Genomic Instability

Genes, something very much part of our identity. However, they are subject to damage throughout life, accumulation of damaged DNA cause numerous diseases. This intrinsic variable nature of the genome, called genomic instability, is one of the key hallmarks of aging.

Genomic instability is a combination of point mutations, translocations, chromosome gain and loss, telomere shortening, etc. Key factors that contribute to DNA damage can be environmental (stress, chronic alcohol consumption, disrupted circadian rhythm- sleep cycle), or from the body within (DNA replication errors, spontaneous hydrolytic reactions and reactive oxygen species). There are, fortunately, treatments that can delay aging. Researchers investigate transcriptional regulators of repair genes, such as non-coding RNAs, hormones, and chromatin modulators. Ongoing research focuses on age-related changes in activation of key DNA repair pathways.

Telomere Attrition

The ends of chromosomes, called telomeres, become shorter every time the cell divides. When telomerase is silenced, that is when the enzyme which adds telomeric repeat sequences become dysfunction, the telomeres become too short for cells to divide.

Telomeres, just like all other sections of DNA, are prone to damage, including double strand breaks (DSBs). And unlike the rest of the chromosomes, telomere DSBs aren’t fixed by the DNA repair pathway, as this would frequently lead to fused chromosomes and genomic instability. That’s why we have telomerase. However, telomerase expression is silenced in many adult cells, and so telomeres get progressively shorter with age. Telomerase deficiency in human is associated with premature development of diseases, such as pulmonary fibrosis, dyskeratosis congenita and aplastic anemia, which involve the loss of the regenerative capacity of different tissues.

Epigenetic Alteration

Epigenetics can be summarized as changes in gene expressions (in turn results in being active or not). It is one of the most exciting fields in life science research in the past thirty years.

Unlike DNA mutation, epigenetic alterations have a higher change of being reversible. Hence, offering opportunities for designing novel anti-aging treatments. Studies suggest that understanding and manipulating the epigenome holds promise for improving age-related pathologies and extending healthy lifespan. Epigenetic alterations include DNA methylation, histone modification, chromatin remodeling, which eventually leads to transcriptional alteration. In general, these changes increase in chromosome fragility and transcriptional noise.

Loss of Proteostasis

As cells age, environmental stresses add up and the mechanisms responsible for maintaining proper protein composition start to decline. Proteins lose their stability, autophagic processes (process in destroying unnecessary or dysfunctional parts of the cells) start to fail, and misfolded proteins accumulate.

Over the years, our bodies are subjected to many environmental inputs that put thermal stress, oxidative stress, and osmotic stress on cells, causing misfolding of proteins. For example, free radicals present in polluted air have been identified as particularly noxious agents, contributing to multiple aging-related pathologies. In younger cells, micro- and macro-autophagy pathways, together with the ubiquitin-proteasome system, take care of clearing these unfolded proteins. However, in aging cells, autophagy induction can be gradually compromised, and lysosomes become less efficient at eliminating cellular waste.

Atherosclerosis & Osteoarthritis

Atherosclerosis is a disease where the arteries are narrowed because of an accumulation of plaque. Osteoarthritis is a common chronic condition of joint, occurs when cartilage between joints break down.

Genomic instability and telomeres shortening at the cellular level can directly affect vascular function, leading to cell cycle arrest, apoptosis and premature vascular senescence. Scientific findings support the concept of prolonged exposure to risk factors (e.g., dyslipidemia, smoking and diabetes mellitus) leading to reactive oxygen species are major stimuli for DNA damage within the plaque.

Chronic Diseases Caused by ROS & Environmental Toxins

Free radicals and oxidants are produced either from normal cell metabolism or from environmental sources such as pollution, cigarette smoke and radiation.

Oxidative stress refers to the accumulation of free radicals in the body and cannot be gradually destroyed. This is the basis of many chronic and degenerative illnesses. Some examples are cancer, cataract, autoimmune disorders, rheumatoid arthritis, cardiovascular and neurodegenerative diseases.

Enhance Cardiovascular & Joints Health

Vitamins and other supplements are efficient in strengthening arteries, and improving cardiovascular health.

DNA methylation, recently revealed, implicates the development of cardiovascular disease. It is heritable but also respond to environmental factors such as nutrition. Vitamin B2, B6, B12, folate and choline produce S-adenosylmethionine, help metabolism, prevent damage of blood vessels’ inner surface, prevent blood clotting and slow down atherosclerosis.

Cellular Antioxidation, Detoxification & Support Immunity

Supporting the liver with its essential nutrients in turn enhances detoxification and immunity.

Antioxidant metabolites and enzymes works together to prevent oxidative damage to DNA, proteins and lipids. Antioxidant prevent reactive species from being formed and remove existing ones before they can damage vital components of the cell. Detoxification characterized by the removal of toxin from a living organism by the liver. Intervention aids excretion toxic molecules from cells and tissues, hence support immunity.


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