Can we reverse the aging process by lengthening our telomeres?

Many countries around the world are experiencing welcome increases in life expectancy as a result of continuing medical advances. However, the outcome of this positive situation is an aging population, with the estimated number of people aged 60 or more set to rise to 1.2 billion by the year 2025. [1] In the U.S., it is predicted that by 2030, one in five citizens will be of retirement age. [2]

Further technological developments are viewed as central to maintaining a fit and healthy population as we age. It is also recognized that we need to develop a better understanding of the biological changes that take place at a molecular level as people age and begin to develop age-related disorders. [1] One of these molecular changes that occurs as we age involves changes to structures called telomeres, which are located at the ends of our chromosomes. Telomeres are thought to play an important role in the aging process and in age-related diseases.

What are telomeres?

what is a telomere ​Chromosomes are long molecules made up of DNA that store our genetic information. Telomeres are short sections of DNA found at the ends of our chromosomes.

Scientists think that telomeres play a key role in various important processes in our body, including aging. In fact, it has been suggested that telomeres act as a “biological clock”, and that they become shorter in a regular, clockwork-like fashion, as cells themselves undergo the aging process. [3] It is also thought that telomeres are involved in a number of serious diseases that are generally associated with the aging process, including cancer and cardiovascular diseases such as coronary heart disease and increased blood pressure. [3]

What do telomeres do?

A chromosome is a long, thin molecule made up of DNA – you can think of it as looking something like a shoelace. We know that the ends of a shoelace can fray and become damaged, which is why shoelaces are manufactured with a small piece of plastic at either end, called an aglet – these aglets protect the ends of a shoelace from damage.

Telomeres and DNAIn the same way that the ends of a shoelace can fray and become damaged, the ends of your chromosomes can also fray and become damaged. This is where telomeres come in. Like the aglets at the ends of a shoelace, telomeres protect the ends of your chromosomes. This is important because chromosomes contain all of the genetic information you need to keep your body functions healthy.

Most cells in our body need to grow and divide regularly to form new cells. A cell must make exact copies of all the chromosomes it contains before it can divide. However, each time a round of cell division takes place, the chromosomes become slightly shorter. This is where an important molecule called telomerase comes in.

What is telomerase?

Telomerase is an enzyme that adds a section of DNA to the ends of your chromosomes after they have been copied for cell division. The addition of new DNA to telomeres reduces (but does not completely stop) the shortening of chromosomes after each round of copying. This decreases the risk of losing key genes as a chromosome shrinks in size. By helping to repair this damage to the ends of chromosomes, telomerase also helps to make sure that a cell’s internal repair mechanisms do not mistake the damaged ends of a chromosome for DNA that is seriously damaged and in need of genuine repair. If these defense mechanisms were to be initiated, they could do serious damage to the chromosomes by trying to repair something that was not broken in the first place, potentially resulting in much more serious damage.

What happens if our telomeres get shorter?

As already mentioned, even with the help of telomerase, telomeres become shorter and shorter as our cells age. This shortening of telomeres can lead to various outcomes:

  • Cellular senescence – this occurs when a cell ceases to divide and effectively goes into a dormant state.
  • Apoptosis – also known as programmed cell death, apoptosis is the process by which a cell undergoes self-destruction.
  • Oncogenic transformation – this is the process that leads to cells dividing uncontrollably and can result in cancer.

How are telomeres linked with aging?

Studies have shown that older individuals with shorter telomeres are not only more likely to die of non-communicable diseases such as heart disease but that they are also more vulnerable to infectious diseases, compared with other older people who have longer telomeres. [4] Lifestyle factors, such as smoking, obesity, lack of exercise, and poor diet can increase the rate at which telomeres become shorter, again potentially leading to an increased risk of disease and early death. [4]

There is a sex variation in the length of telomeres: On average, women have longer telomeres than men, and the rate at which telomeres become shortened is slower in women compared with the rate at which telomeres shorten in men. [5] There is no difference between the sexes at birth [3], so it is likely that these differences arise through environmental factors.

