Biological age acceleration and telomere shortening in Covid-19 surviv

The course of the disease with Covid-19 is astonishingly diverse. The coronavirus not only affects the lungs, but almost all organs such as the kidneys, heart, blood vessels and the nervous system.
The best-known symptom indicating an attack on the nervous system is the reversible disturbance of the sense of taste and smell.
In addition, coagulation problems with a tendency to thrombosis occur, even when the affected person is receiving anticoagulant therapy.

The ACE-2 (angiotensin converting enzyme) concentration can also decrease in the event of an infection - especially in younger patients - resulting in blood pressure-increasing effects such as high blood pressure, cardiac hypertrophy with failure of left ventricular function, cardiac arrhythmias, atherosclerosis, aortic aneurysms, etc.
ACE-2 is relatively common in young people compared to older people.

Significant telomere shortening can occur in young people who have recovered from Covid-19.

The chronological age that is stated on our ID card says little about how fit and healthy our body is. Our biological age can be significantly lower, but it can also be older.
One of these age estimation methods is DNAm-Age. Here, the biological age of a person is determined based on the degree of DNA methylation. The pattern of methylation changes with increasing age. Methylations block the activity of the respective gene and can therefore contribute to the development of diseases.

Another method for determining biological age is telomere length.
In Covid-19 survivors, the younger the patient was, the more severe the telomere shortening was, accompanied by a lower ACE-2 concentration, which leads to the blood pressure-increasing effects with subsequent diseases already mentioned above.

Since TA-65®MD significantly lengthens telomeres, taking it can make an essential contribution to reducing biological age.

Biological age acceleration and telomere shortening in Covid-19 survivors

TA-65® can reduce immunosenescent CD8+CD28- T cells in humans