Scientific work property of Resurgen®.


Any body suffering from a serious illness’ problem can be solved although medicine might tell is irreversible. IRREVERSIBLE in medical terms is SYNONYMOUS with ignorance. Reality is when medicine rate a disease as IRREVERSIBLE what it really means is lacking knowledge or enough information to cure it. We should not see or believe what the doctors tell us is an absolute truth – although we must recognize their good faith- but reality is that is the limit of their current knowledge’s derivatives of the technique they know which still are quite far of the latest science advances.

Every twenty minutes a person dies suddenly from heart failure, 400 persons daily die from cardio vascular disease, totally 150.000 people die each year within our Country.

According to conventional medicine arteriosclerosis is incurable that is to say the arteries semi obstruction have no solution, nevertheless, world most important universities recent studies with controlled clinical trials are proving otherwise and this is a great news what happens is that medicine is extremely slow and perhaps because of obscure interests does not apply them but you must understand dear friend your own health and that of your patients is at stake and I would say even more, life itself.

Basically the problem is that arteriosclerosis affect all of us, howsoever it might be inceptively sometimes from an early age but , its symptoms are observed in elderly, it affects even vegetarians and also to people who has suffered severe shortages of all types feeding including fats, sometimes for years such as concentration camps inmates undergoing severe malnutrition even at death’s door due to consumption.

Therefore the theory this disease is produced by excessive consumption of certain fats must be revised at the light of current knowledge’s. Yourself if done a arterial Doppler may be you could see how your arteries were occupied by atheromatous plaques threatening to obstruct them in a future and yet being an alternative medicine professional perhaps has led an extreme care as far as food is concerned.

Within conventional medicine at no time is spoken to clean arteries, constantly are cited palliative medicines for lowering cholesterol, the LDL or vase dilate arteries, even there are surgical techniques such as cardiac catheterization whereby placing certain stem, a kind of dilators opening the coronary arteries light when there has been a blockage or semi obstruction and the patient has been caught in time, in the case of cardiac infarction or the coronary angina, of course in the case of brain stroke this technique is not valid and may become hemiplegic for the rest of his life.

There are techniques and treatments not only to prevent atheromatous plaques formation but even to eliminate or diminish them when already there are.

With existing treatments in official medicine the patient does survive for a long time based on patches up to when he dies because of lack of irrigation on any part of his body. Hence there is not a causal medicine that is, correcting the real cause driving to the repair of damaged arteries, i.e. up to healing, all of this is due to the fact that this disease cause is unknown affecting to a greater or lessen degree to all human beings even in early life.

As we’ll see in this essay there are ways to clean up these arteries when the atheromatous plaques has already been produced and much better to prevent them. As we’ll see later on treatment with folic acid and vitamin B6 and B12
is advocated and also from my own view point should be added, in men as well as women, soy phyto estrogens, appropriate doses, that is around 90 mgr a day because those are involved with vitamin B6 in homocysteine catabolism as we’ll explain, women are protected while they do rule but when they enter into menopause those fall sharply becoming equal to men as far as suffering from arteriosclerosis, it is well known men androgens increase arteriosclerosis while estrogens reduce it all of which is due to their action over the homocysteine. As well must be administered large doses of vitamin C and E even all types of anti oxidants, we’ll speak about all of this later on.


Association in between homocysteine plasma levels and ahteromatous plaques development


In a recent study carried out by the Neurology Department of Peace University Hospital of Madrid Autonomous University. Over 266 patients affected by arteriosclerosis with a history of heart attacks and some other cardiovascular events to whom carotid doppler was practiced it was found that their carotids were affected by atheromatous plaques and it was found a direct relationship in between the homocysteine level and the number of carotids plaques , so the study concluded with this statement

High homocysteine plasma levels (> 10 mcmol/L) are associated with carotids plaques development registered by carotid doppler ultrasound, independently of age.


This last finding is most important since it is advocating for a treatment, so far unknown, which might be leading to arteriosclerosis healing.