One such environmental factor that may be assisting the slower rate of telomere shortening in women is estrogen. This female reproductive hormone has been found to stimulate telomerase activity.  There are differences among ethnic groups too, with African Americans generally exhibiting longer telomeres than White Americans. [6]

Telomeres and disease

Inflammation and oxidative stress are two key factors involved in the biology of aging andaging-related diseases,and both have been reported to have associations with the shortening of telomeres in white blood cells. [7, 8]

Shortened telomeres have been identified in many types of cancer, although it is difficult to determine whether the shortened telomeres are the cause of cancer or an effect of it because the clinical trials needed to clarify this are technically and ethically challenging.  Laboratory experiments do,however,suggest that short telomeres in human cancer cells play a role in tumor development and chromosomal instability. [9]

In addition to cancer and cardiovascular diseases, there are several other diseases linked to telomere abnormalities, including [9]:

  • Bone marrow failure, which leads to the insufficient production of blood cells.
  • Dyskeratosis congenita, a rare congenital disorder that can cause skin abnormalities and is linked to extremely short telomeres.
  • Acquired aplastic anemia, which again can lead to bone marrow problems and reduced production of blood cells.

Some studies have suggested that longer telomeres are linked with increased longevity, although other studies have suggested this may not be the case; where there does seem to be more agreement is that individuals with longer telomeres showed an increased number of years of healthy life, [1] which is obviously a desirable situation.

Can the aging process be reversed?

So, the question is, can the aging process be reversed by reactivating telomerase and restoring telomeres? As mentioned above, telomere damage is known to be linked with declining organ function and increased susceptibility to disease as we age. There is some evidence to suggest, however, that telomere-related damage can be reversed by the reactivation of telomerase to its full working capacity. Experiments have shown, for example, that the reactivation of telomerase in mice can reverse certain features of aging in the central nervous system (CNS), reduce damage to DNA, and rejuvenate nerve cells. [10]

Telomerase activators

As we age, less telomerase is produced by our body. However, there are lifestyle changes we can make that may help to slow this reduction in telomere length. These lifestyle changes include stopping smoking, taking more exercise, eating a healthier diet, losing weight, and reducing our stress. [4] In addition to lifestyle changes, a study has shown that a new dietary supplement, known as TA-65®, can increase telomere length through the activation of telomerase. [11] The findings of this randomized, double-blind, and placebo-controlled study – the “Gold Standard” for such trials– suggest that TA-65® can lengthen telomeres in a statistically and possibly clinically significant manner.

What is TA-65®?

TA-65 and TelomeresTA-65® is a natural, plant-based compound that transiently activates telomeraseand prevents cells from entering senescence or undergoing programmed cell death, but, crucially, it does not cause any permanent changes that would lead to cells dividing continuously. TA-65® was originally discovered during a screening program that was looking for medically active molecules in traditional Chinese medicines. Artemisinin, the most effective drug currently available for use in the treatment of malaria, was discovered using a similar approach. [12] Since its initial discovery, TA-65® has been refined and is now manufactured under current good management practice (cGMP), is designated as GRAS (generally recognized as safe) for use in a medical food, and is sold as a dietary supplement.

Root Cause Tracker

TA-65® could be a great way to activate your telomerase, keep your telomeres functioning at their best, and help you maintain a fit and healthy lifestyle into old age.

To help you monitor, maintain, and improve your health, there is a brand-new app available, called Root Cause Tracker. This app serves a dual purpose. It helps medical professionals to encourage their patients to keep track of their health, and it helps the general public who wish to take more control of their own health.

So, you can now boost your telomerase activity with a simple dietary supplement, TA-65®, and monitor your health at the same time using the Root Cause Tracker app! Visit the Root Cause Trackerwebsite to find out more.

References

[1] http://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC3733214&blobtype=pdf

[2] https://www.businessinsider.com/aging-population-healthcare?r=US&IR=T

[3] https://link.springer.com/article/10.1007/s00424-009-0728-1

[4] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370421/

[5] https://academic.oup.com/ije/article/44/5/1688/2594582

[6] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2810865/

[7] https://www.ncbi.nlm.nih.gov/pubmed/16303830/

[8] https://www.ncbi.nlm.nih.gov/pubmed/16913878/

[9] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3401586/

[10] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057569/

[11] https://www.liebertpub.com/doi/pdf/10.1089/rej.2015.1793

[12] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4966551/