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  6. <strong>Meat physiology, stress, and degenerative physiology&nbsp;&nbsp;</strong>The US Department of
  7. Agriculture claims that the Pure Food and Drugs Act of 1906 and the Meat Inspection Act of the same year were
  8. passed because the food industry demanded them. Ordinary historians believe that Upton Sinclair's 1905 serial
  9. publication of his novel about the meat industry, The Jungle, caused the public and Theodore Roosevelt to
  10. pressure Congress to pass the laws. Sinclair's descriptions of the use of poisonous preservatives and deodorants
  11. to disguise the smell of rotten meat angered the public and the president enough to overcome the industry
  12. pressure that had kept the US Congress from regulating the commercial food supply long after European
  13. governments had begun regulating food production and sales.Before the government's intervention, it was common
  14. practice to soak all kinds of meat in water or chemical solutions to increase their weight. At present, the US
  15. Department of Agriculture, through the mass media and funding the training of food technologists and "meat
  16. scientists," now takes the position that it is natural for meat to leak water after it is packaged, and says it
  17. is perfectly legal for meat producers to soak the meat in water with chemicals until it has increased its weight
  18. by 8%. The chemicals, such as trisodium phosphate (in a solution strength as high as 12%), are chosen because
  19. they powerfully stimulate swelling and water retention. Considerable amounts of some chemicals, such as sodium
  20. citrate, are allowed to add to the weight of the meat. The use of ozone and hydrogen peroxide to deodorize meat
  21. causes instantaneous oxidative changes, including lipid peroxidation and protein carbonyl formation, as well as
  22. increasing water retention.Most supermarket meat is now packaged with thick diapers so the buyer won't notice
  23. that he is paying for a sizeable amount of pink water. The USDA has an internet site, and consumer hotlines, to
  24. inform angry consumers that they are mistaken if they believe that meat shouldn't leak. They explain that meat
  25. is now "bred" to contain less fat, and so it contains more water, and that it is simply the leanness of the meat
  26. that accounts for its poor flavor.Before the slaughtered animal is put into the soaking solution to gain a
  27. specific amount of weight, the animal has almost always been treated in ways that cause it to go to slaughter in
  28. a state of massive edema. Even before the meat is soaked, the animal has been treated to maximize its water
  29. retention.Muscle physiologists and endocrine physiologists know that fatigue, stress and excess estrogen can
  30. cause the tissues to swell hugely, increasing their weight and water content without increasing their protein
  31. content.As soon as cheap synthetic estrogens, such as DES, became available in the 1940s, their use in animals
  32. was promoted because it was clear that they caused massive water retention. Women who suffer from
  33. hyperestrogenism always have a problem with water retention, but they have never been known to suffer from
  34. over-developed skeletal muscles. In fact, in humans of both sexes, an excess of estrogen has been commonly
  35. associated with sarcopenia, muscular dystrophy, and atrophy of the skeletal muscles. Similar observations have
  36. been made in a variety of animals. Meat scientists are the only people I know of who have ever referred to
  37. estrogen as an anabolic steroid, in the sense of "building muscle."When it was publicized around 1970 that DES
  38. is powerfully carcinogenic, after it had been used for several decades in the meat industry, its use was
  39. outlawed, but its illegal use continued and was overlooked by the US government. The Swiss government has
  40. rejected meat from a large producer in Kansas because it contained DES. Other estrogens are openly used, and the
  41. US government continues to apply pressure to other countries to accept meat exports containing estrogens.There
  42. are many ways to increase the water content of meat, besides feeding estrogen to the animal and soaking the meat
  43. after slaughter. Everything that causes water retention and tissue swelling in the living animal, that is, every
  44. kind of stress, fatigue, poisoning, malnutrition and injury, will make the animal gain weight, without consuming
  45. expensive nutritious food. Crowding, fright, and other suffering increase water retention and accelerate the
  46. breakdown of fats and proteins.The water content of meat shouldn't be increased by any of those methods, not
  47. only because it is a form of stealing from the consumer, but because it makes the product toxic and
  48. unappetizing, and makes the production process a degrading experience.&nbsp;Any chemicals, such as estrogen or
  49. arsenic, that remain in the meat are of course harmful to the consumer, but the changes they produce in the
  50. animals' tissues are the main problem. When grains and soybeans are used for fattening animals, their