It is being advocated Mediterranean diet and, as for myself, where more arteriosclerosis with brain strokes or infarction I’ve seen is within Spanish villages where absolute diet based on vegetables and some pork is strictly observed. Nevertheless those countrymen suffered from a chronic state of deep concern for their camps which could become totally destroyed overnight because of a bad frost or by hail storm. Certainly Mediterranean diet is healthier and that is due to its higher content of antioxidants which prevent or diminish lipoproteins of low density (LDL) oxidation, the real cause of arteriosclerosis, that is, the ones are not the LDL BUT OXIDIZED LDL BY FREE RADICALS.

It is proved certain diets are antioxidants and diminish arteriosclerosis production, the proof is that the index of infarctions among vegetarians is around 24% less than in the rest of population, but something is to reduce atheromatous plaques formation within the arteries by means of the diet, and something else is to eliminate the existing ones, that is to say, to cure arteriosclerosis and this is not achieved neither through Mediterranean diet nor even with vegetarian one. All these diets might serve as preventive since they are antioxidants and arteriosclerosis disease is an oxidative disease by low density proteins (LDL) oxidation. Moreover in an study on hundreds of people who survived concentration camps it was found the atheromas index inside their arteries, or arteriosclerosis, it was about the same either greater than it was in subjects normally fed with opulent diets rich in fat. This gave much matter to think it over, casually it was found in all these patients high homocysteine levels despite not having eaten fats or almost any feeding.

It is well known all these patients underwent a great psychological suffering and to me this is the true genesis of their emotional arteriosclerosis with increased free radicals, homocysteine, lowering of nitric oxide, etc.

All of that is taken by the product RESURGEN and also applied via alveolar as an inhaler so that high doses are acquired in blood i.e. reaching the general blood circulation in adequate doses, to that should be added all types of antioxidants above all vitamin C large dose since this disease is produced by the lipid peroxidation produced by free radicals produced by an uncontrolled metabolism and just about always by our own unbridled emotions as I do demonstrate in those essays before mentioned much less due to fat intake or bad diet although this logically it does contribute but not because of diet type but because of many fats types are more susceptible to oxidation than some others even some of them have the ability to fight those radicals but nevertheless if there is peace with no psychological suffering, which in fact becomes impossible, hardly will be produced free radicals at exorbitant amount to oxidize the LDL It is advised to take RESURGEN as a prophylactic continuously dose 6 inhalations four times a day to avoid suffering this disease or combat it.

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Coronary disease (EC) is the leading cause for death in United States. Conventional risk factors predict less than half of cardiovascular future events and it seems not having the same influence for different ethnic groups. It is seen high homocysteine concentration (HC) in plasma becomes associated with atheromatous plaques formation and blocked arteries.

After several studies was found significant difference in blood homocysteine levels in elders over 65 years age (11,9 +/- 3,5 umol/1) compared with youngters around 20-30 years age (8.73 +/- 1.68 umolQ). Both groups were healthy volunteers, were found levels of 17,4 +/- 7,4 umol/1 in one group of 30-70 years age who has suffered brain stroke .

Current scientific evidences strongly indicate low density lipoproteins oxidative modifications (LDL) constitute the key factor and most important one in arteriosclerosis initiation and development. The oxidized LDL may favour the atheromatous plaque development through a number of mechanisms such as its cytotoxicity, its chemotactic effect over monocytes, its effect over vascular tone, its thrombogenic effects, and finally encouraging their uptake by macrophages to become foam cells.

Actually very little is known on arteriosclerosis being the disease that costs more lives to society, perhaps also because it is silent illness starting in early times in life and little by little produced injuries will worsen

Up to trigger an acute situation life-threatening, such as heart attack and others.
In conventional medicine there are multiple treatments, all of them symptomatic ones in order to lower cholesterol figure or the triglycerides or that of LDL (low density lipoproteins) , all of them side effects even there exists vessels dilators and other attempting to regulate blood pressure but none of them acts on the arteriosclerosis root cause that is to say, over the LDL lipid peroxidation

In an arteriosclerosis patient usually it is easy to find elevation of those LDL, lipoproteins which are the responsible ones for carrying cholesterol to the tissues cells, but these LDL are sick, they became oxidized by the free radicals and do not accomplish their own function depositing on the arteries walls , this makes immunity to become launched and leukocytes migrate up to where they are to destroy them which carries an inflammation; these leukocytes when they digest them become transformed into what is called foam cells and that’s when the atheromatous plaque begins to be formed which in future can block the artery.

