more circumstance: in menopause col- high levels of homocysteine and some apo-
lagen degradation accelerates, therefore proteins. At least 50% of cases of vascular
vessel elasticity and strength drastically disease depend on immune disorders caused
decline. by glycation and autoimmune processes that
can be triggered by Epstein-Barr virus, her-
11 Thelin excessdamagingincreasesactiontheofpermeabilitysugar and insu-and pesvirus,Anyway,cytomegalovirus,atherosclerosis is etc.not just about fat
the risk of vessel wall damage. and weak vessel walls, but also about blood
sugar and insulin fluctuations, as well as gly-
What causes blood vessel damage? Apart cation that changes the activity of certain
from menopause, high homocysteine and vessel dilating enzymes. A priori there is in-
apolipoprotein levels, another adverse factor flammation that results in plaque formation
is glycation. It disables proteins and enzymes, where cholesterol accumulates. This is an it-
impairs detoxification processes and reduces erative process.
the antioxidant status. Impaired detoxifica- When a woman goes through a menopause,
tion leads to an imbalance in the synthesis cholesterol level begins to rise. A man’s low
of sex hormones (if a patient is still in the testosterone level makes the production of
reproductive age). Advanced effects of glyca- nitrous oxide impossible. All of the above re-
tion also include mitochondria defects, their sults in artery damage and plaque formation.
mal-synchronization with the cell nucleus, Plaques become very solid, so one should not
and gene expression changes. This disturbs expect them to disappear by themselves.
the synthesis of matrix metalloproteinases Moreover, scars left after a plaque is removed
and NO-synthase. Glycation triggers endo- distort blood vessels as well.
thelium cell receptor changes, inflammation It is important to distinguish atheroscle-
and tumour necrosis. It correlates with au- rosis from Monckeberg’s sclerosis in which
toimmune processes. In other words, glyca- a muscle layer is damaged, but no plaques
tion leads to enzyme disorders and multistep are formed. This form of sclerotic damage is
uncontrollable inflammatory processes that characterized by lesion of artery middle coat
destroy any tissue or body system. It com- (as opposed to atherosclerosis). For this dis-
plicates all the processes in the vessels. Be- ease degeneration and vessel wall hardening
sides, the inflammation level is measured by processes are relevant, calcium salt accumu-
C-reactive protein levels — the higher the lates in the vessel wall instead of cholesterol.
level, the more active is the process. Thus, Calcification (calcium deposits) and inflam-
the risks of heart and brain strokes and even mation occur in the middle area of the vessel
thrombosis increase. Glycation increases wall, but not in the endothelium. Endothe-
gene expression that controls the work of lium may be affected as well, but for other
mediators in the vessel wall. They are re- reasons (stated above), that is why athero-
sponsible for endothelium stability, spasms, sclerosis can follow. In this case calcinat-
vasoconstriction, and blood coagulability. In ed plaques are formed. In most cases, both
diabetes, lipid metabolism is disturbed, sugar processes affect the same arteries and their
levels become excessive, and the vessel wall segments simultaneously. Often, as calcium
begins to degenerate. accumulates, the vessel wall begins to slough
I personally don’t believe that the main fac- off, which may cause aneurism. So, we should
tor of atherosclerosis is fat accumulation in always bear in mind that calcinated plaques
the vessel wall. I suppose, there is a genet- are a double threat since sclerosis may be
ic predisposition to the vessel wall damage, developing under the plaque
79 // Health territory. PEPTIDES. Atherosclerosis
Для таблиц, дозировок и примечаний сверяйтесь с оригинальным PDF: при извлечении текста порядок колонок может измениться.
Из библиотеки Peptides. Авторство и содержание оригинала сохранены. Размещено с разрешения поставщика.