  51. characteristic fatty acids are present in the meat, and are harmful to the consumer, but their complex
  52. degradation products, such as isoprene, acrolein, and isoprostanes, remain, along with the complex changes they
  53. induce in every aspect of the tissue. The reactive products of oxidative fat degradation stimulate, among other
  54. things, the adaptive/defensive production of polyamines, small molecules derived from amino acids. The
  55. polyamines, in turn, can be oxidized, producing highly toxic aldehydes, including acrolein (Sakata, et al.,
  56. 2003). These molecules stimulate cell multiplication, and alter, at least temporarily, the way the cell's genes
  57. function.An excess of water stimulates cell division, and an important mechanism in producing that effect is the
  58. increased production of polyamines by the enzyme ornithine decarboxylase. This enzyme is activated by an excess
  59. of water (hypotonicity), by estrogen, and by stress.Besides stimulating cell division and modifying the cell's
  60. state of differentiation (including developmental imprinting), the polyamines also contribute to nerve cell
  61. excitation and excitotoxicity. Estrogen and excess water can contribute to nerve cell excitation, for example
  62. producing convulsive seizures. The polyamines are increased during seizures, and they can affect the stability
  63. of the nerve cells, for example contributing to cocaine's seizure-sensitizing action. Although they tend to
  64. block free radicals, they accelerate nerve injury (Yatin, et al., 2001), and can contribute to breakdown of the
  65. blood-brain barrier (Wengenack, et al., 2000, Koenig, et al., 1989).The polyamines are increased in cancers, and
  66. therapies to block their formation are able to stop the growth of various cancers, including prostate, bowel,
  67. and breast cancer. Metabolites of the polyamines in the urine appear to be useful as indicators of cancer and
  68. other diseases. (In pancreatic cancer, Yamaguchi, et al., 2004; in cervical cancer, Lee, et al., 2003; in adult
  69. respiratory stress syndrome, Heffner, et al., 1995.)&nbsp; The quantity of polyamines in the urine of cancer
  70. patients has been reported to be 20 times higher than normal (Jiang, 1990). Polyamines in the red blood cells
  71. appear to indicate prognosis in prostate cancer (Cipolla, et al., 1990).The prostaglandins in semen have been
  72. suspected to have a role in producing cervical cancer (Fernandez, et al., 1995).In protein catabolism, one fate
  73. of the protein's nitrogen is to be converted to the polyamines, rather than to urea. In plants, at least, these
  74. small molecules help cells to balance osmotic stresses.Adding water to meat, or stressing the animals before
  75. slaughter, will increase the meat's content of the polyamines, but the longer the meat is stored, the greater
  76. will be the production of reactive oxygen products and polyamines.&nbsp;The deliberate "aging" of meat is
  77. something that the meat scientists often write about, but it has a peculiar history, and is practiced mainly in
  78. the English speaking cultures. When a supermarket in Mexico City began selling U.S.-style meat for the American
  79. colony, I got some T-bone steaks and cooked them for some of my Mexican friends. The meat wasn't water-logged
  80. (it was 1962, and the beef had been grown in Mexico), but it had been aged for the American customers, and
  81. though my friends ate the steaks for the sake of politeness, I could see that they found it difficult.&nbsp;In
  82. Mexico, even in the present century, butcher shops often don't have refrigeration, and they don't need it
  83. because they sell the meat immediately. The fresh meat tastes fresh. Traditionally, liver is sold only on the
  84. day of slaughter, because its high enzyme content causes it to degrade much faster than the muscle meats. When
  85. it is fresh, it lacks the characteristic bad taste of liver in the US.&nbsp;Both the liver and the muscles
  86. contain a significant amount of glycogen when they are fresh, if the animal was healthy. At first, the lack of
  87. oxygen causes the glycogen to be metabolized into lactic acid, and some fatty acids are liberated from their
  88. bound form, producing slight changes in the taste of the meat. But when the glycogen has been depleted, the
  89. anaerobic metabolism accelerates the breakdown of proteins and amino acids.In the absence of oxygen, no carbon
  90. dioxide is produced, and the result is that the normal disposition of ammonia from amino acids as urea is
  91. blocked, and the polyamines are formed instead. The chemical names of two of the main poly-amines are suggestive
  92. of the flavors that they impart to the aging meat: Cadaverine and putrescine. After two or three weeks of aging,
  93. there has been extensive breakdown of proteins and fats, with the production of very complex new mixtures of
  94. chemicals.Mexicans, despite their low average income, have a very high per capita consumption of meat, as do
  95. several other Latin American countries. Argentina has a per capita meat consumption of nearly a pound a day.