In this plaque there exists inflammation signs hence in blood tests protein C reactive (PCR) is high, i.e arterioscleroris is an inflammatory disease.

As we see the arteriosclerosis true cause is in the excess of free radicals, that is, on the oxidative stress hence try to reduce this stress is essential to prevent and to treat arteriosclerosis. Oxidative stress might be produced because of multiple causes among them, and may be the most important one wayward intensive emotions long-held, that is, psychological chronic stress. Whichever might be the cause it is much better to prevent that early in life, i.e. in young adult that is when they start to be formed atheromatous plaques within the arteries and therefore then is necessary to fight oxidative stress, what means, to practice a real atherosclerosis prevention. Free radicals increase when our Ph becomes closed to acidosis and they are not properly removed out from the body by a malfunction of our antioxidants defences mainly including glutathione and its enzymes besides certain vitamins such as C, E, etc.

To raise glutathione and consequently clean out free radicals must be given the amino acid cysteine, since if we administer pure glutathione

This fails to be risen up according with very specific experiences. That is why in RESURGEN formula we’ve included cysteine besides it is administered alveolar via acquiring high blood concentrations

Currently is being observed a considerable increase of people suffering myocardial infarction or a brain stroke suddenly and unexpectedly in many of them having practiced previously electrocardiograms and blood tests with normal results, i.e. not showing arteriosclerosis signs however many of them were killed or have been left severely damaged. Doctors have realized this and concluded that the medical tests to predict these events which might be leading to grave damage, even to death, are not as exact as they were considered and they are not good enough to predict nor to prevent neither myocardial infarction nor brain stroke. Have not sure and reliable medical tests able to predict these types of acute medical conditions is certainly a very serious problem; otherwise having them quite a number of lives could be saved. At this and to avoid deaths a few years ago began to look for another analytical indexes good enough to get to know if a certain person was suffering arteriosclerosis, what means if she was at risk to suffer suddenly any of these conditions, sometimes, fatal. Consequently they were found certain indexes, blood tests laboratory abnormalities indicating more reliably if a person was at serious risk to develop any of these sudden conditions sometimes even death,
These indexes were high homocysteine and protein C reactive.

What happens is that medicine is extremely slow and even there are multitude of clinical evidence that support the fact that other analytical trials are much more reliable and rigorous have not been put into practice within many hospitals and not even by conventional outpatient medicine, i.e. in health centres. The risk is very large for people of certain age which may have an illness such as arteriosclerosis not knowing it and consequently not having appropriate treatment remedies and standards of living leading to ensure avoiding the fearsome heart attack and other complications which might cost life or left behind serious physical sequelas.

So far apparently there are not reliable routine conventional medicine tests to diagnose arterosclerosis

Usually when in a patient his analytical demonstrates the presence of overall cholesterinemia, cholesterinemia of low density lipoproteins and hyper triglycerinemia it is said he is a high risk patient but there are quite many patients with all their analytical normal besides electrocardiogram unaltered suffering myocardial infarction or cerebral ictus.
Logically if we should submit a certain person to his arteries catheterization to watch them in their inside by sure we would realize some of them were occluded or semi occluded and we would do diagnosis of certainty, but evidently this can’t be routine practiced to the entire population at risk.
Nevertheless there exist another technique non invasive very easy to make which is the carotids arterial echo Doppler or with any other artery through which we can see if there exist atheroma plaques and hence the existing arterosclerosis degree also serve us to see the evolution of the same after taking the adequate treatment.

An article published in le journal The Lancet indicates the treatment with vitamin B6 and folic acid might help to prevent premature arterosclerosis. High concentration of homocysteine (an intermediate in the cysteine biosynthesis) in blood is associated with higher risk to suffer premature arterosclerosis
(Arteries blockade by atheroma plaques)

Homocysteine concentrations might be reduced through folic acid and vitamin B6 treatment, Universitarian Hospital Vrije Universiteit of Amsterdan, Holland doctors say after having studied 158 healthy patients and patients’ relatives with a premature way of the disease. Out of all analyzed people 78 received vitamins and 80 took placebo along two years.

