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Semelhante a Reduce your risk of Breast Cancer
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Reduce your risk of Breast Cancer
- 1. Reduce Your Risk of Breast Cancer
- 27. Cell Membrane Arachidonic Acid cyclooxygenase lipooxygenase Phospholipase A2 Synthetic Modulation of Arachidonic Acid Cascade 2 Series Prostaglandins Thromboxane A2 Leukotrienes SRS-A Cortisone Indomethacin Aspirin Ibuprofen Acetaminophen (weak) Sulfasalazine (topically) Colchicine Sulfasalazine (topically)
- 28. Cell Membrane Arachidonic Acid (AA) cyclooxygenase lipooxygenase Phospholipase A2 Glycyrrhiza glabra Quercetin Quercetin Allium cepa Allium sativum Curcuma longa Boswellia serrata (specific for 5- lipoxygenase) Other Anti-Inflammatory Botanicals Ananas Comosus -- fibrinolysis, inhibits bradykinin, increases Series I Prostaglandins Tanacetum parthenium -- inhibits platelet aggregation Matricaria chamomilla -- unknown Scutellaria baicalensis -- stabilizes mast cell membranes Capsicum Minimum -- depletes substance P Quercetin -- stabilizes mast cell membranes Ammi Visnaga -- stabilizes mast cell membranes : Botanical Modulation of Arachidonic Acid Cascade Potentiates cortisol: Glycyrrhiza glabra Curcuma longa Zingiber officinale Curcuma longa Quercetin (weak) Ananas Comosus (?) Salix nigra Gaultheria procumbens Prostaglandins Series 2 Thromboxane A2 Leukotrienes
- 29. Changing fatty acid intake: omega-6: omega-3 ratios 1:1 4:1 25:1
- 31. Cell Membrane Arachidonic Acid cyclooxygenase lipooxygenase Phospholipase A2 Nutrient Modulation of Arachidonic Acid Cascade EPA/DHA EPA substrate competition 2 Series Prostaglandins Thromboxane A2 EPA substrate competition Leukotrienes SRS-A EPA dihomo-y-linolenic acid (DGLA ) Delta 5 desaturase Vitamin E, C (stabilize membrane) Nonenzymatic Oxidation Leukotrienes SRS-A EPA Vitamin E GS-Px Vitamin E GS-Px Vitamin E
- 66. Thank You
Notas do Editor
- We know that many of the common drugs used today are effective because of their effect on prostaglandin synthesis and inhibition of the AA cascade. This schematic represents some of the known effects of drugs on this inflammatory process Review the slide However, drugs may adversely effect other systems/side effects Steroids-prednisone NSAIDS-Naproxin, ibuprofen, piroxicam----kidney damage, GI bleeding, abdominal pain, indigestion, N/V, ibuprofen Aspirin-may adversely effect glycination, GI Acetominophen-depletes inorganic sulfate (required) for sulfation/Phase II detox of drugs, xenobiotics, and steroid hormones, amine neurotransmitters. Soon to hit the arthritis market is another anti-inflammatory drug (Celebra) by Monsanto Corp.’s Searle unit--expected to ask the FDA for an expedited review by Sept, 1998. If so, it will hit the market early next year with sales expected to top $ 4 billion. (COX2 inhibitor) Global market for prescription painkillers, not including OTC sales is currently $ 5 billion However, ignoring the underlying imbalance does nothing more than treat the symptom
- Additionally, there are a number of botanical medicines that can affect these pathways as well. Wintergreen, meadowsweet(filpendulamia ulmaria), Baikal skullcap(aryuvedic) hammamalis, white oak bark
- 20 The events of inflamm that underlie Sx of pain, swelling, loss of function are induced and regulated by a large number of chemical mediators (including eicosanoids..also kinins, histamine, monokines). The regulation of eicosanoid synthesis is a classic mechanism for controlling inflammation. Eicosanoids (hormone-like substances present in tissues throughout the body) function as mediators of a variety of physiological responses such as inflammation, blood clotting, vascular dilation, and immunity. Eicosanoids can be divided into 4 classes: Prostaglandins, Leukotrienes, thromboxanes, and prostacyclins. A large part of the inflammatory process is regulated by the prostaglandins and leukotrienes. Eicosanoids are produced from omega 6 and omega 3 poly fats present in cell membrane phospholipids. They are also released from cell membranes by the action of phospholipases . LA (seeds/vegetables) Is the predominant omega 6. Converts to AA, the direct precursor of pro-inflam mediators--prostaglandin series 2 (PGE2) and leukotrienes of the 4 series (LTB4). AA also comes directly from the diet (meat/dairy/peanuts). AA is the major fatty acid released in response to injury. Review LA to GLA to DGLA to AA. DGLA leads to (PGE1--anti-inflam). Little DGLA in body compared with AA. But diet (GLA, Borage/Black Current, EPO) can change this. (ALA) Alpha linolenic-also Essential. Goes to EPA to DHA. Harder to find it in diet--flax, pumpkin, walnut, fish. Eicosan oids produced from this fat form PGE3--anti-inflam and leukotrienes of the 5 series. The final conversion of fatty acids to their respective eicosanoids occurs with the help of cycloox and lipooxyg. Enzymatic pathways. As these two pathways use some of the same enzyme systems, there is substrate competition. In some cases there is direct inhibition of enzyme activity. This also means that a relative excess of one fatty acid will dominate an enzyme system , resulting in decreased conversion of the other fatty acids-see previous point Delta 6 desaturase is particularly susceptible to inhibition. This can create a bottleneck in pathway activity, and may be related to chronic inflammatory conditions in certain susceptible individuals. Estimates are that 10% of the population may be deficient in EFAs -this is because we have excessive consumption of AA, low consumption of EPA and ALA, and destruction of EFAs in general by hydrogenation, cooking and oxidation of vegetable oils.
- However, it is also known that nutrients can have a significant modulatory affect on this specific pathway-- In developing UIX, we wanted to address nutrients that modulated these same pathways and enzymes. Vit E, C. glutathione peroxidase--NAC, glutathione, EPA