  96. There is a lot of theorizing about the role of meat in causing cancer, for example comparing Japan's low
  97. mortality from prostate cancer, and their low meat consumption, with the high prostate cancer mortality in the
  98. US, which has a higher meat consumption. But Argentina and Mexico's prostate cancer mortality ranks very
  99. favorably with Japan's.&nbsp;If meat consumption in the US contributes to the very high cancer rate, it clearly
  100. isn't the quantity of meat consumed, but rather the quality of the meat.The polar explorer Vilhjalmur Stefansson
  101. was interested in the health effects of a diet based on meat, because of his observation that fresh meat
  102. prevented scurvy much more effectively than the fruits and vegetables carried by other polar explorers. He
  103. commented on the importance of culture and learning in shaping food preferences:"In midwinter it occurred to me
  104. to philosophize that in our own and foreign lands taste for a mild cheese is somewhat plebeian; it is at least a
  105. semi-truth that connoisseurs like their cheeses progressively stronger. The grading applies to meats, as in
  106. England where it is common among nobility and gentry to like game and pheasant so high that the average
  107. Midwestern American or even Englishman of a lower class, would call them rotten.&nbsp;"I knew of course that,
  108. while it is good form to eat decayed milk products and decayed game, it is very bad form to eat decayed fish. I
  109. knew also that the view of our populace that there are likely to be "ptomaines" in decaying fish and in the
  110. plebeian meats; but it struck me as an improbable extension of the class-consciousness that ptomaines would
  111. avoid the gentleman's food and attack that of a commoner.&nbsp;"These thoughts led to a summarizing query; If it
  112. is almost a mark of social distinction to be able to eat strong cheeses with a straight face and smelly birds
  113. with relish, why is it necessarily a low taste to be fond of decaying fish? On that basis of philosophy, though
  114. with several qualms, I tried the rotten fish one day, and if memory serves, liked it better than my first taste
  115. of Camembert. During the next weeks I became fond of rotten fish."Since Stefansson's observations nearly a
  116. century ago, most Americans have become accustomed to the taste of half-spoiled meat, as part of the process of
  117. adapting to an industrial-commercial food system. Tests done by food technologists have found that most
  118. Americans prefer the taste of synthetic strawberry flavor in ice cream to the taste of ice cream made with real
  119. strawberries. If it took Stefansson only a few weeks to become fond of rotten fish, it isn't surprising that the
  120. public would, over a period of many decades, learn to enjoy a diet of stale foods and imitation
  121. foods.&nbsp;Polyamines are increased in stressed and stored vegetables, as in aged meats. This defensive
  122. reaction retards tissue aging, and researchers are testing the application of polyamines to fruits to retard
  123. their ripening. A plastic surgeon, Vladimir Filatov, discovered that tissue stored in the cold stimulated the
  124. healing process when used for tissue reconstruction, such as corneal transplants. He found that stressed plant
  125. tissues developed the same tissue stimulants. Another pioneer of tissue transplantation, L.V. Polezhaev, saw
  126. that degenerating tissue produced factors that seem to activate stem cells.Although the diffusion of these
  127. stimulating factors from stressed tissues normally functions to accelerate healing and tissue regeneration,
  128. under less optimal conditions they are undoubtedly important factors in tissue degeneration and tumor formation.
  129. For example, the bystander effect (contributing to delayed radiation damage, and producing a field of
  130. precancerous changes around a cancer), in which substances diffusing from injured tissues damage surrounding
  131. cells, involves disturbances in polyamine metabolism.The direct, optimal effects of the polyamines are
  132. protective, but when excessive, prolonged, or without maintained cellular energy, they become harmful.The
  133. expression of genes involves their physical arrangement and accessibility to enzymes and substrates. The
  134. negatively charged nucleic acids are associated with positively charge proteins, the histones. The very small
  135. positively charged polyamines can powerfully modify the interactions between histones and DNA. In recent years
  136. people have begun to speak of the "histone code," as a kind of expansion of the idea of the "genetic code." But
  137. the polyamines, produced in response to stress, might be thought of as a complex expansion of the "histone
  138. code."The addition of small molecules, methyl and acetyl groups, to the large molecules can regulate the
  139. expression of genes, and these patterns can be passed on transgenerationally, or modified by stress. Barbara
  140. McClintock's "controlling factors" were mobile genes that caused the genome to be restructured under the
  141. influence of stress. Her discoveries were the same as those made by Trofim Lysenko decades earlier, and like his
  142. observations, McClintock's were angrily rejected until the 1980s, when the genetic engineering industry needed
  143. some scientific background and natural precedent for their unnatural intervention in the genome.The brain is
  144. extremely different from a malignant tumor, and the derangements produced by stress, by high cortisol and
  145. estrogen and an excess of water, are different in the two types of organ (considering the tumor as an ad hoc
  146. organ), but the polyamines have central roles in the degenerating brain and in the divergent disorganization of
  147. tumors. Their importance in stress physiology is coming to be recognized, along with the meaning of "epigenetic
  148. development," in which the influence of the environment becomes central, rather than just a place in which the
  149. "genotype" is allowed to passively express its "genetic potential." Every developmental decision involves an
