9 Hallmarks define why we age,
In essence, aging is the result of damage to cells, which can cause a range of symptoms, from the most basic wrinkles to more serious illnesses. The ability to slow down the aging process can potentially extend overall health and wellbeing.
In 2013, López-Otín and colleagues developed a framework outlining the "9 Hallmarks of Aging" which encompasses all the known factors contributing to aging. Experimental studies have shown that these hallmarks can either slow down or exacerbate the aging process.
Currently, many scientists are expanding on this framework, identifying molecules and lifestyle habits that target the hallmarks of aging and can potentially reverse the biological clock.
Our products are founded on this scientific research.
We acknowledge that comprehending the 9 Hallmarks of Aging may be challenging for individuals without a biology PhD degree. A simpler approach is to view aging as a result of cell damage, and then categorize it into four primary causes. Additionally, three other causes accelerate the primary causes, while two causes manifest only when there is severe damage.
- DNA errors are classified as genomic instability.
- Loss of DNA protection occurs when telomeres shorten.
- Epigenetic alterations occur when genes are incorrectly activated or deactivated.
- Accumulation of proteins within cells is referred to as loss of proteostasis.
- When cells absorb an excess amount of nutrients, it is referred to as nutrient sensing.
- The breakdown of internal power plants is known as mitochondrial dysfunction.
- Zombie cells are a colloquial term for cellular senescence.
- Reduced tissue maintenance and repair are associated with stem cell exhaustion.
- Altered cellular communication can lead to a cycle of damage.
Genomic instability refers to the tendency of an organism’s DNA to undergo changes or mutations, either spontaneously or as a result of exposure to environmental factors. These mutations can include changes in the sequence of DNA, rearrangements of genetic material, and alterations to chromosome number or structure.
Genomic instability can have serious consequences for the health and survival of an organism. Errors in DNA replication or repair can lead to the accumulation of mutations that can disrupt normal cellular functions, leading to cancer and other diseases.
In addition to environmental factors, genomic instability can also be caused by genetic predisposition or inherited mutations in DNA repair genes. These mutations can make individuals more susceptible to the effects of environmental factors and increase their risk of developing certain diseases.
Understanding the cause and mechanisms of genomic instability is an important area of research in genetics and molecular biology. By identifying the factors that contribute to DNA damage and mutations, researchers can develop strategies to prevent or repair these changes and reduce the risk of disease.
Telomere Shortening is a natural process that occurs as cells divide and DNA is replicated. Telomeres act as protective caps on the ends of chromosomes, preventing them from fraying or stocking to other chromosomes. However, with each cell division, the telomeres become shorter, eventually reaching a point where they can no longer protect the DNA.
When telomeres become too short, the cell can no longer divide, leading to cellular senescence or apoptosis, which is programmed cell death. This process is believed to play a role in aging and age-related diseases, as cells lose their ability to function properly and repair damage.
Telomere Shortening can be accelerated by various environmental and lifestyle factors, such as chronic stress, poor diet, lack of exercise, and exposure to toxins. THis can lead to premature aging and an increased risk of age-related diseases, such as cardiovascular disease, Alzheimer’s disease, and certain types of cancer.
Epigenetic alterations can occur due to various factors such as environmental exposures, diet, lifestyle, and aging. For example, exposure to toxins or chemicals, such as cigarette smoke or pesticides, can cause changes in the epigenome that increase the risk of diseases such as cancer or respiratory diseases. Similarly, a poor diet or sedentary lifestyle can lead to epigenetic changes that increase the risk of obesity, type 2 diabetes, and cardiovascular diseases.
Aging itself is also associated with epigenetic alterations, where certain genes become more active or inactive over time, leading to a decline in the functions of various organs and tissues. However, research has shown that epigenetic alterations are reversible and can be modified through intervention such as dietary changes, exercise, and medications.
Loss of Proteostasis
Loss of proteostasis refers to the disruption of the delicate balance of protein synthesis, folding, and degradation in our cells. This process is essential for maintaining healthy cellular functions and preventing the accumulation of misfolded or damaged proteins that can be toxic to cells.
