-6 polyunsaturated fatty acid ratio on mammary carcinogenesis in rats. Sasaki T, Kobayashi Y, Shimizu J, Wada M, In'nami S, Kanke Y, Takita T. "An increase in the n-3/n-6 ratio did not suppress the incidence or reduce the latency of mammary tumor development. The number and weight of mammary tumors per tumor-bearing rat tended to be large in the group with an n-3/n-6 ratio of 7.84 compared with those in the other groups. As the n-3/n-6 ratios were elevated, the total number and weight of tumors increased gradually."

J. Biol. Chem. 1940 132: 539-551. Essential fatty acids, vitamin B6, and other factors in the cure of rat acrodynia. H. Schneider, H. Steenbock, and Blanche R. Platz

Science. 1988 May 20;240(4855):1032-3. Essential fatty acid depletion of renal allografts and prevention of rejection. Schreiner GF, Flye W, Brunt E, Korber K, Lefkowith JB.

Physiol Bohemoslov. 1990;39(2):125-34. Proportion of individual fatty acids in the non-esterified (free) fatty acid (FFA) fraction in the serum of laboratory rats of different ages. Smidova L, Base J, Mourek J, Cechova I.

Placenta. 2003 Nov;24(10):965-73. Augmented PLA(2)Activity in Pre-eclamptic Decidual Tissue-A Key Player in the Pathophysiology of 'Acute Atherosis' in Pre-eclampsia? Staff AC, Ranheim T, Halvorsen B.

Acta Neurochir Suppl (Wien) 1994;60:20-3. Mechanisms of glial swelling by arachidonic acid. Staub F, Winkler A, Peters J, Kempski O, Baethmann A.

Arch Biochem Biophys. 1991 Aug 15;289(1):33-8. A possible mechanism of mitochondrial dysfunction during cerebral ischemia: inhibition of mitochondrial respiration activity by arachidonic acid. Takeuchi Y, Morii H, Tamura M, Hayaishi O, Watanabe Y.

J Drug Target. 2003 Jan;11(1):45-52. Modulation of tumor-selective vascular blood flow and extravasation by the stable prostaglandin 12 analogue beraprost sodium. Tanaka S, Akaike T, Wu J, Fang J, Sawa T, Ogawa M, Beppu T, Maeda H.

Am J Clin Nutr. 2003 May;77(5):1125-32. Effect of individual dietary fatty acids on postprandial activation of blood coagulation factor VII and fibrinolysis in healthy young men. Tholstrup T, Miller GJ, Bysted A, Sandstrom B.

Biochem Soc Trans. 2003 Oct;31(Pt 5):1075-9. Regression of pre-established atherosclerosis in the apoE-/- mouse by conjugated linoleic acid. Toomey S, Roche H, Fitzgerald D, Belton O.

Int J Biochem Cell Biol. 2003 May;35(5):749-55. Increased muscle proteasome activities in rats fed a polyunsaturated fatty acid supplemented diet. Vigouroux S, Farout L, Clavel S, Briand Y, Briand M. "Changes in the proteasome system, a dominant actor in protein degradation in eukaryotic cells, have been documented in a large number of physiological and pathological conditions." "With the polyunsaturated fatty acid enriched diet, the chymotrypsin-like and peptidylglutamylpeptide hydrolase activities increased by 45% in soleus and extensor digitorum longus (EDL), and by 90% in the gastrocnemius medialis (GM) muscle. Trypsin-like activity of the proteasome increased by 250% in soleus, EDL and GM." "Proteasome activities and level were less stimulated with a monounsaturated fatty acid supplemented diet." "Unsaturated fatty acids are particularly prone to free radical attack. Thus, we suggest that alterations in muscle proteasome may result from monounsaturated and polyunsaturated fatty acid-induced peroxidation, in order to eliminate damaged proteins."

J Am Coll Nutr. 2000 Aug;19(4):478S-486S. Conjugated linoleic acid and bone biology. Watkins BA, Seifert MF. "Recent investigations with growing rats given butter fat and supplements of CLA demonstrated an increased rate of bone formation and reduced ex vivo bone PGE2 production, respectively."

Ups J Med Sci. 1979;84(3):195-201. Effect of nicotinic acid on the posttraumatic increase in free fatty acids and fibrinolysis inhibition activity in the rat. Wegener T, Bagge L, Saldeen T. Nicotinic acid effectively inhibited the posttraumatic increase in both free fatty acids (FFA) and fibrinolysis inhibition activity (FIA) in the blood in rats, indicating that FFA might be involved in the posttraumatic increase of FIA. The FIA in the liver was greater than that in other organs studied and was increased in the posttraumatic phase. The possible role of the liver in the posttraumatic increase of FIA is discussed.

Am J Physiol Regul Integr Comp Physiol. 2001 Mar;280(3):R908-12. CLA reduces antigen-induced histamine and PGE(2) release from sensitized guinea pig tracheae. Whigham LD, Cook EB, Stahl JL, Saban R, Bjorling DE, Pariza MW, Cook ME.

Toxicol Appl Pharmacol 1993 May;120(1):72-9. Essential fatty acid deficiency in cultured human keratinocytes attenuates toxicity due to lipid peroxidation. Wey HE, Pyron L, Woolery 

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. . . . To Be Continued . . . .

 

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