  150. evaluation of resources and their optimal marshaling for adaptation. The polyamines are part of the cytoplasm's
  151. equipment for controlling the genome. The ratio between the different types of polyamine governs the nature of
  152. their regulation of cellular functions.The old idea, "one is what one eats," has evolved far beyond ideas of
  153. simple nutritional adequacy or deprivation, and it's now commonly accepted that many things in foods have fairly
  154. direct effects on our brain transmitters and hormones, such as serotonin, dopamine, adrenalin, endorphins,
  155. prostaglandins, and other chemicals that affect our behavior and physiology.In 1957 James McConnell discovered
  156. that when flatworms were fed other flatworms that had been trained, their performance was improved by 50%,
  157. compared with normal flatworms. Later, similar experiments were done with rats and fish, showing that tissue
  158. extracts from trained animals modified the behavior of the untrained animals so that it approximated that of the
  159. trained animals. Georges Ungar, who did many experiments with higher animals, demonstrated changes in brain RNA
  160. associated with learning, and he and McConnell believed that proteins and peptides were likely to be the type of
  161. substance that transmitted the learning.A dogmatic belief that "memory molecules" would be unable to penetrate
  162. the "blood-brain barrier" allowed most biologists to dismiss their work. Ungar's death, and the hostility of
  163. most biologists to their work, have caused their ideas to be nearly forgotten for the last 30 years. Negatively
  164. charged molecules such as ordinary proteins tend to be repelled by negative charges on the wall of capillaries,
  165. but positively charged molecules spontaneously associate with cellular proteins, and easily penetrate the
  166. barrier. Highly positively charged molecules tend to concentrate in the brain (Jonkman, et al., 1983), and
  167. people are currently attempting to use the principle to deliver antibodies (which are normally excluded from the
  168. brain) therapeutically to the brain by combining them with small positively charged molecules (Herve, et al.,
  169. 2001). This affinity of the brain for positively charged molecules is gradually being recognized as an important
  170. factor in the toxicity of ammonia and guanidine derivatives. As mentioned earlier, even endogenous polyamines
  171. can be involved in disruption of the blood-brain barrier.So, apart from the question of exactly what molecules
  172. were responsible for the learning transfer produced by McConnell and Ungar, there should be no doubt that
  173. polyamines derived from food can enter tissues, especially the brain. People who eat meat from stressed animals
  174. are substantially replicating the experiments of McConnell and Ungar, except that people normally eat a variety
  175. of foods, and each type of food will have had slightly different experiences in its last days of life. But the
  176. deliberate aging of meat is subjecting it to a standardized stress--two or three weeks of cold storage. Because
  177. of the great generality of genetic processes, it wouldn't be surprising if cold storage of vegetables turned out
  178. to produce polyamine patterns similar to those of cold storage meats. Air pollution and other stressful growing
  179. conditions cause vegetables to have very high levels of polyamines.Prolonged exposure to certain patterns of
  180. polyamines might produce particular syndromes, but the mere fact of increasing the total quantity of polyamines
  181. in our diet is likely to increase the incidence of stress-related diseases. Experiments with cells in culture
  182. show that added polyamines can produce a variety of extremely harmful changes, but so far, there has been almost
  183. no investigation of their specific regulatory functions, of their "code."Besides rejecting stale foods produced
  184. under stressful conditions, there are probably some specific ways that we can protect ourselves from polyamine
  185. poisoning.When the organism is functioning efficiently, its respiration is producing an abundance of carbon
  186. dioxide, which protectively modifies many systems and structures. Adequate carbon dioxide protects against
  187. fatigue, cellular and vascular leakiness, edema and swelling.Increasing carbon dioxide will tend to direct
  188. ammonia into urea synthesis, and away from the formation of polyamines. Bicarbonate protects against many of the
  189. toxic effects of ammonia, and since carbon dioxide spontaneously reacts with amino groups, it probably helps to
  190. inactivate exogenous polyamines. This could account for some of the protective effects of carbon dioxide (or
  191. high altitude), for example its anti-seizure, anticancer, and antistress effects.Other things that protect
  192. against excessive polyamines are procaine and other local anesthetics (Yuspa, et al., 1980), magnesium, niacin,
  193. vitamin A, aspirin, and, in some circumstances, caffeine. Since endotoxin stimulates the formation of
  194. polyamines, a diet that doesn't irritate the intestine is important. Tryptophan and methionine contribute to the
  195. formation of polyamines, so gelatin, which lacks those amino acids and is soothing to the intestine, should be a
  196. regular part of the diet.Because the polyamines intensity the neurotoxic and carcinogenic effects of estrogen
  197. and of polyunsaturated fats, those three types of substance should be considered as a functional unit in making
  198. food choices. (Grass-fed organic beef fresh from a local farm would be a reasonable choice.) Unfortunately, the
  199. meat industry has maximized all of those dangers, just for the increased weight of their
  200. product.&nbsp;&nbsp;<strong><h3>REFERENCES</h3></strong>Biull Eksp Biol Med 1993 Jun;115(6):600-2. Ornithine
  201. decarboxylase and malignant growth. Berezov TT.&nbsp;Clin Cancer Res. 1999 Aug;5(8):2035-41. Prognostic value of
  202. ornithine decarboxylase and polyamines in human breast cancer: correlation with clinicopathologic parameters.