At the end of this study participants within the group taking folic acid and vitamin B6 had lessen homocysteine concentrations than those belonging to the placebo group, jet much less showed abnormalities in electrocardiograms (six in folic acid group in contrast with 14 in placebo group).

In the last decade has been clearly documented the association in between arterosclerosis (with coronary obstruction disease cerebral or peripherical) and high total homocysteine concentrations. The involvement of moderate plasmatic homocysteinemia in the pathogenesis of venous thrombosis was not yet suspected or established until recent years.

Treatment with folic acid, B6 and B12 easily reduces, quickly and efficiently (over 40% in about 6 weeks) pathological values of total homocysteine.

Homocysteine has been associated with premature vascular disease as others risk factors such as high levels of cholesterol and triglycerides. This paper wanted to establish parenterally homocysteine administration effect, and folic acid orally in the atheroma plaques formation in rabbits.

To attain that were studied 15 rabbits New Zealand race coming from the Carabobo University vivarium divided into three groups which were fed after the following scheme:

Group 1: Normal food for rabbits
Group 2: Homocysteine subcutaneous injection during 40 days
Group 3: Homocysteine in the same way than group 2 (subcutaneous injection)
plus folic acid orally.


Determinations were made of cholesterol serum levels, lipoproteins, triglycerides, folic acid and homocysteine before and after experimental period.
Rabbits were sacrificed , heart and aorta were extracted to perform histological cuts of the same.

Obtained results showed homocysteine levels were higher in group 2 (homocysteine injection without folic acid) than those obtained in group 1, differences in between those two groups which were significant being observed in group 2 the atheroma plaques more severe grades IV and V.

In group 3 (homocysteine injection plus folic acid) seen homocysteine levels were not higher and folic acid levels in this group were higher compared with the others, as well in this group 3 atheroma plates seen were less severe than those in group 2 with grades I and III.

To conclude the most damage of vascular endothelium was observed in group 2 (homocysteine injection without folic acid)

Results suggest implementation with folic acid prevents the elevation of plasmatic homocysteine therefore reduces injury possibility at vascular level, hence, reduces atheroma plates formation.

Sex hormones. Male hormones are atherogenic, while estrogens protect against atherosclerosis that is why in women diseases rate related with atherosclerosis increase after menopause.

Lack of folic acid is the most frequent vitamin lack in Europe due to the population dietary habits and nutritional as well as the folic acid thermolability during food preparation. Recommended daily allowance is 400 µmg/day. Nevertheless in practice they only ingest as average 170-240 µmg women and 200-235 µmg men. Therapeutic dose in case of homocysteinemia is in between 600 and 1.0 µmg/day.

Among the most important folic acid sources are the Brussels sprouts, kale, asparagus, spinach and wheat germ. Whole grains, legumes, potatoes, chicken, beef and lamb and fish are rich in vitamin B6. The maximum contribution in adults is of 1,5 mg/day.

When there are homocysteine high values it is recommended to intake 10 mg/day. As vitamin B12 source we might have foods of animal origin Mackerel, herning, beef, liver, free fat dairy products and eggs can provide therapeutic needed input of 400 µmg/day.

The recommended amount of vitamin B12 ingestion in healthy adults is only of 3 µmg/day. If it is not possible to achieve sufficient oral intake parenteral replacement should be performed.

To oxidative stress with too high an amount of oxygen free radicals great importance it is attributed in the onset of arteriosclerotic diseases.
To protect against oxidative damage human body needs sufficient antioxidants such as vitamin C and E as well as oligoelements zinc and selenium.

Scientific evidence shows modified LDL, mainly because of oxidative processes have a central role in the development of atherous plates.

Oxidized LDL are the most atherogenic form of LDL taking part on different processes leading to plate formation such as endothelial damage induction, accumulation of monocytes/macrophages, foam cells formation, antibody induction, etc.

Arteriosclerosis is a syndrome characterized by the deposit and infiltration of lipid substances in the arteries of medium and large calibre walls. Is the most common form of arteriosclerosis. Causes an inflammatory reaction and multiplication and smooth muscle cells migration of the wall producing ranging narrowing of the arterial lumen. The concrete nodes are called atheroma plaques.