Accumulation of proteins inside cells can occur due to a number of factors, inducing genetic mutations, environmental toxins, and normal aging processes. As these proteins build up, they can form aggregates or clumps that interfere with normal cellular processes, leading to malfunctioning cells and ultimately contributing to a range of diseases, including Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease.
The build up of proteins can also cause cellular stress, triggering the activation of cellular pathways that can lead to inflammation and oxidative damage, further exacerbating the problem.
Deregulated Nutrient Sensing
This deregulation of nutrient sensing can contribute to a range of health problems including, obesity, type 2 diabetes, and cardiovascular disease. When cells absorb too many nutrients, they can become overloaded with energy, leading to the accumulation of fat and the production of toxic metabolites.
One of the key regulators of nutrient sensing is the hormone insulin, which is produced by the pancreas in response to rising blood glucose levels/ insulin helps to transport glucose from the bloodstream into cells, where it can be used for energy. However, in conditions such as obesity and type 2 diabetes, cells can become resistant to insulin, leading to a buildup of glucose in the bloodstream and increased nutrient uptake by cells.
Maintaining proper nutrient sensing is therefore essential for maintaining healthy cellular function and preventing the onset of age-related disease. This can be achieved through a healthy diet and lifestyle, as well as targeted interventions aimed at restoring the balance of nutrient sensing pathways in the body.
This process of mitochondrial dysfunction can contribute to a range of age-related diseases, including neurodegenerative disorders, cardiovascular disease, and metabolic disorders. Mitochondrial dysfunction can be caused by a range of factors, including genetic mutations, environmental toxins, and normal aging processes.
When mitochondria become damaged, they may produce less energy and more harmful byproducts, leading to cellular stress and oxidative damage. This can trigger a range of cellular responses, including inflammation and apoptosis (programmed cell death), which can further exacerbate the problem.
Maintaining proper mitochondrial function is therefore essential for maintaining healthy cellular function and preventing the onset of age-related diseases. This can be achieved through a range of strategies, including regular exercise, a healthy diet, and targeted interventions aimed at restoring mitochondrial function.
In addition to their role in aging and age-related diseases, cellular senescence has been implicated in a range of other conditions, including cancer, tissue regeneration, and wound healing.
While senescence can serve as a protective mechanism to prevent the formation of cancerous cells, the accumulation of senescent cells can also contribute to the development of cancer by promoting inflammation and disrupting tissue homeostasis.
Efforts to combat the negative effects of cellular senescence are therefore focused on targeted removal of these cells. This can be achieved through a range of strategies, including pharmacological interventions aimed at inducing senescence-specific cell death, or the use of senolytics - compounds that selectively target and eliminate senescent cells.
Stem Cell Exhaustion
Stem cell exhaustion is a condition where the number or duction of stem cells in the body is reduced, resulting in a decrease in tissue maintenance and repair capacity. Stem cells are responsible for repairing and replenishing damaged or old tissues in the body, and their decline can lead to tissue dysfunction and disease.
As we age, our bodies produce fewer stem cells, and those that remain may become less effective due to damage to their DNA or changes in their environment. This can lead to a decrease in the body’s ability to repair and maintain tissues, which can contribute to age-related diseases such as Alzheimer’s, Parkinson’s, and cardiovascular disease.
In addition to aging, stem cell exhaustion can also be caused by factors such as chronic inflammation, exposure to toxins, and certain diseases. Researchers are exploring ways to counteract stem cell exhaustion, such as through the use of stem cell therapies and regenerative medicine.
Altered Intercellular Communication
Altered intercellular communication and vicarious cycle of damage are both key factors in the progression of aging and age-related diseases. As cells and tissues age, they become less efficient at communicating with each other, which can lead to a breakdown in normal physiological processes.
Senescent cells are cells that have stopped dividing due to stress or damage, but they remain active and excrete harmful substances, such as cytokines and growth factors, that can damage nearby healthy cells and tissues. This can create a vicious cycle of damage, where the presence of senescent cells leads to increased inflammation, which in turn leads to more senescent cells and further damage.
Other examples of altered intercellular communication that contribute to aging include changes in hormone levels, alterations in cell signaling pathways, and the accumulation of misfolded proteins. All of these factors can lead to a breakdown in normal cell function and an increase in cellular damage.