  203. Canizares F, Salinas J, de las Heras M, Diaz J, Tovar I, Martinez P, Penafiel R.&nbsp;&nbsp;J Clin
  204. Gastroenterol. 1989 Aug;11(4):434-41. Intestinal autointoxication: a medical leitmotif. Chen TS, Chen PS. The
  205. idea that putrefaction of the stools causes disease, i.e., intestinal autointoxication, originated with
  206. physicians in ancient Egypt. They believed that a putrefactive principle associated with feces was absorbed in
  207. to the general circulation, where it acted to produce fever and pus. This description of the materia peccans
  208. represented the earliest forerunner of our present notion of endotoxin and its effect. The ancient Greeks
  209. extended the concept of putrefaction to involve not only the residues of food, but also those of bile, phlegm,
  210. and blood, incorporating it into their humoral theory of disease. During the 19th century, the early biochemical
  211. and bacteriologic studies lent credence to the idea of ptomaine poisoning--that degradation of protein in the
  212. colon by anerobic bacteria generated toxic amines. Among the leading proponents of autointoxication was
  213. Metchnikoff, who hypothesized that intestinal toxins shortened lifespan. The toxic process, however, was
  214. reversed by the consumption of lactic acid-producing bacteria that changed the colonic microflora and prevented
  215. proteolysis. The next logical step in treatment followed in the early 20th century when surgeons, chief among
  216. them Sir W. Arbuthnot Lane, performed colectomy to cure intestinal autointoxication. By the 1920s, the medical
  217. doctrine fell into disrepute as scientific advances failed to give support. However, the idea persists in the
  218. public mind, probably as an extension of the childhood habit of toilet training.&nbsp;&nbsp; &nbsp;Prog Urol.
  219. 1992 Feb;2(1):50-7. [The diagnostic value of erythrocyte polyamines (EPA) in prostatic adenocarcinoma (PA):
  220. apropos of 100 patients] [Article in French] Cipolla B, Guille F, Quemener V, Leveque JM, Moulinoux JP, Lobel
  221. B.Arch Oral Biol. 2003 Apr;48(4):323-7. Time profile of putrescine, cadaverine, indole and skatole in human
  222. saliva. Cooke M, Leeves N, White C.Hum Reprod. 2003 May;18(5):959-68. Nitric oxide inhibits polyamine-induced
  223. apoptosis in the human extravillous trophoblast cell line SGHPL-4. Dash PR, Cartwright JE, Whitley
  224. GS.Carcinogenesis. 1999 Mar;20(3):493-7. Promotion of intestinal carcinogenesis by dietary methionine. Duranton
  225. B, Freund JN, Galluser M, Schleiffer R, Gosse F, Bergmann C, Hasselmann M, Raul F.Br J Cancer. 1995
  226. Nov;72(5):1194-9. Evaluation of the significance of polyamines and their oxidases in the aetiology of human
  227. cervical carcinoma. Fernandez C, Sharrard RM, Talbot M, Reed BD, Monks N.J Clin Pathol. 1991 May;44(5):410-5.
  228. Seminal polyamines as agents of cervical carcinoma: production of aneuploidy in squamous epithelium. Fletcher S,
  229. Neill WA, Norval M. The effects of several polyamines found in seminal fluid on the cell cycle and ploidy of
  230. three cervical cell lines and of primary epithelial cells cultured from cervical biopsy specimens were monitored
  231. by fluorescent flow cytometry. The rate of cell growth did not change but there were indications of either
  232. hypodiploidy or hyperdiploidy in some cultures at certain concentrations of spermine and spermidine. An
  233. interaction of exogenous polyamines with the DNA of cervical cells was shown to occur, leading to changes in
  234. ploidy with, perhaps, the potential to induce or promote dysplasia.Biochem Biophys Res Commun. 1977 Jul
  235. 11;77(1):57-64. Activation of thyroid ornithine decarboxylase (ODC) in vitro by hypotonicity; a possible
  236. mechanism for ODC induction. Friedman Y, Park S, Levasseur S, Burke G.Anal Biochem. 1988 Oct;174(1):88-96.