They present a central soft core, lumpy and yellow, consisting of lipids (cholesterol and its esters) covered by a fibrous layer. Normally only occur occupying a portion of the circumference of the arterial wall in patches variables along the vessel. Initially scattered but increase in number as the disease progresses. In advanced cases shows a plaques process of calcification increasing the risk of sharp change in the plate:

® may occur plate rupture, erosion or ulceration and might generate the appearance of a thrombus and block a vessel located ahead of the plate zone which would produce a lack of blood supply in the area irrigated by corresponding artery (ischemia) which can be fatal if the blockage occurs in a coronary artery or un a brain artery

® bleeding might occur inside the plate by the breaking of inside existing capillaries which can result in an hematoma and promote the plate rupture;

® vasoconstriction of affected area might as well promote the plate rupture hence is most dangerous arterial hypertension with vasoconstriction.
In this way a place would become thrombogenic and of the degree of the thrombus lability and capacity of local fibrinolysis may derive in three different ways: 1) thrombus organization with plate progressive growth; 2) intermittent occlusions resulting in intermittent ischemias, and 3) total occlusion with necrosis of affected area.

Arteriosclerosis key processes are thickening of the intima and lipids accumulation.

Atheroma plates shows up characteristic distribution since basically they become present within the main arteries, in turbulent blood flow zones above all:

• abdominal aorta more frequently than in thoracic aorta
• especially in the ostial (ostium) of major arterial branches
• in descending order (after abdominal aorta) most frequently affected vessels are:
• coronary arteries
• internal carotids
• vessels of Willis circle, a set of arteries supplying blood to the brain
• normally upper extremities vessels are not affected as well as
mesenteric arteries (upper and lower) and renal arteries except for their
respective ostia.
• in the same individual usually coexist several injuries at different stages of evolution.


Risk factors


This disease is the leading cause of death in West Countries, developed or the first world, such as, United States of America, Europe and Australia, being too frequent in the three South American most developed countries Mexico, Brazil and Argentina and that becomes associated to one unhealthy lifestyle. Risk factors

For the development of arteriosclerosis can be grouped into two categories according with the possibility to act on them


• Age. Age has s dominant influence. Death rates because of heart ischemic diseases (i.e myocardium infarct) increase throughout life even older. Arteriosclerosis normally does not become evident until half life or even later when arteries injuries cause damage to organs. In between 40 up to 60 years age the incidence of myocardium in fact multiplies by five.
• Sex Hormones: Male hormones are atherogenic while estrogens protect against arterosclerosis that is why in women rate for diseases related to arterosclerosis increase after menopause.
• Family history and genetic alterations. Family predisposition to arterosclerosis and cardiac ischemic diseases is quite well defined. Normally genetic susceptibility is associated to another different risk factors such as hypertension or diabetes, less frequently to lipoproteins metabolic alterations which produces high lipid levels in blood as it does in family hypocholesterolemia


• Hyperlipidemia or increased lipids levels in blood Is the greatest risk
Factor towards arterosclerosis. Most evidences refer to hypercholesterolemia, that is to say, cholesterol levels in blood.. The main component of serum cholesterol associated to increased risk are the low density lipoproteins or LDL with a most important physiological role in cholesterol transport toward peripheral tissues. (Nevertheless it is my own believe in agreement with multiple scientific works it goes only with oxidized LDL by free radicals not recognized by the cell and persists in the general circulation becoming accumulated in the arterial walls producing the atheroma plate). Nevertheless high density lipoproteins or HDL protect against arterosclerosis since they remove cholesterol out from the tissues and the atheromas to carry it towards the liver where it is excreted bile through . Hence the HDL is known as the “good cholesterol” : as higher the HDL level less risk and vice verse for the LDL. Exercise and moderate alcohol intake increase the HDL level while obesity and smoking reduce it. A diet rich in cholesterol and saturated fatty acids (present in the eggs yolk, animal fats and butter) increase the LDL levels. Vice verse a low cholesterol diet and as well low in the relationship in between saturated fatty acids and unsaturated causes a reduction in LDL levels. Yet more, fatty acids type omega-3 abundant in fish oils, most probably are beneficial while tran saturated fats produced by vegetable oils artificial hydrogenation (used in baked goods and margarines) might negatively affect cholesterol levels. Drugs known as astatines reduce circulating cholesterol levels by inhibiting one key enzyme of the cholesterol biosynthesis in the liver, the HMG-CoA reductase.
• Arterial hypertension (HTA) one of the main risk factor at any age
responsible by itself for an increase of about 60% risk for cardiovascular
disease. HTA is the main cause of ventricular hypertrophy related to
cardiac failure. Men aged in between 45 and 62 whose blood pressure
(Pa) is over 169/95 mmHg are five times more risky of stroke than those
With a Pa of 140/90 mmHg or even less. As well an increase of systolic
Pressure as diastolic one are important concerning risk increase.
Increase blood pressure causes shear forces that break the fragile
endothelium overlying the inner arteries surface. Anti hypertensive
treatments reduced the incidence of diseases related to arteriosclerosis.
such as brain stokes and cardio vascular accidents.
• Smoking. Toxic substances snuff contained such as nicotine have a
direct toxic effect over the arteries walls causing an inflammatory response. Smoking a pack of cigarettes or even more, doubles death rates because of cardio vascular disease. Give up smoking reduces significantly that risk.
• Diabetes mellitus. Diabetes induces hyper cholesterinemia and increased predisposition to arteriosclerosis. The incidence of myocardial infarction is double in diabetics and it is observed and increase 100 times in lower extremities gangrene frequency induced by arteriosclerosis.

