2014-11-20 18:22:37
Variants of the gene called Apolipoprotein E affect the development of this disease
According to data from the World Health Organization, the leading single cause of death in the world is cardiovascular disease (hereinafter CD), although bacterial and viral infections and parasitism may cause more deaths combined. It is known that there are numerous risk factors for CD, including smoking, lack of exercise, and a diet too high in saturated fats. These risks are modifiable, that is, they can increase or decrease in importance according to our level of information and the commitment we acquire with our own health. However, science has also discovered that there are non-modifiable risks, that is, no matter what we do, we are born and live with them. The most important non-modifiable risks are genetic, as the reader undoubtedly already knows.
In fact, depending on some gene variants that we may have inherited, the risk of suffering from CD varies, and there is nothing we can do to avoid it. Obviously, inherited gene variants not only affect this disease, but are involved in virtually every aspect of our health, including the propensity to become ill from infections and, dare I say, also in our willingness and character to do things. sacrifices that maintain or increase our health, in these postmodern times.
For many years it has been known that gene variants of some proteins responsible for transporting fats in the blood are a risk factor for CD. In particular, variants of the so-called Apolipoprotein E (ApoE) gene affect the development of this disease and, unfortunately, also affect the probability of us developing Alzheimer’s disease.
ApoE is essential for the transport of fats in the blood, particularly cholesterol, and for their incorporation into cells. The liver is the main producer of this protein, although the glial cells of the brain also produce it, presumably to facilitate the incorporation of cholesterol into neurons, which have specific receptor proteins that capture ApoE and the fats it transports. Let us remember that, excluding water, 60% of the brain’s weight is made up of fats, among which cholesterol occupies a prominent place.
The third variant
There are three main gene variants of ApoE, called E2, E3 and E4. Each of us has inherited two of them, one from the father and one from the mother, so we can be homozygous (possessing two copies of the same variant) or heterozygous (possessing two different variants). It has been proven that people homozygous for the E4 variant have around 20 times the risk of developing Alzheimer’s at 75 years of age. On the other hand, people homozygous for the E2 variant have a lower than normal risk of suffering from Alzheimer’s. Consequently, these gene variants constitute either risk factors or protective factors for this disease. Something similar happens with EC. Again, the E4 variant is associated with a higher risk.
To understand why the different variants of a gene so dramatically affect the probability of suffering from a disease, it is always necessary to investigate their effects at the molecular level in depth. These investigations have been carried out both to find the explanation for the effects of ApoE variants on Alzheimer’s and CD. However, while research has borne enough fruit to explain why E4 variants (for those who want to know, only different in two amino acids from E2 and one from E3) affect the development of Alzheimer’s, the same has not happened. with research aimed at explaining the effects of ApoE variants on the cardiovascular system. It is true that the different efficiency of each variant to transport cholesterol can affect the development of CD, but this does not seem to explain everything.
Researchers from the universities of Texas and Cincinnati, USA, address this question and make an interesting discovery with important implications for preventing the development of cardiovascular problems. Scientists find that the cells inside the blood vessels, the so-called endothelium, have receptor molecules for ApoE, as happens with neurons and other cells in the body. This implies that these cells can capture ApoE and react to its presence. Why does this happen? The researchers find that the binding of the E3 variant to the receptor stimulates several important effects, in particular the generation of nitric oxide, a gas with considerable anti-inflammatory effects, as well as the migration of endothelial cells, necessary to repair the damage caused by the normal shear caused by blood on the inside of blood vessels. Both effects are beneficial for maintaining a healthy cardiovascular system.
Surprisingly, the E4 variant is unable to stimulate these effects, which explains why those who have it also suffer from a higher incidence of CD. These results, published in the journal Proceedings, suggest that existing drugs that stimulate the production of nitric oxide could be useful to compensate for the effects of the E4 variant and thus reduce the incidence of CD. Let us sincerely hope that this is the case.
NEW WORK BY JORGE LABORDA.
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Chained circumstances. Ed. Lulu
Other works by Jorge Laborda
One Moon, one civilization. Why the Moon tells us that we are alone in the Universe
One Moon one civilization why the Moon tells us we are alone in the universe
The intelligence funnel and other essays
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