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Action Acid
WORLD IN ACTION - ACID HOUSE REPORT PT.1
Use of omega 3 fatty acids
Interest in omega-3 polyunsaturated fatty acids (PUFAs) has increased sharply in the early 80's, when a Danish research scientists Dyerberg J. and Bang H. found that very low levels of cardiovascular disease (atherosclerosis and coronary heart disease, hypertension), the inhabitants of Greenland, probably due to drinking large amounts of marine fats high in omega-3 PUFA. Scientists have discovered that blood plasma inhabitants of Greenland, as compared with the Danes. These findings were confirmed by epidemiological surveys of the coastal population of Japan, the Netherlands and other countries.
Later it was found that omega-3 fatty acids along with the hypolipidemic effect have hypocoagulation, antiplatelet, anti-inflammatory and immunomodulatory actions.
The mechanism of action and rationale therapeutic use of omega-3 PUFA is partly due to their influence on the state of eicosanoids. Omega-3 fatty acids are competitive antagonists of arachidonic acid - base substrate synthesis of prostaglandins (PG) thromboxanes (Tx) and leukotriene (LT) in the body in the phospholipids of cell membranes.
On admission, EPA and DHA from food (in the body, these acids are not synthesized), they partially replace the omega-6 PUFA in the membranes of platelets, red blood cells, neutrophils, monocytes, hepatocytes and other cells. Competition between arachidonic acid and omega-3 PUFAs on cyclooxygenase-lipooksigenaznom level spectrum shows a modification of PG and LT:
- Decreased production of metabolites of prostaglandin E2;
- Reduces the level of thromboxane A2, a potent vasoconstrictor and activator of platelet aggregation;
- Decreases the formation of LTV4, inducer of inflammation, chemotaxis and adhesion of leukocytes;
- Increases the plasma concentration of thromboxane A3, a weak vasoconstrictor and inducer of platelet aggregation;
- Increased levels of prostacyclin I3 (PGI3) that in the absence of reduction of prostacyclin I2 (PGI2) increases the concentration of total prostacyclin. PGI2 and PGI3 are active vasodilators and inhibit platelet aggregation;
- Concentration LTV5, weak anti-inflammatory agent and a chemo tactic factor.
Mechanisms of action of omega-3 PUFAs in other parts of the hemostatic system (in particular, found a decrease of fibrinogen, activation of the fibrinolysis system) are not fully understood. Hypolipidemic action of fish oil is to suppress the synthesis of lipoproteins of very low and low density, improve their clearance and increasing the excretion of bile. Lately we hear a lot of unflattering words to arachidonic acid (AA). Apparently, you need to cite several arguments in defense of this matter.
In terms of health, when excessive vasoconstriction and bronchoconstriction are not provided, there is no need in excess of vasodilators and bronchodilators.
It should be noted that the release of AA from the cell membrane and subsequent metabolism occurs in response to a variety of factors (stress, hypoxia, catecholamines, collagen, antigen-antibody reaction, etc.). So, in terms of disease under a variety of pathological conditions is a nonspecific compensatory-adaptive reaction is transformed into the pathological. Hyperproduction of constrictor factors, activators trombagregatsii already acquired the clinical significance and requires correction.
Thus, in conditions of disease to humans are more beneficial metabolites EPA, since among them is dominated by chemicals that are inflammatory and inhibit platelet aggregation properties.
If the diet of a healthy person to completely eliminate the AK, it will only bring negative results, since the metabolites of EPA are not fully implemented those functions that perform metabolites of AA. Confirmed by the results of epidemiological studies: the inhabitants of coastal areas, are exclusively products of the sea, do not suffer from atherosclerosis, but they have increased bleeding, frequent development of hemarthrosis in response to the slightest injury, hypotension.
With regard to the sick person, only small change in diet would be something difficult to fix. That's why they need appropriate concentrates or drugs.
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Frequently Asked Questions...
Lexus damages my paint but blames me what is my next step of action?
My car is a 2006 Lexus IS 350 pearl red with only 6,000 miles on it. Lexus told me when I purchased the car and paid additional for Perma Paint (I know its only a layer of wax) to bring the car in at 6 months for another coat. When I dropped off the car and my advisor did the walk through and there were no problems but a few days later they called me to come and look at the car. It was covered on the hood, roof and trunk with mini white spots some all the way through the paint. They tried to blame rock chipping and I have taken the car to another paint shop and came to the conclusion it was some type of acid (battery, wet cement etc...) Now my claim with Lexus has been denied because they call it "Impact damage" and that they took pictures of the circle and it has cracks leading away. I can file a claim with the BAR but thats only a ding to the dealership. Can anyone recommend a lawyer or another course of action? The estimate to repaint which depreciates the car will be aprox. $5000
Answer:
Talk to the regional customer service rep. Start making noise and don't let up. File a complaint with the BBB, bring a civil suit against them. Just keep on going until it starts going your way.