Previously mentioned factors are responsible for about the 80% of cardio vascular diseases. The rest are attributed to other minor factors.

• Inflammation. The presence of inflammation is closely linked to
Arteriosclerosis development being one of the main causing agents for its pathogenesis. Hence the determination of systemic inflammation presence has become an important element for the risk stratification.
One of the most simple and sensitive methods is the determination of protein C reactive level (PCR). This is an acute phase protein synthesized primarily in the liver produced at the end of the cascade of different inflammatory processes. In arteriosclerosis case is synthesized by the damaged endothelial cells and PCR levels in blood accurately predict myocardial infarction risk, cerebral vascular event, peripheral artery disease or sudden cardiac death even in individual apparently with good health. Give up smoking, weight lost and exercise reduce PCR levels as well treatment with astatines reduce PCR.

• Homocysteinemia. Many clinical studies show up stron association in
Between serum homocysteine levels and cardio vascular disease, brain stroke, and venous thrombosis. A decrease in the ingestion of folate and Vit. B12 might produce high blood homocysteine levels

Other factors with a less pronounced effect or more difficult to quantify include:

• Sedentary way of living with reduced physical exercise since this modifies many risk factors and ultimately reduces inflammatory response in the arteries walls.
• Stress, associated to a competitive life style (personality “A type” )
• Obesity, frequently associated to hypertension, diabetes, hyper triglyceridemia and low HDL levels.

Risk factors cause tears in the arteries light of medium and large calibre, where fatty substances become deposited, inflammation and finally narrowing of arteries light and blood flow obstruction. Cholesterol (LDL) is deposited into the atheroma plates when low density lipoproteins or LDL concentration is high (after my own thinking oxidized LDL). The arterial wall cells interpret this deposit as an invasion exciting the immune system which in turn causes inflammation. Excited immunity cells are circulating monocytes penetrating the artery wall, become transformed into macrophages and begin to engulf LDL particles becoming foam cells. As well inflammation forms a capsule of fibrous tissue in between the atheroms plate and the artery. As the atheroma plate advances narrowing occurs or artery stenosis, initially only partial to finally evolve into complete obstruction. Besides that the atheroma plate is fragile and might get broken, bleed and form a thrombus or dispose out from the artery and cause an embolism. Arteries reduce their diameter due to fatty substances accumulation, increasing fragility and arteries hardening. All of this leads to increase blood pressure and in case that might occur within the heart or brain could cause death.