  237. Apparent ornithine decarboxylase activity, measured by 14CO2 trapping, after frozen storage of rat tissue and
  238. rat tissue supernatants. Gaines DW, Friedman L, McCann PP. "Ornithine decarboxylase (ODC) activity of rat
  239. tissues was measured by the standard 14CO2 trapping method after frozen storage (-60 or -70 degrees C) of the
  240. tissues or their 105,000g supernatants." "In the frozen supernatants of liver and spleen, ODC activity changed
  241. only slightly after 1 day but increased 29 and 14%, respectively, by 30 days; activity in kidney supernatant
  242. decreased 17% after 1 day and remained near that level at 30 days." "With AOA, the ODC activities of the fresh
  243. and frozen supernatants were similar, indicating that the large increase in apparent ODC activity in frozen
  244. tissue was due to artifacts from the metabolism of ornithine via the mitochondrial pathway. HPLC analysis of the
  245. reaction products resulting from the incubation of uniformly labeled [14C]ornithine with the fresh and frozen
  246. preparations indicated no increase in putrescine with the frozen preparation."J Dent Res. 1994
  247. Jun;73(6):1168-72. Cadaverine as a putative component of oral malodor. Goldberg S, Kozlovsky A, Gordon D,
  248. Gelernter I, Sintov A, Rosenberg M.Exp Neurol. 2002 Oct;177(2):515-20.&nbsp; Increased red blood cell polyamines
  249. in ALS and Parkinson's disease. Gomes-Trolin C, Nygren I, Aquilonius SM, Askmark H.THE DAILY CITIZEN, April 5,
  250. 1994. Robert Greene, "Soggy Chickens," AP, April 2, 1994; "Interview with Elaine Dodge," "The chickens soak up
  251. to 12 percent of their weight in this water," according to Elaine Dodge of the Government Accountability Project
  252. (GAP).&nbsp;J Anim Sci. 2004 May;82(5):1401-9. Preslaughter stress and muscle energy largely determine pork
  253. quality at two commercial processing plants. Hambrecht E, Eissen JJ, Nooijent RI, Ducro BJ, Smits CH, den Hartog
  254. LA, Verstegen MW.Exp Lung Res. 1995 Mar-Apr;21(2):275-86. Urinary excretion of polyamines in the adult
  255. respiratory distress syndrome. Heffner JE, Ali R, Jeevanandam M.Kumamoto Igakkai Zasshi. 1969 Aug
  256. 25;43(8):661-80. [Studies on relationship between progressive muscular dystrophy and estrogen] [Article in
  257. Japanese] Ideta T.Biomed Chromatogr. 1990 Mar;4(2):73-7. Determination of polyamines in urine of normal human
  258. and cancer patients by capillary gas chromatography. Jiang XC.Int J Biochem. 1990;22(1):67-73. Mitogenic
  259. induction of ornithine decarboxylase in human mononuclear leukocytes: relationships with adenosine diphosphate
  260. ribosyltransferase. Johnson DB, Markowitz MM, Joseph PE, Miller DG, Pero RW. "Inhibitors of ADPRT, nicotinamide,
  261. caffeine and benzamide inhibited the induction of ODC by PHA in a concentration-dependent manner, in the range
  262. (0.6-10 mM) known to inhibit ADPRT."Arzneimittelforschung. 1983;33(2):223-8. Whole body distribution of the
  263. quaternary ammonium compound thiazinamium (N-methylpromethazine) and promethazine in monkey and mice. Jonkman
  264. JH, Westenberg HG, Rijntjes NV, van der Kleijn E, Lindeboom SF.J Neurochem. 1989 Jan;52(1):101-9. Blood-brain
  265. barrier breakdown in cold-injured brain is linked to a biphasic stimulation of ornithine decarboxylase activity
  266. and polyamine synthesis: both are coordinately inhibited by verapamil, dexamethasone, and aspirin. Koenig H,
  267. Goldstone AD, Lu CY. Neurology Service, V.A.Cancer Treat Rep. 1985 Jan;69(1):97-103. Enhancement of the
  268. antiproliferative activity of human interferon by polyamine depletion. Kovach JS, Svingen PA.Cancer Res. 2001
  269. Nov 1;61(21):7754-62. Polyamine depletion in human melanoma cells leads to G1 arrest associated with induction
  270. of p21WAF1/CIP1/SDI1, changes in the expression of p21-regulated genes, and a senescence-like phenotype. Kramer
