FOODS AND FOOD ADDITIVES THAT EFFECT A RISK FACTOR FOR ATHEROSCLEROSIS

The benefits of certain foods that negate a risk factor for atherosclerosis have been touted as having beneficial results in keeping the arteries clear and the mechanism of action has not been addressed.

An example of this is fish oil, a diet rich in fish oil prolongs the bodies ability to keep blood flowing in a manner that does not address clotting, the offending factor is platelets, these tiny healing disc's, promotes an insult to the artery that has plaque build up, this is done by the formation of blood clots.

The following are a list of foods that help eliminate artery clogging plaque.

Chinese food has been found to cause easy bruising after injestion, this is due to the anti platelet effect of the black tree fungus.

An extract of onion can inhibit platelet arachidonic acid metabolism'

Ajoene, a component of garlic inhibits the binding of fibrinogen and platelet aggregation.

Cumin,Tumeric are spices that inhibit platelet aggregation and eichanoid biosynthesis.

The fatty acids of fish oil reduce arachidonic acid and this is done in a competitory fashion by competing with arachidonic acid for cyclooxygenase.

The foods and spices listed above have an effect that is pro healthy and now you know Why.

Reference Williams Hematology, Sixth Edition

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INFLAMMATORY LIPIDS

There are two families of lipids that cause inflammation, and members of these families contribute to proinflammatory actions, the families in question are derived from a substance called arachidonic acid and the pathways that are formed are called the cycloxygenase and lipoxygenase pathway.

Now, a little bit of information about arachidonic acid, it is a 20 carbon polyunsaturated fatty acid that is derived from dietary sources or by conversion from linoleic acid. Interesting that this has an oil base.

Members of both these families enhance platelet aggregation(this means the platelets clump), platelets play a role in clotting and I did touch on this in early posts, you need platelets they heal wounds but when they are in clumps, in the body, this is not normal.

Members of both these families of lipids have been found in inflammatory fluids and so the case for aspirin, aspirin role is to reduce inflamation and by doing so, negates the effect of the cyclooxygenase pathway and a acute inflamatory response.

These two families set off a cascade of other mediators called prostaglandins and leukotrines and in my next post I will go into a short explanation of there lipid role.

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MOLECULES THAT CONTRIBUTE TO THE ATHEROTHROMBOTIC STATE

The major initiator of the clotting system and the bodies ability to achieve hemostatis is tissue factor , it is a component of athersclerotic plaque and is the major contributor in clots that are formed in the arteries. It is associated with acute coronary syndrome.

Tissue factor antigen has been found in abudance in the plaque that is formed on the artery wall.

If you are a patient on an anticoagulant and have your blood tested for protime's or aptt's,if you ever notice how they draw these specimens it is usually done with a tube that is discarded.

The reason the tube is discarded is because of tissue factor, that is in the tissues, in order not to reach the blood flow,tissue factor has to be disengaged.

If not, what will happen is the tissue factor will set off the clotting system and the results will be invalid.

With the rupture of plaque this exposes active tissue factor to circulating blood thus a blood clot is formed.

Tissue factor adheres differently on different surfaces, the majority of tissue factor is inactive, and can be activated by altered phospholipids structures. It is when the active form of TF is released that the body is no longer in a state of homostasis and the arteries are in a procoagulant state.

There are other activators of atherosclerotic plaque and I will touch on these at another time.

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THE DEMOGRAPHICS OF GENETIC CHOLESTEROLS APOLIPOPROTEIN a

Apolipoprotein a circulates in the blood stream in amounts that vary from 1 mg/dl to 100mg/dl, but is usually found in the 20mg/dl range. Higher levels are found in women that are in menopause and in patients that have had a myocardial infarction and patients with diabetes mellitus.

Several large studies have found (apo a), in patients who are at high risk for early coronary heart disease. High levels are also present in patients with Familial hypercholesterolemia.

Apo a has also been associated with an increase incidence for heart disease in the Asian community but not in American Afro Americans.

Several mechanisms have been proposed as to the relationship between apo a and atherosclerosis and thrombus(blood clot).

Apo a displaces plamsminogen from sites on fibrin and fibrinogen and inhibits plamsinogen activation, thereby rendering it's ability to break down clots.

Apo a interferes with the fibrinolytic system.

Inhibits Streptokinase AND TPA both of the latter are needed to break down clots.

Apo a also may enhance the delivery of ldl particles to the artery wall.

APO a has been found in atherosclerotic plaque.

I will be going to my lipid specialist in 2 weeks. I haven't been on a statin or niaspan, for about 8 months. I also will be tested for a Vit D level as I am at higher risk than the normal population and should have a lower value,at this visit I have to remember what a very well known public TV speaker says, "Excuses be Begone".

I was given a prescription by my gynecologist for vit D3. and have been taking the vitamin for about two weeks. I have to say I do feel lot better. I don't know if this is a placebo effect,if it is, I will take the good feeling.

Reference: Williams Hematology, Sixth Edition



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APOLIPOPROTEIN H AND CHOLESTEROL PART 2

I am sure you are all waiting with bated breath to find out how the APL Syndrome came about.

If you remember from my previous post, the laboratory was getting false positive results for syphilis tests, this means that the results were positive but the patient did not have syphilis.

In the early development of coagulation testing a reagent called, Cephalin was being used to speed up coagulation reactions.Cephalin is a phospholipid, this led to abnormailities that were associated with the presence of an anticoagulant in patients with systemic lupus and frequently together with syphilis test. This means that patients with lupus gave a false positive test for syphilis due to the phospholipids in Cephalin.

In 1983 with the development of another phospholipid called Cardiolipin which is the major reagent in the syphilis test, this finding led to a major step in the identification of this syndrome.

Now back to cholesterol, Atherosclerosis was acclerated in mice immunized with anticardiolipin antibodies from an APL syndrome patient(these mice had ldl receptors knocked out).

The antibodies associated with APL can come from different venues. One being cofactor independent antibodies to phospholipis triggered by an infection, also drugs such as procanamide can induce APL antibodies. Also these antibodies can be found in patients that are asymptomatic individuals, there are also patients that are at high risk for developing the disease APL but have not sero converted.

There are co factors that have been identified along with Apo H and these deal mainly with the clotting system.

As you can tell by the above information phospholipids and Apo H have roles that are multi tasked in maintaining hemostasis in the body.

APL antibodies may show cross reactivity against oxidized ldl and this can lead to a risk for atherosclerosis. What else bears mentioning is the impairment of the fibrinolytic system. This is the bodies ability to break down clots.Also, APL antibodies have been associated with increased susceptibility to coronary artery disease and in particular premature atherosclerosis and coronary artery disease appears to be associated with antibodies against oxidized ldl.

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