Schematically, central arteriosclerosis pathogenesis elements are the following:

1. chronic endothelium damage which typically occurs subtly and gradually to end up with the dysfunction of the same, generating an increase of permeability, the adhesion of circulating leukocytes (initially monocytes) and the appearance of thrombus.
2. accumulation of oxidized lipoproteins, mainly LDL with high cholesterol content into the affected blood vessel wall (usually in the innermost layer of a large artery)
3. into lesion accumulated lipoproteins modification because of lipid peroxidation
4. adhesion of blood monocytes (and other leukocytes) to the endothelium followed by their migration toward the innermost and their transformation into macrophages and foam cells.
5. platelets adhesion
6. factors release by activated platelets , macrophages or vascular cells causing migration of smooth muscle cells of the middle artery layer towards the innermost one
7. smooth muscle cells proliferation in the innermost; these cells become
modified and develop extracellular matrix components such as collagen and proteoglycans which are accumulated into the innermost generating the fibrous layer of the atheroma plate.
8. increase lipids accumulation both intracellularly (in the macrophages and
smooth muscle cells) as extracellularly.
9- atheroma plates can remain stable with a dense fibrous layer and
Inflammatory and lipid component not important. These plates although
They might reduce considerably the vessel light generally they do not
Produce an acute lesion, usually plates producing lesions are broken
10. a plate can become unstable (prone to rupture ) if having a thin fibrous
layer, a large lipid core and important inflammatory process . Plaque
rupture can generate a thrombus.

Endothelium chronic damage

As far as hemodynamic disturbances a frequent observation is that atheroma plaques accumulate on the vessels inlet (ostia) , in branching areas, and in the rear wall of abdominal aorta sites where is observed a turbulent blood flow.
In vitro studies have shown the presence of a laminar flow induces the expression of protector genes against the arteriosclerosis (i.e antioxidant enzyme superoxide dismutase) and this would be most important as to the action of glutathione and its enzymes in the arteriosclerosis genesis in such a way that empowering them or increasing their levels (AS RESURGEN DOES ) we could cooperate to combat arteriosclerosis and maybe this shows up the genesis or arteriosclerosis cause might be increased oxidative stress.

• Lipoproteins common alterations are: cholesterol-LDL increase levels,
Decreased cholesterol-HDL levels or increase lipoprotein (a) level.

The mechanisms through which hyper lipidemia contributes to atherogenesis include:

• chronic hyper lipidemia (above all hyper cholesterinemia) might directly
induce endothelial dysfunction by increasing the local production
Of oxygen reactive species (ERO); oxygen free radicals might damage the tissues and to accelerate the disappearance of nitric oxide (NO) reducing its vasodilating action
• In chronic hyper lipidemia the lipoproteins accumulate inside the intima.
These lipids become oxidized by ERO effect generated by the macrophages or endothelial cells. Oxidized LDL are detected by the “scavenger” receptors different ones than those for LDL, ingested by these and accumulate in phagocytes which become known as “foam cells”. Oxidized LDL besides that stimulate the release of growth factors cytokines and chemokines , by endothelial cells recruiting more monocytes to the lesion. Finally oxidized LDL are toxic to endothelial cells and smooth muscle cells and can induce their abnormal functioning.
• Most part of cholesterol is transported by the blood bound to proteins forming particles known as low density lipoproteins o LDL
• When the cell needs cholesterol for the membrane synthesis produces
LDL receptor proteins and insert them in its plasmatic membrane. When
Cholesterol is taken pass to the liposome’s where cholesterol esters are hydrolyzed resulting free cholesterol which thus is available to the cell for the membranes biosynthesis. If too much free cholesterol is accumulated in the cell thus stops cholesterol synthesis as much as LDL receptors proteins synthesis whereby the cell produces and absorbs less cholesterol.
• As it was early mentioned LDL ar not physiologically involved in a net
Cholesterol inflow toward the tissues. Nevertheless in certain pathological circumstances, such as LDL hypercholesterinemia, hypertension, diabetes mellitus, or smoking develops cholesterol exaggerated delivery and unregulated from LDL, chemically modified (oxidized) toward subendothelial macrophages cells which when exceeded in their purification capacity within a process known as “reverse cholesterol transport“ and mediated by the high density lipoproteins (HDL) degenerate into unstable cells, prone to inflammation and pathological cell death (necrosis). The accumulation of these macrophages cholesterol overloaded, known as foam cells, determines the development of atheroma in the artery wall defining pathological fact for the arteriosclerosis disease.

• In postmenopausal woman hepatic lipase activity is increased hence
hormone replacement therapy with estrogens by reducing this enzyme
activity reduces LDL levels.


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