  271. DL, Chang BD, Chen Y, Diegelman P, Alm K, Black AR, Roninson IB, Porter CW.Endokrinologie. 1982 Nov;80(3):294-8.
  272. The effect of androgen and estrogen on food intake and body weight in rats--age dependency. Kuchar S, Mozes S,
  273. Boda K, Koppel J.Endokrinologie. 1982 Nov;80(3):294-8. The effect of androgen and estrogen on food intake and
  274. body weight in rats--age dependency. Kuchar S, Mozes S, Boda K, Koppel J.&nbsp;Cancer Lett. 2003 Nov
  275. 25;201(2):121-31.&nbsp; Altered urinary profiles of polyamines and endogenous steroids in patients with benign
  276. cervical disease and cervical cancer. Lee SH, Yang YJ, Kim KM, Chung BC.Oncol Res. 2005;15(3):113-28. Activation
  277. of cyclin D1 by estradiol and spermine in MCF-7 breast cancer cells: a mechanism involving the p38 MAP kinase
  278. and phosphorylation of ATF-2. Lewis JS, Vijayanathan V, Thomas TJ, Pestell RG, Albanese C, Gallo MA, Thomas
  279. T.Nucleic Acids Res. 2005 Mar 23;33(6):1790-803. Print 2005. Polyamines preferentially interact with bent
  280. adenine tracts in double-stranded DNA. Lindemose S, Nielsen PE, Mollegaard NE. "Polyamines, such as putrescine,
  281. spermidine and spermine, have indirectly been linked with the regulation of gene expression, and their
  282. concentrations are typically increased in cancer cells." "These results provide the first clear evidence for the
  283. sequence-specific binding of polyamines to DNA, and thereby suggest a mechanism by which the cellular effects of
  284. polyamines in terms of differential gene transcriptional activity could, at least partly, be a direct
  285. consequence of sequence-specific interactions of polyamines with promoters at the DNA sequence level."Eur J
  286. Biochem. 1995 Jul 1;231(1):40-4. Regulation of mammalian ornithine decarboxylase. Studies on the induction of
  287. the enzyme by hypotonic stress. Lovkvist-Wallstrom E, Stjernborg-Ulvsback L, Scheffler IE, Persson
  288. L.Gastroenterol Clin North Am 1988 Dec;17(4):931-40. Biochemical markers in colorectal cancer: diagnostic and
  289. therapeutic implications.&nbsp; Luk GD, Desai TK, Conteas CN, Moshier JA, Silverman AL .&nbsp;Proc Natl Acad Sci
  290. U S A. 2003 Jun 24;100(13):7859-64. Pronounced reduction in adenoma recurrence associated with aspirin use and a
  291. polymorphism in the ornithine decarboxylase gene. Martinez ME, O'Brien TG, Fultz KE, Babbar N, Yerushalmi H, Qu
  292. N, Guo Y, Boorman D, Einspahr J, Alberts DS, Gerner EW.Biochem J. 1998 Feb 1;329 ( Pt 3):453-9. Osmotic stress
  293. induces variation in cellular levels of ornithine decarboxylase-antizyme. Mitchell JL, Judd GG, Leyser A, Choe
  294. C.Arch Biochem Biophys. 1964 Apr;105:209-10. Occurrence of polyamines in the germs of cereals. Moruzzi G,
  295. Caldarera CM.Br J Ophthalmol. 2003 Aug;87(8):1038-42. Vitreous polyamines spermidine, putrescine, and spermine
  296. in human proliferative disorders of the retina. Nicoletti R, Venza I, Ceci G, Visalli M, Teti D, Reibaldi
  297. A.Carcinogenesis. 1997 Oct;18(10):1871-5. Dietary polyamines promote the growth of azoxymethane-induced aberrant
  298. crypt foci in rat colon. Paulsen JE, Reistad R, Eliassen KA, Sjaastad OV, Alexander J.Eur J Cancer. 1996
  299. Feb;32A(2):316-21. Red blood cell polyamines, anaemia and tumour growth in the rat. Quemener V, Bansard JY,
  300. Delamaire M, Roth S, Havouis R, Desury D, Moulinoux JP.Anticancer Res 1994 Mar-Apr;14(2A):443-8. Polyamine
  301. deprivation: a new tool in cancer treatment. Quemener V, Blanchard Y, Chamaillard L, Havouis R, Cipolla B,
  302. Moulinoux JP.J Anim Sci&nbsp; 1995 Jul;73(7):1982-6.Effects of ground flaxseed in swine diets on pig performance
  303. and on physical and sensory characteristics and omega-3 fatty acid content of pork: I. Dietary level of
  304. flaxseed. Romans JR, Johnson RC, Wulf DM, Libal GW, Costello WJ.J Anim Sci&nbsp; 1995 Jul;73(7):1987-99. Effects
  305. of ground flaxseed in swine diets on pig performance and on physical and sensory characteristics and omega-3
  306. fatty acid content of pork: II. Duration of 15% dietary flaxseed. Romans JR, Wulf DM, Johnson RC, Libal GW,
  307. Costello WJ.J Clin Invest. 1972 May;51(5):1118-24. Metabolic effects of human growth hormone and of estrogens in
  308. boys with Duchenne muscular dystrophy. Rudman D, Chyatte SB, Patterson JH, Gerron GG, O'Beirne I, Barlow J,
  309. Jordan A, Shavin JS.Biochem Biophys Res Commun. 2003 May 23;305(1):143-9. Increase in putrescine, amine oxidase,
  310. and acrolein in plasma of renal failure patients. Sakata K, Kashiwagi K, Sharmin S, Ueda S, Irie Y, Murotani N,
  311. Igarashi K.Biochem Soc Trans. 2003 Apr;31(2):375-80. Polyamines and prostatic cancer. Schipper RG, Romijn JC,
  312. Cuijpers VM, Verhofstad AA.Nitric Oxide. 2000 Dec;4(6):583-9. Nitric oxide synthase inhibition promotes
  313. carcinogen-induced preneoplastic changes in the colon of rats. Schleiffer R, Duranton B, Gosse F, Bergmann C,
  314. Raul F. "l-Arginine is metabolized either to polyamines through arginase and ornithine decarboxylase (ODC)
  315. activities or to citrulline and nitric oxide (NO, nitrogen monoxide) through the NO synthase (NOS) pathway.
  316. Polyamine levels and ODC activity are high in tumor cells. The aim of this study was to test whether
  317. N(G)-nitro-l-arginine methyl ester (l-NAME), an inhibitor of NOS, modulates colon carcinogenesis." "In
  318. l-NAME-treated rats, the number of ACF was higher than in controls by 47%. ODC activity was enhanced by 11-fold.
  319. S-Adenosyl-methionine-decarboxylase activity and putrescine concentration were significantly increased in the
  320. colonic mucosa of l-NAME-treated rats. The data suggest that l-NAME promotes carcinogen-induced preneoplastic
  321. changes in the colon by inhibiting NOS activity and by stimulating polyamine biosynthesis."Brain Res. 1997 Nov
  322. 14;775(1-2):198-202. Role of cerebral spermidine in the development of sensitization to convulsant activity of
  323. cocaine and lidocaine. Shimosato K, Watanabe S, Katsura M, Ohkuma S.Melanoma Res. 1994 Aug;4(4):213-23. Cellular
  324. pathways leading to melanoma differentiation: therapeutic implications. Soballe PW, Herlyn M.Rev Can Biol. 1959
  325. Apr;18(1):23-52. Studies on the mechanism of the catabolic action of estrogens. Sternberg J, Pascoe-Dawson E.<a
  326. href="http://www.fsis.usda.gov/wps/portal/fsis/topics/food-safety-education/get-answers/food-safety-fact-sheets/meat-preparation/water-in-meat-and-poultry/CT_Index"
  327. >http://www.fsis.usda.gov/wps/portal/fsis/topics/food-safety-education/get-answers/food-safety-fact-sheets/meat-preparation/water-in-meat-and-poultry/CT_Index</a
  328. >J Neurol Sci. 1989 Feb;89(2-3):189-97. Hyperestrogenemia in neuromuscular diseases. Usuki F, Nakazato O, Osame
  329. M, Igata A.&nbsp;&nbsp; &nbsp;Rinsho Shinkeigaku. 1985 Jun;25(6):711-5. [Hyperestrogenemia in Duchenne muscular
  330. dystrophy (DMD)] [Article in Japanese] Usuki F, Nakazato O, Osame M, Igata A.Neurosci Lett. 2001 Aug
  331. 17;309(1):62-6. Increase of the ornithine decarboxylase/polyamine system and transglutaminase upregulation in
  332. the spinal cord of aged rats. Virgili M, Necchi D, Scherini E, Contestabile A.Nat Biotechnol. 2000
  333. Aug;18(8):868-72. Targeting alzheimer amyloid plaques in vivo. Wengenack TM, Curran GL, Poduslo JF.Rinsho Byori.
  334. 2004 Apr;52(4):336-9. [Urine diacetylspermine as a novel tumor marker for pancreatobiliary carcinomas] [Article
  335. in Japanese] Yamaguchi K, Nagano M, Torada N, Hamasaki N, Kawakita M, Tanaka M.J Neurosci Res. 2001 Mar
  336. 1;63(5):395-401. Role of spermine in amyloid beta-peptide-associated free radical-induced neurotoxicity. Yatin
  337. SM, Yatin M, Varadarajan S, Ain KB, Butterfield DA.Mol Endocrinol. 2003 May;17(5):831-44. Epub 2003 Jan 23.
  338. Estrogen enhances depolarization-induced glutamate release through activation of phosphatidylinositol 3-kinase
  339. and mitogen-activated protein kinase in cultured hippocampal neurons. Yokomaku D, Numakawa T, Numakawa Y, Suzuki
  340. S, Matsumoto T, Adachi N, Nishio C, Taguchi T, Hatanaka H.Poult Sci. 2004 Mar;83(3):400-5. Water-holding
  341. capacity in chicken breast muscle is enhanced by pyruvate and reduced by creatine supplements. Young JF,
  342. Karlsson AH, Henckel P.&nbsp;Proc Natl Acad Sci U S A. 1980 Sep;77(9):5312-6. Local anesthetics inhibit
  343. induction of ornithine decarboxylase by the tumor promoter 12-O-tetradecanoylphorbol 13-acetate. Yuspa SH,
  344. Lichti U, Ben T.&nbsp;Exp Oncol. 2004 Sep;26(3):221-5. Role of polyamines in the function of nuclear
  345. transcription factor NF-kappaB in breast cancer cells. Zaletok S, Alexandrova N, Berdynskykh N, Ignatenko N,
  346. Gogol S, Orlovsky O, Tregubova N, Gerner E, Chekhun V.Arkh Patol 1995 Jul-Aug;57(4):89-92. Biological markers of
  347. precancer of the large intestine. Zagrebin VM. © Ray Peat Ph.D. 2014. All Rights Reserved. www.RayPeat.com
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